American Journal of Cardiovascular Disease Research»Articles

Article

Coronary Artery Disease in Overweight and Obese Women in Gaza- Palestine: An Observational Study

1AL Shifa Hospital, Cardiology department, Gaza, Palestine

2Al Quds University, Faculty of Public Health, Gaza, Palestine


American Journal of Cardiovascular Disease Research. 2014, 2(2), 23-26
DOI: 10.12691/ajcdr-2-2-2
Copyright © 2014 Science and Education Publishing

Cite this paper:
Amal Jamee, Yehia Abed. Coronary Artery Disease in Overweight and Obese Women in Gaza- Palestine: An Observational Study. American Journal of Cardiovascular Disease Research. 2014; 2(2):23-26. doi: 10.12691/ajcdr-2-2-2.

Correspondence to: Amal  Jamee, AL Shifa Hospital, Cardiology department, Gaza, Palestine. Email: dr_amal08@yahoo.fr

Abstract

Coronary artery disease risk factors are increasing worldwide, the increase is more prominent among young women due to increase of unfavorable coronary risk factors mainly related to increase in Body mass index rates(BMI). Coronary events predominate in obese women with other associated coronary risk factors. Increase BMI increases risk of fatal or non-fatal coronary events 1.5 to 3 times. Our study aimed to identify risk factors for coronary artery disease among obese and overweight Palestinian women, to plan for interventions policies. The study design is an observational based on 500 overweight and obese women (BMI greater than or equal 25 kg/m2). Coronary angiography was performed for all the study population, and revealed 250 patients with approved CAD, the rest of the study population consist of 250 cases with normal coronary. Socio demographic data, traditional cardiovascular risk factors, blood glucose, hemoglobin and clearance creatinine measurement were collected. We excluded all patients with history of prior cardiac surgery or percutaneous coronary intervention. Statistical analysis was performed using SPSS version 20.0. Our findings indicate that the mean age for cases is (63.5 ±8.7) vs. (58.2±9.8) for control and the difference is statically significant (Pvalue= 0.001). Other risk factors include rise of systolic and diastolic blood pressure, high blood sugar and impaired clearance creatinine are present in overweight and obese women with documented coronary artery disease. Regression analysis shows that advancing ages, and diabetes, are the main factors for development of coronary artery disease in obese women. Conclusion: Diabetes Mellitus is the major risk factor for the development of CAD and measures to control diabetes will minimize the chances of CAD among overweight and obese women in Palestine.

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References

[[[[[[[[[[[[[[[[[[[[[[[
[[1]  Okrainec K, Banerjee DK, Eisenberg MJ, “Coronary artery disease in the developing world, Quebec Canada”. Am Heart J, 148. 7-15. 2004.
 
[[2]  Ministry of health. “Annual Report”, Palestine, 2012.
 
[[3]  Eveline Oestreicher Stock, Rita Redberg. “Cardiovascular Disease in Women”. Curr Probl Cardiol, 450.526-537. 2012.
 
[[4]  Mosca L,Mochari H,Christian A, et al. “National study of women’s awareness, preventive action, and barriers to cardiovascular health”. Circulation, 113.525-34.2006.
 
[[5]  Natalie Bello, Lori Mosca. ‘Epidemiology of Coronary Heart Disease in Women”. Progress in Cardiovascular Diseases, 46. 287-295. 2004.
 
Show More References
[6]  World Health Organization Fact Sheet. Obesity and Overweight. Geneva: WHO 2011.
 
[7]  Pogorelov D, Lazarenko AI, Khuratora BG. “Overweight an actual problem in modern world”. Vopr Pitan, 72.36-39. 2003.
 
[8]  Jousilahti P, Tuomilehto J, Vartiainen E, Pekkanen J, Puska P. “Body weight, cardiovascular risk factors, and coronary mortality, 15-year follow-up of middle-aged men and women in eastern Finland”. Circulation, 93.1372-1379. 1996.
 
[9]  Mokdad AH, Ford ES, Bowman BA, et al. “Prevalence of obesity, diabetes, and obesity-related health risk factors 2001”, JAMA, 289.76-79. 2003.
 
[10]  Bethesda. “Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults”, National Institutes of Health 1998.
 
[11]  Manson JE, Colditz GA, Stampfer MJ, et al. “A prospective study of obesity and risk of coronary heart disease in women”, N Engl J Med, 322.882-889. 1990.
 
[12]  Rexrode KM, Carey VJ, Hennekens CH, et al. “Abdominal adiposity and coronary heart disease in women”. JAMA, 280.1843-1848. 1998.
 
[13]  Folsom AR, French SA, Zheng W, et al. “Weight variability and mortality: the Iowa Women’s Health Study”. Int J Obes Relat Metab Disord, 20. 704-709. 1996.
 
[14]  Poirier P, Giles TD, Bray GA, et al. “Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the American Heart Association”. Scientific Statement on Obesity and Heart Disease 1997.
 
[15]  McGill Jr. HC, McMahan CA, Herderick EE et al. “Obesity accelerates the progression of coronary atherosclerosis in young men”. Circulation, 105. 2712-2718. 2002.
 
[16]  Lerner DJ, Kannel WB. “Patterns of coronary heart disease morbidity and mortality in the sexes: a 26-year follow-up of the Framingham population”. Am Heart J, 111. 383-390. 1986.
 
[17]  Pinsky JL, Jette AM, Branch LG, et al. “The Framingham Disability Study: relationship of various coronary heart disease manifestations to disability in older persons living in the community”. Am J Public Health, 80. 1363-1367. 1990.
 
[18]  Wilson PW, D’Agostino RB, Sullivan L, Parise H, Kannel WB.”Overweight and obesity as determinants of cardiovascular risk: the Framingham experience”. Arch Intern Med, 162. 1867-1872. 2002.
 
[19]  Yang P, Zhou Y, Chen B et al. “Overweight, obesity and gastric cancer risk: results from meta-analysis of cohort studies”. Eur J Cancer, 45. 2867-2873.2009.
 
[20]  Krauss RM, Winston M, Fletcher BJ, Grundy SM. “Obesity: impact on cardiovascular disease”. Circulation, 98. 1472-1476. 1998.
 
[21]  Kerstyn C. Zalesin, MDa,*, Barry A. Franklin, PhDb, Wendy M. Miller, MDc, Eric D. Peterson, MD, MPHd, Peter A. McCullough, MD, MPHe. “Impact of Obesity on Cardiovascular Disease”. Med Clin N Am, 95. 919-937. 2011.
 
[22]  Wang Y, Lobstein T. “Worldwide trends in childhood overweight and obesity”. Int J Pediatr Obes, 1.1-25. 2006.
 
[23]  HF Abdul-Rahim, NME Abu-Rmeileh, A Husseini, G Holmboe-Ottesen, J Jervell, E Bjertness. “Obesity and selected co-morbidities in an urban Palestinian population” International Journal of Obesity, 25. 1736-1740. 2001.
 
[24]  Amal Jamee, Yehia Abed, Marwan O. Jalambo. “Gender Difference and Characteristics Attributed to Coronary Artery Disease in Gaza-Palestine”. Global Journal of Health Science, 5.51-56. 2013.
 
[25]  Must A, Spadano J, Coakley EH, Field AE, Colditz G, Dietz WH. “The disease burden associated with overweight and obesity”. JAMA, 282. 1523-1529. 1999.
 
[26]  Garrison RJ, Kannel WB, Stokes J 3rd, Castelli WP. “Incidence and precursors of hypertension in young adults: the Framingham Offspring Study”. Prev Med, 16. 235-251. 1987.
 
[27]  Sarah H Wild, Christopher D Byrne.” Risk factors for obesity and coronary heart disease” BMJ, 333.1009-1011. 2006.
 
[28]  M. Chinikar, M. Maddah, S. Hoda. “Coronary artery disease in Iranian overweight women”. International Journal of Cardiology, 113. 391-394. 2006.
 
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Article

Viscum Album Versus Bleomycin for Pleurodesis among Patients with Malignant Pleural Effusion

1Cardiothoracic Surgery Department, Suez Canal University, Ismailia, Egypt


American Journal of Cardiovascular Disease Research. 2014, 2(2), 17-22
DOI: 10.12691/ajcdr-2-2-1
Copyright © 2014 Science and Education Publishing

Cite this paper:
Marawan H. Elkasas, Hamdy D. Elayouty. Viscum Album Versus Bleomycin for Pleurodesis among Patients with Malignant Pleural Effusion. American Journal of Cardiovascular Disease Research. 2014; 2(2):17-22. doi: 10.12691/ajcdr-2-2-1.

Correspondence to: Hamdy  D. Elayouty, Cardiothoracic Surgery Department, Suez Canal University, Ismailia, Egypt. Email: h.dosoky@yahoo.com

Abstract

OBJECTIVE: To compare between mistletoe(Viscum album) and bleomycin as chemical agents for pleurodesis in malignant pleural effusions. METHODS: In this study 50 patients with pathologically confirmed, symptomatic, malignant pleural effusion irrespective of the primary tumor were studied at Suez Canal University hospital in the period of 3 years from January 2009 to December 2012. Patients were divided into 2 groups; 25 patients each: group A(pleurodesis with Mistletoe using 100mg – 5 ampoules-repeated two or three times, injected every other day) and group B(pleurodesis with Bleomycin1 iu/kg average-4 ampoules-or maximally 60 units). follow-up included postero-anterior and lateral chest radiography done after one week, month and 3 months. RESULTS: Most of the patients among both groups show complete remission defined as no effusion detected within four weeks of pleurodesis (72% and 56% among bleomycin and Viscum groups respectively). Significant difference was found between both groups. Recurrences were more frequent among group A (20% versus 8% in group B), P < 0.05. Hospital stay was shorter in the bleomycin group of patients, with a mean of (6.2) day. CONCLUSION: Both bleomycin and Viscum album are effective and safe agents for chemical pleurodesis, however bleomycin has some advantages over Viscum album due to its lower incidence of failure, and being more economic and for the shorter hospital stay.

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References

[[[[[[[[[[[[[[[[[[[[[[[[
[[1]  Sahn SA: The differential diagnosis of pleural effusions. West J Med 1982 Aug; 137: 99-108.
 
[[2]  Lynch TJ.: Management of malignant pleural effusions. Chest 1993; 103(suppl): 385S-389S.
 
[[3]  Sahn SA: Malignancy metastatic to the pleura. Clin Chest Med. 1998 Jun; 19(2): 351-61.
 
[[4]  F. Rodriguez-Panadero, V.B. Antony: Pleurodesis: state of the art. Eur Respir J 1997; 10: 1648-1654.
 
[[5]  Walker-Renard P, Vaughan LM, Sahn SA. Chemical pleurodesis for malignant pleural effusions. Ann Intern Med 1994; 120: 56-64.
 
Show More References
[6]  Ruckdeschel JC, Moores D, Lee JY, et al. Intrapleural therapy for malignant pleural effusions. A randomized comparison of bleomycin and tetracycline. Chest 1991; 100: 1528-35.
 
[7]  Zimmer PW, Mark H, Kenneth C, Eric H and Low DE. Prospective Randomized Trial of Talc Slurry vs Bleomycin in Pleurodesis for Symptomatic Malignant Pleural Effusions.Chest 1997; 112; 430-434.
 
[8]  Diacon AH, Wyser C, Bolliger CT, et al. Prospective randomized comparison of thoracoscopic talc poudrage under local anesthesia versus bleomycin instillation for pleurodesis in malignant pleural effusions. Am J Respir Crit Care Med 2000; 162: 1445-1449.
 
[9]  Robinson LA, Fleming W7H, Galbraith TA. Intrapleural doxycycline control of malignant pleural effusions. Ann Thorac Surg 1993; 55: 1115-22.
 
[10]  Patz EF Jr, McAdams, P, Erasmus, JJ, et al: Sclerotherapy for malignant pleural effusions: a prospective randomized trial of bleomycin vs doxycycline with small-bore catheter drainage.Chest1998; 113, 1305-1311.
 
[11]  Antony VB, Rothfuss KJ, Godbey SW, Sparks JA, Hott JW. Mechanism of tetracycline hydrochloride-induced pleurodesis: tetracycline hydrochloride-stimulated mesothelial cells produce a growth factor-like activity for fibroblasts. Am Rev Respir Dis 1992; 146: 1009-1013.
 
[12]  Vargas FS, Wang N-S, Lee HM, Gruer SE, Sassoon CSH, Light RW.: Effectiveness of bleomycin in comparison to tetracycline as pleural sclerosing agent in rabbits. Chest 1993; 104: 1582-1584.
 
[13]  Kienle G. S., Kiene H: Complementary cancer therapy: a systematic review of prospective clinical trials on anthroposophic Mistletoe extracts. Eur J Med Res (2007) 12: 103-119.
 
[14]  Molassiotis A. , Fernandez-Ortega P., Pud D., et al.: Use of complementary and alternative medicine in cancer patients: a European survey. Ann Oncol. 2005; 16: 655-663.
 
[15]  Kienle GS, Berrino F, Büssing A, Portalupi E, Rosenzweig S, Kiene H.: Mistletoe in Cancer a Systematic Review on Controlled Clinical Trails. European Journal of Medical Research 2003; 8: 109-19.
 
[16]  Horneber M, Bueschel G, Huber R, Linde K, Rostock M.: Mistletoe therapy in oncology. Cochrane Database of Systematic Reviews 2008, Issue 2. Art. No.: CD003297.
 
[17]  Becker H.: European mistletoe: Taxonomy, host trees, parts used, physiology. In: Büssing A editor(s). Mistletoe: The Genus Viscum. Harwood Academic Publishers, 2000:31-41.
 
[18]  Kim M-H, Park Y-K, Lee S-H, et al: Comparative study on the effects of a Viscum album (L.) extract (mistletoe) and doxycycline for pleurodesis in patients with malignant pleural effusion. Translation by Helixor Heilmittel GmbH. Korean Journal of Medicine 1999, 57:S121.
 
[19]  Stump P C and A. Büssing: Stimulation of antitumour immunity by intrapleural instillation of a Viscum album L. extract. Anti cancer drugs 1997, 8 (suppl 1) S23-S26.
 
[20]  Stirpe F., Sandvig K., Olsnes S., Pihl A. Action of viscumin, a toxic lectin from mistletoe, on cells in culture . J Biol Chem. 1982; 257: 13271-13277.
 
