Coronary Disease Death Research Articles

Coronary Disease Deaths: From Birth Cohorts to Prevention

Cardiovascular diseases remain the number one cause of death in most of the western world. However, mortality from coronary disease nonetheless started to decline in several countries including the United States and part of western Europe 4 decades ago, and this decline has continued until the present time. Conceptually, the decline in coronary disease mortality could reflect a decrease in the incidence of coronary disease with fewer new cases occurring, or a decline in its case fatality, or a combination thereof. Progress in the primary prevention of coronary disease would decrease incidence while improvement in medical care and secondary prevention would increase survival. Hence, describing temporal trends in different populations and examining their causes is important and can help to design interventions, deploy prevention strategies, and advocate for policy changes. Despite the importance of this endeavor, quantifying the role of each of the aforementioned components in coronary mortality decline remains a difficult task and the determinants of the decline are still incompletely understood. This matter is further complicated by the fact that the respective contribution of potential determinants likely evolved over time and across countries. Within this context, studies of trends according to person, place, and time have the potential to shed some light on this subject. The article by Ocana-Riola et al reports an in-depth analysis of temporal trends in mortality from ischemic heart disease in southern Spain, aiming at separating age, birth cohort, and period effects. In epidemiology, age effect can be defined as a change in the outcome rate according to age, irrespective of birth cohort and calendar time; cohort effect can be defined as a change in the outcome rate according to year of birth, irrespective of age and calendar time; and period effect can be defined as a change in the outcome rate affecting an entire population at some point in time, irrespective of age and birth cohort. The study pertains to 145 539 deaths from ischemic heart disease that occurred in Andalusia between 1981 and 2008 among individuals aged between 30 and 84 years. For age effect, as expected, mortality from ischemic heart disease increased substantially with age for both men and women. Concerning birth cohort effect, the risk of

President’s Column

It has been my pleasure to serve as President of the American Society for Preventive Cardiology (ASPC) over the past 2 years. During my tenure, we have revitalized our Society and strengthened our relationship with our journal, Preventive Cardiology. In November 2009 we held a joint symposium with the National Lipid Association prior to the American Heart Association’s Annual Meeting in Orlando, Florida. This symposium on “Overcoming Challenges in Cardiovascular Disease (CVD) Prevention: A Focus on the Cardiometabolic Risk Continuum,” enabled our Society to contribute our own special expertise to the proceedings, while strengthening our relationship with a partner society. My section, on treatment of hypertension based on global risk, was directly targeted at a key element of prevention and an example of how we convey our insights to the broader medical community. On March 5, 2010, we again reached out to partner organizations by participating in the Joint Conference–50th Cardiovascular Disease Epidemiology and Prevention and Nutrition, Physical Activity and Metabolism 2010, in San Francisco, California. We conducted a session on what has become a tradition for the ASPC, a debate on prevention guidelines that illustrated the range of opinion and depth of approach embraced by our field. We will continue to team up and partner with organizations that share our goals and mission and strengthen our Society while we enhance our branch of medicine. Note that there is an application for membership in the ASPC included in this journal and we invite you to apply for membership. We are looking forward to an active year in 2010, as health care is on the national agenda and prevention is in the spotlight and central to improving care and reducing costs and burden. By now our lawmakers are familiar with the grim statistics: over a third of adult Americans will experience coronary heart disease in their lifetimes. Whether the condition is angina pectoris, myocardial infarction, or coronary disease death, predicting the onset and occurrence of these events is critical in our clinical decision making. Going forward, practitioners should be thoroughly familiar with traditional approaches, as the multivariable prediction model developed by the Framingham investigators has been extensively validated with cohort studies and captures a range of factors, including age, sex, cholesterol level, and smoking status. Increasingly, we are seeing practitioners test the limits of our science. Physicians and other health care professionals are examining alternative measures of coronary heart disease and surrogate markers that may help to predict clinical events and guide preventive care in cardiology. Our task is to add to the body of knowledge and help researchers and clinicians alike gain greater insight into the process and theory of risk estimation. By gauging additional variables in models that include traditional risk assessment criteria, the statistical significance of alternate approaches may be clarified as to their predictive value. While there is room for improvement, our current standards for coronary heart disease risk assessment are proven to be relatively accurate. The value of new factors for assessment should be judged also for their applicability; traditional approaches are by now well understood and familiar to both clinicians and patients, and recommendations for medical therapy and lifestyle modification are practical and low in cost. Thus, while caution is warranted, we can also be cautiously optimistic that new developments now emerging from studies in omega 3 fatty acids and high-density lipoprotein cholesterol therapeutics will change and improve the landscape for diagnosis and prevention.

