Psychosocial and other features of coronary heart disease: insights from the Framingham Study

Contributors to CHD include atherogenic personal attributes, living habits which promote these, signs of preclinical disease, and host susceptibility to these influences. Atherogenic traits include the blood lipids, blood pressure, and glucose tolerance. High LDL cholesterol is positively and high HDL cholesterol inversely related to CHD incidence. Hypertension, whether systolic or diastolic, labile or fixed, casual or basal, at any age in either sex contributes powerfully to coronary heart disease. The impact of diabetes on CHD is greater for women than for men and varies according to the level of the foregoing risk factors. The faulty life-style is typified by a diet excessive in calories, fat, and salt, a sedentary habit, unrestrained weight gain, and cigarettes. Alcohol used in moderation may be beneficial. Oral contraceptives worsen atherogenic traits and, when used for long periods beyond age 35 in conjunction with cigarettes, predispose to thromboembolism. Type A persons with an overdeveloped sense of time urgency, drive, and competitiveness develop an excess of angina pectoris. Men married to more highly educated women are at increased risk, as are men married to women in white-collar jobs. Preclinical signs of a compromised coronary circulation include silent MI, ECG-LVH, blocked intraventricular conduction, and repolarization abnormalities. Exercise ECG may elicit still earlier evidence. Measures of innate susceptibility include a family history of premature cardiovascular disease, diabetes, hypertension, and gout. Optimal prediction of CHD requires a quantitative combination of risk factors in multiple logistic risk formulations that identify high-risk persons with multiple marginal abnormalities. Preventive management should also be multifactorial.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sudden death risk in overt coronary heart disease: the Framingham Study

Over 30 years of surveillance of 5127 subjects free of CHD, 760 men and 574 women developed overt CHD, and there were 160 sudden deaths in men and 73 in women. Among those who sustained clinically manifest CHD, the sudden death risk was increased 6.7 times that of those without an interim event. Although the relative risk was comparable in the two sexes, CHD did not eliminate the female advantage over men. Myocardial infarction imposed a greater sudden death risk than angina pectoris, and silent infarctions were as dangerous as symptomatic infarctions. Onset of CHD put young and old at equal risk of sudden death. Some 40% of sudden deaths occurred in the 4% of the general population with overt CHD. The proportion of coronary attacks presenting as sudden death increased from 13% at ages 35 to 64 years to 20% at ages 65 to 94 years. The fraction of CHD deaths classified as sudden deaths was lower in those with than without interim CHD. In those with established CHD, factors reflecting ischemic myocardial damage and cardiac failure were the chief predictors of sudden death. The proportion of CHD deaths presenting as sudden deaths has not declined in subjects with prior CHD over three decades, despite a national decline in the overall CHD mortality rate.     

Metabolic risk factors for coronary heart disease in women: perspective from the Framingham Study

In over 30 years of surveillance of 2873 women, 574 developed initial clinical manifestations of CHD. A number of antecedent metabolic risk factors proved atherogenic, including blood lipids, glucose tolerance, uric acid, and menopause. Serum total cholesterol predicts as strongly in women as in men. The predictive power of cholesterol is strengthened when the total cholesterol is partitioned into its atherogenic LDL and protective HDL fractions. Contrary to the case in men, triglyceride may be a contributor to risk in older women. A total-to-HDL cholesterol ratio exceeding 7.5 equalizes the risk in men and women. Impaired glucose tolerance also eliminates the female CHD risk advantage over men, conferring a three-fold increased risk. Serum uric acid, although lower in women than in men, is equally predictive in the sexes. Central obesity confers an increased CHD risk in women and predisposes to diabetes, hyperuricemia, hypertension, and an unfavorable LDL/HDL cholesterol ratio. A combination of obesity, low HDL cholesterol, and impaired glucose tolerance predisposes especially. Age-adjusted risk of CHD is increased two- to threefold compared to pre menopausal women, even when induced surgically without removing the ovaries. It is not clear whether post menopausal estrogen replacement eliminates this excess risk. Fibrinogen is higher in women than in men, and is increased with hypertension, diabetes, hypercholesterolemia, high hematocrit, and cigarette smoking. At any level of multivariate risk, fibrinogen added to the CHD risk in women.     

