SUSPICIUOS BUT SUDDEN CARDIOVASCULAR DEATHS

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ISSN No. 2394-3971

Original Research Article SUSPICIUOS BUT SUDDEN CARDIOVASCULAR DEATHS Nnoli Martin A., Chukwuegbo Cornelius, Jegede Olushola, Nwabuko Collins.

University of Calabar/Teaching hospital Calabar. Calabar. Cross-River State. Nigeria.

Abstract: Aim: To determine the causes of sudden deaths while asleep and in motion (activity). Materials & Method: Two cases of middle aged male Negroid adults were autopsied and analyzed in the department of anatomic pathology for the cause of sudden death at rest and in activity-while eating. Results: They were both found to be class 1(one) and 3(three) obsessed with estimated BMI’s of 43.5kg/m2 and 50.6kg/m2 respectively. The major features were on the cardiovascular as both had a massive cardiomegaly of 900 gm/500gms respectively. ( Normal for normal adult male of 75kg weight:300-350gms). This feature was compromised with other lesions like florid arteriomatous plaques. Conclusion: We found to our opinion that both died of hypertensive cardiovascular diseases following long standing hypertension though with good management but lack of compliance on the patients side. Keywords: Suspected poisoned, cardiovascular death, autopsy. Introduction: deaths as they noted that most death peaks In USA, Cardiovascular disease appears to up at 7am and 9 am respectively. They be common cause of deaths; as it is a major further found that most deaths from cause of deaths of men within the ages of cardiovascular ailment peaks up to 70 % 20-65 years. Zipes and wallen ( 1988), during the day than at night (rest periods).2 found that 80% of patients that died of Deaths resulting from cardiovascular causes sudden cardiac deaths are mainly due to are often natural and unexpected as the diseases of coronary artery like in built occur within 60minutes of onset of final arteriomatous plaques narrowing the symptoms.3 At times, there will be need for 1 lumen. Willich et al 1987, attributed this a detailed forensic autopsy with deaths to circadian variation in the time of toxicological analysis especially like in our Nnoli M.A. et al., Med. Res. Chron., 2015, 3 (1), 59-63

Medico Research Chronicles, 2016

Submitted on: January 2016 Accepted on: February 2016 For Correspondence Email ID:

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Case fatality rates following coronary events also increases with antecendent heart rate and fraction of coronary deaths as sudden death increases strikingly with heart rate in men 35-64 years of age.7 These days clinicians assessed patients on individuals total burden of risk than on the level of particular risk factor.8-14 This is to the fact that arteriosclerotic cardiovascular disease often times are associated with many risk factors that results to sudden deaths. This is sequel to those risk factors producing a total risk which clinician should have been able to estimate in any cardiovascular disease. Summary of Cases: Case A: This is class 1 obese, middle aged Negroid race of 55 years of age, an estate developer who was found dead while resting. An inquest was requested by his family members because they suspected he could have been poisoned by people around him before he decided to take a short rest. Case B: This is class 3 obese (estimated BMI= 43.5kg/m2) fairly elderly Negroid race of 63 years academician. He was said to have died while eating but had cardiovascular accidents (stroke) a few months ago though fully recovered.

Figure 1: Depicts A section of abdominal aorta with Shinny areas of fatty flakes and arteriomatous plaques with distinct obliteration of vessel lumen with various sizes.

Nnoli M.A. et al., Med. Res. Chron., 2015, 3 (1), 59-63

Medico Research Chronicles, 2016

cases where one is an estate developerchances of toxins from sites of building ranging from asbestos and other obnoxious materials. The toxicology could have excluded toxic causes of sudden deaths like occupational or drug related as amphetamine, cocaine or anabolic steroids abuse.4 Vincent Dimaio 1993 found that 13.4% of deaths in such patients are due to acute thrombosis. He further elucidated this from outcome of autopsy cases of left coronary and its branches showing much higher incidence in thrombosis in comparison to the right coronary vessel.5 However, this is hidden in hypertensive cardiovascular disease due to plaque formation which results to thickening of the walls by arteriosclerotic deposits. In later life, the vessels are noted to be more rigid with patent lumen though calcified. This is probably due to deposit of calcium in the vascular walls. At times epicardial coronary vessels may not be occluded but examination under the microscope of sections of myocardium will show severe occlusive dysplasia of coronary vessles.6

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Figure 3: Depicts a section of heart with enlarged chambers, concentric hypertrophy and focal areas of hemorrhages. Autopsy Findings: Case A: The finding was of class 1 obese Negroid middle aged man with displaced apical heart and massive

cardiomegaly (Heart weighed 900gms) Normal: 300-350gms. Section of heart showed left ventricular hypertrophy

Nnoli M.A. et al., Med. Res. Chron., 2015, 3 (1), 59-63

Medico Research Chronicles, 2016

Figure 2: Depicts a massive cardiomegaly weighing 900g with areas of bulging epicardial fat on the anterior wall.