Challenges to Improve Coronary Heart Disease Risk Assessment

CORONARY HEART DISEASE (CHD) IS COMMON AND includes the diagnoses angina pectoris, myocardial infarction, and coronary disease death. Predicting the first occurrence of these events is important and may affect clinical decisions and care. It can be expected that more than a third of adult Americans will develop CHD during their lifetime, and improvements in diagnosis and care may provide great benefits. The article by Tzoulaki and colleagues assesses the scientific literature concerning efforts to improve the prediction of CHD over and above the Framingham risk score. The authors report that many articles have provided information on new risk factors, but the study designs and data analyses in those reports raise concerns about the usefulness of the new information and about how improvement over the Framingham risk score was assessed. Researchers and clinicians should understand how CHD risk estimation is undertaken and evaluated, as these methods are frequently used to assess risk of developing disease across a variety of health disciplines. Risk estimates for initial CHD events should be derived from studies based on complete information for carefully measured risk factors at baseline, adequate follow-up, and reliable outcome data. A common initial step is to use proportional hazards univariate or age-adjusted regression models. When possible, the variables of interest are analyzed as continuous measures. Factors that are significant in the univariate analyses are then considered for inclusion in multivariable prediction models. With this approach, a set of variables was developed by Framingham investigators and included age, sex, systolic blood pressure, cholesterol level, high-density lipoprotein cholesterol level, diabetes mellitus, and current smoking. This approach was further evaluated with external validation sets from cohort studies across the United States. Including newer variables is of considerable interest because factors might improve the prediction of CHD and prevention strategies might be more effective. A variety of performance criteria are used to evaluate the usefulness of CHD risk prediction and a brief summary explains the terms used to interpret these studies, including relative risk, discrimination, calibration, and reclassification. For each risk factor, proportional hazards modeling yields regression coefficients for a study cohort. The relative risk of a variable is computed by exponentiating the regression coefficient in the multivariable regression models. This measure estimates the difference in risk for an individual with a given risk factor such as cigarette smoking compared with the risk for an individual who does not smoke. An analogous approach can be undertaken to estimate effects for continuous variables by showing effects for a specific number of units for the variable or by identifying differences in risk associated with a difference in the number of units associated with a standard deviation for the factor. Discrimination is the ability of a statistical model to separate those who experience clinical CHD events from those who do not. The C statistic, analogous to the area under a receiver operating characteristic curve, is the typical performance measure used. This statistic represents an estimate of the probability that a model assigns a higher risk to those who develop CHD within a specified follow-up than to those who do not and represents a composite of the overall sensitivity and specificity of the prediction equation. Values for the C statistic range from 0.00 to 1.00; 0.50 reflects discrimination by chance. Higher values generally indicate a good level of agreement between observed and predicted risks. The average C statistic for the prediction of CHD is typically in the 0.70 range. The error associated with Cstatistic estimates can be estimated and used to compare differences in risk prediction models. Calibration measures how closely predicted estimates of absolute risk agree with actual outcomes. To present calibration analyses, the data are often separated into deciles of risk, and observed rates are tested for differences from what was expected from the estimating equation. A version of the Hosmer-Lemeshow 2 statistic can be used to evaluate how well the observed and expected agree; smaller 2 values generally indicate good calibration. A CHD prediction model might be recalibrated if it provides relatively good ranking of risk and discrimination, but the model sys-

Acute coronary syndromes, heart failure, and diabetes in the Gulf Registry of Acute Coronary Events

This editorial refers to the paper entitled 'Heart failure in patients hospitalized with acute coronary syndromes: observations from the Gulf Registry of Acute Coronary Events (Gulf RACE)' by Alawi A. Alsheikh-Ali et al., on page 1135.

