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Sudden cardiac death

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presentation of sudden death and death due to cardiac causes

presentation of sudden death and death due to cardiac causes

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  • Today I will be presenting on sudden cardiac death. I will be looking to define sudden death.. Look at the principles of examination in a case of sudden death. I will also be looking at the causes of sudden death and finally I will be discussing on the cardiac causes of sudden death.
  • WHO define sudden death as any death that occurs within 24 hours from the onset of symptoms. Sudden death can be misleading in terms that someone who dies from meningitis might be thought to have died suddenly and unexpectedly for the family members. However, the attending physician might think of the death as neither sudden nor unexpected. Most cases of sudden unexpected death can be attributed to failure of medical intervention. As such, following proper medical care, the deaths could have been predictable as well as preventable.
  • Most cases of sudden death occur either between the ages of 1 month to 30 years or more than 70 years of age. Most common aetiological causes of sudden death in the infancy can be attributed to congenital anomalies just as most cases of sudden death in the older age group can be attributed to arteriosclerotic heart disease. Clinically silent degenerative diseases are the most common cause of sudden death in the entire population. Some deaths that could be labelled as sudden and unexpected are due to electrocution with household current. The confusion may arise due lack of any injuries on the body, the individual may have removed the appliance from the plug. The deceased may have walked to another room before he died thereby removing the obvious implications of his surroundings. Another case of mistaken labelling as sudden death is where death is due to unsuspected drug overdose or poisoning. Yet another case is of concealed trauma where clinical examination of the deceased revealed no abnormalities at the time.
  • The examination of a dead body in case of sudden death will comprise of gross anatomical examination of the body. The examination may reveal any disease or injury that might be attributable to the death. Following gross examination, microscopic examination should be done. Microscopic examination may reveal disease or pathology that was completely unrecognised on gross. Following microscopic examination, toxicological studies of the body fluids should be carried out to rule out any drug overdose or poising. Further lab studies should be carried out ???? Microbiogical cultures may demostrated disease processes not seen on gross or microscopy.
  • Some common mistakes made by medical examiners in cases of sudden death resulting in an obscure or negative autopsies include the following. Failure to examine the sinuses of valsalva and the coronary ostia could lead to failure to detect obstructing lesions at these sites. Similarly, failure to section coronary arteries at regular close intervals in its’ entire course may lead to failure to locate the site of thrombosis or occlusion. Failure to examine all the coronary arteries may lead to failure to locate the site of occlusion.
  • The aetiology of sudden death can be divided into two broad categories. Sudden deaths occurring due to cardiac disease and those occurring due to non-cardiac causes. Some common cardiac causes of sudden unexpected death are :
  • Some common non-cardiac causes of sudden death are:
  • Cardaic causes of sudden death accounts for more than 300k deaths every year in the U.S. out of which 80% are due to coronary arteriosclerosis. Hypertensive cardio-vascular disease accounts for far less deaths. This could be due to the lack of evidence in cases of these deaths. This leading to physicians being reluctant to diagnose HCVD as the cause of death in view of the lack of supporting evidence.
  • The 2004 WHO Disability adjusted life years report gives the figures as follows.
  • Death can be attributed to the lack of functionality of the tissues. The state of death is conferred by absent electro chemical intercellular communication in the brain and heart. This electro-physiological disturbance leaves no anatomical traces or records except in cases where the individual had been monitored before death. Therefore, one should consider the circumstances before death as well as the surroundings of the body. Another important medical tool that should be availed of is the medical history of the deceased. These can help in determining the cause of death in cases where there are no anatomical abnormalities.
  • As I said earlier, death is due to the electro-mechanical decoupling in the body. Some common mechanisms for these are: Increased excitability of the myocardium causing propagation of ectopics. These ectopic beats cause ventricular tachycardia or premature ventricular contractions. In the presence of circus pathways, these ectopics may lead to development of ventricular fibrillation causing ineffective circulation with lead to rapid death. Ventricular excitability can be enhanced by Myocardial hypertrophy, Ethanol intoxication, Ischaemia, Sympathetic discharge, Hyper-thyroidism. Ventricular excitability is also enhance by Drugs like Caffeine, Sympathomimetic drugs, Epinephrine, Norepinephrine, Theophylline, Mono-Amine Oxidase inhibitors, Tri-cyclic Anti-depressants, Depression of the myocardial contractility causeing failure of the propagation of impulses. In case of failure of propagation of electrical impulse from the SA node, the ectopic pacemakers start producing impulses. The failure of this safety mechanism will lead to cardiac asystole and death. Myocardial depression can be caused by Parasympathetic discharge, Myxoedema, Hypothermia, Hyperkalemia
  • In addition to the causes mentioned above, the nervous system itself can produce strong electrochemical discharges that cause death by causing cardiac asystole, ventricular fibrillation or vascular redistribution. These are controlled by the vasomotor and the respiratory centers in the brain. The important vasomotor centers are present in the mid-brain, region of the third ventricle and in the medulla oblongata. The centers influence the heart through the sympathetic and the parasympathetic pathways. The sympathetic pathways involve the intermediolateral columns of the spinal cord from where fibers pass to the sympathetic ganglia especially the stellate ganglion and finally via the sympathetic branches passing along the base of the heart to supply the heart. The parasympathetic fibers pass via the vagus nerve, passing through the mediastinum to supply the heart The important respiratory centers are present in the medulla and are under the influence of the dorsal pontine centers. The respiratory center exert their influence via fibers in the upper spinal cord and the phrenic nerves originating from c3,c4 and c5 passing along the neck and through the pericardial sac to supply the diaphragm. Any abnormal discharge could cause either increased excitability or depression of the myocardium.
