The role of acute myocardial infarction in sudden cardiac death—a statistician's nightmare

Lovegrove, T; Thompson, Peter L.

doi:10.1016/0002-8703(78)90002-9

Cited by 50 publications

(9 citation statements)

References 7 publications

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“…In recent studies using durations≤1 hour 33,34 and detecting thrombi by cross‐sectioning major coronary arteries every 0.5 cm, 22,23 acute thrombi were detected in only ≤14% of the victims 22,23 . The authors of these studies concluded that acute coronary occlusion was not an important mechanism of SCD, confirming earlier studies using SCD definitions with brief antemortem symptom durations 24 , 26 . We previously reported that ICD recipients very rarely (<3%) develop acute coronary syndromes suggestive of atherothromboses in the wake of successful shocks for electrogram‐verified rapid highly lethal fast ventricular tachycardia (VT; >240/min) or ventricular fibrillation (VF) 35…”

Section: Cardiomegaly and Coronary Artery Disease In Patients With Scdsupporting

confidence: 60%

“…In western countries, autopsy studies of adult SCD victims have shown, without exception, increased heart weights compared with variously selected concurrent control groups 22–29 . A second constant feature is severe coronary atherosclerosis 22–29 . The Framingham investigators were among the first to point out that there was a close correlation between heart weight and the severity of coronary artery disease 30 .…”

Section: Cardiomegaly and Coronary Artery Disease In Patients With Scdmentioning

confidence: 99%

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Structural Pathways and Prevention of Heart Failure and Sudden Death

Pacifico

Henry

2003

Cardiovasc electrophysiol

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We review the macroscopic and microscopic anatomy of myocardial disease associated with heart failure (HF) and sudden cardiac death (SCD) and focus on the prevention of SCD in light of its structural pathways. Compared to patients without SCD, patients with SCD exhibit 5‐ to 6‐fold increases in the risks of ventricular arrhythmias and SCD. Epidemiologically, left ventricular hypertrophy by ECG or echocardiography acts as a potent dose‐dependent SCD predictor. Dyslipidemia, a coronary disease risk factor, independently predicts echocardiographic hypertrophy. In adult SCD autopsy studies, increases in heart weight and severe coronary disease are constant findings, whereas rates of acute coronary thrombi vary remarkably. The microscopic myocardial anatomy of SCD is incompletely defined but may include prevalent changes of advanced myocardial disease, including cardiomyocyte hypertrophy, cardiomyocyte apoptosis, fibroblast hyperplasia, diffuse and focal matrix protein accumulation, and recruitment of inflammatory cells. Hypertrophied cardiomyocytes express “fetospecific” genetic programs that can account for acquired long QT physiology with risk for polymorphic ventricular arrhythmias. Structural heart disease associated with HF and high SCD risk is causally related to an up‐regulation of the adrenergic renin‐angiotensin‐aldosterone pathway. In outcome trials, suppression of this pathway with combinations of beta‐blockers, angiotensin‐converting enzyme inhibitors, angiotensin‐II receptor blockers, and mineralocorticoid receptor blockers have achieved substantial total mortality and SCD reductions. Contrarily, trials with ion channel‐active agents that are not known to reduce structural heart disease have failed to reduce these risks. Device therapy effectively prevents SCD, but whether biventricular pacing‐induced remodeling decreases left ventricular mass remains uncertain. (J Cardiovasc Electrophysiol, Vol. 14, pp. 764‐775, July 2003)