Vitamin D Status and the Risk of Cardiovascular Disease Death

Accumulating evidence suggests that inadequate vitamin D levels may predispose people to chronic diseases. The authors aimed to investigate whether serum 25-hydroxyvitamin D (25(OH)D) level predicts mortality from cardiovascular disease (CVD). The study was based on the Mini-Finland Health Survey and included 6,219 men and women aged > or =30 years who were free from CVD at baseline (1978-1980). During follow-up through 2006, 640 coronary disease deaths and 293 cerebrovascular disease deaths were identified. Levels of 25(OH)D were determined from serum collected at baseline. Cox's proportional hazards model was used to assess the association between 25(OH)D and risk of CVD death. After adjustment for potential confounders, the hazard ratio for total CVD death was 0.76 (95% confidence interval (95% CI): 0.60, 0.95) for the highest quintile of 25(OH)D level versus the lowest. The association was evident for cerebrovascular death (hazard ratio = 0.48, 95% CI: 0.31, 0.75) but not coronary death (hazard ratio = 0.91, 95% CI: 0.70, 1.18). A low vitamin D level may be associated with higher risk of a fatal CVD event, particularly cerebrovascular death. These findings need to be replicated in other populations. To demonstrate a causal link between vitamin D and CVD, randomized controlled trials are required.

Severity of Myocardial Infarction

Cardiovascular disease constitutes a burden of epidemic proportion,1 and understanding its determinants is essential to designing effective interventions. Doing so requires the ability to track disease burden at the population level. In the United States, without national registries, community surveillance is the method of choice.2 Community surveillance studies are mostly retrospective by design, rely on diagnostic codes for case finding, and require a defined population in which events can be consistently and reliably captured and validated with standardized approaches. Applied to cardiovascular disease, community surveillance measures its burden in communities by tracking the incidence of events, their severity, and their mortality, thereby enabling the appraisal of the components of cardiovascular diseases in a given population.2 Because of the aforementioned methodological requirements, few surveillance studies exist in the United States. They include the Atherosclerosis Risk in Communities (ARIC) Study,3 the Minnesota Heart Survey,4 the Olmsted County Study,5 and the Worcester Heart Attack Study.6 The data from these studies indicate that, although deaths from coronary disease have declined, the incidence of myocardial infarction in the United States has remained mostly stable. Thus, the decline in mortality can be envisioned as reflecting an improvement in survival, which may be mediated by a declining severity of myocardial infarction. Article p 503 The article by Myerson et al7 in this issue of Circulation specifically addresses this important and understudied issue in ARIC between 1987 and 2002. They examined a large, multiracial population and relied on several indicators, including the composite Predicting Risk of Death in Cardiac Disease Tool (PREDICT) score to conclude that the severity of infarction declined over time. Indeed, the proportion of infarctions with major ECG abnormalities, ST-segment elevation, and Q waves decreased, as did biomarker values and the proportion of persons presenting with shock. …

The Burden of Blood Pressure-Related Disease

The importance of high blood pressure as a major cause of common serious diseases has been recognized in most Western countries for ≈50 years. Before that, malignant hypertension was a frequent reason for hospital admission and a common cause of death.1 Safe and effective antihypertensive drugs were first developed in the 1960s and were shown to dramatically improve the prognosis associated with malignant hypertension.2,3 Over the next few decades, the widespread use of an expanding armamentarium of blood pressure–lowering drugs to patients at risk of malignant hypertension effectively eradicated this condition from most developed countries. Subsequently, the provision of blood pressure–lowering treatments to a much broader group of patients at risk of serious cardiovascular diseases, such as stroke and coronary heart disease, among whom blood pressure levels were often only modestly elevated, contributed importantly to the declines in stroke and coronary disease deaths rates experienced by most Western populations.4 However, the situation in higher-income countries stands in stark contrast to that experienced by their lower-income neighbors. The overall burden of blood pressure–related diseases is rapidly rising in countries such as India and China as a consequence of the aging population, increasing urbanization, and increases in age-specific rates of conditions such as stroke.5,6 Even war-torn countries and those ravaged by HIV/AIDS, such as some in sub-Saharan Africa, incur a huge burden of blood pressure–related diseases. In several such populations, cerebral hemorrhage is the leading cause of death in adults.7 Although safe and effective antihypertensive treatment could be provided in these regions with a range of generic products from <1 cent per person per day, the reality is that most people for whom such drugs are clearly indicated receive no treatment whatsoever. In this regard, the antihypertensive care available for a large proportion of the world’s population …