  • Following cessation of circulation due to whatever cause, consciousness is lost within 15 seconds, and cerebral function becomes irreversibly ceases within 5 minutes. In case of respiratory arrest, cerebral function is the same in that consciousness is lost in 15 seconds and death occurs with 5 minutes. However, cardiac function is not disturbed initially so that there is initial tachycardia followed by bradycardia and then complete electromechanical dissociation with presence of electrical activity but no circulation till death occurs.
  • Other biochemical changes that could lead to cessation of vital functions including electrolyte disturbances, diabetic ketoacidosis, drug overdosages and poisoning which might produce alterations of the intracellular composition causing death.
  • Sudden death can basically be divided into 2 groups: those with functional abnormality and those with structural abnormality. In cases of sudden death due to functional disturbance, the cases can again be divided into those that has a significant anatomic alteration for which functional disturbance can be attributed or referred and those in which no anatomic alteration is evident at autopsy. Those cases where there is no anatomic alteration are designated functional death. Examples of functional death are: Vagal Cardiac Inhibition – this is sudden death that occurs within seconds to within a minute or two after minor trauma or peripheral or internal stimulation of a relatively simple and ordinarily innocuous nature. These cases are often categorised as accidental in nature. Eg: Blow to the larynx, Blow to the solar plexus, Kick in the scrotum, Carotid sinus pressure, Cannulation of the cervix Spontaneous ventricular fibrillation – history is of non-suspicious circumstances surround death associated with pre-mortem exertion, exercise or intense emotional situation. On complete autopsy, including toxicology and microscopy, no abnormalities are noted. Studies have shown that these cases are associated with patients with electrically unstable hearts that suffer a fatal dysrhythmia following adrenergic discharge. Sudden Nocturnal Cardiac Death – There is a particular type of sudden cardiac death that was prevalent on in east and south asia that has now been discovered to have occurred in the US as well following migration of Hmongs to the US. This syndrome is called by various names, in Japan it is called Pokkuri, in phillipines it is called Bangungut, and in the thailand, vietnam, laos and cambodia it is called laitai and nonlaitai. It is a case of sudden nocturnal cardiac death where ventricular dysrhythmias are demostrated. This could be attributed to the night terrors occurring in non-REM sleep or due to the increased adrenergic discharge during the nocturnal cycle. These cases show negligible gross changes. Another group of functional death are the ECG syndromes. These are syndromes that may clinically show evidences on ECG but are not associated with any gross abnormalities. Three common variants of this group are: Pre-excitation syndromes – most importantly Wolf-Parkinson-White syndrome. Long Q-T syndrome and lastly Sick sinus syndrome. Wolf Parkinson White syndrome: In this syndrome, there are extra pathways communicating between the atria and ventricles. This leads to re-entry of impulses, which gets recirculated and thereby causes ventricular tachycardia and ventricular fibrillations. The ECG findings are Wide QRS complex and Delta wave with a short P- δ interval. Long Q-T syndrome – This is characterised by prolonged recovery phase from depolarisation of the cardiac muscles. This leads to a tendency to syncope and could lead to death due to ventricular tachydysrhythmias. They are of two types: Congenital and acquired. Congenital long Q-T syndrome is seen in Romano-Ward syndrome and Jervell and Lange-Nielsen syndrome. Acquired cases are seen with drugs, electrolyte abnormalities, anorexia nervosa, Hypothermia, Toxic substances, Liquid diet. Sick sinus syndrome – This can be seen in cases of surgical manipulation in the region of the SA node. May lead to spontaneous sinus bradycardia, syncope and rarely sudden death.
  • This is a diagrammatic sketch of the right side of the heart, showing the conduction system. RA – Right atrium; RV – Right ventricle; L – Limbus fossae ovalis; C – Coronary sinus; SVC – Superior vena cava; IVC – Inferior vena cava; M – medial leaflet of the tricuspid valve; AV – AV node; PB – Bundle of His, pentration portion; BB – Bundle of His, branching portion; RBB – Right bundle branch; PA – Pulmonary artery; Ao – Aorta; SA – SA node; PV – Pulmonary valve; S – Septal band; CBF – Central fibrous body.