[21]  Klein R, Classen K, Berg PA, Ludtke R, Werner M, Huber R. In vivo-induction of antibodies to mistletoe lectin-1 and viscotoxin by exposure to aqueous mistletoe extracts: a randomised double-blinded placebo controlled phase I study in healthy individuals. Eur J Med Res 2002;7(4): 155-163.
 
[22]  Heinzerling L, Von BV, Liebenthal C, Von BR, Volk HD. Immunologic Effector Mechanisms of a Standardized Mistletoe Extract on the Function of Human Monocytes and Lymphocytes in vitro, ex vivo, and in vivo. Journal of Clinical Immunology 2006; Jul 26(4): 347-59
 
[23]  Antony VB, Godbey SW, Kunkel SL, et al. Recruitment of inflammatory cells to the pleural space: chemotactic cytokines, IL-8, and monocyte chemotactic peptide-1 in human pleural fluids. J Immunol 1993; 151: 7216-7223.
 
[24]  Antony VB, Hott JW, Kunkel SL, Godbey SW, Burdick MD, Strieter RM. Pleural mesothelial cell expression of C-C (monocyte chemotactic peptide) and C-X-C (interleukin 8) chemokines. Am J Respir Cell Mol Biol 1995; 12: 581-588.
 
[25]  Rodriguez-Panadero F, Segado A, Martin Juan J, Ayerbe R, Torres Garcia I, Castillo J. Failure of talc pleurodesis is associated with increased pleural fibrinolysis. Am J Respir Crit Care Med 1995; 151: 785-790.
 
[26]  Harrison LH Jr. In some cases - avoid talc pleurodesis. Chest 1995; 108: 289.
 
[27]  Balassoulis G, Sichletidis L, Spyratos D, Chloros D, Zarogoulidis K, Kontakiotis T, Bagalas V, Porpodis K, Manika K, Patakas D. Efficacy and safety of erythromycin as sclerosing agent in patients with recurrent malignant pleural effusion. Am J Clin Oncol. 2008 Aug; 31(4): 384-9.
 
[28]  Rodriguez-Panadero F, Lopez Mejias J. Low glucose and pH levels in malignant pleural effusions: diagnostic significance and prognostic value in respect to pleurodesis. Am Rev Respir Dis 1989; 139: 663-667.
 
[29]  Rodriguez-Panadero F, Sanchez Gil R, Martin Juan J, Castillo Gomez J.: Prediction of results of talc pleurodesis in malignant pleural effusions. Am J Respir Crit Care Med 1994; 149: (4, 2): A1103.
 
Show Less References

Article

The Role of Calcium-Sensitizer Levosimendan for the Treatment of Heart Failure

1Department of Pharmacy, GRD (PG) IMT, Dehradun, (Uttarakhand), India


American Journal of Cardiovascular Disease Research. 2014, 2(1), 9-16
DOI: 10.12691/ajcdr-2-1-3
Copyright © 2014 Science and Education Publishing

Cite this paper:
Mohammad Asif. The Role of Calcium-Sensitizer Levosimendan for the Treatment of Heart Failure. American Journal of Cardiovascular Disease Research. 2014; 2(1):9-16. doi: 10.12691/ajcdr-2-1-3.

Correspondence to: Mohammad  Asif, Department of Pharmacy, GRD (PG) IMT, Dehradun, (Uttarakhand), India. Email: aasif321@gmail.com

Abstract

In the treatment of heart failure, clinical signs are low cardiac output, therapy with positive inotropic agents in an acute cardiac care is mandatory. Three classes of inotropic drugs are currently used, including beta-adrenergic agonists (especially dobutamine), phosphodiesterase inhibitors (such as milrinone) and the recently developed calcium sensitizers such as levosimendan. The classic inotropic drugs offer short-term haemodynamic enhancement in heart failure patient and their use has been connected with poor prognosis. The inotropic drugs, the Ca2+-sensitizers, may offer a choice of long-lasting result.

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References

[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[
[[1]  Sakata Y. Clinical significance of calcium sensitizer. Clin Calcium. 2013; 23 (4): 575-82.
 
[[2]  Arai M. Calcium mobilizers and calcium sensitizers. Nihon Rinsho. 2011; 69 Suppl 9: 417-22.
 
[[3]  Giglioli C, Cecchi E, Landi D, Chiostri M, Spini V, Valente S, Gensini GF, Romano SM. Levosimendan produces an additional clinical and hemodynamic benefit in patients with decompensated heart failure successfully submitted to a fluid removal treatment. Congest Heart Fail. 2012; 18 (1): 47-53.
 
[[4]  van Hees HW, Andrade Acuña G, Linkels M, Dekhuijzen PN, Heunks LM. Levosimendan improves calcium sensitivity of diaphragm muscle fibres from a rat model of heart failure. Br J Pharmacol. 2011; 162 (3): 566-73.
 
[[5]  Robertson IM, Sun YB, Li MX, Sykes BD. A structural and functional perspective into the mechanism of Ca2+-sensitizers that target the cardiac troponin complex. J Mol Cell Cardiol. 2010; 49 (6): 1031-41.
 
Show More References
[6]  Follath F. Newer treatments for decompensated heart failure: focus on levosimendan. Drug Des Devel Ther. 2009; 3:73-8.
 
[7]  Meyer K, Klocke RC, Schipke JD, Gams E, Korbmacher B. Ca2+ sensitizer superior to catecholamine during myocardial stunning? Eur J Cardiothorac Surg. 2008; 34 (2): 326-31.
 
[8]  Parissis JT, Andreadou I, Bistola V, Paraskevaidis I, Filippatos G, Kremastinos DT. Novel biologic mechanisms of levosimendan and its effect on the failing heart. Expert Opin Investig Drugs. 2008; 17 (8): 1143-50.
 
[9]  Endoh M. Could Ca2+ sensitizers rescue patients from chronic congestive heart failure? Br J Pharmacol. 2007; 150 (7): 826-8. Epub 2007 Feb 26.
 
[10]  Endoh M. Cardiac Ca2+ signaling and Ca2+ sensitizers. Circ J. 2008; 72 (12): 1915-25.
 
[11]  Antoniades C, Tousoulis D, Koumallos N, Marinou K, Stefanadis C. Levosimendan: beyond its simple inotropic effect in heart failure. Pharmacol Ther. 2007; 114 (2): 184-97.
 
[12]  Kasikcioglu HA, Uyarel H, Tartan Z, Kasikcioglu E, Ozturk R, Cam N. Do calcium sensitizers affect right ventricular functions in patients with chronic heart failure? Int J Cardiol. 2007; 118 (2): 246-8. Epub 2006 Sep 28.
 
[13]  Papp JG, Pollesello P, Varró AF, Végh AS. Effect of levosimendan and milrinone on regional myocardial ischemia/reperfusion-induced arrhythmias in dogs. J Cardiovasc Pharmacol Ther. 2006; 11 (2): 129-35.
 
[14]  González-Chon O, García López SM, Chacón Mercado MA, Arias Sánchez EA, Vega Zapata RE. Levosimendan: a new strategy in the treatment of heart failure. Arch Cardiol Mex. 2005; 75 Suppl 3: S3-130-9.
 
[15]  Perrone SV, Kaplinsky EJ. Calcium sensitizer agents: a new class of inotropic agents in the treatment of decompensated heart failure. Int J Cardiol. 2005; 103 (3): 248-55.
 
[16]  Haikala H, Pollesello P. Calcium sensitivity enhancers. IDrugs. 2000; 3 (10): 1199-205.
 
[17]  Bonnefoy E, Trindade PT. Levosimendan, a revolution in the world of inotropic agents. Rev Med Suisse. 2005; 1 (21): 1425-6, 1428-9.
 
[18]  Andersen GO, Eritsland J, Bjørnerheim R, Kløw NE, Jonassen A, Mangschau A. Cardiogenic shock-new therapeutic strategies. Tidsskr nor Laegeforen. 2005; 125 (10): 1318-21.
 
[19]  Ng TM.Levosimendan, a new calcium-sensitizing inotrope for heart failure. Pharmacotherapy. 2004; 24 (10): 1366-84.
 
[20]  Papp Z, Van Der Velden J, Borbély A, Edes I, Stienen GJ. Effects of Ca2+-sensitizers in permeabilized cardiac myocytes from donor and end-stage failing human hearts. J Muscle Res Cell Motil. 2004; 25 (3): 219-24.
 
[21]  Sorsa T, Pollesello P, Rosevear PR, Drakenberg T, Kilpeläinen I. Stereoselective binding of levosimendan to cardiac troponin C causes Ca2+-sensitization. Eur J Pharmacol. 2004; 486 (1): 1-8.
 
[22]  Follath F. Levosimendan in patients with low-output heart failure: lessons from the LIDO trial. Ital Heart J. 2003; 4 Suppl 2: 34S-38S.
 
[23]  Erhardt LR. Is calcium sensitization the best strategy to improve myocardial contractility in acute heart failure? Ital Heart J. 2003; 4 Suppl 2: 27S-33S.
 
[24]  Lehmann A, Boldt J, Kirchner J. The role of Ca2+-sensitizers for the treatment of heart failure. Curr Opin Crit Care. 2003; 9 (5): 337-44.
 
[25]  Endoh M. Mechanisms of action of novel cardiotonic agents. J Cardiovasc Pharmacol. 2002; 40 (3): 323-38.
 
[26]  Teerlink JR. The development of new medical treatments for acute decompensated heart failure. Heart Fail Monit. 2002; 2 (4): 129-37.
 
[27]  Nawarskas JJ, Anderson JR. Levosimendan: a unique approach to the treatment of heart failure. Heart Dis. 2002; 4(4):265-71.
 
[28]  Endoh M. Mechanism of action of Ca2+ sensitizers--update 2001. Cardiovasc Drugs Ther. 2001; 15 (5): 397-403.
 
[29]  Kleerekoper Q, Putkey JA. Drug binding to cardiac troponin C. J Biol Chem. 1999 Aug 20; 274 (34): 23932-9.
 
[30]  Bowman P, Haikala H, Paul RJ. Levosimendan, a calcium sensitizer in cardiac muscle, induces relaxation in coronary smooth muscle through calcium desensitization. J Pharmacol Exp Ther. 1999; 288 (1): 316-25.
 
[31]  Zimmermann N, Boknik P, Gams E, Herzig JW, Neumann J, Scholz H. Calcium sensitization as new principle of inotropic therapy in end-stage heart failure? Eur J Cardiothorac Surg. 1998; 14 (1): 70-5.
 
[32]  Haikala H, Kaivola J, Nissinen E, Wall P, Levijoki J, Lindén IB. Cardiac troponin C as a target protein for a novel calcium sensitizing drug, levosimendan. J Mol Cell Cardiol. 1995; 27 (9): 1859-66.
 
[33]  Haikala H, Levijoki J, Lindén IB. Troponin C-mediated calcium sensitization by levosimendan accelerates the proportional development of isometric tension. J Mol Cell Cardiol. 1995; 27 (10): 2155-65.
 
[34]  Haikala H, Linden IB. Mechanisms of action of calcium-sensitizing drugs. J Cardiovasc Pharmacol. 1995; 26 Suppl 1: S10-9.
 
[35]  Haikala H, Nissinen E, Etemadzadeh E, Levijoki J, Lindén IB. Troponin C-mediated calcium sensitization induced by levosimendan does not impair relaxation. J Cardiovasc Pharmacol. 1995; 25 (5): 794-801.
 
[36]  Nielsen-Kudsk JE, Aldershvile J. Will calcium sensitizers play a role in the treatment of heart failure? J Cardiovasc Pharmacol. 1995; 26 Suppl 1: S77-84.
 
[37]  Lehtonen L, Mills-Owens P, Akkila J. Safety of levosimendan and other calcium sensitizers. J Cardiovasc Pharmacol. 1995; 26 Suppl 1: S70-6.
 
[38]  Hasenfuss G, Pieske B, Kretschmann B, Holubarsch C, Alpert NR, Just H. Effects of calcium sensitizers on intracellular calcium handling and myocardial energetics. J Cardiovasc Pharmacol. 1995; 26 Suppl 1: S45-51.
 
[39]  Varro A, Papp JG. Classification of positive inotropic actions based on electrophysiologic characteristics: where should calcium sensitizers is placed? J Cardiovasc Pharmacol. 1995; 26 Suppl 1: S32-44.
 
[40]  Rusca M, Liaudet L. Inotropic agents for treatment of acute heart failure syndromes in intensive care. Rev Med Suisse. 2009; 5 (229): 2512-5.
 
Show Less References

Article

Anemia Prevalence and Sociodemographic Factors among Patient with Cardiovascular Disease in Gaza-Palestine

1AL Shifa Hospital, Cardiology department, Gaza, Palestine

2Al Quds University, Faculty of Public Health, Gaza, Palestine


American Journal of Cardiovascular Disease Research. 2014, 2(1), 4-8
DOI: 10.12691/ajcdr-2-1-2
Copyright © 2014 Science and Education Publishing

Cite this paper:
Amal Jamee, Yehia Abed. Anemia Prevalence and Sociodemographic Factors among Patient with Cardiovascular Disease in Gaza-Palestine. American Journal of Cardiovascular Disease Research. 2014; 2(1):4-8. doi: 10.12691/ajcdr-2-1-2.

Correspondence to: Amal  Jamee, AL Shifa Hospital, Cardiology department, Gaza, Palestine. Email: dr_amal08@yahoo.fr

Abstract

Chronic anemia is a risk factor for cardiovascular diseases outcome in patients with heart failure, dilated cardiomyopathy and uncontrolled hypertension. This study was performed to analyze the prevalence of anemia among cardiac patients and to determine the relationship between anemia and socio demographic characteristics. The study design is a cross sectional based on 300 cardiac patients ( ≥ 19 years) who were hospitalized in ALShifa hospital (Gaza) for 3 months period during the year 2012. The analysis includes socio demographic data, traditional risk factors for cardiovascular diseases (CVD), and Laboratory test included (hemoglobin and clearance creatinine measurement). Collected data was analyzed by using statistical package for social science version 20.0. Anemia was defined as Hemoglobin less than < 12 g/dl in female and less than 13 g/dl in male based on World health organization criteria. Among 300 patients, 181patients (60.3%) were anemic and 119 (39.7%) were non-anemic. The mean age for all population was 61.4 years. Mean age of patients with anemia tends to be higher (63.9 years) than non-anemic (57.7 years) and the differences between the two means reached statistical significant level (P value < 0.001). Anemia was more common in female (71.4%), older age (71.1%), diabetics (70%), impaired clearance creatinine (70%), hypertensive’s (65%) and low education level (64.5%). The highest proportion belonged to valvular heart disease (77.8%), congestive heart failure (74.6%) followed by hypertension (54%), and the lowest is coronary artery disease (46%). Logistic regression reveals that low education, low clearance creatinine level, smoking and diabetes are independently associated with anemia. We conclude that Anemia is common among cardiovascular disease patients, and worsens the prognosis of their clinical condition. Intervention policies to minimize anemia risk factors are needed.

