Case report Silent myocardial ischaemia: A cause for sudden death in young people M.D.

Nithin, Smitha Rani,* Varun Pai Department of Forensic Medicine, J.S.S. Medical College (Affiliated to J.S.S. University), Mysore, Karnataka, India *Corresponding Author Email: smitha_2444@yahoo.co.in Abstract Sudden death is natural unexpected death occurring within an hour of the onset of acute symptoms. Sudden cardiovascular death is a catastrophic event in young people throughout the world. In about half of the young people who die suddenly, the first presentation of their disease is often at autopsy. Herein, we report a case where a young man died due to silent myocardial ischaemia and sudden death was the first presentation. Keywords: Young individuals; Sudden death; Autopsy; Atherosclerotic cardiovascular disease. Introduction Cardiac disorders constitute the most common causes of sudden natural death. Among adolescents and young adults, the incidence of sudden cardiac death is approximately 1 in 100000 population per year.1 Death due to coronary atherosclerosis accounts for approximately 50% of all cardiac deaths, and 50% of coronary atherosclerosis deaths are sudden and

unexpected.2 The number of deaths due to coronary artery disease in India is projected to increase from 1.591miliion in year 2000 to 2.034 million by year 2010 (WHO report 1999).3 Atherosclerotic cardiovascular disease is not rare as a cause of death in young adults.4,5 Coronary disease can remain silent and sudden death can be its first presentation.6 Herein, we report a case of death of a young man due to coronary atherosclerosis, where first presentation is the sudden death. Case report A 28-year-old man boarded the bus and was found dead by the conductor within 10 minutes when he went to issue a boarding ticket. He was shifted immediately to the hospital, where he was declared brought dead. The relatives revealed that the deceased was healthy before this incidence. He was a non-smoker and non-hypertensive. There was no previous history of chest pain and significant illness. Further, there was a history of frequent consumption of red meat (beef) by the deceased and hypercholesterolaemia in the family. On postmortem examination, length of the body measured 169 cm and weighed 75 kg. There were no external injuries on the body. The brain weighed 1100 gm and was congested. Heart weighed 250 gm. The thickness of the right and left ventricular walls measured 0.4 cm and 1.3 cm, respectively and were unremarkable. The circumference of the tricuspid, pulmonary, mitral and aortic valves measured 10.5 cm, 8 cm, 10 cm and 9.5 cm, respectively and were healthy. The anterior descending branch of left coronary artery showed thickening of wall due to atherosclerosis with complete occlusion by a thrombus (Fig. 1). The other coronaries were patent. The root, ascending and descending parts of aorta showed moderate degree of atherosclerosis. The right and left lungs weighed 410 gm and 370 gm, respectively and were

congested. Stomach contained 300 ml of yellowish coloured fluid with out any abnormal odour. Small and large intestines were intact and healthy. The spleen, liver and kidneys were intact and healthy. Histopathological examination of the heart revealed normal myocardium and valves. The serial sections of anterior descending branch of left coronary artery showed narrowing of the lumen by atherosclerotic plaque, which consists of lipid-laden macrophages and inflammatory cells with secondary hemorrhage (Fig. 2). Sections from lungs showed dilated alveolar spaces with congested vessels in the alveolar wall. Sections from the liver, spleen and kidneys showed normal histology. The cause of death was opined as ischemia of heart secondary to atherosclerotic occlusion of the anterior descending branch of left coronary artery. Discussion Atherosclerosis is a chronic, progressive, inflammatory disease with a long asymptomatic phase. Coronary atherosclerosis may present as angina pectoris, acute myocardial infarction or sudden death. The myocardial ischemia impairs the arterial baroreflex and lead to hemodynamic instability, and even lethal dysarrhythmia.7,8 In the absence of infarction, coronary artery disease may cause regional left ventricular dysfunction.9 In majority of the sudden coronary deaths, there will be an active coronary artery lesion.10 An active coronary lesion is defined as a disrupted plaque, luminal fibrin/platelet thrombus, or both. An inactive lesion is defined as having a cross-sectional luminal stenosis of 75% with out plaque disruption or luminal thrombus.2 Arterial thrombosis, most often with underlying plaque rupture was the mechanism of sudden cardiac death in > 80% of the cases.11 Vulnerable plaques

