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American Journal of Cardiovascular Disease Research

ISSN (Print): ISSN Pending

ISSN (Online): ISSN Pending

Editor-in-Chief: Dario Galante




“Requiring Intravenous Nitroglycerin” Should be considered a High Risk Feature in Patients with Non-ST Elevation Myocardial Infarction and Unstable Angina

1Department of Medicine, Harlem Hospital Center in affiliation with Columbia University Medical Center New York, NY 10037

2Division of Cardiology, Department of Medicine, Harlem Hospital Center in affiliation with Columbia University Medical Center New York, NY 10037

American Journal of Cardiovascular Disease Research. 2015, 3(1), 9-12
doi: 10.12691/ajcdr-3-1-3
Copyright © 2015 Science and Education Publishing

Cite this paper:
Olusegun Sheyin, Melissa Fajardo, Oladapo Igandan, Bredy Pierre-Louis. “Requiring Intravenous Nitroglycerin” Should be considered a High Risk Feature in Patients with Non-ST Elevation Myocardial Infarction and Unstable Angina. American Journal of Cardiovascular Disease Research. 2015; 3(1):9-12. doi: 10.12691/ajcdr-3-1-3.

Correspondence to: Olusegun  Sheyin, Department of Medicine, Harlem Hospital Center in affiliation with Columbia University Medical Center New York, NY 10037. Email:


Introduction: Early risk stratification of patients with unstable angina (UA) and non-ST elevation myocardial infarction (NSTEMI) is crucial to identify those at high risk for further cardiac events as they may benefit from an early invasive strategy of coronary angiography and revascularization. The TIMI score, a widely used predictive model to guide management strategy in UA and NSTEMI may not accurately stratify risk. Case description: A 63-year-old man, who is an active smoker with past medical history of hypertension and dyslipidemia, presented with severe sub-sternal, crushing chest pain, which began four hours prior to presentation. His EKG revealed sinus tachycardia, without ST segment deviations or Q waves. He received aspirin, three doses of sublingual nitroglycerin and metoprolol, but continued to have chest pain, thus he was commenced on intravenous nitroglycerin infusion. His chest pain went away after two hours on nitroglycerin infusion. His initial serum troponin I was 0.31 ng/mL and 3.60 ng/mL four hours after presentation. He was admitted for NSTEMI and started on clopidogrel, atorvastatin and intravenous heparin. Echocardiogram revealed inferio-septal wall a kinesis and severely reduced left ventricular systolic function. His troponin I continued to rise, peaking at 37.4 ng/mL. He was started on eptifibatide and was referred for coronary angiography and percutaneous coronary intervention, with finding of fifty percent proximal and distal left anterior descending artery (LAD) lesions. Discussion: With a TIMI score of 2, our patient was classified as low risk at presentation. The need for intravenous nitroglycerin infusion for continuing chest pain in the management of UA or NSTEMI may suggest a greater degree of myocardial ischemia and a higher risk for adverse cardiovascular outcomes. This case demonstrates that UA and NSTEMI patients requiring intravenous nitroglycerin initially planned for conservative therapeutic approach need continuous risk stratification which may dictate a change to the invasive management strategy.