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References

[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[[
[[1]  World Health Organization. Proceedings of the 15th Annual Conference of the Indian Society of Hypertension and 4th International CME on Atherosclerosis, “Hypertension and Coronary Artery Disease,” WHO New Delhi India, November. 2005.
 
[[2]  UNRWA United Nations Relief and Work Agency for “Palestine Refugees in the Near East,” Annual Report of the Department of Health. 2006.
 
[[3]  Joyce A, Wahr, “Anemia and Cardiovascular Disease,” Transfusion alternative in transfusion medicine, (2). 24-30. 2008.
 
[[4]  Fauci A, Braunwald E, Kasper D, Hauser S, Longo D, Jameson J, et al. Harrison, “Principle’s of internal medicine,” 17 Ed. New York: McGraw publishing Co. 2008.
 
[[5]  Mark J, Sarnak, Hocine Tighiouart, Guruprasad Manjunath, et al, “Anemia as a Risk Factor for Cardiovascular Disease in the Atherosclerosis Risk in Communities (ARIC) Study,” J Am Coll cardiology, 40 (1). 27-33. 2002.
 
Show More References
[6]  Chaves PH, Semba RD, Leng SX, Woodman RC, Ferrucci L, Guralnik JM, Fried LP, “Impact of Anemia and Cardiovascular Disease on Frailty Status of Community-Dwelling Older Women: The Women's Health and Aging Studies II and I,” Journals of Gerontology Series A: Biological Sciences & Medical, 60 (6). 729-735. 2005.
 
[7]  Patel KV, “Epidemiology of anemia in older adults,” Seminars in Hematology, 45 (4). 210-217. 2008.
 
[8]  DeMaria R, Ripamonti V, Sandri R, et al ,“The negative prognostic synergism of anemia and heart disease in female nursing home residents,” Am J Cardiol, 96 (10). 1460-1462. 2005.
 
[9]  Komajda M, “Prevalence of anemia in patients with chronic heart failure and their clinical characteristics,” J Cardiac Failure, 10. 1-4. 2004.
 
[10]  Ble A, Fink JC, Woodman RC, Klausner MA, Windham BG, Guralnik TM, et al, “Renal function, erythropoietin and anemia of older persons: the In Chianti Study,” Arch Intern Med, 165. 2222-2227. 2005.
 
[11]  Guralnik JM, Eisenstaedt RS, Ferrucci L, Klein HG, Woodman RC, “Prevalence of anemia in persons 65 years and older in the United States: evidence for a high rate of unexplained anemia,” Blood, 104 (8). 2263-2268. 2004.
 
[12]  Salive ME, Cornoni-Huntley J, Guralnik JM, Phillips CL, Wallace RB, Ostfeld AM, et al., “Anemia and hemoglobin levels in older persons: relationship with age, gender, and health status,” J Am Geriatr Soc, 40. 489-496. 1992.
 
[13]  Azin Alizadehasl, Zahra Golmohammadi, Lale Panjavi, Siamak Mahmoodmoradi, Rasoul Azarfarin, “The incidence of anemia in adult patients with cardiovascular diseases in northwest Iran,” Cardiovascular Research Centre, 61 (11). 1091-1095. 2011.
 
[14]  Raed Odeh, M.B. Bdeir, Tara Conboy, “Prevalence of anemia in a Saudi population with chronic heart failure,” Journal of the Saudi Heart Association, 24 (4). 277-278. 2012.
 
[15]  Varat MA, Adolph RJ, Fowler NO, “Cardiovascular effects of anemia,” Am Heart Journal, 83 (3). 415-426. 1972.
 
[16]  Gerry JL, Baird MG, Fortuin NJ, “Evaluation of left ventricular Function in patients with sickle cell anemia,” Am J Med, 60 (7). 968-972. 1976.
 
[17]  Riva E, Tettamanti M, Mosconi P, Apolone G, Gandini F, Nobili A, et al, “Association of mild anemia with hospitalization and mortality in the elderly: the Health and Anemia population-based study,” Haematologica, 94 (1). 22-28. 2009.
 
[18]  Hegde N, Rich MW, Gayomali C, “The cardiomyopathy of iron deficiency,” Text Heart Inst Journal, 33 (3). 340-344. 2006.
 
[19]  Anand IS, Chandrashekhar Y, Ferrari R, et al, “Pathogenesis of oedema in chronic severe anemia: studies of body water and sodium renal function, hemodynamic variables, and plasma hormones,” Br Heart Journal, 70 (4). 357-362. 1993.
 
[20]  Pocock SJ, Wang D, Pfeffer MA, Yusuf S, McMurray JJ, Swedberg KB, et al, “Predictors of mortality and morbidity in patients with Chronic heart failure,” Eur Heart Journal, 27 (1). 65-75. 2006.
 
[21]  Velavan P, Khan NK, Goode K, Rigby AS, Loh PH, Komajda M, et al, “Predictors of short term mortality in heart failure-insights from the Euro Heart Failure survey,” Int J Cardiol, 138 (1). 63-69. 2010.
 
[22]  Groenveld HF, Januzzi JL, Damman K, van Wijngaarden J, Hillege HL, van Veldhuisen DJ, et al, “Anemia and mortality in heart failure patients a systematic review and meta-analysis,” J Am Coll Cardiol, 52 (10). 818-827. 2008.
 
[23]  Silverberg DS, Wexler D, Iaina A, “The importance of anemia and its correction in the management of severe congestive heart failure,” Eur J Heart Failure, 4. 681-686. 2002.
 
[24]  Pocock SJ, Wang D, Pfeffer MA, Yusuf S, McMurray JJ, Swedberg KB, et al, “Predictors of mortality and morbidity in patients with chronic heart failure,” Eur Heart J, 27. 65-75. 2006.
 
[25]  Velavan P, Khan NK, Goode K, Rigby AS, Loh PH, Komajda M, et al, “Predictors of short term mortality in heart failure-insights from the Euro Heart Failure survey,” Int J Cardiol, 138: 63-69. 2010.
 
[26]  Salisbury AC, Kosiborod M, “Outcomes associated with anemia in patients with heart failure,” Heart Fail Clin, 6. 359-372. 2010.
 
[27]  Silverberg DS, Wexler D, Iaina A, and Schwartz D, “The role of correction of anemia in patients with congestive heart failure: a short review,” Eur J Heart Fail, 10 (9). 819-823. 2008.
 
[28]  Adams KF, Patterson JH, Oren RM, Mehra MR, O'Connor CM, Pina IL, et al, “Prospective assessment of the occurrence of anemia in patients with heart Failure: results from the Study of Anemia in a Heart Failure Population, STAMINA-HFP Registry,” Am Heart J, 157 (5). 926-932. 2009.
 
[29]  daSilveira AD, Ribeiro RA, Rossini AP, Stella SF, Ritta HA, Stein R, et al, “Association of anemia with clinical outcomes in stable coronary artery disease,” Coron Artery Disease, 19 (1). 21-26. 2008.
 
[30]  Bassand JP, Hamm WC, Ardissino D, Boersma E, Budaj A, Ferna´ ndez-Aviles F, et al, “Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes,” Eur HeartJ, 28. 1598-1660. 2007.
 
[31]  Bassand JP, Hamm WC, Ardissino D, Boersma E, Budaj A, Ferna´ ndez-Avile F, et al, “Guıa de Practica Clınica para el diagnostico y tratamiento del sındrome coronario agudo sin elevacion del segmento ST,” Rev Esp Cardiol, 60. 1070-1080. 2007.
 
[32]  Gonzalez-Ferrer JJ, Garcıa-Rubira JC, Vivas-Balcones D, Nunez-Gil I, Carda Barrio R, Fuentes-Ferrer M, et al, “[ Pronostico intrahospitalario de la hemoglobina en pacientes con sındrome coronario agudo,” Rev ESP Cardiol,; 61. 945-952. 2008.
 
[33]  Oona M, Merce C, Lluis R, “In-hospital Acquired Anemia in Acute Coronary Syndrome. Predictors, In-hospital Prognosis and One-year Mortality,” Rev Esp Cardiol, 65 (8). 742-748. 2012.
 
[34]  Salisbury AC, Amin AP, Reid KJ, Wang TY, Masoudi FA, Chan PS, et al, “Hospital acquired anemia and in-hospital mortality in patients with acute myocardial Infarction,” Am Heart J, 162. 300-309. 2011.
 
[35]  Salisbury AC, Alexander KP, Reid KJ, Masoudi FA, Rathore SS, Wang TY, et al, “Incidence, correlates and outcomes of acute, hospital-acquired anemia in Patients with acute myocardial infarction,” Circ Cardiovascular Qual Outcomes, 3. 337-346. 2010.
 
[36]  Shaffer C, “Diagnostic blood loss in mechanically ventilated patients,” Heart Lung, 36. 217-222. 2007.
 
[37]  Thavendiranathan P, Bagai A, Ebidia A, Detsky AS, Choudhry NK, “Do blood tests cause anemia in hospitalized patients? The effect of diagnostics phlebotomy on hemoglobin and hematocrit levels,” J Gen Intern Med, 20. 520-524. 2005.
 
[38]  James S, Oldgren J, Lindback J, Johnston N, Siegbahn A, Wallentin L 2005 An acute Inflammatory reaction induced by myocardial damage is superimposed on a chronic inflammation in unstable coronary artery disease,” Am Heart J, 149. 619-626. 2005.
 
[39]  Sa´nchez PL, Morinigo JL, Pabo´n P, Martı´n F, Piedra I, Palacios IF, et al, “Prognostic relations between inflammatory markers and mortality in diabetic patients With non-ST elevation acute coronary syndrome,”. Heart, 264-269. 2004.
 
[40]  Mueller C, Buettner HJ, Hodgson JM, Marsch S, Perruchoud AP, et al, “Inflammation and long-term mortality after non-ST elevation acute Coronary syndrome treated with a very early invasive strategy in 1042 consecutive Patients,” Circulation, 105. 1412-1415. 2002.
 
[41]  Hasan F, O'Brien CS, Sanyal A, Dalton HR, “Aortic stenosis and gastrointestinal bleeding,” J R Soc Med, 97 (2). 81-82. 2004.
 
[42]  Maria M, Alexandros P, Fragiskos P, Evangelos Z, DimitrisA, George K, Gregory C, Panos V, “Systemic blood pressure profile in hypertensive patients with low hemoglobin concentrations,” International Journal of Cardiology, 142 (1). 95-96. 2010.
 
[43]  Paul B, Wilfred NC, Woodman R, Depasquale C, “Prevalence and correlates of anemia in essential hypertension,” Clin Exp Pharmacol Physiol, 35 (12). 1461-1464. 2008.
 
Show Less References

Article

Correction of Aortic Valve Stenosis: Is it Effective to Improve Left Ventricular Functions and Reduce Its Mass?

1Department of Cardiothoracic Surgery, Suez Canal University, Ismailia, Egypt

2Department of Cardiology, Ismailia General Hospital, Ismailia, Egypt


American Journal of Cardiovascular Disease Research. 2014, 2(1), 1-3
DOI: 10.12691/ajcdr-2-1-1
Copyright © 2014 Science and Education Publishing

Cite this paper:
Hamdy D. Elayouty, Magdy Ibrahim Wahdan, Marwan Hassan Elkasas, Hany Salman Fiesal, Eiman M. Altahawi. Correction of Aortic Valve Stenosis: Is it Effective to Improve Left Ventricular Functions and Reduce Its Mass?. American Journal of Cardiovascular Disease Research. 2014; 2(1):1-3. doi: 10.12691/ajcdr-2-1-1.

Correspondence to: Hamdy  D. Elayouty, Department of Cardiothoracic Surgery, Suez Canal University, Ismailia, Egypt. Email: h.dosoky@yahoo.com

Abstract

Background: Aortic valve stenosis causes gradual obstruction to left ventricular outflow tract. It is a common valvular disease that carries many life threatening complications. We hypothesized that the reduction or elimination of the pressure gradient across the aortic valve after correction of the stenotic lesion would lead to regression of left ventricular mass and improve left ventricular functions. Aim of the work is to assess the effectiveness of the correction and factors controlling these changes in left ventricular mass index and functions. Methods: preoperative and postoperative Electro-cardiography and echocardiography were performed for all patients. The corrective procedures included aortic valve replacement, balloon aortic valvuloplasty and open valve repair. Results: Sixty patients had correction of aortic valve stenosis (44 males, 16 females). ECG score preoperatively ranged between3 and 9 with a mean of 6 ± 1.63. Postoperatively, it ranged between 0 and 6 and mean of 3 ± 0.7. The mean LVED/BSA was reduced from 32.52 preoperatively to 30.41 postoperatively. The mean interventricular septal thickness index was reduced by 1.03. The mean left ventricular posterior wall thickness index was reduced by 0.99. Mean left ventricular mass index was reduced by 31.86 gm. The mean ejection fraction increased by 6.45. Mean trans-aortic peak gradient was reduced by 41.36 mmHg. Conclusions: Correction of aortic valve stenosis improves systolic and diastolic left ventricular function and a reduction in left ventricular mass index. Aortic root enlargement procedures can be safely avoided.

Keywords

References

[[[[
[[1]  Chambers J. Aortic stenosis. BMJ 2005, 330:801-2.
 
[[2]  Connolly H M, Orszulak TA, Osborn SLand Roger Hodge DO: Aortic vave replacement for aortic stenosiswith severe left ventricular dysfunction; prognostic indicators. Circulation 1997, 95:395-400.
 
[[3]  Gonzalez-Juanatey JR, Garacia-Acuna JM and Fernandez MV: Influence of the size of aortic valve prostheses on hemodynamics and change in left ventricular mass; implication for surgical management of aortic stenosis. J Thoracic Cardiovascular Surg 1996, 112: 273-80.
 
