Sudden_Cardiac_Death_Forensic_Perspective.pptx

sudden cardiac death forensic perspective by Dr. Roshan vyasabhat

1. Sudden Cardiac Deaths: A Forensic Perspective Unraveling the Cause of Unexpected Cardiac Death . Dr. Roshan Vyasabhat -post graduate. Dept of Forensic Medicine & Toxicology. Gandhi Medical College.

2. What is Sudden Cardiac Death? Definition: SCD is most commonly defined as unexpected death from cardiac causes, either without symptoms or within 24 hours of symptom onset. (different authors use different criteria)

3. Learning Objectives: Understand the key causes of SCD. Detail forensic investigation protocol. Role of histology, toxicology and etc. Examine medicolegal aspects and differential diagnoses.

4. The Scope of the Problem Major public health issue worldwide. Accounts for a significant percentage of all natural deaths. Incidence varies with age, gender, geography .

5. Causes of SCD in Adults Coronary Artery Disease (Most common, >80%) Atherosclerotic plaque rupture with thrombosis. Severe coronary atherosclerosis causing critical stenosis and ischemia(> 75%).

6. Coronary Artery Disease Progressive luminal narrowing of coronary arteries caused by development of atheromatous plaque composed of lipids, inflammatory cells and connective tissue Pathophysiology: Divided in 3 phases Initiation : Deposit of cholesterol rich, low density lipoprotein (LDL) particles in the intima (fatty streak) Endothelial activation secondary to proinflammatory signals and mechanical stress Progression : Recruitment of leukocytes and SMC production of extracellular matrix molecules contribute to thickening of the intimal layer Variable accumulation of calcium, large mineralization decreases risk of thrombotic event Complication: Plaque rupture: thrombus formation in plaques with large lipid core and thin fibrous cap Plaque erosion: plaques with rich extracellular matrix, little lipid content and thin friable fibrous cap Buried caps are evidence of prior rupture and healing

7. Coronary Artery Disease Gross description Fatty streaks are flat yellow discoloration in the intima surface Early plaque is raised yellow, well defined lesion, focal in distribution and irregular in shape Complicated plaques show ulcers, protrusions and thrombus

8. Coronary Artery Disease Microscopic (histologic) description Fatty streak: subendothelial accumulation of foam cells without necrotic core or fibrous cap Fibrous cap atheroma: Well formed necrotic core with overlying fibrous cap; smooth muscle cells, macrophages, lymphocytes and connective tissue components may be present Fibrocalcific plaque: collagen rich plaque, contains large areas of calcification with few inflammatory cells, necrotic core may be present

9. (A) Absence of atherosclerosis. (B) Grade 1, non-confluent plaques without ulcerations and protrusions. (C) Grade 2, confluent areas or/and an area of ulceration with minimal protrusion. (D) Grade 3, confluent plaques with multifocal ulcerations or protrusions.

10. ISCHEMIC HEART DISEASE-MI IHD represents an imbalance between myocardial supply (perfusion) and cardiac demand for oxygenated blood. Ischemia not only limits tissue oxygenation ( and thus ATP generation), but also reduces the availability of nutrients and the removal of metabolic wastes. In approximately 10% of cases, MI occurs in the absence of the typical coronary atherothrombosis .

11. IHD can declare itself through one or more of the following clinical presentations: • Myocardial infarction (MI), in which ischemia causes cardiac necrosis • Angina pectoris • Chronic IHD with heart failure • Sudden cardiac death (SCD)

12. The gross and microscopic appearance of an infarct depends on the interval of time between the MI and death. DAMAGED MYOCARDIUM UNDERGOES A PROGRESSIVE SEQUENCE OF MORPHOLOGIC CHANGES INVOLVING TYPICAL ISCHEMIC COAGULATIVE NECROSIS,THE PREDOMINANT MECHANISM OF CELL DEATH IN MI and apoptosis also.

13. GROSS

14. MICROSCOPIC

15. Causes of SCD in Adults Cardiomyopathies : Hypertrophic Cardiomyopathy (HCM ) . Dilated Cardiomyopathy (DCM ) -heart often appears globulaar due to biventricular dilation . Ventricular dilation approx 4cm.

16. Hypertrophic Cardiomyopathy (HCM) -fatal greater than 1.5cm Pressure overload hypertrophy Volume overload hypertrophy Spontaneous gene mutes- FOS,JUN , MYC, and EGR1 ) The proposed sequence of initially adaptive—and later harmful. LVH grater than 1.3cm can be fatal.