Fish intake and risk of incident atrial fibrillation

Study Question: Does fish intake influence the incident rate of atrial fibrillation? Methods: The Cardiovascular Health Study, a population-based prospective cohort study, was used to prospectively identify subjects with new-onset atrial fibrillation (AF) on the basis of hospital discharge records and annual electrocardiograms. The fish consumption and usual dietary intake was assessed at baseline in 4815 adults ≥age 65 years in 1989 and 1990, with a mean follow-up of 12 years. Results: Mean age was 72 years, 95% were white, about 20% had diabetes and 20% had coronary disease; mean sBP was 135 mm Hg and 45% were treated for hypertension. Incident AF was detected in 980 subjects. In multivariate analyses, consumption of tuna or other broiled or baked fish was inversely associated with incidence of AF, with a 28% lower risk with intake 1 to 4 times per week (HR=0.72; 95% CI=0.58–0.91; p=0.005), and 31% lower risk with intake ≥5 times per week (HR=0.69; 95% CI=0.52–0.91; p=0.008), compared with <1 time per month (p trend=0.004). Results were not materially different after adjustment for preceding myocardial infarction (MI) or congestive heart failure. In similar analyses, fried fish/fish sandwich consumption was not associated with lower risk of AF. Conclusions: Among elderly adults, consumption of tuna or other broiled or baked fish, but not fried fish or fish sandwiches, is associated with lower incidence of AF. Fish intake may influence risk of this common cardiac arrhythmia. Perspective: The study results are consistent with the clinical studies demonstrating less sudden death in coronary disease and the putative anti-arrhythmic effects of n-3 fatty acids including decreased ventricular myocyte excitability, and termination of induced asynchronous contraction in atrial myocytes. Fish oil intake can result in replacement of cardiac cellular membrane arachidonic acid by eicosapentaenoic acid. Why not fried fish? It is not the beer because alcohol intake was not greater in the fried fish/fish sandwich group. Frying can change the n-3 to n-6 PUFAs and lead to formation of trans-fatty acids. MR

The platelet PlA2 and angiotensin-converting enzyme (ACE) D allele polymorphisms and the risk of recurrent events after acute myocardial infarction

Chromosome 17q21-23 harbors genes for platelet glycoprotein IIIa and angiotensin-converting enzyme (ACE), which are polymorphic for alleles PlA2 and ACE “D.” These alleles have been independently and often associated with ischemic coronary artery disease (CAD). We sought to determine if the PlA2 and ACE D polymorphisms were risk factors for recurrent coronary events. In the Cholesterol And Recurrent Events (CARE) trial, 4,159 men and women with documented myocardial infarction (MI) were randomized to receive either placebo or pravastatin, and were followed prospectively for 5 years. PlA and ACE genotypes were determined in 767 patients: 385 cases who had experienced a recurrent primary event (death due to coronary disease or nonfatal MI), and 382 age- and gender-matched controls. In patients receiving placebo, the PlA1,A2 genotype conferred a relative risk (RR) of 1.38 (confidence intervals [CI] 1.04 to 1.83; p = 0.028; adjusted RR = 1.32, CI = 0.99 to 1.76; p = 0.058]) for the primary end point. Compared with the placebo group, pravastatin reduced the excess RR of coronary disease death and recurrent MI in the PlA1,A2 patient population by 31% (p = 0.06). The ACE D allele appeared to have modestly additive effects on the PlA1,A2 risk. Among the PlA1,A2 patients, pravastatin had little effect on the risk of recurrent events with the ACE II genotype, but reduced the adjusted RR from 1.42 (placebo) to 0.58 for ACE ID patients, and from 1.56 (placebo) to 0.83 for ACE DD. The PlA1,A2 genotype was associated with an excess of recurrent coronary events in patients after MI who did not receive pravastatin, and the ACE D allele added to this risk. These data suggest that it would be important to perform a larger study to address the potential role of these genotypes in therapeutic decision making.