  • This is a diagrammatic sketch of the left side of the heart showing the conduction system of the heart. LA – Left atrium; LV – Left ventricle; Ao – Aorta; CM – central fibrous body and pars membranacea; BB – Bundle of His, branching portion; MLB – Main left bundle branch; AR – anterior radiation of the left bundle branch; PR – Posterior radiation of the left bundle branch; MS – Midseptal fibers of the left bundle branch; P – Peripheral Purkinje nets; M – Mitral valve; PT – Pulmonary trunk
  • Some lesions of the conducting system which may be seen on either gross or microscopic examination are: Fibrous replacement of the bundle branches – This is commonly seen in aged and hypertrophied hearts. It present as premature sclerosis of basal septum and can be diagnosed by microscopic examination of the conducting system. Calcification of mitral anulus – This is commonly seen in elderly females and is commonly associated with Rheumatoid Arthritis, Ankylosing spondylitis and scleroderma. There is impingement of the AV node by calcific deposits. Commonly seen in the presence of ventricular endocardial disease, left bundle branch being the most commonly involved.
  • Congenital anomalies of the conducting system may be compatible or incompatible with life. Those that are compatible with life may cease to be so following external insult. Some common anomalies found in healthy individuals are Persistent fetal dispersion of AV node, Ectopic connections between the node and ventricles. Ectopic His bundle, Ectopic AV tracts, Marked sclerosis of the artery to AV node. Role of these anomalies in sudden cardiac death is debatable and undecided.
  • Congenital anomalies in the development of the coronary arteries. These are compatible with life till the These are some common developmental anomalies – Origing of the left coronary artery from the right sinus of Valsalva with the artery passing between the aorta and pulmonary artery; Only a single coronary ostium in the right sinus of Valsalva with the left coronary artery arising from the proximal right coronary artery; Origin of the right coronary artery from the left sinus of Valsalva; Origin of the left coronary artery from the right sinus of Valsalva with the artery passing dorsal to the aorta rather than between the aorta and pulmonary artery; Coronary artery hypoplasia No diagnostic criteria has been set forth for this entity. Sudden death is more likely when the anomalous artery forms an acute angle with the sinus of Valsalva or produces a right angle in the artery itself.
  • Other congenital anomalies that are less compatible with life are bridging of the coronary arteries, Dissecting coronary aneurysm and coronary artery spasm. Bridging of coronary arteries – This refers to the anomalous pathway of the epicardial arteries where the artery runs an intramural couse. Therefore, on contraction of myocardium, the artery gets occluded, leading to ischemia and thereby may be a cause of sudden death. Dissecting coronary aneurysm – may be primary or secondary to extension of the aortic root dissection. The extension of the aortic root dissection may be spontaneous or due to trauma. Seen more commonly in peri-partal females. Coronary artery spasm – In this, the coronary artery undergoes spasms which cause significant constriction and decrease in blood supply leading to ischemia. Angina associated with acute MI-like symptoms are the primary complaints. However, on autopsy, infarct is not seen and neither is there any significant atherosclerosis. This is seen in Printzmetal’s angina and unstable angina.
  • The illustration in the left upper corner is the most common and clinically significant anomaly. There is an anomalous origin of the LCA from the right sinus of Valsalva and the LCA courses between the aorta and pulmonary artery. This interarterial course can lead to compression of the LCA (yellow arrows) resulting in myocardial ischemia. The other anomalies shown do not produce hemodynamic instabilities.
  • Interarterial LCA On the left images of a patient with an anomalous origin of the LCA from the right sinus of Valsalva and coursing between the aorta and pulmonary artery. Sudden death is frequently observed in these patients.
  • ALCAPA On the left images of a patient with an anomalous origin of the LCA from the pulmonary artery, also known as ALCAPA. ALCAPA results in the left ventricular myocardium being perfused by relatively desaturated blood under low pressure, leading to myocardial ischemia. ALCAPA is a rare, congenital cardiac anomaly accounting for approximately 0.25-0.5% of all congenital heart diseases.  Approximately 85% of patients present with clinical symptoms of CHF within the first 1-2 months of life.
  • Myocardial bridging Myocardial bridging is most commonly observed of the LAD (figure). The depth of the vessel under the myocardium is more important that the lenght of the myocardial bridging. There is debate, whether some of these myocardial bridges are hemodynamically significant.
  • Cardiomyopathy is a group of diseases that is characterised by myocardial dysfunction. The cause may be known or unknown. And the cardiomyopathy is not the result of arteriosclerotic, hypertensive, congenital or valvular diseases. It can be divided into 3 broad categories. Dilated or congestive, Hypertrophic and restrictive or onliterative.