[1]  Rojer V, Go A, Lloyd-Jones D, et al. Heart Disease and Stroke Statistics--2012 Update: A Report From the American Heart Association. Circulation. 2012; 125: e2-e220.
[2]  Amsterdam EA, Wenger NK, Brindis RG, Casey Jr DE, Ganiats TG, Holmes Jr DR, Jaffe AS, Jneid H, Kelly RF, Kontos MC, Levine GN, Liebson PR, Mukherjee D, Peterson ED, Sabatine MS, Smalling RW, Zieman SJ, 2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary Syndromes, Journal of the American College of Cardiology (2014).
[3]  Bertrand ME, Simoons ML, Fox KA, et al. Management of acute coronary syndromes: acute coronary syndromes without persistent ST segment elevation; recommendations of the Task Force of the European Society of Cardiology. Eur Heart J 2000; 21:1406.
[4]  Mehta SR, Cannon CP, Fox KA, et al. Routine vs selective invasive strategies in patients with acute coronary syndromes: a collaborative meta-analysis of randomized trials. JAMA 2005; 293: 2908.
[5]  Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA 2000; 284: 835.
Show More References
[6]  Aragam K, Tamhane U, Kline-Rogers E, Li J, Fox K, Goodman S,Eagle K, Gurm H. Does Simplicity Compromise Accuracy in ACS Risk Prediction? A Retrospective Analysis of the TIMI and GRACE Risk Scores. PLoS One. 2009 Nov 23; 4 (11): e7947.
[7]  Borzak S, Cannon CP, Kraft PL, et al. Effects of prior aspirin and anti-ischemic therapy on outcome of patients with unstable angina. TIMI 7 Investigators. Thrombin Inhibition in Myocardial Ischemia. Am J Cardiol 1998; 81:678
[8]  Granger CB, Goldberg RJ, Dabbous O, Pieper KS, Eagle KA, Cannon CP, Van de Werf F, Avezum A, Goodman SG, Flather MD, Fox KAA, for the Global Registry of Acute Coronary Events Investigators. Predictors of hospital mortality in the Global Registry of Acute Coronary Events. Arch Intern Med 2003; 163: 2345-53.
[9]  Boersma E, Pieper KS, Steyerberg EW, et al. Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation: results from an international trial of 9461 patients. The PURSUIT Investigators. Circulation. 2000; 101: 2557-2567.
[10]  Cannon CP, Weintraub WS, Demopoulos LA, Vicari R, Frey MJ, Lakkis N, Neumann FJ, Robertson DH, DeLucca PT, Di Battiste PM, Gibson CM, Braunwald E; TACTICS (Treat Angina with Aggrastat and Determine Cost of Therapy with an Invasive or Conservative Strategy)-Thrombolysis in Myocardial Infarction 18 Investigators. Comparison of early invasive and conservative strategies inpatients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med. 2001 Jun 21; 344 (25): 1879-87.
Show Less References


The Metabolic Syndrome in Offspring of Women with a Family History of Early Onset Type 2 Diabetes Mellitus Who Developed Gestational Diabetes Mellitus

1Department of Basic Medical Sciences, Faculty of Medical Sciences, University of the West Indies, Mona, Jamaica

American Journal of Cardiovascular Disease Research. 2016, 4(1), 1-6
doi: 10.12691/ajcdr-4-1-1
Copyright © 2016 Science and Education Publishing

Cite this paper:
R Irving. The Metabolic Syndrome in Offspring of Women with a Family History of Early Onset Type 2 Diabetes Mellitus Who Developed Gestational Diabetes Mellitus. American Journal of Cardiovascular Disease Research. 2016; 4(1):1-6. doi: 10.12691/ajcdr-4-1-1.

Correspondence to: R  Irving, Department of Basic Medical Sciences, Faculty of Medical Sciences, University of the West Indies, Mona, Jamaica. Email:


Objective: To evaluate for the metabolic syndrome (MS) in offspring of women with family history of early onset type 2 diabetes mellitus (T2DM) who developed gestational diabetes mellitus (GDM) using as controls offspring of women with no family history of diabetes and normal glucose tolerance (NGT). Methods: Anthropometric and biochemical measurements were evaluated for 30 offspring age 10-16 years of women with family history of early onset T2DM who developed GDM. Obstetrical records of these mothers were also noted. Thirty offspring of women (30) with NGT and no family history of diabetes served as controls. Measurements included: Total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), fasting and postprandial glucose, insulin, waist circumference, weight and height. For analyses, MS was defined as ≥3 of 4 features: glucose intolerance, dyslipidemia, obesity and hypertension in the childhood/adolescence criteria as recommended by the National Cholesterol Education Program Adult Treatment Panel Third (NCEP-ATP III) modified standard. Cox regression analysis was used to determine the independent hazard (risk) of developing MS attributable to GDM with a family history of early onset T2DM. Results: Offspring of women with GDM and family history of early onset T2DM had significantly more (≥ 2, p<0.05) features of MS than offspring of women with NGT and no family history of diabetes. Thirty percent (30.0%), 29.5% and 39.0% of the offspring of these GDM women had glucose intolerance, obesity and dyslipidemia respectively. These offspring had a hazard of 3.33 (95% CI: 2.12-9.15) of having MS compared to offspring of women with NGT and no family history of diabetes. Conclusion: Offspring of women with GDM and family history of early onset T2DM are at increased risk for MS.