[[4]  Sim EK, Orszulak TA, Schaff HV: Influence of prosthesid size on change in left ventricular mass following aortic valve replacement Eur J Cardiothorac Surg 1994, 8: 293-7.
 
[[5]  Penta de Peppo A, Zeitani J and Nardi P: small functional size after aortic valve replacement; no risk in young to middle-age patients. Ann Thoracic Surg. 2005, 79: 1915-20.
 
Show More References
[6]  Dare AJ, Veinot JP, Edwards WD, Tazelaar HD and Schaff HV: New observation on the etiology of aortic valve disease a surgical pathology study of 236 cases. Hum Pathol. 1993, 24:1330-8.
 
[7]  Misawa Y: left ventricular mass index in aortic valve surgery; a new index for early valve replacement. Eur J Cardiothoracic Surg, 24: 667-8.
 
[8]  Rajappan K, Bellenger NG, Di Terlizzi M, Yacoub MH, Sheridan DJ and Pennell DJ:Assessment of left ventricular mass regression after aortic valve replacement- cardiovascular magnetic resonance versus M-mode echocardiography. Eur J Cardiothoracic Sur.2003, 24:59-65.
 
[9]  Knez I, Maier R, Rehak P and Rigler B: left ventricular architecture after valve replacement due to critical aortic stenosis, an approach to disqualify the myth of valve prosthesis- patient mismatch. Eur. J Cardiothoracic Surg. 2001, 19:797-805.
 
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Article

Relation of Cardiovascular Risk Factors with Coronary Angiographic Findings in Iraqi Patients with Ischemic Heart Disease

1Department of Medicine, Duhok College of Medicine, Kurdistan Region, Iraq

2Cardiologist and fellow in Interventional Cardiology, Azadi Heart Center, Azadi Teaching Hospital, Duhok Governorate, Iraq

3Department of Medicine, Mosul College of Medicine, Iraq

4Cardiologist, Ibn-Sina Teaching Hospital, Mosul Governorate, Iraq


American Journal of Cardiovascular Disease Research. 2013, 1(1), 25-29
DOI: 10.12691/ajcdr-1-1-6
Copyright © 2013 Science and Education Publishing

Cite this paper:
Ameen Mosa Mohammad, Sabri Khalif Sheikho, Jasim Mohammed Tayib. Relation of Cardiovascular Risk Factors with Coronary Angiographic Findings in Iraqi Patients with Ischemic Heart Disease. American Journal of Cardiovascular Disease Research. 2013; 1(1):25-29. doi: 10.12691/ajcdr-1-1-6.

Correspondence to: Ameen  Mosa Mohammad, Department of Medicine, Duhok College of Medicine, Kurdistan Region, Iraq. Email: doctoramb@yahoo.com

Abstract

Background: Atherosclerotic coronary artery disease is a major cause of death all over the world. Among patients with coronary artery disease, there are different cardiovascular risk factors which may exhibit their effects on coronary angiographic findings. This work aimed to study the relation of different cardiovascular risk factors with coronary angiographic findings in patients with ischemic heart disease (IHD). Methods: This case-series prospective study involved 220 patients with IHD who underwent coronary angiography in Mosul Cardiac Catheterization Unit in Ibn-Sina Teaching Hospital over a period of five months from April 1st through August 31st 2006. Patients with different coronary risk factors including smoking, positive family history of IHD, type 2 diabetes mellitus (T2DM), hypertension (HT), dyslipidemia, obesity and physical inactivity who presented with IHD were categorized and compared according to presentations into; ST-elevation myocardial infarction (STEMI) ( n = 72), Non-ST-elevation myocardial infarction (NSTEMI) and/or unstable angina (n = 98) and chronic stable angina (n = 50) and then the patients were re-grouped according to the number of cardiovascular risk factors into patients with < 3 risk factors (n = 125) vs. those with > 3 risk factors (n = 95). Results: There were significant associations between the risk factors and the angiographic characteristics in patients with IHD. There were more significantly stenosed lesions among patients with > 3 risk factors compared to patients with < 3 risk factors (p < 0.05). Lesions were more diffused (p < 0.01), with higher incidence of left ventricular dysfunction (p < 0.001) among former patients compared to later ones. Conclusions: Significant findings were observed in the angiographic profile of patients with multiple risk factors. There were more multi-vessels and diffused angiographic findings among patients with chronic stable angina.

Keywords

References

[[[[[[[[[[[[[[[[[[[
[[1]  Lee G, Dennis A. Acute myocardial infarction. In: Cecil textbook of medicine, 22nd edition, EB. Saunders Company 2004:304-24.
 
[[2]  Pająk A, Kozela M. Cardiovascular Disease in Central and East Europe. Public Health Reviews. 2012; 33:416-35.
 
[[3]  Eugene B, Doughles Z, Peter L. Acute myocardial infarction. In: Braunwald heart disease. Textbook of Cardiovascular Medicine, 6th edition, WB. Saunders Company 2001:1114-1211.
 
[[4]  Dennis LK, Eugene B, Arthony F. Pathogenesis of atherosclerosis. In: Harrisons principles of Internal Medicine, 16th edition, Mccraw-hill companies 2005:1430-34.
 
[[5]  Troiano RP, Berrigan D, Dodd KW, Masse LC, Tilert T, McDowell M. Physical activity in the United States measured by accelerometer. Med Sci Sports Exerc. 2008; 40:181-8.
 
Show More References
[6]  Umesh N. Khot, Monica B. Khot, Christopher T. Bajzer, Shelly K. Sapp, E. Magnus Ohman, Sorin J. Brener, Stephen G. Ellis, A. Michael Lincoff, Eric J. Topol. Prevalence of conventional risk factors in patients with coronary heart disease. JAMA. 2003; 290 (7):898-904.
 
[7]  Hasson L, Zanchetti A, Camithers SG. Principal results of the hypertension optimal treatment (HOT) randomized trial, lancet 1998; 351:1755.
 
[8]  Hjemann I, Valve BK, Holme I, Leren P. Effect of diet and smoking intervention on the incidence of coronary artery disease, Lancet 1991; 2:1303-10.
 
[9]  Lawrence MT, Stephan J. Mcphee. Coronary artery disease. In: Current medical diagnosis and treatment, 44th edition, Lange medical company 2004:328-330.
 
[10]  Kenichi O, Toshiyuki N, Masahiko L. Angiographic and coronary risk factor analysis of Japanese patients with ischemic heart disease before age of 40. A multicenter cooperative study, JCJ 1996; 60: 822-30.
 
[11]  Gaspardone A, Crea F, Perino M, Iamle M, Tomai F, Versaci F and Borini R. Risk factors in patients with different clinical and angiographic manifestations of ischemic heart disease, Cardiologia 1995; 40(9): 679-84.
 
[12]  Dunker K, Lind L, Lagerqvist B, Zetbelius B, Vessby B and Lithell H. Cardiovascular risk factors for stable angina pectoris versus unheralded myocardial infarction, AM Heart J 2004 Mar; 147(3):502-8.
 
[13]  Wagar H, Braunwald E. Relation between clinical presentation and angiographic findings in unstable angina pectoris, and comparison with that in stable angina, AMJ Cardiol 1993;72:544.
 
[14]  Thomas CS, Varghese K, Habib F, Abrahim MT, Hayat NJ and Cherian G. Extent and severity of atherosclerotic vascular disease in patients undergoing coronary angiography.. The Kuwait vascular study, Angiology 2003Jan; 54(1):85-92.
 
[15]  Kunihisa M, Keiko N. Risk factors that discriminate high risk from low risk Japanese patients with coronary artery disease, Jpn Circ J 2000;64:825-830.
 
[16]  Charles CJ, Robert CG, Joseph L. Acute coronary syndromes. In: Cecil Essentials of Medicine, 6th edition, WB. Saunders company 2004:98-109.
 
[17]  Zoller P, Halmai I, Horvath T. Correlation between clinical picture and coronary angiography in unstable angina, Orv-Hetil 1996; 137:19-22.
 
[18]  Cianflone D, Ciccirillo F, Buffon A, Trani C, Scabbia EV, Finocchiaro ML and Crea F. Comparison of coronary angiographic narrowing in stable angina pectoris, unstable angina pectoris and in acute myocardial infarction, AMJ Cardiol 1995;76(4):215-9.
 
[19]  Mona AE, Ayman SM, Ramzy H. Comparison between stable angina and unstable angina: Clinical and coronary angiographic correlation, Egypt Heart J 1998; 50(1):97-106.
 
[20]  Shunji K, Famio K, Akira S, Toshiro M, Michihiro K, Takashi K and Kazuhiro F. Effects of coronary risk factors on angiographic morphology in patients with ischemic heart disease, JPC Circ J1997;61:390-395.
 
[21]  Satyendra T, Sudeep K, Aditya K. Premature coronary artery disease in north India: An angiography study of 1971 patients, Indian Heart J 2005; 57:311-318.
 
[22]  Scott MG, Gary JB, Michael HC. Primary prevention of coronary heart disease: Guidance from Framingham. Circulation 1998; 97:1876-1887.
 
[23]  Lexin W, Jingtian Li, Shukai S, Rongguo Y and Gouqin F. Management of cardiovascular risk factors in type 2 diabetic patients undergoing coronary angiography, CMJ 2003; 44(6):712-15.
 
[24]  Gera S, Harsh W. Percutaneous coronary interventions: a clinical-angiographic study, JIACIM 2004; 5 (4):322-6.
 
Show Less References

Article

Risk Factors of Metabolic Syndrome among Clinic Patients in Gaza - Palestine

1AL Shifa Hospital, Cardiology department, Gaza, Palestine

2Al Quds University, Faculty of Public Health, Gaza, Palestine

3Private clinic, Former Director General AL Shifa Hospital Gaza, Palestine


American Journal of Cardiovascular Disease Research. 2013, 1(1), 20-24
DOI: 10.12691/ajcdr-1-1-5
Copyright © 2013 Science and Education Publishing

Cite this paper:
Amal Jamee, Yehia Abed, Hassan Abutawila. Risk Factors of Metabolic Syndrome among Clinic Patients in Gaza - Palestine. American Journal of Cardiovascular Disease Research. 2013; 1(1):20-24. doi: 10.12691/ajcdr-1-1-5.

Correspondence to: Amal  Jamee, AL Shifa Hospital, Cardiology department, Gaza, Palestine. Email: dr_amal08@yahoo.fr

Abstract

Metabolic syndrome is a term, which refers to a combination of medical disorders that are associated with a higher risk for cardiovascular disease and diabetes. The syndrome is more common in female than males. This study was conducted to estimate the prevalence of the metabolic syndrome among patients with cardiovascular diseases in Gaza and to examine the association between traditional risk factors for the non-communicable diseases and each of the component of the metabolic syndrome. We used the Adult Treatment Protocol III National cholesterol Education Programme of America (ATPIII) indicators for diagnosis and determination of metabolic syndrome. The syndrome was met if an individual had three or more criteria: waist circumference >102cm in men and >88cm in women, fasting plasma glucose ≥110mg/dl, Blood pressure ≥130/85mmhg, serum Triglycerides ≥150mg/dl and serum HDL cholesterol <40mg/dl in male and <50mg/dl in female. Statistical analysis was performed using SPSS version 20. The prevalence of metabolic syndrome was 59.5%, without difference between male and female. The main risk factors for metabolic syndrome were high blood pressure (78.8% for systolic and 73.8% for diastolic Blood Pressure), large waist circumference (67.9%), high Triglycerides (78.6%), and high fasting blood sugar (86.4%). HDL cholesterol was protective but not statistically significant. The risk factors of metabolic syndrome in both sexes in descending order were as follows, high fasting blood sugar, large waist circumference, high Triglycerides, high Blood Pressure, and low HDL cholesterol. We conclude that high level of prevalence of metabolic syndrome in our study population indicates the need for an active health programme to reduce the factors influencing the prevalence. Therefore, preventive interventions must be taken seriously.

Keywords

References

[[[[[[[[[[[[[[[[[[[[[[[[[[[[[
[[1]  Eva Kassi, Panagiota Pervanidou, Gregory Kaltsas and George Chrousos “Metabolic syndrome: definitions and controversies,” BMC Medicine, 9. 48. 2011.
 
[[2]  Jaber LA, Brown MB, Hamm ad A, Zhu Q, Herman WH, “The prevalence of the metabolic syndrome among Arab Americans,” Diabetes Care, 27 (1). 234-238. 2004.
 
[[3]  Reaven GM, “Role of insulin resistance inhuman disease” Banting lecture Diabetes, 37. 1595-1607.1988.
 
[[4]  DeFronzo RA, Ferrannini E, “Insulin resistance, a multifaceted Syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease,” Diabetes Care, 14. 173-194. 1991.
 
[[5]  Kaplan NM, “The deadly quartet, Upper-body obesity, glucose intolerance hypertriglyceridemia, and hypertension,” Arch Intern Med, 149. 1514-1520. 1989.
 
Show More References
[6]  Aguilar-Salinas CA, Rojas R, Gomez-Perez FJ, Mehta R, Franco A, Olaiz G, et al, “The metabolic syndrome: a concept hard to define,” Arch Med Res, 36 (3). 223-231. 2005.
 
[7]  Abu Sham’s RA, Dawazah AK, Kufri FH, Yassin IH, Torok NI, “Metabolic syndrome and cardiovascular risk factors among Palestinian of east Jerusalem,” East Mediterr Health J, 15. 1464-1473. 2009.
 
[8]  Einhorn D, Reaven GM, Cobin RH, Ford E, Ganda OP, Handelsman Y, et al, “American College of Endocrinology position statement on the insulin resistance syndrome,” Endocr Pract, 9. 237-252. 2003.
 
[9]  Alberti KG, Zimmet P, Shaw J, IDF Epidemiology Task Force Consensus Group, “The metabolic syndrome a new worldwide definition,” Lancet, 366. 1059-1062. 2005.
 
[10]  Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al, “Diagnosis and Management of the Metabolic Syndrome. An American Heart Association/ NationalHeart,Lung, and Blood Institute Scientific Statement,” Circulation,112. 2735-2752. 2005.
 
[11]  Balkaua B, Valensic P, Eschwègea E, Slam G, “A review of the metabolic syndrome,” Diabetes Metab, 33. 405-413. 2007.
 
