Mechanism of death and prevalence of myocardial ischemic symptoms in the terminal event after acute myocardial infarction

doi:10.1016/0002-9149(88)91295-7

The American Journal of Cardiology

Volume 61, Issue 1, 1 January 1988, Pages 8-15

https://doi.org/10.1016/0002-9149(88)91295-7 Get rights and content

Abstract

A prospective study to determine prognostic factors for risk stratification in 867 patients surviving the coronary care unit phase of acute myocardial infarction (AMI) is reported. During a 48-month follow-up, 144 patients (17%) died. The deaths were examined for the chronology, cause, mechanism, location and presence of myocardial ischemia in the terminal event. A classification previously proposed by Hinkle and Thaler was used to define the mechanism of cardiac death and the presence of ischemia. There were 113 deaths due to coronary atherosclerotic coronary artery disease, including 5 due to complications of coronary artery bypass graft surgery. Of the remaining 108 of these deaths, 74% were classified as due to an arrhythmic mechanism and 26% as myocardial failure. Of the deaths due to an arrhythmia or to myocardial failure, 56 (52%) occurred out of hospital. The ratio of arrhythmic: myocardial failure deaths was not different for the patients who died within 3 months after the Index AMI compared with later deaths. Sudden death (≤1 hour of new symptoms) was strongly associated with arrhythmic death but 32 (54%) of patients who died >1 hour after the onset of symptoms were also classified as having an arrhythmic cause of death. Previously described risk factors, including an ejection fraction <0.40 and ≥10 ventricular premature complexes/hour, were independent predictors of mortality but did not differentially predict the mechanism of cardiac death. Evidence of myocardial ischemia before the terminal event was found in about 50 (60%) patients whose deaths were witnessed and who died from an arrhythmia or myocardial failure.

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Citation Excerpt :
Mortality after MI has decreased in the contemporary era. In the prethrombolytic era, rates during the first 2½ years after MI were higher than 15%, and 75% of deaths were attributed to arrhythmia105 compared with 5% in the thrombolytic era.106,107 Reperfusion strategies to limit infarct size are most likely responsible for the observed decrease in mortality after MI and SCD rates, the mechanism for which may relate to improved overall electrical stability in the myocardium or specifically in the myocytes adjacent to the infarcted territory.
Sudden cardiac death accounts for approximately 50% of all deaths attributed to cardiovascular disease in the United States. It is most commonly associated with coronary artery disease and can be its initial manifestation or may occur in the period after an acute myocardial infarction. Decreasing the rate of sudden cardiac death requires the identification and treatment of at-risk patients through evidence-based pharmacotherapy and interventional strategies aimed at primary and secondary prevention. For this review, we searched PubMed for potentially relevant articles published from January 1, 1970, through March 1, 2014, using the following key search terms: sudden cardiac death, ischemic heart disease, coronary artery disease, myocardial infarction, and cardiac arrest. Searches were enhanced by scanning bibliographies of identified articles, and those deemed relevant were selected for full-text review. This review outlines various mechanisms for sudden cardiac death in the setting of coronary artery disease, describes risk factors for sudden cardiac death, explores the management of cardiac arrest, and outlines optimal practice for the monitoring and treatment of patients after an acute ST-segment elevation myocardial infarction to decrease the risk of sudden death.
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La muerte súbita probablemente sea el desafío más importante de la cardiología moderna. En este artículo, después de realizar una revisión histórica de la muerte súbita, se comentan la epidemiología y las enfermedades asociadas a ella y se hace énfasis en los aspectos fisiopatológicos, especialmente los factores desencadenantes que actuando sobre un miocardio vulnerable precipitan la arritmia final, que en general lleva a la fibrilación ventricular y en menor medida a bradiarritmia y muerte súbita. Se comentan especialmente la importancia de la isquemia aguda y la disfunción ventricular y el papel de la genética, no sólo en las cardiopatías de origen genético, sino también su posible efecto desencadenante en la cardiopatía isquémica aguda y crónica. Por último, se describe cuál es la mejor forma de identificar a los pacientes en riesgo, cómo prevenir la muerte súbita y qué conducta seguir ante un paciente resucitado de una parada cardiaca.
Sudden death is probably the greatest challenge in modern cardiology. After reviewing its history, we describe the epidemiology of sudden death and its associated diseases. We highlight its physiopathologic aspects, including the factors that act on vulnerable myocardium triggering the final arrhythmia, mainly ventricular fibrillation and, to a lesser extent, bradycardia and sudden death. We emphasize the relevance of acute ischemia, ventricular dysfunction and genetic factors, not only in genetic heart disease, but also as triggers of sudden death in acute and chronic ischemic heart disease. Finally, we describe the best way to identify candidates at risk, discuss how to prevent sudden death, and outline the best approach to managing a patient resuscitated from cardiac arrest.
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There are conflicting findings from observational studies of the arrhythrogenic potential of azithromycin. Our aim was to quantify the association between azithromycin use and the risk of ventricular arrhythmia.
We conducted a nested case–control study within a cohort of new antibiotic users identified from a network of 7 population-based health care databases in Denmark, Germany, Italy, the Netherlands and the United Kingdom for the period 1997–2010. Up to 100 controls per case were selected and matched by age, sex and database. Recency of antibiotic use and type of drug (azithromycin was the exposure of interest) at the index date (occurrence of ventricular arrhythmia) were identified. We estimated the odds of ventricular arrhythmia associated with current azithromycin use relative to current amoxicillin use or nonuse of antibiotics (≥ 365 d without antibiotic exposure) using conditional logistic regression, adjusting for confounders.
We identified 14 040 688 new antibiotic users who met the inclusion criteria. Ventricular arrhythmia developed in 12 874, of whom 30 were current azithromycin users. The mean age of the cases and controls was 63 years, and two-thirds were male. In the pooled data analyses across databases, azithromycin use was associated with an increased risk of ventricular arrhythmia relative to nonuse of antibiotics (adjusted odds ratio [OR] 1.97, 95% confidence interval [CI] 1.35–2.86). This increased risk disappeared when current amoxicillin use was the comparator (adjusted OR 0.90, 95% CI 0.48–1.71). Database-specific estimates and meta-analysis confirmed results from the pooled data analysis.
Current azithromycin use was associated with an increased risk of ventricular arrhythmia when compared with nonuse of antibiotics, but not when compared with current amoxicillin use. The decreased risk with an active comparator suggests significant confounding by indication.

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Mechanism of death and prevalence of myocardial ischemic symptoms in the terminal event after acute myocardial infarction

Abstract

J Roy Statist Soc B

Adv Cardiol

JACC

Acta Med Scand

On sudden death

Circulation

Clinical classification of cardiac deaths

Circulation

Risk stratification and survival after myocardial infarction

N Engl J Med

The relationships among ventricular arrhythmias, left ventricular dysfunction and mortality in the 2 years after myocardial infarction

Circulation