  • Dilated or congestive cardiomyopathy is associated with enlargement of the heart with dilatation of all four chambers on gross examination. It usually presents with presence of endocardial thrombi. Microscopically, it presents as extensive interstitial and perivascular fibrosis. Most common causes being chronic alcoholism, peripartum cardiomyopathy, chronic myocarditis and idiopathic. In chronic alcoholism , the effects are due to direct toxicity of alcohol on the cardiac musculature, nutritional effects of alcohol on the body and toxic effect of additives like cobalt. Heart failure with gross enlargement of the chambers in the last month of pregnancy or in the first six months post-partum is designated Peripartum cardiomyopathy. In about half of the individuals, the enlarged heart returns to normal in 6-12 months post partum. If however, the failure becomes incompatible with life and death occurs, the finding on gross examination would be presence of grossly dilated heart with flabby myocardium. Presence of mural thrombosis is a common finding in these cases. Microscopically, signs of degeneration and/or hypertrophy may be present. It may also present as focal or diffuse interstitial myocardial fibrosis. Microscopically, one can find scattered mono-nuclear infiltrates as well as occasional fatty infiltrates. In chronic myocarditis, the common cause is the exposure to toxic substances like cobalt and adriamycin. The mechanism in these cases is due to the direct toxicity of the substance to the cardiac musculature, due to atypical reaction to the toxin and due to excessive dosage of the drug. This is clinically associated with arrhythmias leading to sudden death.
  • Hypertrophic cardiomyopathy is the single most common cause of sudden death in adolescent and young adults. It shows an autosomal dominant genetic inheritance. On gross, the left ventricle is hypertrophied without dilatation. The hypertrophy is disproportionate, asymmetrical in the septum as compared to the left ventricle. This causes obstruction to the outflow tract. Rarely, it may also present as concentric hypertrophy of the left ventricle similar to that seen in hypertensive patients. On microscopy, the myocardial fibers are in dissary with presence of bypertrophied bizarre myocardial cell. This is typically seen in the septal myocardium.
  • This is a microscopic view of the myocardium seen under 160 x magnification that shows groups of myocardial fibers that are arrange haphazardly as well as replacement of some myocardial fibres by connective tissue.
  • This is a microscopic section of the myocardium showing a cross-section of a small branch of the coronary arteries seen under 160 x magnification. The artery is seen to have thick walls and reduced luminal cross-sectional area. Presumably the arterial wall changes are secondary to the myocardial disease.
  • This is a microscopic view of a cut section of the heart seen at 160 x magnification. This shows the bizarre arrangement of clusters of myocardial fibers as seen in hypertrophic cardiomyopathy. This section is from a 7 year old girl who died suddenly and unexpectedly.
  • The commonest valvular diseases are mitral valve prolapse, aortic stenosis and acute bacterial valvulitis Mitral valve prolapse also know as floppy mitral valve, myxomatous degeneration of the mitral valve or Barlow’s syndrome is one of the commonest cardiac conditions in the world. It is thought that 15% of the world’s population is inflicted with symptomatic or asymptomatic mitral valve prolapse. It is generally an asymptomatic condition that continues to remain undetected unless it becomes symptomatic due to some associated insult. Generalised cardiac symptoms are the primary indicators like angina, palpitation, shortness of breath etc. Aortic stenosis has become more prevalent than mitral stenosis in todays world. This is due to the decrease in mitral stenosis of rhematic fever as well as advancement in the field of surgery for mitral stenosis. Congenital aortic stenosis is the commonest aetiology followed by Rheumatic, secondary calcification of congenital bicuspid valves and Primary degenerative calcification of normal aortic valves. Thrombo-embolic accident following acute bacterial valvulitis is another common cause of sudden death that might be missed. It most commonly involved the tricuspid valve and is seen common in IV drug abusers.
  • This is a case of a 45-year old physician who had a long history of palpitations and was found dead in bed. His ECG showed normal sinus rhythm, normal PR and QT intervals, inverted T-waves in lead 3 and normal QRS morphology. A 24-hour Holter monitor revealed frequent premature ventricular contractions and several episodes of non-sustained (three to five beats) ventricular tachycardia. The heart weighed 483 grams. All chambers especially the left atrium were hypertrophied and enlarged. THe posterior leaflet of the mitral valve (PM) was redundant, markedly thickened, nodose and calcified at the annulus. The annulus of this leaflet was elongated and the valve was moored on the left atrial side.
  • This is a case of a nineteen year old stable college student who while watching television was startled when her mother entered the living room and she exclaimed that her mother had scared her because she thought she had gone to bed and didn’t expect to see her come in the room. She then fell to the floor dead. She had recurrent dizzy spells a few days before death. Her father died suddenly at age 36 and his father died a few months later, apparently of heart failure with a history of repeated episodes of passing out. Two of the father’s sisters had heart problems. Her two younger sisters were diagnosed as having mitral valve prolapse but are asymptomatic and are now on small doses of propanolol. The heart weighed 220 grams. There was slight hypertrophy and enlargement of the left atrium and right ventricle. The mitral origice was normal in size. The valve showed distinct prolapse of the posterior leaflet which was redundant and nodose. This redundancy extended to the posterior part of the anterior leaflet. All other valves and the coronaries were normal.
  • This is a microscopic cut section of the heart including the mitral valve at ?x magnification. The first picture shows the degenerative process
  • This is a microscopic section of the myocardium at 400 x magnification showing the mucoid degenerative area of mitral valve.
  • Clinical features of myocarditis could range from being asymptomatic to non-specific symptoms and could result in death.