[1]  Metzger B.E., Coustan D.R (Eds.): Proceedings of the Fourth International Work-shop-Conference on gestational diabetes mellitus. Diabetes Care (1998), 21 (2): B1–B167.
[2]  Lawlor D.A., Relton C., Sattar N., Nelson S.M. Maternal adiposity—a determinant of perinatal and offspring outcomes? Nat Rev Endocrinol (2012), 8:679-88.
[3]  Sridhar S.B., Ferrara A., Ehrlich S.F., Brown S.D., Hedderson M. M. Risk of large-for-gestational-age newborns in women with gestational diabetes by race and ethnicity and body mass index categories. Obstet Gynecol (2013), 121:1255-62.
[4]  Barrett H., Nitert M., McIntyre D.,Callaway L. Disturbances of lipoprotein metabolism with hypercholesterolemia have been reported in offspring of GDM pregnancies. Diabetes Care (2014), 37(5):1484-1493.
[5]  Friedemann C., Heneghan C., Mahtani K., Thompson M., Perera R., Ward A.M. Cardiovascular disease risk in healthy children and its association with body mass index: systematic review and meta-analysis. BMJ (2012), 345:e4759.
Show More References
[6]  West N.A., Crume T.L., Maligie M.A., Dabelea D. Cardiovascular risk factors in children exposed to maternal diabetes in utero. Diabetologia (2011), 54(3):504-7.
[7]  Ghosh A., Liu T., Khoury MJ., Valdez R. Family history of diabetes and prevalence of the metabolic syndrome in U. S. adults without diabetes: 6-year results from the National Health and Nutrition Examination Survey (1999-2004). Public Health Genomics (2010),13:353-9.
[8]  Eisenmann J.C., Welk G.J., Wickel E.E., Blair S.N. Stability of variables associated with the metabolic syndrome from adolescence to adulthood: the Aerobics center longitudinal study. Am J Hum Biol. (2004), 16(6):690-96.
[9]  International Diabetes Federation [IDF]. IDF definition of metabolic syndrome in children and adolescents [updated 2013 Feb; cited 2015 Nov 12]. Available from:
[10]  Cook S., Weitzman M., Auinger P., Nguyen M., Dietz W.H., et al. Prevalence of a metabolic syndrome phenotype in adolescents: findings from NHANES-III, 1988-1994. Arch Pediatr Adolesc Med. (2003), 157:821-7.
[11]  de Ferranti S., Gauvreau K., Ludwig D., Neufeld E.J., Newburger J.W., Rifai N. Prevalence of the metabolic syndrome in American adolescents. Circulation (2004), 110:2494-7.
[12]  Das M., Pal S., Ghosh A. Family history of type 2 diabetes and prevalence of metabolic syndrome in adult Asian Indians. J Cardiovasc Dis Res. (2012), 3(2):104-108
[13]  Doria A., Yang Y., Malecki M. Phenotypic characteristics of early-onset autosomal-dominant type 2 diabetes unlinked to known maturity-onset diabetes on the young (MODY) genes. Diabetes Care (1999), 229(2): 253-26.
[14]  James J., Irving R., Choo-Kang E., Wright-Pascoe R., McLaughlin W., Mullings A., Gabay L., Kulkarni S. Multigenerational inheritance and clinical characteristics of three large pedigrees with early onset type 2 diabetes in Jamaica. Pan Am J Public Health (2010), 27(6):435-441.
[15]  Matthews D.R., Hosker J.P., Rudenski A.S., Naylor B.A., Treacher D.F., Turner R.C. Homeostasis Model Assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia (1985), 28(7):412-419.
[16]  Centers for Disease Control [CDC]. Clinical growth charts. Available at:,retreived on 1/12/2016.
[17]  National Heart Lung and Blood Institute (NHLBI). Available at:, retrieved on 12/14/2015.
[18]  Landon M., Rice M.M., Yarner M., Casey B., Reddy U., Wapner R., et al. Mild Gestational Diabetes Mellitus and Long-Term Child Health. Diabetes Care (2014).
[19]  Kaplan N.M. The deadly quartet. Upper-body obesity, glucose intolerance, hypertriglyceridemia, and hypertension. Arch Intern Med (1989), 149(7):1514-20.
[20]  Tracy R.E., Newman W.P., Wattigney W.A., Srinivasan S.R., Strong J.P., Berenson G.S. Histologic features of atherosclerosis and hypertension from autopsies of young individuals in a defined geographic population: the Bogalusa Heart Study. Atherosclerosis (1995), 116:163-79.