The duration of the association between serum cholesterol and coronary mortality: a 35-year experience.

Our purpose was to study the time-related association between a single measurement of total serum cholesterol and the occurrence of coronary deaths in a population sample of middle-aged men. This is a longitudinal population study with multiple measurements of serum cholesterol and a 35-year follow-up for coronary mortality in 1622 coronary disease-free men aged 40-59 years belonging to the Italian rural cohorts of the Seven Countries Study. A single measurement of serum cholesterol (plus those of five other risk factors as possible confounders) was considered. During 35 years of follow-up, 214 men died from coronary heart disease. Annual partitioned proportional hazards models were solved, one for each independent year of follow-up, to predict the risk of coronary heart disease deaths. Single-year hazard functions were cumulated and smoothed. Similar analyses were made starting from cholesterol measurements taken at years 5, 10 and 20 of follow-up. The resulting hazard curves showed regularly increasing risk for coronary events and fitted straight lines with large correlation coefficients, demonstrating a strong association of serum cholesterol with both early and late events. The slopes were steeper for cholesterol measurements taken at younger ages. The slope for cholesterol measurement taken at year 20 (age 60-84 years) was flat. In slopes starting at an early age, two components could be isolated corresponding to different associations with events (stronger for early events when measurements were taken around the age of 50 years and for late events when measurements were taken around the age of 55 or 60 years). A single measurement of total serum cholesterol in middle-aged men maintains a relatively monotone relationship with the occurrence of coronary heart disease deaths over 35 years. In the study population, measurements taken in late adulthood had smaller or null association with coronary disease deaths.

Trends in Heart Disease Deaths in Olmsted County, Minnesota, 1979-1994

Although age-adjusted heart disease mortality has declined since the 1960s, this decline may not have applied equally to all subgroups. To examine recent trends in heart disease mortality, specifically in women and in the elderly. Age- and sex-specific heart disease mortality (International Classification of Diseases, Ninth Edition, Clinical Modification [ICD-9-CM] codes 390-398, 402, 404-429) in Olmsted County, Minnesota, between 1979 and 1994 were studied. The total number of heart disease deaths was 3095; 1578 (51%) occurred in women and 1984 (64%) in persons aged 75 years or older. Most heart disease deaths (77%) were coronary disease deaths (ICD-9-CM codes 410-414). Age-adjusted heart disease mortality rates declined from 123 per 100,000 (95% confidence interval [CI], 102-144/100,000) in 1979 to 81 per 100,000 (95% CI, 67-95/100,000) in 1994. Poisson regression analyses indicated that the trends differed according to sex and age. For women, the relative risk (RR) of heart disease death in 1994 compared with 1979 was 0.69 vs 0.53 for men (P = .06). This equates to a decline in heart disease mortality of 2.5% per year in women or 32% over the period and 4.2% per year in men or 47% over the period. The decline was less pronounced as age increased (P < .001). For 60-year-old women, the RR for 1994 compared with 1979 was 0.59, whereas for 80-year-old women, the RR for 1994 compared with 1979 was 0.76. For men, the RR for 1994 compared with 1979 was 0.60 for 80-year-old men vs 0.46 for 60-year-old men. Between 1979 and 1994, in Olmsted County, the decline in heart disease mortality was of lesser magnitude in women and in the elderly, emphasizing the importance of age- and sex-specific trends to characterize time patterns in heart disease deaths to target preventive measures.

Prospective association between lipid soluble antioxidants and coronary heart disease in men. The Multiple Risk Factor Intervention Trial.