[12]  Balkau B, Vernay M, Mhamdi L, Novak M, Arondel D, et al, “The incidence and persistence of the NCEP (National Cholesterol Education Program) metabolic syndrome. The French D.E.S.I.R. study,” Diabetes Metab, 29 (5).526-532. 2003.
 
[13]  Ramachandran A, Snehalatha C, Satyavani K, Sivasankari S, Vijay V, “ Metabolic syndrome in urban Asian Indian adults, a population study using modified ATP IIIcriteria,” Diabetes Res Clin Pract, 60 (3).199-204. 2003.
 
[14]  Giulia D’Agostini, Mariantonietta Cicoira, Corrado Vassanelli, “Heart Failure in Women: A Disease with Peculiar Path physiological Mechanisms and Clinical Presentation,” American Journal of Cardiovascular Disease Research, 1(1). 1-6.2013.
 
[15]  Isomaa B, Almgren P, Tuomi T, et al, “Cardiovascular morbidity and mortality associated with the metabolic syndrome,” Diabetes Care, 24. 683-689. 2001.
 
[16]  Lakka HM, Laaksonen DE, Lakka TA, et al, “The metabolic syndrome and total cardiovascular disease mortality in middle aged men,” JAMA, 288. 2709-2716. 2002.
 
[17]  Robert H Eckel, Scott M Grundy, Paul Z, “The metabolic syndrome,” Lancet, 365. 1415-1428.2005.
 
[18]  Stern M, Williams K, Gonzalez, Villalpando C et al, “Does the metabolic syndrome improve identification of individuals at risk of type 2 diabetes and or cardiovascular disease?” Diabetes Care, 27(11. 2676-81. 2004.
 
[19]  Deepa M, Farooq S, Datta M, Deepa R, Mohan V, “Prevalence of metabolic syndrome using WHO, ATPIII and IDF definitions in Asian Indians: the Chennai Urban Rural Epidemiology Study (CURES-34), ” Diabetes Metab Res Rev, 23 (2). 127-134. 2007.
 
[20]  Azizi F, Salehi P, Etemadi A, Zahedi-Asl S, “Prevalence of metabolic syndrome in an urban population: Tehran Lipid and Glucose Study” Diabetes Res Clin Pract, 61(1). 29-37. 2003.
 
[21]  Dunstan DW, Zimmet PZ,Welborn TA et al, “The rising prevalence of diabetes and impaired glucose tolerance. The Australian Diabetes, Obesity and Lifestyle Study,”Diabetes Care, 25. 829-834. 2002.
 
[22]  Hamdy A S, Seham A, Nader N, and Iman ES, “Metabolic syndrome in the Middle East,”Indian J Endocrinol Metab olisme,16(1). 2012.
 
[23]  Khader Y, Bateiha A, El-Khateeb M, Al- Shaikh A, Ajlouni K, “ High prevalence of the metabolic syndrome among Northern Jordanians,” J Diabetes Complications, 21 (4).214-219.2007.
 
[24]  Kozan O,Oguz A, Abaci A, Erol C ,Ongen Z, Temizhan A et all, “Prevalence of the metabolic syndrome among Turkish adults,” EUR journal Clin N utr, 61. 548-553. 2007.
 
[25]  Bouguerra R, Alberi H, Smida H ,Salem LB, Rayana CB, et al, “WC cut off points for identification of abdominal obesity among the Tunisian adult population,” Diabetes Obese Meta, 9.859-868.2007.
 
[26]  Suhad M. Bahijri, Rajaa M. Al Raddadi, “The Importance of Local Criteria in the Diagnosis of Metabolic Syndrome in Saudi Arabia,” Ther Adv in Endo and Metab 4 (2).51-59.2013.
 
[27]  Eytan C, Han K, Abigail, Elad G and Moshe G, “Hyperuricemia and Metabolic Syndrome: Lessons from a Large Cohort from Israel,” IMAJ, 14. 2012.
 
[28]  Ford ES, Giles WH, Dietz WH, “Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey,” JAMA, 287. 356-359. 2002.
 
[29]  Park YW, Zhu S, Palaniappan L, Heshka S, Carnethon MR, Heymsfield SB, “The metabolic syndrome: Prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 1988-1994,” Arch Intern Med, 163.427-436. 2003.
 
[30]  Grundy SM, Cleeman JI, Daniels SR, et al, “Diagnosis and management of the metabolic syndrome: An American Heart Association/Nation Heart, Lung, and Blood Institute scientific statement,”.Curr Opin Cardiol, 21.1-6.2006.
 
[31]  Ervin RB, “Prevalence of metabolic syndrome among adults 20 years of age and over, by sex, age, race and ethnicity, and body mass index: United States, 2003-2006,” Natl Health Stat Report, 131-7. 2009.
 
[32]  G. Mancia, G. Parati, C. Borghi et al, “Hypertension prevalence, Awareness, control and association with metabolic abnormalities in the San Marino population: the SMOOTH study,” Journal of Hypertension, 24 (5) .837-843.2006.
 
[33]  Athyros VG, Bouloukos VI, Pehlivanidis AN, Papageorgiou AA, Dionysopoulou SG, Symeonidis AN, et al, “The prevalence of the metabolic syndrome in Greece: the MetS-Greece Multicentre Study,” Diabetes Obese Metab, 7. 397-405. 2005.
 
[34]  Gami AS, Witt BJ, Howard DE, et al, “Metabolic syndrome and risk of incident cardiovascular events and death: a systematic review and meta-analysis of longitudinal studies,” J Am Coll Cardiol, 49(4). 403-414.2007.
 
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Article

A Chronic Disorder in the Emergency Room: A Descriptive Analysis of Paroxysmal Atrial Fibrillation Cases Requiring Urgent Treatment

1Department of Cardiology, University Hospital Center ‘Mother Theresa’, Faculty of Medicine, University of Medicine in Tirana, Albania

2Biomedical and Experimental Department, Faculty of Medicine, University of Medicine in Tirana, Albania


American Journal of Cardiovascular Disease Research. 2013, 1(1), 16-19
DOI: 10.12691/ajcdr-1-1-4
Copyright © 2013 Science and Education Publishing

Cite this paper:
Petrit Bara, Sokol Myftiu, Gentian Vyshka. A Chronic Disorder in the Emergency Room: A Descriptive Analysis of Paroxysmal Atrial Fibrillation Cases Requiring Urgent Treatment. American Journal of Cardiovascular Disease Research. 2013; 1(1):16-19. doi: 10.12691/ajcdr-1-1-4.

Correspondence to: Gentian  Vyshka, Biomedical and Experimental Department, Faculty of Medicine, University of Medicine in Tirana, Albania. Email: gvyshka@yahoo.com

Abstract

Atrial fibrillation (AF) is the most frequent arrhythmia, and patients frequently visit emergency departments, where the condition might be diagnosed for the first time. An analysis of factors that might lead a chronic patient to seek urgent medical treatment is important, especially in terms of preventing long-term disability and morbidity. This is even truer for atrial fibrillations, whose complications have a known notoriety and are source of important mortality figures, mainly related to ischemic stroke or more serious consequential cardiac arrhythmias. We have studied paroxysmal AF cases treated during a period of two months in an emergency facility of the University Hospital Centre of Tirana, with 106 patients recruited sequentially in a prospective, open-label and descriptive study. Our data confirmed an important association between overweight and obesity and paroxysmal AF in general, since more than 80% of the patients suffering from this condition had a high body mass index. A thorough discussion of the data, confronted with much larger studies reported from several sources and available actually, is made at the end of the paper. The necessity to re-confirm findings through larger groups of study and through a multi-centre design is formulated.

Keywords

References

[[[[[[[[[[[[[[[[[[[[[[
[[1]  Colilla S, Crow A, Petkun W, Singer DE, Simon T, Liu X. Estimates of Current and Future Incidence and Prevalence of Atrial Fibrillation in the U.S. Adult Population. Am J Cardiol. 2013 Jul 4.
 
[[2]  Todaro MC, Choudhuri I, Belohlavek M, Jahangir A, Carerj S, Oreto L, Khandheria BK. New echocardiographic techniques for evaluation of left atrial mechanics. Eur Heart J Cardiovasc Imaging. 2012 Dec; 13(12):973-84.
 
[[3]  Barrett TW, Self WH, Jenkins CA, Storrow AB, Heavrin BS, McNaughton CD, Collins SP, Goldberger JJ. Predictors of Regional Variations in Hospitalizations Following Emergency Department Visits for Atrial Fibrillation. Am J Cardiol. 2013 Aug 22.
 
[[4]  Atzema CL, Austin PC, Miller E, Chong AS, Yun L, Dorian P. A Population-Based Description of Atrial Fibrillation in the Emergency Department, 2002 to 2010. Ann Emerg Med. 2013 Jun 26.
 
[[5]  Atzema CL, Dorian P, Ivers NM, Chong AS, Austin PC. Evaluating early repeat emergency department use in patients with atrial fibrillation: a population-based analysis. Am Heart J. 2013 Jun; 165(6):939-48.
 
Show More References
[6]  Boiarintsev VV, Alekseeva LA, Stazhadze LL, Bulanova NA, Bazarova MB, Mikhaĭlovskaia IV. [Atrial fibrillation registered for the first time: characteristics of clinical course, treatment, prognosis]. Kardiologiia. 2013; 53(2):25-9.
 
[7]  Atzema CL, Austin PC, Chong AS, Dorian P. Factors associated with 90-day death after emergency department discharge for atrial fibrillation. Ann Emerg Med. 2013 May; 61(5):539-548.e1.
 
[8]  Ball J, Carrington MJ, Wood KA, Stewart S; SAFETY Investigators. Women versus men with chronic atrial fibrillation: insights from the Standard versus Atrial Fibrillation spEcific managemenT studY (SAFETY). PLoS One. 2013 May 29; 8(5):e65795.
 
[9]  Bhusri S, Ansell J. New anticoagulants in atrial fibrillation: an update for clinicians. Ther Adv Chronic Dis. 2012 Jan; 3(1):37-45.
 
[10]  Salhadin P, Bran M, De Marneffe M, Denolin H. Management of patients with chronic atrial fibrillation. Br J Clin Pharmacol. 1982; 13(Suppl 2):295S-296S.
 
[11]  Olshansky B, Heller EN, Mitchell LB, Chandler M, Slater W, Green M, Brodsky M, Barrell P, Greene HL. Are transthoracic echocardiographic parameters associated with atrial fibrillation recurrence or stroke? Results from the Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) study. J Am Coll Cardiol. 2005 Jun 21; 45(12):2026-33.
 
[12]  Rovellini A, Folli C, Cardani F, Monzani V. Thromboembolic and haemorrhagic events in permanent atrial fibrillation: observational study in an emergency department. Eur J Intern Med. 2009 Dec; 20(8):756-9.
 
[13]  Ki CS, Jung CL, Kim HJ, Baek KH, Park SJ, On YK, Kim KS, Noh SJ, Youm JB, Kim JS, Cho H. A KCNQ1 mutation causes age-dependant bradycardia and persistent atrial fibrillation. Pflügers Arch. 2013 Aug 30. [Epub ahead of print].
 
[14]  Lemmens R, Hermans S, Nuyens D, Thijs V. Genetics of atrial fibrillation and possible implications for ischemic stroke. Stroke Res Treat. 2011; 2011:208694.
 
[15]  Conway DS, Lip GY. Ethnicity in relation to atrial fibrillation and stroke (the West Birmingham Stroke Project). Am J Cardiol. 2003 Dec 15; 92(12):1476-9.
 
[16]  Bosch RF, Pittrow D, Beltzer A, Kruck I, Kirch W, Kohlhaussen A, Bonnemeier H. Gender differences in patients with atrial fibrillation. Herzschrittmacherther Elektrophysiol. 2013 Sep; 24(3):176-183.
 
[17]  Michelena HI, Powell BD, Brady PA, Friedman PA, Ezekowitz MD. Gender in atrial fibrillation: Ten years later. Gend Med. 2010 Jun; 7(3):206-17.
 
[18]  Overvad TF, Rasmussen LH, Skjøth F, Overvad K, Lip GY, Larsen TB. Body mass index and adverse events in patients with incident atrial fibrillation. Am J Med. 2013 Jul; 126(7):640.e9-17.
 
[19]  Zhuang J, Lu Y, Tang K, Peng W, Xu Y. Influence of body mass index on recurrence and quality of life in atrial fibrillation patients after catheter ablation: a meta-analysis and systematic review. Clin Cardiol. 2013 May; 36(5):269-75.
 
[20]  Guijian L, Jinchuan Y, Rongzeng D, Jun Q, Jun W, Wenqing Z. Impact of body mass index on atrial fibrillation recurrence: a meta-analysis of observational studies. Pacing Clin Electrophysiol. 2013 Jun; 36(6):748-56.
 
[21]  Badheka AO, Rathod A, Kizilbash MA, Garg N, Mohamad T, Afonso L, Jacob S. Influence of obesity on outcomes in atrial fibrillation: yet another obesity paradox. Am J Med. 2010 Jul; 123(7):646-51.
 
[22]  Crystal E, Connolly SJ. Atrial fibrillation: guiding lessons from epidemiology. Cardiol Clin. 2004 Feb; 22(1):1-8.
 
[23]  Iguchi Y, Kimura K, Shibazaki K, Aoki J, Sakai K, Sakamoto Y, Uemura J, Yamashita S. HbA1c and atrial fibrillation: a cross-sectional study in Japan. Int J Cardiol. 2012 Apr 19; 156(2):156-9.
 
[24]  Agmon Y, Khandheria BK, Meissner I, Schwartz GL, Petterson TM, O'Fallon WM, Gentile F, Spittell PC, Whisnant JP, Wiebers DO, Covalt JL, Seward JB. Association of atrial fibrillation and aortic atherosclerosis: a population-based study. Mayo Clin Proc. 2001 Mar; 76(3):252-9.
 
[25]  Potpara TS, Polovina MM, Licina MM, Mujovic NM, Marinkovic JM, Petrovic M, Vujisic-Tesic B, Lip GY. The impact of dilated left atrium on rhythm control in patients with newly diagnosed persistent atrial fibrillation: the Belgrade atrial fibrillation project. Int J Clin Pract. 2011 Nov; 65(11):1202-3.
 
[26]  Lévy S. Factors predisposing to the development of atrial fibrillation. Pacing Clin Electrophysiol. 1997 Oct; 20(10 Pt 2):2670-4.
 