[21]  Napoli C., D’Armiento F.P., Mancini F.P., Postiglione A.,Witzhum J.L., Palumbo G .,et al. Fatty streak formation occurs in human fetal aortas and is greatly enhanced by maternal hypercholestemia. Intimal accumulation of low density lipoprotein and its oxidation precede monocyte recruitment into early atherosclerotic lesions. Journal of Clinical Investigation (1997), 100(11): 2680-90.
[22]  Yuan G., AL-Shaki KZ., Hegele R. Hypertriglyceridemia: Its etiology, effects and treatment. CMAJ (2007), 176(8):1113-1120.
[23]  Dalleck L.C., Kjelland E.M. The prevalence of metabolic syndrome and metabolic syndrome risk factors in college-aged students. Am J Health Promot. (2012), 27(1): 37-42.
[24]  Uckun-Kitapci., Firat S., Sipahi T., Barrier R., Edwards L.J., Calikoglu A.S. Obesity and type 2 diabetes mellitus: A population-based study of adolescents Pediatr Endocrinol Metab (2004), 17(12):1633-40.
[25]  Kim S., England J., Sharma A., Njoroge T. Gestational diabetes mellitus and risk of childhood overweight and obesity in offspring: A systematic review. Experimental Diabetes Research (2011), 2011: 541308.
[26]  Savona-Ventura C., Schranz A.G., Chircop M. Family history in the aetiology of gestational diabetes mellitus and type 2 diabetes. Malta Medical Journal (2003), 15 (2): 25-30.
[27]  Zhong-Chang L., Delvin E., Frazer W., Audibert F., Deal C., Julien P., et al. Maternal glucose tolerance in pregnancy affects fetal insulin sensitivity. Diabetes Care (2010), 33(9):2055-2061.
[28]  Vaarasmaki M., Pouta A., Elliott P., Tapanairan D., Sovio U., Ruokonen A., et al. Adolescent manifestations of metabolic syndrome amongst children born to women with GDM in a general population birth cohort. Am J Epid. (2009), 169(10): 1209:1215.
[29]  Tsadok M.A., Friedlander Y., Paltiel O., Manor O., Meiner V., Hochner H., et al. Obesity and blood pressure in 17-year-old offspring of mothers with gestational diabetes: insights from the Jerusalem perinatal study. Exp Diabetes Res. (2011), 2011:906154.
[30]  Bunt J., Tateranni A., Salbe A. Intrauterine exposure to diabetes is a determinant of Hemoglobin A1c and systolic blood pressure in Pima Indian children. J Clin Endocrinol Metab (2005), 90(6): 3225-3229.
[31]  Tam W.H., Yang X., Ko G.T., Tong PC., Cockram C.S., Sahota D.S., Rogers M.S., Chan J.C. Glucose intolerance and cardiometabolic risk in children exposed to maternal gestational diabetes mellitus in utero. Pediatrics (2008), 122:1229-1234.
[32]  Ding G., Haung H. Paternal transgenerational glucose intolerance with epigenetic alterations in second generation offspring of GDM. Asian J Androl. (2013), 15(4): 451-452.
[33]  Dabelea D., Hanson R., Lindsay R, Pettitt D., Imperatore G., Gabir M. Intrauterine exposure to diabetes conveys risk for type 2 diabetes and obesity: a study of discordant sibships. Diabetes. (2000), 49: 2208-2211.
[34]  Savona-Ventura C., Schranz AG., Chircop M. Risk factors for gestational impaired glucose tolerance in the Maltese population: a cross-sectional study. J. Obstet. Gynaecol (2001), 21 (6): 591-594.
[35]  Rodriquez B., Fujimoto W., Mayer-Davis E., Imperatore G., Williams D.,Bell R. Prevalence of cardiovascular disease risk factors in U.S. children and adolescents with diabetes. The search for diabetes in youth study. Diabetes Care (2006), 29(8): 1891-1896.
[36]  da Silva R., Miranda W., Chacra A., Dib S. Metabolic Syndrome and Insulin Resistance in Normal Glucose Tolerant Brazilian Adolescents With Family History of Type 2 Diabetes. Diabetes Care (2005), 28(2):716-718
[37]  Rodden A., Diaz V., Mainous11 A.G., Koopman R., Geesey M.E. Insulin resistance in adolescents. Journal of Pediatrics (2007), 151 (3): 275-279.
[38]  Yajnik C. Nutrient-mediated teratogenesis and fuel-mediated teratogenesis: Two pathways of intrauterine programming of diabetes. Intern J Gynec & Obstretrics (2009), S27-31.
[39]  Malcolm J.C., Lawson M.L., Gaboury I., Lough G., Keely E. Glucose tolerance of offspring of mother with gestational diabetes mellitus in a low-risk population. Diabetic Medicine (2006), 23(5): 565-570.
Show Less References