A nested case-control study was performed using participants enrolled in the Multiple Risk Factor Intervention Trial (MRFIT). The cases involved nonfatal myocardial infarction or death from coronary heart disease. Serum samples (n = 734) obtained at baseline and frozen for approximately 20 years were analyzed for the antioxidants, carotenoids, retinol, and alpha-, gamma-, and total tocopherol. The concentrations of antioxidants were in the expected range and their association with low density lipoprotein (LDL) cholesterol reflected their absorption and transport mechanisms. Among nonsmokers, the odds ratios (95% confidence intervals (CI)) for quartile IV versus quartile I were 1.40 (0.40-4.89), 0.77 (0.20-2.96), 1.45 (0.38-5.56), 2.34 (0.56-9.81), and 2.40 (0.52-11.07) for retinol, total carotenoids, and alpha-, gamma-, and total tocopherol, respectively. The equivalent odds ratios (95% CI) for smokers were 0.90 (0.34-2.41), 0.66 (0.23-1.84), 0.67 (0.21-2.13), 2.04 (0.88-4.73), and 0.52 (0.16-1.67), respectively. This analysis of antioxidant concentrations by quartiles indicated no significant association of antioxidant levels with the risk of coronary disease death or nonfatal myocardial infarction.

Association of serum total cholesterol with coronary disease and all-cause mortality: multivariate correction for bias due to measurement error.

Measurement error in the exposure under investigation is an important but often ignored source of bias in observational studies. The authors examined the impact of measurement error in the association between total serum cholesterol and 16-year coronary heart disease and all-cause mortality in a cohort of 6,137 middle-aged men of Japanese descent in the Honolulu Heart Program (1973-1988). A Cox regression model that enables modeling of survival time with correction for measurement errors in multiple covariates was employed. After controlling for age, body mass index, systolic blood pressure, smoking status, alcohol consumption, dietary cholesterol, and total calorie intake, a difference of one standard deviation (38 mg/dL) in total cholesterol was associated with a significant increase in the risk of coronary disease death (uncorrected hazard ratio = 1.35). After correction for measurement errors in total cholesterol and covariates (except smoking and age), the estimated hazard ratio increased to 1.65 (a 22% increase). A U-shaped relation was observed between total cholesterol levels and the risk of all-cause mortality. This association was then examined with a quadratic model and with a two-slope or V-shaped regression model. In the quadratic fit, the magnitude of the quadratic total cholesterol term increased threefold after the adjustment for measurement error. In the V fit, the hazard ratio of all-cause death corresponding to a change in one standard deviation above 214 mg/dL (the nadir of the V) was 1.15, and increased to 1.49 (by 29%) after the correction. The corresponding hazard ratio of a change in one standard deviation below 214 mg/dL was 1.11, and increased to 1.37 (by 23%) after the correction. The authors conclude that the impact of elevated total cholesterol on the risk of coronary disease and all-cause mortality may be greater than previously estimated with standard methods of analysis. In addition, the correction for measurement error in total cholesterol and covariates did not explain the excess mortality associated with low total cholesterol. More research is needed to elucidate the fundamental issues underlying the U-shaped association, i.e., confounding versus causal implications.

Cardiovascular diseases during and after World War II: A comparison of the Federal Republic of Germany with other European countries