  • The causes could be infective in nature, secondary to connective tissue disorders, due to physical agents, chemical poisons or drugs.
  • Coronary arteriosclerosis has been associated with a 9 fold increase in the mortality. It shows increased incidence with increase in age and affects men more than women in all age groups. A postiive stress test, is associated with increased risk of myocardial infarction. Symptoms range from vague symptoms like tiredness and fatigue, generalised cardiac symptoms like to chest pain, palpitations and shortness of breath. In one-fourth of patients, the first sign is death. Estimated half of all sudden death victims present with the history of atherosclerotic heart disease.
  • The diktat for coronary arteriosclerosis is that it can result in death at any time and any any place. Sudden death is the first and last symptom in ¼ of individuals with cardiovascular disease. Half of individuals with coronary atherosclerosis die suddenly. Sudden dysarythmias occur in people with no distress previously.
  • The mechanism of sudden death in an individual can be attributed to Myocardial ischemia which leads to an acute elecrical event, most commonly a ventricular tachydysrhythmia, in the presence of a super-imposed transient risk factor.
  • Hypertension is the most important risk factor for sudden death in individuals with coronary arteriosclerosis. Hypertension and arteriosclerosis are risk factors for myocardial infarction and hence have a multi-fold increased risk of sudden death. Other risk factors include stimulation of vagal discharge, coronary artery spasm, thromboembolism, sympathomimetic drugs like caffeine, epinephrine.
  • Exercise is associated with increased incidence of sudden death. Exercise causes increased heart rate which increases the myocardial oxygen demand. Exercise also increases the catecholamine levels in the body. This causes the myocardium to get hyper-excitable. Majority of cases of acute cardiac event presents with only electrical instability with only a few showing signs of infarction. Only a small percentage of sudden death is associated with acute coronary artery occlusion with thrombus and myocardial infarct Majority of cases of coronary artery disease who die in the hospital are associated with thrombotic occlusion and infarct.
  • Hypertensive cardiovascular disease is associated with concentric thickening of the arterial wall. In case of plaque formation there is eccentric thickening of the wall. In case of elderly, the vessel wall are rigidly calcified. However, the lumen remains patent. Most individuals who die due to coronary arteriosclerosis have involvement of at least 2 vessels. The most commonly involved arteries are left main coronary artery and proximal left anterior descending coronary artery. For diagnosis of death due to coronary arteriosclerosis, the circumstances of death should be taken into account. After ruling out other causes beyond reasonable doubt, the diagnosis may be give as death due to coronary arteriosclerosis.
  • Even on microscopy, it is impossible to detect MI on Hematoxylin and Eosin stains if less than five hours has occurred. However, it is possible to detect by Para-amino schiff stain. There is decreased glycogen in the myocardium. In 5 – 24 hours, neutrophils appear in the myocardium follwed by appearance of degenerating neutrophils. In 1 – 3 days extensive neutrophil infiltrate and their degenarating forms as well is present in the myocardium. 4 – 6 days, Neutrophils, eosinophils, macrophages, pigment, fibroblasts, capillaries ( NO lymphocytes) 7 – 14 days, Neutrophils, eosinophils, macrophages, pigment, fibroblasts, capillaries, lymphocytes, plasma cells 2 – 8 weeks, Eosinophils, macrophages, pigment, fibroblasts, capillaries, lymphocytes, plasma cells ( NO neutrophils) > 2 months, Connective tissue condensed; minute foci of necrosis may still persist. Exudate has essentially disappeared, but a small number of lymphocytes and pigmented macrophages may be seen until one year
  • This is a microscopic section of the myocardium at magnification of 160 x showing wavy myocardial fibers in very early myocardial infarction.
  • This is a microscopic section of the myocardium at a magnification of 400 x showing pyknotic myocardial fiber nuclei. The wide spacing between adjacent myocardial fibers is indicative of myocardial oedema. These are both signs of very early myocardial infarction.
  • This is a microscopic section of the myocardium at a magnification of 1000 x showing contraction bands and granularity of cytoplasm in very early myocardial infarction.
  • This is a cut section of the myocardium at magnification of 160 x showing spotty scarring with isolated clusters of myocardial fibers . These are findings present in late myocardial infarction and could be the source of dysrhythmias and sudden unexpected death.
  • This is a microscopic section of the myocardium at magnification of 160 X showing radial zone of preserved myocardial fibers surrounding an obviously diseased small artery near a point of branching. The degree of myocardial ischaemia is less near the artery as compared to the area further away that shows only scar tissue. This can be seen in late myocardial infarction.