have a large number of foam cells, extracellular lipid, thin fibrous caps and clusters of inflammatory cells and are more prone to rupture.12 Serum lipid abnormality is a key risk factor in the development of plaque rupture, which results from exposure of the lipid core to the lumen.13 However, calcification stabilizes the plaques and protects against rupture.12 In the present case, the deceased was young and died suddenly while travelling. There was absence of risk factors such as smoking and hypertension except the excess consumption of red meat and familial hypercholesterolaemia. Postmortem examination revealed the occlusion of a major coronary artery due to complicated atherosclerotic lesion. Histopathology examination of coronary sections confirmed the presence of active coronary atherosclerotic lesion with almost complete narrowing of lumen. Haemorrhage into the plaque may occur from rupture of either the overlying endothelium or the thin-walled capillaries that vascularise the plaque. The resulting haematoma may remain localised with in the intima and occlude the lumen. A significant coronary pathology with absence of any pathology in the other organs suggests that the deceased died due to myocardial ischaemia. Since the earliest significant histological features of acute myocardial infarction under light microscope takes about 4 to 12 hours after the onset of ischemic injury, the death in the present case was considered to be sudden. The early recognition of coronary atherosclerosis is very important. Increased plasma cholesterol, triglycerides, low-density lipoproteins, and apolipoprotein-B are the important biochemical markers for the development of early and apparently clinically silent coronary artery disease.14 Also, the subclinical stage of coronary atherosclerosis can be identified by several methods such as coronary angiography, intravascular ultrasonography, B-mode ultrasonography, computed tomography and magnetic resonance imaging.15

We conclude that the role of forensic expert in the investigation of sudden death is very important. Though it is rare, coronary atherosclerosis should be considered in the diagnosis of sudden death in the young, even in the absence of major risk factors. As identification of group at risk is so difficult and death occurs so quickly, emphasis has to be given for educational programs on cardiopulmonary resuscitation for normal population and for primary preventive measures. References

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7. Yuda S, Fang ZY, Marwick TH. Association of severe coronary stenosis with subclinical left ventricular dysfunction in the absence of infarction. J Am Soc Echocardiogr 2003;16:11631170. 8. Naghavi M, Libby P, Falk E, Casscells SW, Litovsky S, Rumberger J, et al. From vulnerable plaque to vulnerable patient: A call for new definitions and risk assessment strategies: Part II. Circulation 2003;108:1772-1778. 9. Lie JT. Histopathology of the conduction system in sudden death from coronary heart disease. Circulation 1975;51:446-452. 10. Tousoulis D, Davies G, Stefanadis C, Toutouzas P, Ambrose JA. Inflammatory and thrombotic mechanisms in coronary atherosclerosis. Heart 2003;89:993-997. 11. Schmermund A, Schwartz RS, Adamzik M, Sangiorgi G, Pfeifer EA, Rumberger JA, et al. Coronary atherosclerosis in unheralded sudden coronary death under age 50: histo-pathologic comparison with 'healthy' subjects dying out of hospital. Atherosclerosis 2001;155:499-508. 12. Sudha ML, Sundaram S, Purushothaman KR, Kumar PS, Pratibha D. Coronary atherosclerosis in sudden cadiac death: An autopsy study. Indian J Pathol Microbiol 2009;52:486-489. 13. Virmani R, Burke AP, Farb A. Sudden cardiac death. Cardiovasc Pathol 2001;10:211-218. 14. Hiserodt JC, Perper JA, Koehler SA, Orchard TJ. A comparison of blood lipid and lipoprotein values in young adults who die suddenly and unexpectedly from atherosclerotic coronary artery disease with other noncardiac deaths. Am J Forensic Med Pathol 1995;16:101-106. 15. Toth PP. Subclinical atherosclerosis: what it is, what it means and what we can do about it. Int J Clin Pract 2008;62:1246-1254.

Fig. 1. Cross section of anterior descending branch of left coronary artery showing occlusion.

Fig. 2. Microscopy of the narrowed coronary lumen by atherosclerotic lesion with secondary haemorrhage (Haematoxylin and Eosin 100x).