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Science and Education Publishing (SciEP) is a multidisciplinary open access publisher of Journals covering the fields of Science, Technology and Medicine. All SciEP publications are subject to high-quality peer review, editorial and production processes and are freely available online.

Welcome to the April, 2013 edition of SciEP newsletter, providing monthly summaries of articles on science & education related topics of interest to scientist and professionals. The mission of our journals is to provide an open access forum for publishing new findings on issues pertinent to scientific and academic field. We also invite you to submit original research papers, review articles, short reports, or case studies are considered for publication in our Multidisciplinary Journals.

American Journal of Public Health Research
DOI: 10.12691/ajphr-1-1-3

The Implementation of a Tele-Homecare System with Service Oriented Architecture and HL7 Message Transmission Standard
Ching-Sung Wang

American Journal of Medical and Biological Research
DOI: 10.12691/ajmbr-1-1-2

The Influence of Ethanol on Pyruvate Kinases Activity in Vivo, in Vitro, in Silico
Lelevich Sergey Vladimirovich, Khrustalev Vladislav Victorovich, Barkovsky Eugene Victorovich, Shedogubova Tatyana Aleksandrovna

American Journal of Medical Sciences and Medicine
DOI: 10.12691/ajmsm-1-1-1

Clinical and Histological Features in Wegener Granulomatosis
Li Cavoli Gioacchino, Passantino Rita, Bono Luisa, Tortorici Calogera, Ferrantelli Angelo, Giammarresi Carlo, Rotolo Ugo

American Journal of Infectious Diseases and Microbiology
DOI: 10.12691/ajidm-1-1-2

The Curse of Lymphatic Filariasis: Would the Continual Use of Diethylcarbamazine Eliminate this Scourge in Papua New Guinea?
Anne Lanham, Lillian Mwanri

We have released issues of some journals on February 2013.
American Journal of Public Health Research
American Journal of Medical Sciences and Medicine
American Journal of Medical and Biological Research
American Journal of Pharmacological Sciences
American Journal of Clinical Medicine Research
American Journal of Nursing Research
American Journal of Cancer Prevention
American Journal of Medicine Studies
American Journal of Infectious Diseases and Microbiology
American Journal of Cardiovascular Disease Research
American Journal of Biomedical Research
American Journal of Mechanical Engineering
American Journal of Microbiological Research
Journal of Preventive Medicine
American Journal of Food and Nutrition
American Journal of Hypertension Research
American Journal of Sports Science and Medicine
Journal of Cancer Research and Treatment
American Journal of Zoological Research
Journal of Biomedical Engineering and Technology
American Journal of Microbiological Research
Biomedical Science and Engineering

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A Rare Presentation of Acute Coronary Syndrome with Posterior Fossa Intracranial Bleed

Shazia Yasir

ER Physician (PG), Ziauddin University Hospital

Abstract: Without significant coronary artery stenosis, ischemic ECG changes including ST segment elevation, segmental wall abnormality & elevated serum cardiac specific markers may develop after central nervous system injuries. Misdiagnosing these patients as acute MI may result in catastrophic outcomes. By reporting case of 56 year old male with posterior cranial fossa haemorrhage mimicking ST segment elevation MI, we hope to underline that careful attention to neurological abnormalities is critical in making correct diagnosis.

Keywords: myocardial infarction, posterior cranial fossa haemorrhage

Received November 09, 2013; Revised December 29, 2013; Accepted January 16, 2014

Citation: Shazia Yasir, A Rare Presentation of Acute Coronary Syndrome with Posterior Fossa Intracranial Bleed. American Journal of Medical Case Reports, 2 (1). 10-11. January 2014. doi:10.12691/ajmcr-2-1-3

1. Introduction

ECG Changes are common in patients with cerebrovascular diseases, including subarachnoid haemorrhage, subdural haematoma & ischemic stroke [1,2,3], but typical ST segment elevation is rare. The exact phenomenon is not clear but the changes can be caused predominantly in the subendocardium of the left ventricle due to ischemia, which, in turn, can be caused by centrally mediated release of catecholamines induced by hypo-perfusion of posterior hypothalamus. Mild elevation in serum cardiac enzymes is often associated with ECG changes [4]. We would like to emphasize careful attention to abnormalities in neurological events, which can enable better evaluation and management.

2. Case Presentation

A 56-year old male patient presented to the emergency department with complaint of chest heaviness for several hours associated with vertigo and 6–8 episodes of vomiting. Clinical examination of the patient showed good general conditions with rhythmic pulse. The additional risk factor found along with the above mentioned complaint was hypertension. On arrival, he had no neurological symptoms and his blood pressure was 213/103, pluses 77 beats/minute, body temperature was 99F, respiratory rate was 18 breaths/minute, O2 saturation was 99% on room air and plasma glucose was 4.6619 mmol/l. On initial examination, we did not find any head trauma, abnormal respiratory sound or cardiac murmur. The ECG on presentation had ST segment elevation from leads V2–V4, & T-wave inversions in V6, II, AVL & AVF.