[27]  Selmer C, Olesen JB, Hansen ML, Lindhardsen J, Olsen AM, Madsen JC, Faber J, Hansen PR, Pedersen OD, Torp-Pedersen C, Gislason GH. The spectrum of thyroid disease and risk of new onset atrial fibrillation: a large population cohort study. BMJ. 2012 Nov 27; 345:e7895.
 
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Article

Cardiac Resynchronization Therapy: Effects on Mitral Regurgitation in Heart Failure Patients

1Cardiovascular Research Center, Heshmat Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran


American Journal of Cardiovascular Disease Research. 2013, 1(1), 12-15
DOI: 10.12691/ajcdr-1-1-3
Copyright © 2013 Science and Education Publishing

Cite this paper:
Jalal Kheirkhah, Vahid Toulabi, Hassan Moladoust, Mohammad Asadian Rad, Hamid Reza Bonakdar, Anoosh Barzigar, Fardin Mirbolouk, Bijan Shad, Vahid Nikseresht. Cardiac Resynchronization Therapy: Effects on Mitral Regurgitation in Heart Failure Patients. American Journal of Cardiovascular Disease Research. 2013; 1(1):12-15. doi: 10.12691/ajcdr-1-1-3.

Correspondence to: Hassan Moladoust, Cardiovascular Research Center, Heshmat Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran. Email: hmoladost@yahoo.con

Abstract

Background: Cardiac resynchronization therapy (CRT) has been introduced as a promising therapeutic choice in heart failure patients (HF) with ventricular dyssynchrony, shown with a wide QRS. Objective: This study aimed to evaluate the effect of CRT on the severity of mitral regurgitation (MR) quantitatively using the volumetric Doppler method in HF patients. Patients and methods: This was a prospective before-after survey in which 22 HF patients with wide QRS (≥120 ms) and NYHA class III who were included. All patients were evaluated initially for QRS width, NYHA class, MR volume, MR fraction HF and mitral valve area (MV area). Biventricular pacing was done through cardiac-resynchronization device along with three pacing leads and same evaluations were done after CRT. Results: The mean (SD) QRS width and NYHA class were significantly decreased after CRT in HF patients (P<0.001). Also MR volume (46.9±30.2cc vs. 27.0±26.4cc, P<0.001) and fraction (40.1±25.5% vs. 26.8±22.7%, P=0.002) were improved following CRT. The decrease of MV area after CRT was also significant (10.6±3.0cm2 vs. 8.6±2.6cm2, P<0.001). Conclusion: As MR is associated with morbidity and mortality in HF patients and the standard surgical therapy may not be practical for a majority of them, this novel treatment may improve their disease condition significantly.

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References

[[[[[[[[[[[[[[[[[[[
[[1]  Roger VL, Go AS, Lloyd-Jones DM, Adams RJ, Berry JD, Brown TM, et al. Heart Disease and Stroke Statistics--2011 update: A report from the American Heart Association. Circulation 2011; 123: 18-209.
 
[[2]  Hekmatpour D, Mohammadi E, Ahmadi F, Arefi SH. Noncompliance factors of congestive heart failure patients readmitted in cardiac care units. Iranian Journal of Critical Care Nursing 2009; 2: 91-97.
 
[[3]  Linde C, Leclercq C, Rex S, Garrigue S, Lavergne T, Cazeau S, et al. Long-Term benefits of biventricular pacing in congestive heart failure: Results from the Multisite Stimulation In Cardiomyopathy (MUSTIC) study. J Am Coll Cardiol 2002; 40:111-118.
 
[[4]  Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E, et al. Cardiac resynchronization in chronic heart failure. N Engl J Med 2002; 346: 1845-1853.
 
[[5]  Farwell D, Patel NR, Hall A, Ralph S, Sulke AN. How many people with heart failure are appropriate for biventricular resynchronization? Eur Heart J 2000; 21: 1246-1250.
 
Show More References
[6]  Aaronson KD, Schwartz JS, Chen TM, Wong KL, Goin JE, Mancini DM. Development and prospective validation of a clinical index to predict survival in ambulatory patients referred for cardiac transplant evaluation. Circulation 1997; 95: 2660-2667.
 
[7]  Acosta H, Viafara L M, Izquierdo D, Adams D, Pothula V R, Wallner H, et al. Reduction of mitral regurgitation by biventricular pacing with intraventriuclar timing optimization in patients without a standard indication: A potential new indication for Cardiac Resynchronization Therapy. The Journal of Innovations in Cardiac Rhythm Management 2012; 3: 784-790.
 
[8]  St.John Sutton MG, Plappert T, Abraham WT, Smith AL, DeLurgio DB, Leon AR, et al. Effect of cardiac resynchronization on left ventricular size and function in chronic heart failure. Circulation 2003; 107: 1985-1990.
 
[9]  Horwich T, Foster E, De Marco T, Tseng Z, Saxon L. Effects of resynchronization therapy on cardiac function in pacemaker patients upgraded to biventricular devices. J Cardiovasc Electrophysiol 2004; 15: 1284-1289.
 
[10]  Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, Tavazzi L. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005; 352: 1539-1549.
 
[11]  Eskesen K, Kanagalingam S, Abraham TP. Mitral Regurgitation in Cardiac Resynchronization. Solving another piece of puzzle. Circ Cardiovasc Imaging 2009; 2: 427-428.
 
[12]  Ypenburg C, Lancellotti P, Tops LF, Bleeker GB, Holman ER, Pierard LA, et al. Acute effects of initiation and withdrawal of cardiac resynchronization therapy on papillary muscle dyssynchrony and mitral regurgitation. J Am Coll Cardiol 2007; 50: 2071-2077.
 
[13]  Lancellotti P, Melon P, Sakalihasan N, Waleffe A, Dubois C, Bertholet M, Pierard LA. Effect of cardiac resynchronization therapy on functional mitral regurgitation in heart failure. Am J Cardiol 2004; 94: 1462-1465.
 
[14]  Kanzaki H, Bazaz R, Schwartzman D, Dohi K, Sade LE, Gorcsan J 3rd. A mechanism for immediate reduction in mitral regurgitation after cardiac resynchronization therapy. J Am Coll Cardiol 2004; 44: 1619-1625.
 
[15]  Disney PJ, Ashby DT, Young GD, Bradley JA. Ventricular pacing for severe mitral regurgitation following atrioventricular nodal ablation. Pacing Clin Elecrophys 2003; 26: 643-644.
 
[16]  Breithardt OA, Sinha AM, Franke A, Hanrath P, Stellbrink C. Echocardiography in cardiac resynchronization therapy: Identification of suitable patients, follow-up and therapy optimization. Herz 2003; 28: 615-627.
 
[17]  Irwin JM, Glover MU, Barold SS. Treatment of pacemaker induced severe mitral regurgitation with biventricular pacing in two patients with a normal left ventricular ejection fraction. Pacing Clin Electrophysiol 2003; 26: 2333-2335.
 
[18]  Sutton MG, Plappert T, Hilpisch KE, Abraham WT, Hayesn DL, Chinchoy E. Sustained reverse left ventricular structural remodeling with cardiac resynchronization at one year is a function of etiology: Quantitative Doppler echocardiographic evidence from the Multicenter InSync Randomized Clinical Evaluation (MIRACLE). Circulation 2006; 113: 266-272.
 
[19]  Auricchio A, Stellbrink C, Sack S, Block M, Vogt J, Bakker P, et al. Long-lerm clinical effect of hemodynamically optimized cardiac resynchronization therapy in patients with heart failure and ventricular conduction delay. J Am Coll Cardiol 2002; 39: 2026-2033.
 
[20]  Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, De Marco T, et al. Comparison of medical therapy, pacing, and defibrillation in heart failure (COMPANION) investigators: Cardiacresynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med 2004; 350: 2140-2150.
 
[21]  Young JB, Abraham WT, Smith AL, Leon AR, Lieberman R, Wilkoff B, et al. Combined cardiac resynchronization and implantable cardioversion defibrillation in advanced chronic heart failure. JAMA 2003; 289: 2685-2694.
 
[22]  Gras D, Leclercq C, Tang AS, Bucknall C, Luttikhuis HO, Kirstein-Pedersen A. Cardiac resynchronization therapy in advanced heart failure. Eur J Heart Fail 2002; 4: 311-320.
 
[23]  Etienne Y, Mansourati J, Touiza A, Gilard M, Bertault-Valls V, GuilloPh, et al. Evaluation of left ventricular function and mitral regurgitation during left ventricular-based pacing in patients with heart failure. Eur J Heart Fail 2001; 3: 441-447.
 
[24]  Breithardt OA, Sinha AM, Schwammenthal E, Bidaoui N, Markus KU, Franke A, Stellbrink C. Acute effects of cardiac resynchronization therapy on functional mitral regurgitation in advanced systolic heart failure. J Am Coll Cardiol 2003; 41: 765-770.
 
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Article

Evaluation of Asymptomatic Patients with Median Arcuate Ligament Syndrome (Mals) Using Color Duplex Ultrasound and Computed Tomographic (Ct) Angiography

1Department of Radiodiagnosis, Faculty of medicine, Fayoum University, Egypt


American Journal of Cardiovascular Disease Research. 2013, 1(1), 7-11
DOI: 10.12691/ajcdr-1-1-2
Copyright © 2013 Science and Education Publishing

Cite this paper:
Ashraf Talaat Youssef. Evaluation of Asymptomatic Patients with Median Arcuate Ligament Syndrome (Mals) Using Color Duplex Ultrasound and Computed Tomographic (Ct) Angiography. American Journal of Cardiovascular Disease Research. 2013; 1(1):7-11. doi: 10.12691/ajcdr-1-1-2.

Correspondence to: Ashraf Talaat Youssef, Department of Radiodiagnosis, Faculty of medicine, Fayoum University, Egypt. Email: ashraftalaat1@yahoo.com

Abstract

Median arcuate ligament syndrome is considered as rare syndrome manifested by variety of symptoms. Aim of the Work: To assess the presence of asymptomatic patients showing the typical color duplex ultrasound and CT angiographic features of MAL syndrome and the impact of these findings on the pathogenesis and management of the syndrome. Material and Methods: 200 asymptomatic patients were examined with color duplex ultrasound and further CT angiography was performed to all patients with color duplex findings of arcuate ligament syndrome. Results: 8 patients showed typical color duplex findings and CT angiographic features of MALS. Conclusion: The diagnosis of MAL syndrome shouldn't depend only on the imaging criteria and should be strongly linked to the unexplained patient symptoms after meticulous exclusion of other etiologies. The management shouldn’t depend only on relieving the arterial stenosis but also on dissection of peri arterial nerve plexus.

Keywords

References

[[[[[[[[[[[[[[[[[[[[[[[[
[[1]  Dunbar, W. Molnar, F. F. Beman, and S. A. Marable, “Compression of the celiac trunk and abdominal angina,” The American Journal of Roentgenology, Radium Therapy, and Nuclear Medicine, vol. 95, no. 3, pp. 731-744, 1965.
 
[[2]  P. T. HARJOLA, “A rare obstruction of the coeliac artery. Report of a case,” AnnalesChirurgiae et GynaecologiaeFenniae, vol. 52, pp. 547-550, 1963.
 
[[3]  P. Martinez and G. J. Hogan, “Mesenteric ischemia,” Emergency Medicine Clinics of North America, vol. 22, no. 4, pp. 909-928, 2004.
 
[[4]  Edwards, A. J.; Hamilton, J. D.; Nichol, W.D.; Taylor, G.W. compression syndrome .Br. Med. J., 1:342-5, 1970.
 
[[5]  Reuter, S. R. Accentuation of celiac compression by the median arcuate ligament of the diaphragm during deep expiration. Diagn.Radiol., 98:561-4,1971.
 
Show More References
[6]  Hongsakul, SorrachaRookkapan, JitpreedeeSungsiri, and TeeravutTubtawee.Case Reports in Vascular Medicine, Severe Case of Median Arcuate Ligament Syndrome with Successful Angioplasty and stenting.Article ID 129870, 4 pages. Volume 2012 (2012).
 
[7]  Harjola, P. T.Arare obstruction of the coeliac artery. An. Chir.Gynaecol.Fenn., 52:547-570, 1963.
 
[8]  Harjola, P. T. Coeliac axis constriction and abdominal angina. Bull. Soc. Intern. Chir., 27:464-7, 1968.
 
[9]  Harjola, P.T. &Lahtiharju, A.Celiac axis syndrome. Abdominal angina caused by external compression of the celiac artery. Am. J. Surg., 115:864-9, 1968.
 
[10]  PETRELLA, S. & PRATES J. C, Celiac trunk compression syndrome .A review. Int. J. Morphol., 24(3):429-436, 2006.
 
[11]  Duffy AJ, Panait L, Eisenberg D, Bell RL, Roberts KE, SumpioB, Management of median arcuate ligament syndrome: a new paradigm.. Ann Vasc Surg.; 23(6):778-84.2009.
 
[12]  Jimenez JC, Harlander-Locke M, Dutson EP, Open and laparoscopic treatment of median arcuate ligament syndrome.J Vasc Surg.; 56(3):869-73. sep 2012.
 
[13]  Ayşe Erden,MehmetYurdakul,TurhanCumhur, Marked increase in flow velocities during deep expiration: A duplex doppler sign of celiac artery compression syndrome. CardioVascular and Interventional Radiology, Volume 22, Issue 4, pp 331-332, july 1999.
 
[14]  Wolfman D, Bluth EI, Sossaman J. Median arcuate ligament Syndrome. J Ultrasound Med 2003; 22: 1377-1380.
 
[15]  Horton KM, Talamini MA, Fishman EK. "Median arcuate ligament syndrome: evaluation with CT angiography". Radiographics 25 (5): 1177-82, 2005.
 
[16]  R. S. Okten, F. Kucukay, M. Tola, B. Bostanci, and T. Cumhur, “Is celiac artery compression syndrome genetically inherited? A case series from a family and review of the literature,” European Journal of Radiology, vol. 81, no. 6, pp. 1089-1093, 2012.
 
[17]  S. Q. H. Chou, K. Y. Kwok, L. S. Wong, D. H. S. Fung, and W. K. Wong, “Imaging features of median arcuate ligament syndrome,” Journal of the Hong Kong College of Radiologists, vol. 13, no. 2, pp. 101-103, 2010.
 