  • Mallory described that histological features could be determined on gross examination as well: In the First 72 hours the infarction appears pale and drier. Sometimes, hemorrhage is observed. On the 4 th days, Yellow line appears at the periphery due to leukocytic infiltration. Infarct becomes yellow brown. In 6 – 8 days, Band becomes broader and sometime yellow-green In 8-10 days, Granulation tissue is formed around the infarct forming a reddish-purple zone. Size of infarct decreases, depression may be seen around the infarct. In 2 – 3 weeks: healing continues, band of granulation tissue increases and central mass of necrotic muscles decrease. Infarct appears pale and red-brown color. 3-4 weeks: small islands of necrotic muscle surrounded by granulation tissue. >1 month: granulation tissue become older, collagen content increases, capillaries become compressed and less prominent. Infarct appears paler and gelatinous. 2 – 3 months Infarct contracts to form a white fibrous shrunken and firm scar.
  • One of the complications of myocardial infarction that could result in sudden unexpected death is perforation resulting in massive hemopericardium with cardiac tamponade. On opening the chest, one can immediately see a distended, taut, blue pericardial sac. This has been called the blue sign by some pathologists. This is usually associated with a transmural myocardial infarct that is extremely necrotic and inflamed. The commonest time period is between 5 – 7 days post-MI right before the connective tissue replaces the necrotic muscle.
  • In conclusion, Sudden death has been defined as any death that occurs within twenty four hours of the onset of symptoms. Sudden death is commonly due to cardiac origin. Among cardiac deaths, the most commonly occuring based on the age it affects are: Congenital in infants In adults it is mainly due to coronary insufficiency caused by coronary artery disease, valvular diseases, myocardial diseases and disease of the conduction system.
  • Transcript

    • 1. Rijen ShReStha 21-09-2066M.D. ReSiDent, 1St YeaR
    • 2.  Define sudden death Principles of examination in case of a sudden death Causes of sudden death Discussion on cardiac causes of sudden death
    • 3.  Sudden death is any death that occurs within 24 hours of onset of symptoms. ▪ Primary or unpredictable or unexpected ▪ Predictable ▪ Most cases of sudden unexpected death are due to failure to seek timely medical intervention. ▪ If proper medical attention was availed of, death might have been not only predictable but also preventable.
    • 4.  Age: ▪ 1 month – 30 years ▪ > 70 years Aetiology ▪ Most common: clinically silent degenerative diseases ▪ May be over-looked if evidences are not supportive ▪ Electrocution with household current ▪ Unsuspected drug overdose / poisoning ▪ Concealed trauma with no findings.
    • 5.  Anatomical examination ▪ Disease ▪ Injury ▪ Evidence of temporal cause Microscopic examination ▪ Disease completely unrecognized on gross Toxicology Lab studies Microbiological cultures
    • 6.  Failure to examine the sinuses of valsalva and coronary ostia Failure to section coronary arteries at regular, close intervals. Failure to examine entire length of the coronary arteries. Failure to examine ALL the coronary arteries.
    • 7. Cardiac Causes  Coronary artery disease ▪ Coronary atherosclerosis ▪ Developmental anomalies ▪ Coronary artery embolism ▪ Others ▪ Vasculitis ▪ Dissection  Myocardial diseases ▪ Cardiomyopathies ▪ Myocarditis and other infiltrative processes ▪ Right ventricular dysplasis  Valvular diseases ▪ Mitral valve prolapse ▪ Aortic stenosis and other forms of left ventricular outflow obstruction ▪ Endocarditis  Conduction system abnormalities Modified from Virmani R, Roberts WC: Sudden cardiac death. Hum Pathol 18:485,
    • 8. Non-cardiac causes Hemorrhage Intra cranial hemorrhage Diseases of the aorta G.I. bleeding Respiratory tract bleeding Intra-cranial causes other than hemorrhage Epilepsy Intracranial Tumors Meningitis Miscellaneous Primary Pulmonary Hypertension Bronchial Asthma Psychiatric Pulmonary thrombo-embolism Epiglottitis Senescence
    • 9. > 300,000 deaths per year ▪ 80% of which are due to Coronary arterioscleriosisLess due to ▪ Hypertensive Cardio-vascular disease ▪ Cardio-myopathies ▪ Valvular diseases ▪ Myocarditis ▪ Others including Congenital Deformities.
    • 10.  WHO DALY Report 2004 Nepal India U.S.ACardio-vascular disease 49.9 2810.0 922.7Rheumatic Heart Disease 1.6 103.9 3.5Hypertensive Heart Disease 6.2 49.7 43.7Ischaemic Heart Disease 23.3 1531.5 514.4Inflammatory Heart Disease 0.8 57.8 33.4
    • 11.  Electrophysiological disturbances leave no anatomical traces, gross or microscopic.  Circumstances  Surroundings  Medical History
    • 12. Common mechanisms for electro-mechanical decoupling: Myocardial hyper-excitability causing propagation of ectopics.  Ectopic beats causing ventricular tachycardia or premature ventricular contractions.  Presence of circus pathways leads to development of ventricular fibrillation  Ineffective circulation leading to rapid death. Myocardial depression causing failure of propagation of electrical impulses.  Ectopic pace-maker may produce impulse ▪ Failure to establish ectopic pace-maker leads to cardiac asystole and death.