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evidenced by left ventricular wall thickness of 2cm (Normal 1-1.5cm). Multiple foci of rheumatic vavulitis with massive arteriomatous plaques-aorta, basilar artery. The lungs had extensive bilateral severe pleural adhesion/pulmonary oedema; with fatty liver change. Other systems/organs showed no pathological changes. Case B: The finding was of class 3obese elderly man with estimated BMI – 43.5kg/m2. The cardiovascular showed enlarged heart of 500 gm with left ventricular hypertrophy and massive areas of healed rheumatic valvulitis and hemorrhages (clots). There is still massive arteriomatous plaques- aorta, basilar artery. Both kidneys showed multiple foci of healed scars evidence of chronic pyelonephritis. There is mild to moderate anemia in virtually all organs with mild fatty change of the liver. Also seen is mild to moderate cerebral oedema. Limitations: Toxicology analysis could have been vital as to allay the fears of his relatives who were suspecting food and to exclude use of drugs like cannabis, amphetamine or industrial pollutions as in the case of the estate developer. However, we are constrained by unavailability of the gas chromatography and mass spectrometer for the analysis of such samples as gastric contents, bile fluids or vitreous humor. Discussions: In both Cases we concluded in our own opinion that the cause of death was due to hypertensive cardiovascular diseases following long standing systemic hypertension – that is being poorly managed by the two patients despite adequate medication from experts-cardiologists. It is not surprisingly as most if not all in this status of management often time comedown with sudden death as in both cases. In Kragol AH ( 1988) studies, they found that most of these cardiac related deaths are due to left ventricular hypertrophy and minimal coronary atherosclerosis that

resulted to the sudden deaths.7 It is known clinically that such patients with left ventricular hypertrophy often have more ventricular premature contractions than without left ventricular hypertrophy or normal people.15-17 These could have been the factor in our own case as both not only having features of hypertensive cardiovascular disease and massive arteriomatous plaques but with left ventricular hypertrophy. However, in all of the cases we had the major issue of ignorance to seek an expert management from both patients. Even where the expert treatment was given there was lack of compliance. It is also pertinent to mention at the instances of the patients visiting the cardiologist, the physicians should have identified all asymptomatic patients at high risk of sudden death as to prevent any disease symptoms. That is having measures of use of anti-arrhythmic agents or even cardioverter defibrillator implants; and to go further liaising with a forensic pathologist as to identify the incidence, causes and circumstances that surrounds any cardiac related sudden deaths the physicians must have managed.18 References: 1. Zipes DP and Wallens HJJ: (1988). Sudden Cardiac death: Circulation 8(21):2234-2351 2. Willich SN, Levy D, Rocco MB: (1987).Circadian Variation in the incidence of Sudden Cardiac death in Framingham heart Study Population. Am Cardiol60:801-806. 3. G.L. de la Grandmaison. Am Durigon: (2002) Sudden death, a medico-legal Series of 77 Cases between 1995 and 2000, Med. Sci. Law. 42:225-232. 4. SB Karch :( 2002). Pathology of Drug Abuse. CRC Preas. 183-187. 5. Dimaio VJM, Dimaio JM: (1993). Incidence of Coronary thrombosis in

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Sudden death due to coronary artery disease. AM J Med & Path 14 (4) 273-5. 6. Burke AP, Virmani R: (1998). Intramural Coronary dysplasia of the Ventricular Septum and Sudden death. Hum Path.29(10):1124-7 7. Kragol AH, Robert WC: (1988). Sudden Death and Cardiomegaly unassociated with Coronary, Valvular Congenital or Specific Myocardial disease. Am J Cardiol61:659-660. 8. Pyoralok, Debacker G: (1994).Prevention of Coronary heart disease in Clinical Practice. Recommendation of the task force of European Society of Cardiology European Artherosclerosis Society and European Society of Hypertension. Eur Heart J.15:1300-331. 9. Grundy SM: (1998) Primary Prevention of Coronary heart disease. Guidance from Framingham: A statement for health care Professionals from the AHA Task force on risk reduction. AHA Circulation. 97:1876-1887. 10. Anonymous: (1998). Joint British recommendations on Prevention of Coronary heart disease in Clinical Practice. British Cardiac Society. British hyperlipidaemia Association, British Hypertension Society endorsed by British diabetic Assoc. Heart. 80 (suppl):51-29 11. Robson J, Fender G.: (2001). Predicting and reducing cardiovascular risk. Heart.85:487-488.

12. Blair SN, Penon TA: (2002). AHA Guidelines for Primary Prevention of Cardiovascular disease and Stroke: Update: Consensus Panel Guide to Comprehensive risk reduction for adults Patients without Coronary or other atherosclerotic vascular disease. AHA Science Advisory and Co-ordinating committee. Circulation.106:388-391. 13. Wood DA, Debacker G, Faergeman O: (1998). Prevention of Coronary Heart disease in Clinical Practice. Recommendation of Second Joint Task Force of European and other Societies on Coronary Prevention. Eur Heart J.19:1434-1503. 14. Jackson R.: (2000). Guidelines on Preventing Cardiovascular disease in Clinical Practice. BMJ.320:659-661 15. Messer Li FH, Ventural Ho, Elizardi DJ.: (1984) Hypertension and Sudden death. Am J Med.77:18-22 16. Haider AW, Larson MG, Benjamin EJ.:(1988). Increased Left Ventricular mass and hyoertrophy associated with increased risk for Sudden death. JACC 32 (5): 1454-9. 17. Frolich ED. :( 1988). Left Ventricular Hypertrophy and Sudden death (Editorial Comment) JACC 32 (5): 1460-2. 18. Vincent J. Dimaio. Forensic Pathology 2nd Edition. Deaths due to Natural disease Pg 65.

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