[18]  Mohammed Muqeetadnan, Syed Amer, Ambreen Rahman, Salman Nusrat, and Syed Hassan.Case Reports in Gastrointestinal Medicine, Celiac Artery Compression Syndrome Article ID 934052,3 pages, volume 2013 (2013).
 
[19]  Gander, S., Mulder, D.J., Jones, S., Ricketts, J.D., Soboleski, D.A., Justinich, C.J.Recurrent abdominal pain and weight loss in an adolescent: Celiac artery compression syndrome Canadian Journal of Gastroenterology ;Volume 24, Issue 2,pages 91-93 February 2010.
 
[20]  A. S. van Petersen, B. H. Vriens, A. B. Huisman, J. J. Kolkman, and R. H. Geelkerken, “Retroperitoneal endoscopic release in the management of celiac artery compression syndrome,” Journal of Vascular Surgery, vol. 50, no. 1, pp. 140-147, 2009.
 
[21]  Kuntsevich GI, Shilenok DV.Duplex scanning of hemodynamic parameters of the celiac trunk and superior mesenteric artery in healthy volunteers. Khirurgiia (Mosk); (7):48-51,1993.
 
[22]  Matthews, B Carbonell, A. M.; Kercher, K.W.; Heniford, B.T.22-Matthews, B D.Laparoscopie management of median ligament syndrome. Surg. Endosc., 19:729, 2005.
 
[23]  J. W. Chou, C. M. Lin, C. L. Feng, C. F. Ting, K. S. Cheng, and Y. F. Chen, “Celiac artery compression syndrome: an experience in a single institution in Taiwan,” Gastroenterology Research and Practice, vol. 2012, Article ID 935721, 6 pages, 2012.
 
[24]  P. Baccari, E. Civilini, L. Dordoni, G. Melissano, R. Nicoletti, and R. Chiesa, “Celiac artery compression syndrome managed by laparoscopy,” Journal of Vascular Surgery, vol. 50, no. 1, pp. 134-139, 2009.
 
[25]  D. Grotemeyer, M. Duran, F. Iskandar, D. Blondin, K. Nguyen, and W. Sandmann, “Median arcuate ligament syndrome: vascular surgical therapy and follow-up of 18 patients,” Langenbeck's Archives of Surgery, vol. 394, no. 6, pp. 1085-1092, 2009.
 
[26]  Geelkerken RH, van Bockel JH, de Roos WK, Hermans J. Coeliac artery compression syndrome: the effect of decompression. Br J Surg; 77:807.1990.
 
[27]  Balaban DH, Chen J, Lin Z, Tribble CG, McCallum RW.Median arcuate ligament syndrome: a possible cause of idiopathic gastroparesis. Am J Gastroenterol; 92(3):519-23.1997.
 
[28]  Carey JP, Stemmer EA, Connolly JE. Median arcuate ligament syndrome. Experimental and clinical observations. Arch Surg. 99(4):441-446, 1969.
 
[29]  Ward, E. M.; Rorie, D.K.; Nauss, L. A. &Bahn, R.C. The celiac ganglia in man: normal anatomic Variations. Anesth.Analg., 58:461-5, 1979.
 
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Article

Heart Failure in Women: A Disease with Peculiar Pathophysiological Mechanisms and Clinical Presentation

1Section of Cardiology, Dept. of Medicine, University of Verona, Verona, Italy


American Journal of Cardiovascular Disease Research. 2013, 1(1), 1-6
DOI: 10.12691/ajcdr-1-1-1
Copyright © 2013 Science and Education Publishing

Cite this paper:
Giulia D’Agostini, Mariantonietta Cicoira, Corrado Vassanelli. Heart Failure in Women: A Disease with Peculiar Pathophysiological Mechanisms and Clinical Presentation. American Journal of Cardiovascular Disease Research. 2013; 1(1):1-6. doi: 10.12691/ajcdr-1-1-1.

Correspondence to: Giulia D’Agostini, Section of Cardiology, Dept. of Medicine, University of Verona, Verona, Italy. Email: dagostini.giu@gmail.com

Abstract

Heart Failure (HF) is a disease whose prevalence is increasing in developed countries, involving up to 10% of the older population; the increase is due both to better therapy and to the aging population. Fifty percent (50%) of these patients are women, most of them presenting with preserved systolic function and diastolic dysfunction. Female patients show different etiology to males; they present several comorbidities and at an older age. Despite this, women appear to have a lower mortality risk, and female gender is an independent prognostic factor for better survival. An explanation for this different presentation and prognosis may be different ventricular remodeling in response to pressure burden on the left ventricle, leading to completely different left ventricular geometry and compliance mechanisms. These differences are not only detectable at macroscopic examinations but also appear in microscopic gene and molecular expression, with a reduction in apoptosis during lifetime and a lower myocyte volume. Although all these mechanisms have a protective role in chronic HF, different remodeling in women leads to a weak balance in the acute setting, with an imbalance between compensatory mechanisms and higher cardiac output requirements. This impairment goes along with the loss of “female gender advantage” after hospitalization. Despite the peculiar presentation of HF in women, there is little evidence about therapy in this setting, due to under-representation of women in clinical trials and the absence of sex-specific, prospective randomized trials.

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References

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[[1]  McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Böhm M, Dickstein K, Falk V, Filippatos G, Fonseca C, Gomez-Sanchez MA, Jaarsma T, Køber L, Lip GY, Maggioni AP, Parkhomenko A, Pieske BM, Popescu BA, Rønnevik PK, Rutten FH, Schwitter J, Seferovic P, Stepinska J, Trindade PT, Voors AA, Zannad F, Zeiher A; ESC Committee for Practice Guidelines, “ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC” EHJ, 33. 1787-1847. 2012.
 
[[2]  Rosamond W, Flegal K, Furie K, Go A, Greenlund K, Haase N, Hailpern SM, Ho M, Howard V, Kissela B, Kittner S, Lloyd-Jones D, McDermott M, Meigs J, Moy C, Nichol G, O'Donnell C, Roger V, Sorlie P, Steinberger J, Thom T, Wilson M, Hong Y; American Heart Association Statistics Committee and Stroke Statistics Subcommittee, ”Heart Disease and Stroke Statistics-2008 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee” Circulation, 117. e25-146. Jan.2008.
 
[[3]  Galvao M, Kalman J, DeMarco T, Fonarow GC, Galvin C, Ghali JK, Moskowitz RM, “Gender differences in in-hospital management and outcomes in patients with decompensated heart failure: analysis from the Acute Decompensated Heart Failure National Registry (ADHERE)” J Card Fail, 12. 100-7. Mar.2006.
 
[[4]  Roger VL, Weston SA, Redfield MM, Hellermann-Homan JP, Killian J, Yawn BP, Jacobsen SJ. “Trends in heart failure incidence and survival in a community-based population”, JAMA, 292. 344-50. Jul. 2004.
 
[[5]  Blauwet LA, Hayes SN, McManus D, Redberg RF, Walsh MN, “Low rate of sex-specific result reporting in cardiovascular trials”, Mayo Clin Proc., 82. 166-70. Feb. 2007.
 
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[6]  Luczak ED, Leinwand LA, “Sex-based cardiac physiology,” Annu Rev Physiol., 71. 1-18. 2009.
 
[7]  Konhilas JP, Leinwand LA, “The effects of biological sex and diet on the development of heart failure,” Circulation, 116. 2747-59. Dec. 2007.
 
[8]  O'Meara E, Clayton T, McEntegart MB, McMurray JJ, Piña IL, Granger CB, Ostergren J, Michelson EL, Solomon SD, Pocock S, Yusuf S, Swedberg K, Pfeffer MA; CHARM Investigators, “Sex differences in clinical characteristics and prognosis in a broad spectrum of patients with heart failure: results of the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) program,” Circulation, 115. 3111-20. 2007.
 
[9]  Kannel WB, “Incidence and epidemiology of heart failure,” Heart Fail Rev., 5. 167-73. 2005.
 
[10]  Martínez-Sellés M, Doughty RN, Poppe K, Whalley GA, Earle N, Tribouilloy C, McMurray JJ, Swedberg K, Køber L, Berry C, Squire I; Meta-Analysis Global Group In Chronic Heart Failure (MAGGIC), “Gender and survival in patients with heart failure: interactions with diabetes and aetiology. Results from the MAGGIC individual patient meta-analysis,” Eur J Heart Fail., 14. 473-9. May.2012.
 
[11]  Cleland JG, Swedberg K, Follath F, et al, “The EuroHeart Failure survey programme-a survey on the quality of care among patients with heart failure in Europe. Part 1: characteristics and diagnosis,“ Eur Heart J, 24. 442-63. 2003.
 
[12]  Shafazand M, Schaufelberger M, Lappas G, Swedberg K, Rosengren A., “Survival trends in men and women with heart failure of ischaemic and non-ischaemic origin: data for the period 1987– 2003 from the Swedish Hospital Discharge Registry,” I Eur Heart J., 30. 671-678. 2009.
 
[13]  Iribarren C, Karter AJ, Go AS, Ferrara A, Liu JY, Sidney S, Selby JV, “Glycemic control and heart failure among adult patients with diabetes,” Circulation, 103. 2668-2673. 2001
 
[14]  Redberg R, Schiller N., “Gender and valvular surgery,” J Thorac Cardiovasc Surg., 127. 1-3. 2004.
 
[15]  Kenchaiah S, Evans JC, Levy D, Wilson PW, Benjamin EJ, Larson MG, Kannel WB, Vasan RS et al., “Obesity and the risk of heart failure,” N Engl J Med., 347. 305-313. 2002.
 
[16]  Cesare Russo, Zhezhen Jin, Vittorio Palmieri, Shunichi Homma, Tatjana Rundek, Mitchell S.V. Elkind, Ralph L. Sacco and Marco R. Di Tullio, “Arterial Stiffness and Wave Reflection : Sex Differences and Relationship With Left Ventricular Diastolic Function,” Hypertension, 60. 362-368. 2012.
 
[17]  Ginghină C, Botezatu CD, Șerban M, Jurcuț R, “A personalized medicine target: heart failure in women” Journal of Medicine and Life, 4. 280‐286. 2011.
 
[18]  Nanchen D, Gussekloo J, Westendorp RG, Stott DJ, Jukema JW, Trompet S, Ford I, Welsh P, Sattar N, Macfarlane PW, Mooijaart SP, Rodondi N, de Craen AJ; PROSPER Group, “Subclinical thyroid dysfunction and the risk of heart failure in older persons at high cardiovascular risk,” J Clin Endocrinol Metab, 97. 852-61. 2012.
 
[19]  Lam CS, Carson PE, Anand IS, Rector TS, Kuskowski M, Komajda M, McKelvie RS, McMurray JJ, Zile MR, Massie BM, Kitzman DW, “Sex differences in clinical characteristics and outcomes in elderly patients with heart failure and preserved ejection fraction: the Irbesartan in Heart Failure with Preserved Ejection Fraction (I-PRESERVE) trial,” Circ Heart Fail.5. 571-8. 2012.
 
[20]  Cil H, Bulur S, Türker Y, Kaya A, Alemdar R, Karabacak A, Aslantaş Y, Ekinözü I, Albayrak S, Ozhan H; MELEN Investigators, “Impact of body mass index on left ventricular diastolic dysfunction,” Echocardiography, 29. 647-51. 2012.
 
[21]  Mohammed SF, Borlaug BA, Roger VL, Mirzoyev SA, Rodeheffer RJ, Chirinos JA, Redfield MM, “Comorbidity and ventricular and vascular structure and function in heart failure with preserved ejection fraction: a community-based study,” Circ Heart Fail. 5(6).710-9. Nov. 2012.
 
[22]  Brouwers FP, Hillege HL, van Gilst WH, van Veldhuisen DJ, “Comparing new onset heart failure with reduced ejection fraction and new onset heart failure with preserved ejection fraction: an epidemiologic perspective,” Curr Heart Fail Rep., 9.363-8. 2012.
 
[23]  Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ, “Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factorbased approach: the Euro Heart Survey on atrial fibrillation,” Chest, 137. 263-272. 2010.
 
[24]  Adams KF, Sueta CA, Gheorghiade M, O’Connor CM, Schwartz TA, Koch GG, Uretsky B, Swedberg K, McKenna W, Soler-Soler J, Califf RM, “Gender differences in survival in advanced heart failure: insights from the FIRST study” Circulation, 99. 1816-1821. 1999.
 
[25]  Simon T, Mary-Krause M, Funck-Brentano C, Jaillon P, “Sex differences in the prognosis of congestive heart failure: results from the Cardiac Insufficiency Bisoprolol Study (CIBIS II)” Circulation, 103. 375-380. 2001.
 
[26]  Liao Y, Cooper RS, Mensah GA, McGee DL, “Left ventricular hypertrophy has a greater impact on survival in women than in men,” Circulation, 92. 805-10. 1995.
 
[27]  Krumholz HM, Larson M, Levy D, “Sex differences in cardiac adaptation to isolated systolic hypertension,” Am J Cardiol, 72. 310-3. 1993.
 
[28]  Kostkiewicz M, Tracz W, Olszowska M, Podolec P, Drop D, “Left ventricular geometry and function in patients with aortic stenosis: gender differences,” Int J Cardiol, 71. 57-61. 1999.
 
[29]  Pfeffer JM, Pfeffer MA, Fletcher P, Fishbein MC, Braunwald E, “Favorable effects of therapy on cardiac performance in spontaneously hypertensive rats,” Am J Physiol, 242. H776-84. 1982.
 
[30]  Weinberg EO, Thienelt CD, Katz SE, et al, “Gender differences in molecular remodeling in pressure overload hypertrophy,” J Am Coll Cardiol, 34. 264-73. 1999.
 
[31]  Scheuer J, Malhotra A, Schaible TF, et al, “Effects of gonadectomy and hormonal replacement on rat hearts,” Circ Res, 61. 12-9. 1987.
 
[32]  Levin ER, “Cell localization, physiology, and nongenomic actions of oestrogen receptors,” J Appl Physiol, 91. 1860-7. 2001.
 
[33]  Novotny JL, Simpson AM, Tomicek NJ, et al., “Rapid oestrogen receptor- activation improves ischemic tolerance in aged female rats through a novel protein kinase C_-dependent mechanism,” Endocrinology, 150. 889-96. 2009.
 