Figure 1. CT scans of the patient

Laboratory examination showed: LDH 281 (range: 24-195 u/l), CK-MB: 34 (< 25 u/l), SGOT (AST): 24 (upto 37 u/l). The echocardiogram showed symmetrically hypertrophied normal sized left ventricle with mild segmental left ventricular systolic dysfunction. Grade 1 diastolic dysfunction with ejection fraction: 50%. During patient’s stay in emergency department, he vomited again and his blood pressure was continuously around 210/102. The CT scan brain (without contrast) was performed immediately, which showed posterior cranial fossa haemorrhage. After undergoing craniotomy and ventriculoperitoneal (VP) shunt placement, the patient’s condition improved and he was discharge in 15 days without any neurological deficit.

Figure 2. ECG of the patients

3. Discussion

Abnormalities of ECG, echocardiography and serum cardiac specific markers are related with cerebrovascular disease [5,6,7,8,9]. Hypertension is usual cause of primary haemorrhage into pons or cerebellum due to displacement of vessels specially in the absence of trauma. The incidence of hypertension is greater than one fifth of all spontaneous intra-cerebral haemorrhage (10). Some patients have abnormalities on ECG including a prolonged QT interval, depressed ST segment, rarely elevated ST segment, inverted or flat T waves, tall peaked T waves & U waves. These changes are most likely due to centrally mediated release of catecholamine induced by hypoperfusion of posterior hypothalamus. The autopsies of patients have revealed that patients with posterior fossa hemorrhage also have characteristics subendocardial myocardial lesion called contraction band necrosis in the heart [11,12,13]. In spite of all these studies the exact phenomena is still uncertain & future studies are needed.

When patient present in emergency department with no typical neurological symptoms but with initial reading of very high blood pressure and ECG show ST segment elevation, we may misdiagnose as acute MI and treat with multiple antiplatelet & anticoagulant agents, which may lead to harmful effects [14]. Moreover, by delaying the accurate diagnosis, it may result in catastrophic outcome. In this patient there is one reflecting point is his continuous raised blood pressures and we all are well known that stress or chronic hypertension induced cardiomyopathy may developed by cerebrovascular accidents. So even patient is present with acute ST elevation MI, we should consider a cerebral insult and act promptly to save the life of patient.

References

[1]   | Cardiac manifestations of acute neurological lesions. (Oppenheimer S, Norris JW.) In: Aminoff MJ, editor. Neurology and General Medicine: the Neurological Aspects of Medical Disorder. 2nd ed. New York, NY: Churchill-Livingstone; 1995. pp. 183-200.
[2]   | Van der Bilt IAC, Visser FC. Neurogenic induced myocardial dysfunction. Heart Metab. 2004; 24:27-30.
[3]   | Zaroff JG, Rordorf GA, Newell JB, Ogilvy CS, Levinson JR. Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurgery. 1999; 44: 34-39. discussion 39-40.
[4]   | The annual incidence of non traumatic intracranial haemorrhage varies from 2-22/100,000. (Ingalls T, Asplundh K, Mahoney M, Bonita R. A multinational comparison of subarachnoid haemorrhage epidemiology in the WHO MONICA stroke study. Stroke 2000: 31: 105).
[5]   | Elrifai AM, Bailes JE, Shih SR, Dianzumba S, Brillman J. Characterization of the cardiac effects of acute subarachnoid hemorrhage in dogs. Stroke. 1996; 27: 737-741. discussion 741-2.
[6]   | Yuki K, Ko ama Y, Onda J, Emoto K, Morimoto T, Uozumi T. Coronary vasospasm following subarachnoid hemorrhage as a cause of stunned myocardium: case report. J Neurosurg. 1991; 75: 308-311.
[7]   | Zaroff JG, Rordorf GA, Newell JB, Ogilvy CS, Levinson JR. Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurgery. 1999; 44: 34-39. discussion 39-40.
[8]   | Chen YL, Yu TH, Fu M. Takotsubo cardiomyopathy: transient left ventricular apical ballooning mimicking acute myocardial infarction. J Formos Med Assoc. 2006; 105: 839-843.
[9]   | Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol. 2001; 38: 11-18.
[10]   | A study of primary cerebellar & pontine hemorrhage with observation on their pathogen by Henry B. D INSDALE. MD in JAMA Neurology Journal.
[11]   | Brouwers PJ, Wijdicks EF, Hasan D, et al. Serial electrocardiographic recording in aneurysmal subarachnoid hemorrhage. Stroke. 1989; 20: 1162-1167.
[12]   | Doshi R, Neil-Dwyer G. Hypothalamic and myocardial lesions after subarachnoid hemorrhage. J Neurol Neurosurg Psychiatry. 1977; 40: 821-826.
[13]   | Greenhoot JH, Reichenbach DD. Cardiac injury and subarachnoid hemorrhage: a clinical, pathological and physiological correlation. J Neurosurg. 1969; 30: 521-531.
[14]   | Blood pressure levels in acute myocardial infarction. http://www.ncbi.nlm.nih.gov/pubmed/696568.