17. gross Left ventricular hypertrophy with and without dilation

18. microscopic Normal myocardium Hypertrophied myocardium

19. Pathophysiology Important changes at the tissue and cell level occur with cardiac hypertrophy. Significantly , myocyte hypertrophy is not accompanied by a proportional increase in capillary numbers . As a result, the supply of oxygen and nutrients to the hypertrophied heart is more tenuous than in the normal heart. T he same time, cardiac hypertrophy is associated with heightened metabolic demands due to increases in mass. As a result of these changes, the hypertrophied heart is vulnerable to ischemia , which can evolve to cardiac failure.

20. Dilated Cardiomyopathy (DCM) DCM is characterized by morphologically and functionally progressive cardiac dilation and contractile ( systolic) dysfunction , usually with concomitant hypertrophy . Although an exhaustive evaluation may not be able to pinpoint a specific etiology (“idiopathic DCM ”). DCM is probably familial in up to 50% of cases, caused by mutations in a diverse group of more than 20 genes. Heart size will be enlarged and globular in shape.

21. GROSS

22. MICROSCOPIC V ariable myocyte hypertrophy and interstitial fibrosis E nlarged , bizarre, hyperchromatic nuclei (likened to “Ninja stars”)

23. Causes of SCD in the Young Hypertrophic Cardiomyopathy (HCM): Most common in young athletes. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC). Congenital Coronary Artery Anomalies . Myocarditis (often viral ).

24. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC). Arrhythmogenic right ventricular cardiomyopathy is an autosomal dominant disorder that classically manifests with right-sided heart failure and rhythm disturbances, which can cause sudden cardiac death . Mutations involve genes encoding desmosomal junctional proteins at the intercalated disk (e.g., plakoglobin ) Classically, the right ventricular wall is severely attenuated due to loss of myocytes , accompanied by massive fatty infiltration and focal fibrosis

25. Gross & microscopic R eplacement of the right ventricular free-wall by fat and fibrosis.

26. Congenital Coronary Artery Anomalies some, like  anomalous left coronary artery from the pulmonary artery  (ALCAPA) or those with an interarterial course, can lead to serious complications, including  sudden cardiac death , especially in young athletes

27. Myocarditis The inflammation of the heart muscle can cause life-threatening arrhythmias and heart failure, especially during the acute phase

28. 'Negative Autopsy' Cases SCD without structural disease: E lectrical disorder . Long QT Syndrome (LQTS). Brugada Syndrome. Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT). Wolf-Parkinson-White syndrome.

29. The Initial Scene Investigation Scene Documentation: Body position, environment. Circumstances: At rest, exercise, emotional event? Evidence: Medications, drugs, bottles. Witness Interviews: Medical history, symptoms.

30. NON GENETIC RISK FACTORS OF MOST CARDIAC DISEASES High Blood Pressure (Hypertension) High cholestrol Smoking risk Diabetes Over weight and obesity Unhealthy Diet : Lack of Physical Activity:  Insufficient physical activity or being too sedentary increases Harmful Use of Alcohol Air Pollution  

31. The Crucial Autopsy Examination 1. External Examination Look for trauma, injection marks, or poison indicators. Check for stigmata of chronic disease ( xanthelasma , obesity, cyanosis, clubbing).

32. The Crucial Autopsy Examination 2. Internal Examination Weight: Increased in cardiomyopathy. Coronary arteries: Open longitudinally. Look for atherosclerotic plaques, thrombosis, stenosis (>75%). Myocardium: Pale areas (acute infarct <12 hrs ). Yellow-soft areas (1–7 days old infarct). Fibrosis/scarring (old infarct). Valves: Calcification, vegetations , prolapse. Conduction system (special dissection): Histology if no gross cause found.

33. Beyond the Naked Eye 3.Ancillary Investigations Histopathology: Myocarditis, fibrosis, hypertrophic fibers. Toxicology: Drugs, alcohol, poisons. Microbiology/virology: Infective causes. Molecular autopsy (genetic testing): Channelopathies (e.g., long QT, Brugada ).

34. The Verdict: Natural vs. Unnatural SCD = natural death (mostly) . Differential Diagnosis: Poisoning (e.g., CO). Trauma (blunt chest force). Drug overdose. Death in Custody: struggle & stress may precipitate SCD.

35. Summary & Future Outlook SCD: Common, complex cause of unexpected death. Meticulous forensic investigation required. Negative autopsy → molecular and electrolytes . Future Directions: Wider use of molecular autopsies. Genetic forensic databases. Improved public health screening.

36. References Robbins & cotran pathologic basics of disease 10 th international edition-2021. The essentials of forensic medicine & toxicology 35 th edition.

37. Questions & Discussion Thank You !