[34]  Williams JK, Adams MR, Herrington DM, Clarkson TB, “Short-term administration of oestrogen and vascular responses of atherosclerotic coronary arteries,” J Am Coll Cardiol, 20. 452-7. 1992.
 
[35]  Higashi Y, Sanada M, Sasaki S, et al, “Effect of oestrogen replacement therapy on endothelial function in peripheral resistance arteries in normotensive and hypertensive postmenopausal women,” Hypertension, 37. 651-7. 2001.
 
[36]  Grohe C, Kahlert S, Lobbert K, et al, “Cardiac myocytes and fibroblasts contain functional oestrogen receptors,” FEBS Lett, 416. 107-12. 1997.
 
[37]  Camper-Kirby D, Welch S, Walker A, et al, “Myocardial Akt activation and gender: increased nuclear activity in females versus males,” Circ Res, 88. 1020-7. 2001.
 
[38]  Sugden PH, Clerk A., “Akt like a women: gender differences in susceptibility to cardiovascular disease,” Circ Res, 88. 975-7. 2001.
 
[39]  Brunet A, Bonni A, Zigmond MJ, et al., “Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor,” Cell, 96. 857-68. 1999.
 
[40]  Zha J, Harada H, Yang E, et al, “Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X,” Cell, 87. 619-28. 1996.
 
[41]  Vanhaesebroeck B, Alessi DR, “The PI3K-PDK1 connection: more than just a road to pkb,” Biochem J, 346. 561-76. 2000.
 
[42]  Zhai P, Eurell TE, Cotthaus R, et al, “Effect of estrogen on global myocardial ischemia-reperfusion injury in female rats,” Am J Physiol Heart Circ Physiol, 279. H2766-75. 2000.
 
[43]  Richards RG, DiAugustine RP, Petrusz P, Clark GC, Sebastian J., “Estradiol stimulates tyrosine phosphorylation of the insulin-like growth factor-1 receptor and insulin receptor substrate-1 in the uterus,” Proc Natl Acad Sci USA, 93. 12002-7. 1996.
 
[44]  Wang L, Ma W, Markovich R, Lee WL, Wang PH, “Insulin-like growth factor I modulates induction of apoptotic signaling in H9C2 cardiac muscle cells,” Endocrinology, 139. 1354-60. 1998.
 
[45]  Huang A, Sun D, Koller A, Kaley G, “Gender difference in myogenic tone of rat arterioles is due to estrogen-induced, enhanced release of NO,” Am J Physiol, 272.H1804-9. 1997.
 
[46]  Olivetti G, Giordano G, Corradi D, et al, “Gender differences and aging:effects on the human heart,” J Am Coll Cardiol, 26. 1068-79. 1995.
 
[47]  Mallat Z, Fornes P, Costagliola R, et al., “Age and gender effects on cardiomyocyte apoptosis in the normal human heart,” J Gerontol A Biol Sci Med Sci, 2001; 56: M719-23.
 
[48]  Biondi-Zoccai GG, Abbate A, Bussani R, et al., “Reduced postinfarction myocardial apoptosis in women: a clue to their different clinical course? “ Heart, 91. 99-101. 2005.
 
[49]  Guerra S, Leri A, Wang X, et al, “Myocyte death in the failing human heart is gender dependent,” Circ Res, 85. 856-66. 1999.
 
[50]  Cavasin MA, Tao Z, Menon S, Yang XP, “Gender differences in cardiac function during early remodeling after acute myocardial infarction in mice,” Life Sci, 75. 2181-92. 2004.
 
[51]  Wong SC, Sleeper LA, Monrad ES, et al, “Absence of gender differences in clinical outcomes in patients with cardiogenic shock complicating acute myocardial infarction. A report from the SHOCK trial registry,” J Am Coll Cardiol, 38. 1395-401. 2001.
 
[52]  Shah AN, Mentz RJ, Gheorghiade M, Kwasny MJ, Fought AJ, Zannad F, Swedberg K, Maggioni AP, Konstam MA, “Gender Does Not Affect Postdischarge Outcomes in Patients Hospitalized for Worsening Heart Failure With Reduced Ejection Fraction (from the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study With Tolvaptan [EVEREST] Trial),” Am J Cardiol., 110. 1803-8. 2012.
 
[53]  Jong P, Vowinckel E, Liu PP, Gong Y, Tu JV, “Prognosis and determinants of survival in patients newly hospitalized for heart failure: a population-based study,” Arch Intern Med., 162. 1689-94. 2002.
 
[54]  Charlson ME, Pompei P, Ales KL, MacKenzie CR., “A new method of classifying prognostic comorbidity in longitudinal studies: development and validation,” J Chronic Dis., 40(5). 373-83. 1987.
 
[55]  Niall G. Mahon, MD, Eugene H. Blackstone, MD, FACC, Gary S. Francis, MD, FACC, Randall C. Starling III, MD, FACC, James B. Young, MD, FACC, Michael S. Lauer, MD, FACC, ”The Prognostic Value of Estimated Creatinine Clearance Alongside Functional Capacity in Ambulatory Patients With Chronic Congestive Heart Failure,” J Am Coll Cardiol, 40. 1106-13. 2002.
 
[56]  Anju Nohria, MD, Vic Hasselblad, PHD, Amanda Stebbins, PHD, Daniel F. Pauly, MD, PHD, Gregg C. Fonarow, MD, Monica Shah, MD, Clyde W. Yancy, MD, Robert M. Califf, MD, Lynne W. Stevenson, MD, James A. Hill, MD, “ Cardiorenal Interactions. Insights From the ESCAPE Trial,” J Am Coll Cardiol 51. 1268-74. 2008.
 
[57]  Eileen M. Hsich, MD, Ileana L. Piña, MD, “Heart Failure in Women. A Need for Prospective Data,” J Am Coll Cardiol, 54. 491-8. 2009.
 
[58]  The CONSENSUS Trial Study Group, “Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS),” N Engl J Med, 316.1429-1435. 1987.
 
[59]  The SOLVD Investigators, “Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions,” N Engl J Med 327. 685-691. 1992.
 
[60]  Packer M, Poole-Wilson PA, Armstrong PW, Cleland JG, Horowitz JD, Massie BM, Ryden L, Thygesen K, Uretsky BF, “Comparative effects of low and high doses of the angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure. ATLAS Study Group,” Circulation, 100. 2312-2318. 1999.
 
[61]  Milton Packer, MD; Michael B. Fowler, MD; Ellen B. Roecker, PhD; Andrew J.S. Coats, MD; Hugo A. Katus, MD; Henry Krum, MB, BS, PhD; Paul Mohacsi, MD; Jean L. Rouleau, MD; Michal Tendera, MD; Christoph Staiger, MD; Terry L. Holcslaw, PhD; Ildiko Amann-Zalan, MD; David L. DeMets, PhD; for the Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS) Study Group, “Effect of carvedilol on the morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized cumulative survival (COPERNICUS) study,” Circulation, 106. 2194-2199. 2002.
 
[62]  MERIT-HF Study Group, “Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF),” Lancet, 353. 2001-2007. 1999.
 
[63]  CIBIS-II Study Group, “The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial,” Lancet, 353. 9-13. 1999.
 
[64]  Dobre D, van Veldhuisen DJ, Mordenti G, Vintila M, Haaijer-Ruskamp FM, Coats AJ, Poole-Wilson PA, Flather MD; SENIORS Investigators, “Tolerability and dose-related effects of nebivolol in elderly patients with heart failure: data from the Study of the Effects of Nebivolol Intervention on Outcomes and Rehospitalisation in Seniors with Heart Failure (SENIORS) trial,” Am Heart J, 154. 109-15. 2007.
 
[65]  Anderson JL, Krause-Steinrauf H, Goldman S, Clemson BS, Domanski MJ, Hager WD, Murray DR, Mann DL, Massie BM, McNamara DM, Oren R, Rogers WJ; Beta-Blocker Evaluation of Survival Trial (BEST) Investigators, “Failure of Benefit and Early Hazard of Bucindolol for Class IV Heart Failure,” J Card Fail, 9. 266-77. 2003.
 
[66]  Poole-Wilson PA, Swedberg K, Cleland JG, Di Lenarda A, Hanrath P, Komajda M, Lubsen J, Lutiger B, Metra M, Remme WJ, Torp-Pedersen C, Scherhag A, Skene A; Carvedilol Or Metoprolol European Trial Investigators, “Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET): randomised controlled trial,” Lancet, 362. 7-13. 2003.
 
[67]  Faiez Zannad, M.D., Ph.D., John J.V. McMurray, M.D., Henry Krum, M.B., Ph.D., Dirk J. van Veldhuisen, M.D., Ph.D., Karl Swedberg, M.D., Ph.D., Harry Shi, M.S., John Vincent, M.B., Ph.D., Stuart J. Pocock, Ph.D., and Bertram Pitt, M.D., for the EMPHASIS-HF Study Group, ”Eplerenone in Patients with Systolic Heart Failure and Mild Symptoms,” N Engl J Med, 364. 11-21. 2011.
 
[68]  Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A, Palensky J, Wittes J, “The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators,” N Engl J Med, 341. 709-17. 1999.
 
[69]  Pitt B, Williams G, Remme W, Martinez F, Lopez-Sendon J, Zannad F, Neaton J, Roniker B, Hurley S, Burns D, Bittman R, Kleiman J, “The EPHESUS trial: eplerenone in patients with heart failure due to systolic dysfunction complicating acute myocardial infarction. Eplerenone Post-AMI Heart Failure Efficacy and Survival Study,” Cardiovasc Drugs Ther, 15(1). 79-87. Jan. 2001.
 
[70]  Cohn JN, Tognoni G, Glazer R, Spormann D., “Baseline demographics of the Valsartan Heart Failure Trial. Val-HeFT Investigators,” Eur J Heart Fail, 2. 439-46. 2000.
 
[71]  McMurray JJ, Ostergren J, Swedberg K, Granger CB, Held P, Michelson EL, Olofsson B, Yusuf S, Pfeffer MA, “Effects of candesartan in patients with chronic heart failure and reduced left-ventricular systolic function taking angiotensin-converting-enzyme inhibitors: the CHARM-Added trial,” Lancet, 362. 767-771. 2003.
 
[72]  Bertram Pitt, Philip A Poole-Wilson, Robert Segal, Felipe A Martinez, Kenneth Dickstein, A John Camm, Marvin A Konstam, Günter Riegger, George H Klinger, James Neaton, Divakar Sharma, Balasamy Thiyagarajan,on behalf of the ELITE II investigators, “Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure: randomised trial-the Losartan Heart Failure Survival Study ELITE II,” Lancet 355. 1582-87. 2000.
 
[73]  Konstam MA, Neaton JD, Dickstein K, Drexler H, Komajda M, Martinez FA, Riegger GA, Malbecq W, Smith RD, Guptha S, Poole-Wilson PA, “Effects of highdose versus low-dose losartan on clinical outcomes in patients with heart failure (HEAAL study): a randomised, double-blind trial,” Lancet, 374. 1840-1848. 2009.
 
[74]  Velazquez EJ, Pfeffer MA, McMurray JV, Maggioni AP, Rouleau JL, Van de Werf F, Kober L, White HD, Swedberg K, Leimberger JD, Gallo P, Sellers MA, Edwards S, Henis M, Califf RM; VALIANT Investigators, “VALsartan In Acute myocardial iNfarcTion (VALIANT) trial: baseline characteristics in context,” Eur J Heart Fail, 5. 537-44. 2003.
 
[75]  Dickstein K, Kjekshus J; OPTIMAAL Trial Steering Committee and Investigators, “Optimal Trial in Myocardial Infarction with the Angiotensin II Antagonist Losartan. Comparison of baseline data, initial course, and management: losartan versus captopril following acute myocardial infarction (The OPTIMAAL Trial). OPTIMAAL Trial Steering Committee and Investigators. Optimal Trial in Myocardial Infarction with the Angiotensin II Antagonist Losartan,” Am J Cardiol, 87. 766-71. 2001.
 
[76]  Swedberg K, Komajda M, Bohm M, Borer JS, Ford I, Dubost-Brama A, Lerebours G, Tavazzi L, “Ivabradine and outcomes in chronic heart failure (SHIFT): a randomised placebo-controlled study,” Lancet, 376. 875-88. 2010.
 
[77]  Fox K, Ford I, Steg PG, Tendera M, Ferrari R; BEAUTIFUL Investigators, “Ivabradine for patients with stable coronary artery disease and left-ventricular systolic dysfunction (BEAUTIFUL): a randomised, double-blind, placebo-controlled trial,” Lancet, 372(9641). 807-16. Sep. 2008.
 
[78]  Daubert JP, Zareba W, Hall WJ, Schuger C, Corsello A, Leon AR, Andrews ML, McNitt S, Huang DT, Moss AJ; MADIT II Study Investigators, ”Predictive value of ventricular arrhythmia inducibility for subsequent ventricular tachycardia or ventricular fibrillation in Multicenter Automatic Defibrillator Implantation Trial (MADIT) II patients,” J Am Coll Cardiol, 47. 98-107. 2006.
 
[79]  Mark DB, Nelson CL, Anstrom KJ, Al-Khatib SM, Tsiatis AA, Cowper PA, Clapp-Channing NE, Davidson-Ray L, Poole JE, Johnson G, Anderson J, Lee KL, Bardy GH; SCD-HeFT Investigators, “Cost-effectiveness of defibrillator therapy or amiodarone in chronic stable heart failure: results from the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT),” Circulation, 114. 135-42. 2006.
 
[80]  Feldman AM, de Lissovoy G, Bristow MR, Saxon LA, De Marco T, Kass DA, Boehmer J, Singh S, Whellan DJ, Carson P, Boscoe A, Baker TM, Gunderman MR., “Cost effectiveness of cardiac resynchronization therapy in the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) trial,” J Am Coll Cardiol, 46. 2311-21. 2005.
 
[81]  Calvert MJ, Freemantle N, Yao G, Cleland JG, Billingham L, Daubert JC, Bryan S; CARE-HF investigators, “Cost-effectiveness of cardiac resynchronization therapy: results from the CARE-HF trial,” Eur Heart J, 26. 2681-8. 2005.
 
[82]  Blauwet LA, Hayes SN, McManus D, Redberg RF, Walsh MN, “Low rate of sex-specific result reporting in cardiovascular trials,” Mayo Clin Proc, 82. 166-70. 2007.
 
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