    • 13. Nervous system can produce strong or electro- chemical discharges that cause ▪ Asystole ▪ Ventricular fibrillation ▪ Vascular redistribution
    • 14.  On cessation of circulation,  Consciousness lost within 15 seconds  Irreversible cessation of cerebral function within 5 minutes. In case of respiratory arrest, cerebral response is the same. Cardiac function will continue  Initial tachycardia  Bradycardia  Electromechanical dissociation with presence of electrical activity but no circulation.
    • 15.  Other bio-chemical changes leading to sudden cessation of vital functions:  Electrolyte disturbances  Diabetic ketoacidosis  Drugs
    • 16. Death due to functional abnormality  Deaths in which there is a significant anatomic alteration from which functional disturbance is obvious or can be referred.  Deaths in which no anatomic alteration can be demostration by routine autopsyThe term ‘functional death’ is used for the latter i.e. apparentsudden cardiac deaths that occur withour any anatomicallysignificant findings by customary autopsy techniques.
    • 17.  Lesions of the conducting system ▪ Fibrous replacement of the bundle branches (Lev’s Disease) ▪ Aged and hypertrophied hearts ▪ Premature sclerosis of basal septum ▪ Diagnosed following microscopy of conducting system ▪ Calcification of mitral anulus ▪ Impingement of the atrio-ventricular node by calcific deposits ▪ Elderly women ▪ Rheumaroid arthritis, ankylosing spondylitis and scleroderma ▪ ventricular endocardial disease may involve left bundle branch. ▪ Collagen vascular diseases ▪ Infiltrative and inflammatory conditions
    • 18. Common anomalies found in healthy individuals ▪ Persistent fetal dispersion of atrio-ventricular node. ▪ Ectopic connections between the node and ventricles ▪ Ectopic His bundle ▪ Ectopic atrio-ventricular tracts ▪ Marked sclerosis of artery to the atrio-ventricular node.Role of these anomalies in sudden cardiac death is debatable and undecided.
    • 19.  Origin of the left coronary artery from the right sinus of Valsalva with the artery passing between the aorta and pulmonary artery. Only a single coronary ostium in the right sinus of Valsalva with the left coronary artery arising from the proximal right coronary artery Origin of the right coronary artery from the left sinus of Valsalva. Origin of the left coronary artery from the right sinus of Valsalva with the artery passing dorsal to the aorta rather than between the aorta and pulmonary artery. Coronary artery hypoplasia  no diagnostic criteria has been set forth for this entity.
    • 20.  Bridging of coronary arteries: ▪ anomalous pathway of the epicardial arteries ▪ intramural course. ▪ On contraction of the myocardium, the artery gets occluded causing ischaemia. Dissecting coronary aneurysm ▪ Primary ▪ secondary to extension of aortic root dissection ▪ Could be spontaneous ▪ Could be due to trauma Coronary artery spasm ▪ Angina coupled with symptoms similar to acute MI ▪ Autopsy shows no infarct ▪ Coronary artery patent without significant atherosclerosis, narrowing or coronary spasm
    • 21.  A diverse group of disease of both known and unknown aetiology, characterised by myocardial dysfunction. Diseases not the result of arteriosclerotic, hypertensive, congenital or valvular disease.3 types ▪ Dilated or congestive ▪ Hypertrophic ▪ Restrictive or obliterative
    • 22.  Gross ▪ Enlargement of the heart with dilatation of all four chambers ▪ Endocardial thrombi is commonly seen Microscopically ▪ Extensive interstitial and peri-vascular fibrosis ▪ Most common cause: ▪ Chronic alcoholism  Direct toxic effects of alcohol  Nutritional effects of alcohol  Toxic effects of additives – E.g. Cobalt ▪ Peripartum cardiomyopathy ▪ Chronic myocarditis ▪ Idiopathic
    • 23.  Genetic inheritance – autosomal dominant Most common cause of sudden death in adolescents and young adults Gross ▪ Hypertrophied, non-dilated left ventricle ▪ Disproportionate, asymmetrical hypertrophy of inter-ventricular septum as compared to free left ventricular wall ▪ Obstruction of the outflow track ▪ May also present as concentric left ventricular hypertrophy Microscopically ▪ disarray of ventricular myocardial fibers ▪ hypertrophied bizzare myocardium cells. ▪ Seen typically in the septum
    • 24.  Mitral Valve prolapse  Floppy mitral valve  Myxomatous degeneration of the mitral valve  Barlow’s Syndrome Aortic stenosis  Congenital  Rheumatic inflammation with fusion of cusps  Secondary calcification of congenital bicuspid valves  Primary degenerative calcification of normal aortic valves Acute bacterial valvulitis ▪ involves the tricuspid valve ▪ IV drug abusers
    • 25.  Clinical Features Could range from no symptoms to non-specific symptoms and may also result in death.  None  Acute fulminating Congestive Heart Failure  Sudden Death
    • 26.  Aetiology  Infective: ▪ Bacterial ▪ Rickettsial ▪ Viral ▪ Protozoal ▪ Fungal  Connective tissue disorders: ▪ Rheumatic Disease ▪ Rheumatoid Arthritis  Physical agents  Chemical poisons or drugs  Idiopathic
    • 27.  Associated with a 9x increase in mortality Increased incidence with increasing age. More in men than in women of all ages. Positive Treadmill/Exercise Stress Test associated with increased riskSymptoms: ▪ Vague symptoms including tiredness and fatigue ▪ Chest pain ▪ Palpitations ▪ Shortness of breathIn one-fourth of patients, first symptom is sudden death.Approximately Half of all sudden death victims present with history of Atherosclerotic Heart Disease.