The Statistische Bundesamt (Federal Office for Statistics) has released information which shows a steep increase of atherosclerosis and coronary sclerotic deaths since 1949–1950 throughout West Germany. This upturn is observed to a different extent among all age groups and with a lesser effect among normally menstruating women. During the years 1950 to 1970, the epidemic proportions could hardly be overlooked. Since 1970, the increase has been more gradual, and since 1975 coronary deaths have plateaued. A reduction in the prevalence of coronary disease deaths could possibly have occurred for men ages 40–45. Also, the number of fatal strokes has decreased in the FRG for the last 3 reporting years. Clinical and pathoanatomical investigations in Germany prove that coronary heart disease deaths between 1945 and 1948 were rare—a paucity of global statistics precludes adequate comparison with other countries. These data are supported by the study of the pathoanatomical protocols showing very few cases of accluding coronary sclerosis. Comparative pathoanatomical studies conducted for the years 1939–1953 in Basel and Marburg and ranked according to progression disclosed no significant differences in atherosclerotic disorders. Yet, autopsy reports of the University of Marburg for the years 1945–1948 indicate an increased prevalence of premature fatty streaks and edema. This probably could be due to higher numbers of critically injured and chronically ill soldiers. In another Swiss study, a substantial increase of coronary atherosclerosis was found among active duty soldiers in 1939–1945 and 50 accident deaths examined at the Zürich Institute of Pathology in 1964. This process can be related to the nutritional situation of the 60s as opposed to the war years. The less dramatic reduction of calorie intake in neutral Switzerland should be considered when compared with European countries at war. Thromboembolism in the FRG was considerably lower during the lean postwar years than during the prewar years and the years following 1948. Perhaps the only benefit resulting from the World War II years was that they contributed to our understanding of the roles of nutrition, smoking, obesity and physical activity in the pathogenesis of arteriosclerosis.

Identification of sudden death risk factors in acute and chronic coronary artery disease

Because of their potential role in the pathogenesis of sudden death, cardiac arrhythmias in patients with coronary artery disease have become the subject of increasing concern and investigation. A series of studies on the problem of ventricular ectopy as it relates to the entire spectrum of sudden death in coronary disease were carried out utilizing continuous portable electrocardiographic monitoring systems. Evaluation of arrthymias during the entire 3 week in-hospital period after acute myocardial infarction in 83 patients revealed that absence of premature ventricular contractions, including their serious forms (multifocal, paired, R on T phenomenon, frequency 5/min or greater) and ventricular tachycardia in the coronary care unit did not exclude their high incidence rate (premature ventricular contractions 30 percent, serious forms 41 percent, ventricular tachycardia 6 percent) in the late hospital phase. Because late hospital serious forms of ventricular ectopy correlated with arterial hypoxia and elevated left ventricular filling pressure in the coronary care unit and with persistent S-T abnormalities, the extent of left ventricular dysfunction and ischemia with acute myocardial infarction appeared precursors to these arrhythmias. Study of ventricular ectopy in the late hospital phase of acute myocardial infarction indicated that ventricular ectopy and particularly its serious forms and prognostic significance relative to subsequent sudden death after discharge; the extent of predischarge S-T segment alterations was greater in subjects who died suddenly than in survivors, suggesting that persistent ischemia or segmental dyssynergy, or both, predisposed to lethal arrhythmias. Among 86 patients with chronic coronary disease documented by catheterizerization, 87 percent had ventricular ectopy and 62 percent serious ventricular arrhythmias, in contrast to 34 percent and 9 percent, respectively in normal subjects; frequency of serious forms of ventricular ectopy was related to extent of coronary atherosclerosis. Correlation of standard electrocardiograms with continuous Holter electrocardiograms in 101 patients with chronic coronary disease over 24 months revealed that the former modality was insensitive in arrhythmia detection; patients free of ventricular ectopy by serial standard electrocardiograms had a 62 percent incidence rate of serious forms of ventricular ectopy and 6 percent ventricular tachycardia on portable continuous monitoring. Additional studies of patients with chronic coronary disease showed that assessment of both the type of ventricular ectopy and the setting in which it occurs provides the most meaningful characterization of risk of sudden death. These systematic series of observations identify premature ventricular ectopic beats as important and separate risk factors in coronary disease...

Cigarette smoking and geographic variation in coronary heart disease mortality in the United States

Striking geographic variation in death rates for coronary heart disease has been observed to occur within the United States. Coronary disease death rates for states are strongly correlated with per capita cigarette sales, estimated from state cigarette tax revenues. The correlation noted was as high as +0.76 if only the states with the most accurate cigarette consumption information were used. This correlation could not be attributed either to urbanization or to softness of the local water supply. It is suggested that accompanying the search for new hypotheses to explain geographic variation in coronary heart disease mortality should be an attempt to determine whether any of the established risk factors are responsible.