Fibrinogen, cigarette smoking, and risk of cardiovascular disease: insights from the Framingham Study

During the tenth biennial examination, 1315 Framingham study participants free of cardiovascular disease had fibrinogen measured along with other major cardiovascular risk factors including cigarette smoking. The fibrinogen values were significantly higher in smokers than in nonsmokers, increased with the amount smoked in each sex, and exsmokers had values as low as those of nonsmokers. Over 10 years of follow-up, 165 men and 147 women developed cardiovascular disease, the risk in both sexes increasing progressively in relation to antecedent fibrinogen values over the 180 to 450 mg/dl range. Risk gradients for cardiovascular disease in men diminished with advancing age. In men, risk of cardiovascular disease was related to cigarette smoking. This was true in the multivariate case taking all standard risk factors into account. As for fibrinogen, the impact diminished with advancing age. Regression coefficients were actually larger in the multivariate than in the univariate case because of a negative correlation between smoking and blood pressure. Fibrinogen contributed to cardiovascular disease, risk taking into account both cigarette smoking and other risk factors. When fibrinogen is added to the multivariate model for prediction of cardiovascular disease the coefficient for smoking becomes much reduced and is no longer statistically significant. However, each independently contributed to risk in cross-sectional analysis. These data provide another mechanism whereby cigarette smoking influences the occurrence of atherocardiovascular disease and also another reason for prohibiting cigarette use.     

Lipids and coronary heart disease in Asia

In Western countries, it has been shown that coronary heart disease (CHD) is related to high serum total cholesterol (TC) levels. In less developed continents such as Asia and Africa, serum lipid levels are low and CHD incidence is much lower as compared with Western countries. With growing urbanization and industrialization in Asia, it has been shown that there is a concomitant rise in the level of serum TC and with it a rise in CHD. In all the Asian countries, serum TC levels are also higher in the urban compared with the rural population. Singapore, the only Asian country which is 100% urbanized since 1980, showed a rise of serum TC similar to that seen in the US and UK from the 1950s to the 1980s followed thereafter by a fall. This is reflected in the trend (rise followed by a fall) of CHD morbidity and mortality as well. In spite of a declining trend in serum TC level, CHD morbidity and mortality are still high in Singapore and comparable to the Western countries. The rest of the Asian countries show a different pattern from Singapore. In general, there is still a rising trend in serum TC level and in CHD mortality in most Asian countries. However, Japan is considered an exception in having a decreasing CHD mortality in spite of an increasing trend in serum TC. This may be attributed to a better control of other CHD risk factors such as hypertension and smoking. The rising trend in serum TC level remains a cause for concern, as this will emerge as a major problem for CHD morbidity and mortality in the future.     

Lipids, lipoproteins, and coronary heart disease: Implications for antihypertensive therapy

There is now considerable evidence that treatment of abnormalities of lipids and lipoproteins reduces the incidence of coronary heart disease (CHD). Treatment of hypertension, another major cardiovascular risk factor, has not been shown to have the same impact on CHD. Possible explanations for this are that cardiovascular risk factors may occur in combination in an individual or that therapy for hypertension has adversely affected one or several of the other risk factors for CHD, thereby effuetting the benefit gained by lowering blood pressure.This article reviews the relationship between lipids, lipoproteins, and coronary heart disease, and the impact of cholesterol lowering on CHD. The evidence that antihypertensive drugs are associated with lipid and lipoprotein abnormalities is introduced by a critical appraisal of the several studies for such evidence. Implications for the treatment of the hypertensive patient are discussed.     

Risk of coronary heart disease in subjects with chest discomfort: the Framingham Heart Study

PURPOSE: To examine the risk of coronary heart disease (CHD) events in subjects of the Framingham Study reporting new chest discomfort. SUBJECTS AND METHODS: Original cohort subjects with chest discomfort were classified by their history into three groups: definite angina, possible angina, or nonanginal chest discomfort. Subjects were followed for 2 years for CHD events, including coronary insufficiency, myocardial infarction, or CHD death. RESULTS: Compared to that in subjects without chest discomfort, the relative odds of a CHD event was 3.7 (95% confidence interval [CI] 2.11, 6.60) in men with definite angina and 3.0 (95% CI 1.33, 6.69) in men with possible angina. Comparable increased CHD risk was also observed in women with definite or possible angina, with relative odds of 5.4 (95% CI 3.08, 9.30) and 2.9 (95% CI 1.13, 7.17), respectively. The increase in CHD risk associated with definite or possible angina persisted after adjustment for cardiac risk factor profile. There was no increase in risk associated with nonanginal chest discomfort. CONCLUSION: CHD risk is increased in subjects with new chest discomfort that on the basis of history is consistent with definite or possible angina, whereas CHD risk is not increased in subjects with nonanginal chest discomfort. The presence of chest discomfort and its characteristics facilitate the classification of subjects into meaningful categories that offer prognostic information beyond that provided by traditional CHD risk factors.     