Severe Cardiomyopathy from Limb Girdle Muscular Dystrophy: A Nidus for a Catastrophic Cascade

1Department of Medicine, Overlook Medical Center, Summit, NJ, USA

2Department of Cardiology, Morristown Medical Center, Morristown, NJ, USA

American Journal of Cardiovascular Disease Research. 2016, 4(1), 7-10
doi: 10.12691/ajcdr-4-1-2
Copyright © 2016 Science and Education Publishing

Cite this paper:
Glenmore Lasam, Jenny Lam. Severe Cardiomyopathy from Limb Girdle Muscular Dystrophy: A Nidus for a Catastrophic Cascade. American Journal of Cardiovascular Disease Research. 2016; 4(1):7-10. doi: 10.12691/ajcdr-4-1-2.

Correspondence to: Glenmore  Lasam, Department of Medicine, Overlook Medical Center, Summit, NJ, USA. Email:


We report a case of a 57-year-old female with Limb Girdle Muscular Dystrophy (LGMD) who initially presented to her outpatient physician a year ago with progressive shoulder and pelvic girdle muscle weakness associated with slight limitation of movement, gradual onset of easy fatigability, intermittent episodes of exertional dyspnea, and trace bipedal edema. On the day of admission, she had sudden onset of unresponsiveness due to massive cerebral infarct likely cardioembolic as evidenced by left ventricular thrombus, in the setting of severe cardiomyopathy associated from LGMD. The patient was treated with hemodynamic support and systemic anticoagulation but did not show any signs of neurologic improvement. Comfort care measures were initiated, eventually, the patient succumbed to death.