    • 28. “ANY TIME and ANY PLACE” Sudden death is the first and last symptom in ¼ of individuals with cardiovascular disease. Half of individuals with coronary atherosclerosis die suddenly. Sudden dysarythmias occur in people with no distress previously.
    • 29.  Sudden death, in an individual with significant coronary atherosclerosis, occurs due to  Myocardial ischemia  Acute electrical event – a ventricular tachydysrhythmia  “Super-imposed transient risk factor”
    • 30.  Transient rise in Blood pressure Sympathetic discharge Coronary artery spasm Embolism Sympathomimetic stimulation of heart ▪ Caffeine ▪ Epinephrine ▪ Cocaine
    • 31.  Exercise ▪ Increased heart rate ▪ Increased myocardial oxygen demand ▪ Increased catecholamine levels – ‘hyper-excitability’ Majority of cases of acute cardiac event presents with only electrical instability with only a few showing signs of infarction. Only a small percentage of sudden death is associated with acute coronary artery occlusion with thrombus and myocardial infarct Majority of cases of coronary artery disease who die in the hospital are associated with thrombotic occlusion and infarct.
    • 32.  Hypertensive cardiovascular disease – concentric thickening Plaque formation – eccentric thickening In elderly, vessel walls rigidly calcified but with patent lumina. Most individuals, 2 vessel involvement  Left main coronary artery  Proximal left anterior descending coronary artery Consider terminal circumstances of death and exclude other causes beyond reasonable doubt.
    • 33. < 5 hours: Impossible by H&E : possible by PAS (decreased glycogen)5 – 24 hours: Appearance of neutrophils to appearance of degenerating neutrophils1 – 3 days: Exclusively neutrophils and their degenerating forms4 – 6 days: Neutrophils, eosinophils, macrophages, pigment, fibroblasts, capillaries (NO lymphocytes)7 – 14 days: Neutrophils, eosinophils, macrophages, pigment, fibroblasts, capillaries, lymphocytes, plasma cells2 – 8 weeks: Eosinophils, macrophages, pigment, fibroblasts, capillaries, lymphocytes, plasma cells (NO neutrophils)> 2 months: Connective tissue condensed; minute foci of necrosis may still persist. Exudate has essentially disappeared, but a small number of lymphocytes and pigmented macrophages may be seen until one year
    • 34. Hours Days Weeks1 5 6 12 24 2 3 4 5 6 10 12 14 18 3 4 8 52 Mural Thrombus (Completely organized after 3 weeks) Fibrinous Pericarditis (Organisation beginning at 5 days) Lymphocytes, Plasma Cells Fibroblasts Capillaries Scar Tissue Necrosis Collagen Pigmented Macrophages Eosinophils Neutrophils (with degenerating forms beginning at 24 hours) Adapted from Mallory et al. American Heart Journal 18:647-71, 1939
    • 35.  Mallory describes that histological features could be determined on gross examination as well:  First 72 hours: Infarction appears pale and drier. Sometimes, hemorrhage is observed.  4 days: Yellow line appears at the periphery due to leukocytic infiltration. Infarct becomes yellow brown.  6 – 8 days: Band becomes broader and sometime yellow-green  8-10 days: Granulation tissue is formed around the infarct forming a reddish-purple zone. Size of infarct decreases, depression may be seen around the infarct  2 – 3 weeks: Healing continues, band of granulation tissue increases and central mass of necrotic muscles decrease. Infarct appears pale and red-brown color.  3-4 weeks: Small islands of necrotic muscle surrounded by granulation tissue.  >1 month: Granulation tissue become older, collagen content increases. Capillaries become compressed and less prominent. Infarct appears paler and gelatinous.  2 – 3 months Infarct contracts to form a white fibrous shrunken and firm scar.
    • 36.  Perforated Myocardial infarct forming massive hemopericardium with cardiac tamponade.  Distended, taut, blue pericardial sac.  Usually associated with transmural myocardial infarct that is extremely necrotic and inflamed  Occurs between 5 – 7 days before connective tissue replaces necrotic muscle.  History of minimal or no chest discomfort.  Rapid death
    • 37.  Sudden death – any death that occurs within twenty four hours of onset of symptoms. Common causes of sudden death are cardiac in nature.  In infants – congenital  In children, adolescents and young adults ▪ Cardiomyopathies ▪ Myo carditis ▪ Coronary artery anomalies  In adults – coronary insufficiency caused by coronary artery disease. – Valvular diseases – Myocardial diseases – Diseases of the conduction system