Silent myocardial ischemia and infarction: insights from the Framingham Study

More than one in four myocardial infarctions that occurred over 30 years in the Framingham Study were detected only because of routine biennial electrocardiographic examinations. Of these, almost half were completely silent. The fraction of infarctions unrecognized was higher in women (35 per cent) than in men (28 per cent). Such infarcts were uncommon in persons with angina and recurrent infarctions. Unrecognized infarctions were as likely as recognized ones to result in eventual death, heart failure, or strokes. Thus, unrecognized infarctions are common and have as serious a prognosis as typically symptomatic infarctions.     

Risk stratification of dyslipidemia: insights from the Framingham Study

Dyslipidemia, fundamental to the atherosclerotic process, is now a readily correctable risk factor with established efficacy of treatment for reducing risk of CHD and strokes. The current focus on LDL-cholesterol for risk assessment needs to be broadened to accommodate the two-way traffic of cholesterol entering and leaving the arterial intima reflected by the LDL/HDL ratio or the Total/HDL ratio. The choice of lipid therapy should be individualized to take into account the presence of the metabolic syndrome and the lipid profile of the patient. The intensity of therapy and goals should be linked to multivariable risk, particularly in those with modest lipid values. Cardiovascular risk factor clustering is pronounced for each lipid, is promoted by adiposity and greatly influences its CHD hazard. Global risk assessment taking clustering into account is essential for efficient preventive management of lipids. More attention needs to be afforded the absolute risk reduction attainable and must recognize that the number needed to treat to prevent one event increases the lower the lipid value, the lower global risk and the healthier the subject.     

Community surveillance for coronary heart disease: The Framingham Cardiovascular Disease Survey: Comparisons with the Framingham Heart Study and previous short-term studies

It appears likely that intervention trials on a community scale against one or more coronary heart disease risk factors will begin in the near future. Prerequisite to the evaluation of the effectiveness of these trials is the accurate determination of coronary heart disease incidence rates. The Framingham Cardiovascular Disease Survey was undertaken to test the hypothesis that a short-term surveillance study of a defined population can generate accurate incidence rates for at least some categories of cardiovascular disease and that these rates are comparable with those obtained by longitudinal survey of the same population. In conjunction with the 1970 U.S. census, a 1 year survey was made of all new coronary heart disease events occurring in the town of Framingham, Mass. Surveillance was performed by several methods that were intentionally overlapping. During the study period, 244 coronary heart disease events occurred. Despite the relatively small size of the population, many of the well established epidemiologic characteristics of this disease were evident. The rates obtained by the cardiovascular disease survey were comparable with those obtained by the Framingham Heart Study, for the harder end points of myocardial infarction and death from coronary heart disease, but much smaller for the softer end point of angina pectoris, especially in women. These data and those from similar studies indicate that periodic short-term surveillance studies of target populations of major intervention programs can provide an economic method of generating incidence data for the evaluation of the impact of such programs on myocardial infarction and death from coronary heart disease.     

Metabolic syndrome vs Framingham Risk Score for prediction of coronary heart disease, stroke, and type 2 diabetes mellitus

BACKGROUND: We sought to compare metabolic syndrome (MetS) with the Framingham Risk Score (FRS) as predictors of coronary heart disease (CHD), stroke, and type 2 diabetes mellitus (DM2) in middle-aged men. METHODS: A prospective study of 5128 men aged 40 to 59 years with no history of cardiovascular disease (CVD) (CHD or stroke) or DM2 drawn from general practices in 24 British towns and observed for 20 years. Metabolic syndrome was defined as the presence of 3 or more metabolic abnormalities based on modified National Cholesterol Education Program criteria. RESULTS: Men with MetS at baseline (26%) showed significantly higher relative risk (RR) than men without MetS of developing CHD (RR, 1.64; 95% confidence interval [CI], 1.41-1.90), stroke (RR, 1.61 95% CI, 1.26-2.06), and DM2 (RR, 3.57; 95% CI, 2.83-4.50). The probability of developing CVD or DM2 over 20 years increased from 11.9% in those with no abnormalities to 31.2% in those with 3 abnormalities to 40.8% in those with 4 or 5 abnormalities. The FRS was a better predictor of CHD and stroke than MetS but was less predictive of DM2. Areas under the receiver-operating characteristic curves for FRS vs the number of metabolic abnormalities were 0.68 vs 0.59 for CHD, 0.60 vs 0.70 for DM2, and 0.66 vs 0.55 for stroke (P< .001 for all). CONCLUSIONS: Presence of MetS is a significant predictor of CVD and DM2 but is a stronger predictor of DM2 than of CHD. Although MetS does not predict CHD as well as the FRS, it serves well as a simple clinical tool for identifying high-risk subjects predisposed to CVD or DM2.