Sudden Death from Coronary Disease

Five hundred consecutive sudden deaths ascribed to coronary arteriosclerotic heart disease after complete autopsy were studied, with special attention to coronary vessels and myocardium. In 184 cases, new disease (recent thrombosis, acute myocardial infarct, or both) explained the sudden catastrophe. The remaining cases presented only chronic degenerative coronary disease, frequently associated with healed infarcts. The cardiac mechanisms responsible for sudden death in coronary disease must of necessity differ in these two groups with such disparate morbid anatomy. The presence of an intact myocardium in many of these patients suggests that the potentiality for good cardiac function exists if the heart beat can be restored. Such positive measures as intermittent rhythmic manual compression (cardiac massage), electrical defibrillation, or both in association with artificial respiration are indicated when the physician is present at deaths occurring under these circumstances.

IMPENDING MYOCARDIAL INFARCTION

Article1 September 1944IMPENDING MYOCARDIAL INFARCTIONLEO WAITZKIN, M.D.LEO WAITZKIN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-21-3-421 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn 1937 Feil,1 and Sampson and Eliaser2 described "preliminary" or "premonitory" pain in 15 (50 per cent) and 29 (48.1 per cent)† of their cases of acute myocardial infarction.Since this subject is deemed of considerable importance, we are recording our experience and impressions. Of 61 consecutive cases of acute infarction treated in the past two years, 17 had premonitory symptoms. They are summarized in table 1. Additional data are given in 5 cases.The symptoms have the following characteristics:1. There may be one or more episodes of spontaneous prolonged cardiac pain, mild or severe, with or without a...Bibliography1. FEIL H: Preliminary pain in coronary thrombosis, Am. Jr. Med. Sci., 1937, cxciii, 42-48. CrossrefGoogle Scholar2. SAMPSONELIASER JJM: The diagnosis of impending acute coronary artery occlusion, Am. Heart Jr., 1937, xiii, 675-686. CrossrefGoogle Scholar3. ECKSTEINGREGGPRITCHARD RWDEWH: The magnitude and time of development of the collateral circulation in occluded femoral, carotid, and coronary arteries, Am. Jr. Physiol., 1941, cxxxii, 351-361. CrossrefGoogle Scholar4. ALLEN EV: Sudden occlusions of the arteries of the extremities, Proc. Staff Meet. Mayo Clin., 1935, x, 678. Google Scholar5. FALK OP: The causes and prevention of sudden death in coronary disease, Jr. Am. Med. Assoc., 1942, cxix, 1250-1252. CrossrefGoogle Scholar6. LINDERKATZ ELN: Papaverine hydrochloride and ventricular fibrillation, Am. Jr. Physiol., 1941, cxxxiii, 155-160. CrossrefGoogle Scholar7. LEROYSNIDER GVSS: The sudden death of patients with few symptoms of heart disease, Jr. Am. Med. Assoc., 1941, cxvii, 2019-2023. CrossrefGoogle Scholar8. SALLEY SM: Unusual atropine effect on ventricular tachycardia, Am. Jr. Med. Sci., 1932, clxxxiii, 456. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Baltimore, Maryland*Received for publication April 16, 1943.From the Medical Service, U. S. Marine Hospital, Norfolk, Virginia.†The validity of this percentage is questioned, since it is not based on the total number of cases, but on an unstated fraction—27 cases. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byApproach to the management of unstable anginaCoronary anatomy and arteriography in patients with unstable angina pectorisUnstable angina pectoris: National cooperative study group to compare medical and surgical therapyCoronary Heart Disease: Some Historical, Nosological, and Clinical AspectsAccelerated Angina PectorisSTUDIES ON THE SEVERE TYPE OF ANGINA PECTORISIntermediate Coronary SyndromeThe Effects of Intravenous Aminophylline upon the Coronary Blood-Oxygen ExchangeChanges in the precordial electrocardiogram produced by extension of anteroseptal myocardial infarction 1 September 1944Volume 21, Issue 3Page: 421-430KeywordsAcute myocardial infarctionArmed forcesInfarctionMedical servicesMyocardial infarction Issue Published: 1 September 1944 PDF downloadLoading ...