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Section: Cardiomegaly and Coronary Artery Disease In Patients With Scdsupporting

confidence: 60%

Section: Cardiomegaly and Coronary Artery Disease In Patients With Scdmentioning

confidence: 99%

Structural Pathways and Prevention of Heart Failure and Sudden Death

Pacifico

Henry

2003

Cardiovasc electrophysiol

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Section: Sudden Cardiac Deathmentioning

confidence: 82%

“…Autopsy data indicate that approximately one-third of sudden cardiac deaths are caused by acute total coronary occlusion by thrombosis as the hallmark of myocardial infarction. [11][12][13] Findings in patients resuscitated from sudden cardiac death support these pathologic findings. 14 Thus, in many cases, the only difference between non-fatal myocardial infarction and sudden cardiac death is that the patients dying suddenly experienced a fatal arrhythmia or immediate heart failure during what would otherwise have been a non-fatal myocardial infarction.…”

Section: Sudden Cardiac Deathmentioning

confidence: 82%

Circadian variation and triggering of cardiovascular events

Willich

1999

Vasc Med

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Myocardial infarction and sudden cardiac death demonstrate a marked circadian variation with an increased risk during the morning after awakening and arising. The recognition of the morning increase of acute cardiovascular events has convinced many that they may be triggered by morning activities. It is of note, however, that cardiovascular events occur throughout the day -even if at lower frequency compared with the morning.There is a strong association between external triggers and the onset of myocardial infarction and sudden cardiac death beyond what is to be expected by chance alone. The magnitude of this association (relative risk two-to threefold) is comparable with the known long-term risk factors of cardiac disease. Trigger factors occur relatively frequently and may play a causative role in up to 20% of cases of acute coronary syndromes. Physical exertion, bursts of anger and sexual activity have been proved to have triggering potential. Other possible triggers include external and environmental events such as earthquakes, war threat and climatic factors.The pathophysiological links between external triggers and the onset of cardiovascular events are important in addressing the question of a causal relationship between triggers and disease onset and in perhaps improving preventive strategies.

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“…It must be underlined that this diagnosis can explain death only with a certain probability when there is a high grade stenosis (>75%) of at least one segment of a major epicardial coronary artery (Sheppard and Davies, 1998) without other cardiac lesions. In most of the series, the rate of recent infarcts is usually low, between 12 and 41% (Liberthson et al, 1974;Myers and Dewar, 1975;Lovergrove and Thompson, 1978;Baroldi et al, 1979;Aizaki et al, 1997). More sensitive techniques like immunohistochemistry could detect earlier ischemic myocardial lesions (Edston and Kawa, 1995;Piercecchi-Marti et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Sudden Adult Death: A Medico-Legal Series of 77 Cases between 1995 and 2000

Grandmaison

Durigon

2002

Med Sci Law

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Among all the autopsies performed between 1995 and 2000 in our Department, 77 adult cases of sudden death were selected. Sex, age, place of death, circumstances of death, causes of death and heart weight were reported from these 77 post-mortem records. A complete forensic autopsy was performed in every case. Sudden death occurred more frequently in males at rest. Strenuous activity was rarely involved in sudden death and 72.7% of the cases died from cardiovascular disease, mainly coronary atherosclerosis. Non-cardiac causes were dominated by pulmonary and neurological diseases. Cardiomegaly was a frequent finding in cases who died from cardiac pathology. This study underlines the importance of complete medico-legal investigations in case of sudden death. Multiple heart samples are required in order to detect focal microscopic lesions, such as myocarditis and some forms of cardiomyopathy with minimal gross abnormalities. The post-mortem diagnosis of such cardiomyopathies is very important because the family of the deceased may undergo a possible screening. Toxicology is useful in the diagnosis of epileptic seizure and in identifying drugs like metamphetamine as a risk factor for some lethal cardiovascular pathologies such as aortic dissection. Molecular biology can also be helpful when limits of morphological diagnosis have been reached.

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The role of acute myocardial infarction in sudden cardiac death—a statistician's nightmare

Cited by 50 publications

References 7 publications

Structural Pathways and Prevention of Heart Failure and Sudden Death

Structural Pathways and Prevention of Heart Failure and Sudden Death

Circadian variation and triggering of cardiovascular events

Sudden Adult Death: A Medico-Legal Series of 77 Cases between 1995 and 2000

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