[1]  Narayanaswami P, Weiss M, Selcen D, et al. Evidence-based guideline summary: diagnosis and treatment of limb-girdle and distal dystrophies: report of the guideline development subcommittee of the American Academy of Neurology and the practice issues review panel of the American Association of Neuromuscular & Electrodiagnostic Medicine. Neurology 2014; 83(16):1453.
[2]  Wicklund MP, Kissel JT. The limb-girdle muscular dystrophies. Neurol Clin 2014; 32:729.
[3]  Bushby KM. Limb-Girdle Muscular Dystrophies. National Organization of Rare Disorders. Accessed March 8, 2016.
[4]  Norwood FL, Harling C, Chinnery PF, Eagle M, Bushby K, Straub V. Prevalence of genetic muscle disease in Northern England: in-depth analysis of a muscle clinic population. Brain 2009;132: 3175-3186.
[5]  Darras BT. Limb-girdle muscular dystrophy. UpToDate, Waltham, MA. (Accessed on March 10, 2016.).
Show More References
[6]  Okere A, Reddy S, Gupta S, et al. A Cardiomyopathy in a Patient With Limb Girdle Muscular Dystrophy Type 2A. Circulation: Heart Failure. 2013; 6: e12-e13.
[7]  Norwood F, de Visser M, Eymard B, Lochmϋller H, Bushby K. EFNS guideline on diagnosis and management of limb girdle muscular dystrophies. Eur J Neurol. 2007; 14:1305-1312.
[8]  Hong JS, Ki CS, Kim JW, et al. Cardiac Dysrhythmias, Cardiomyopathy and Muscular Dystrophy in Patients with Emery-Dreifuss Muscular Dystrophy and Limb-Girdle Muscular Dystrophy Type 1B. J Korean Med Sci. 2005 Apr;20(2):283-290.
[9]  van der Kooi A, de Voogt W, Barth P, et al. The heart in limb girdle muscular dystrophy. Heart 1998;79:73-77.
[10]  Verhaert D, Richards K, Rafael-Fortney JA, Raman SV. Cardiac Involvement in Patients With Muscular Dystrophies: Magnetic Resonance Imaging Phenotype and Genotypic Considerations. Circ Cardiovasc Imaging. 2011;4:1 67-76.
[11]  Kalaria VG, Passannante MR, Shah T, et al. Effect of mitral regurgitation on left ventricular thrombus formation in dilated cardiomyopathy. Am Heart J. 1998;135 2 pt 1:215-220.
[12]  Falk RH, Foster E, Coats MH et al. Ventricular thrombi and thromboembolism in dilated cardiomyopathy: a prospective follow-up study. Am Heart J. 1992;123:136-142.
[13]  Stratton JR, Resnick AD. Increased embolic risk in patients with left ventricular thrombi. Circulation. 1987;75:1004-1011.
[14]  Lip GY, Manning WJ, Weissman NJ. Left ventricular thrombus after acute myocardial infarction. UpToDate, Waltham, MA. (Accessed on March 10, 2016.).
[15]  Vaitkus PT, Barnathan ES. Embolic potential, prevention and management of mural thrombus complicating anterior myocardial infarction: a meta-analysis. J Am Coll Cardiol. 1993;22(4):1004.
[16]  Finsterer J, Stöllberger C: Atrial fibrillation/flutter in myopathies. Int J Cardiol 2008, 128:304-310.
[17]  Chen C-H, Tang S-C, Su Y-N, Yang C-C, Jeng J-S. Cardioembolic stroke related to limb-girdle muscular dystrophy 1B. BMC Research Notes. 2013;6:32.
[18]  Ambrosi P, Mouly-Bandini A, Attarian S, et al. Heart transplantation in 7 patients from a single family with limb-girdle muscular dystrophy caused by lamin A/C mutation. Int J Cardiol. 2009;137(3):e75.
[19]  Margeta M, Connolly AM, Winder TL, et al. Cardiac pathology exceeds skeletal muscle pathology in two cases of limb-girdle muscular dystrophy type 2I. Muscle Nerve. 2009;40(5):883.
[20]  Meune C, Van Berlo JH, Anselme F, Bonne G, Pinto YM, Duboc D: Primary prevention of sudden death in patients with lamin A/C gene mutations.N Engl J Med 2006, 354:209-210.
Show Less References