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Biomedical subjects

W B Kannel

Publications and source records attributed to W B Kannel.

At least 73 records · Page 4Linked to original sources
PubMed1996

Cardioprotection and antihypertensive therapy: the key importance of addressing the associated coronary risk factors (the Framingham experience).

Hypertension directly predisposes to all of the major atherosclerotic cardiovascular disease outcomes, including coronary artery disease, stroke, cardiac failure, and peripheral artery disease. Coronary artery disease deserves a high priority in treatment of hypertension because it is the most common and lethal sequela. However, reduction of blood pressure as the sole therapeutic goal of antihypertensive therapy is no longer appropriate. Hypertension tends to cluster with other atherogenic risk factors, including dyslipidemia, glucose intolerance, insulin resistance, obesity, and elevated uric acid. Hypertension is only one of the many risk factors for atherosclerotic cardiovascular disease and is variably hazardous, depending on the number and severity of these coexistent metabolically linked risk factors. The presence of coexistent, already overt cardiovascular disease and left ventricular hypertrophy also greatly influence the hazard and choice of therapy. The urgency for, and choice of, therapy should be based on the multivariate cardiovascular risk profile rather than relying solely on the character and severity of the blood pressure elevation. In this way at-risk hypertensive persons can be more appropriately targeted for treatment designed to improve their multivariate risk profile and to provide maximum benefit and cost effectiveness.

Adult↗
PubMed1996

Sex and time trends in cardiovascular disease incidence and mortality: the Framingham Heart Study, 1950-1989.

Variations in cardiovascular disease mortality between sexes, over time, and across regions point to population differences in the biologic, behavioral, and environmental factors influencing cardiovascular health. The authors examined 20-year trends in risk factors, incidence, and mortality among women and men in Framingham, Massachusetts, who were members of the Framingham Heart Study and aged 50-59 years in 1950, 1960, and 1970. The incidence declined 21% between the female cohorts (p < 0.01 for trend) with the greatest decline occurring between the 1950 and 1960 cohorts. The 20-year incidence declined only 6% between the male cohorts despite an 18% decline (p < 0.05 for trend) during the first 10 years of follow-up. Cardiovascular disease mortality declined 59% between the female cohorts and 53% between the male cohorts (both p < 0.001 for trend). The largest mortality declines occurred between the 1950 and 1960 female cohorts during the second 10 years of follow-up and between the 1960 and 1970 male cohorts during both follow-up periods. Obesity, hypercholesterolemia, and high blood pressure were significantly lower at baseline and 10 years later in the 1970 female cohort compared with the 1950 cohort (all p < 0.001). Smoking and high blood pressure were significantly lower at baseline and 10 years later in the 1970 male cohort compared with the 1950 cohort (both p < 0.001). More than half of the 51% decline in coronary heart disease mortality observed in women between 1950 and 1989 and one third to one half of the 44% decline observed in men could be attributed to improvements in risk factors in the 1970 cohorts.

Adult↗
PubMed1996

Secular trends in long-term sustained hypertension, long-term treatment, and cardiovascular mortality. The Framingham Heart Study 1950 to 1990.

BACKGROUND: Cardiovascular morbidity and mortality result from the chronic processes involved in hypertension. However, long-term sustained (LTS) hypertension has received little attention. METHODS AND RESULTS: Trends in the prevalence of LTS hypertension and its treatment were assessed in 1950, 1960, and 1970 among three cohorts of men and women in the Framingham Heart Study (Mantel-Haenszel test). Cardiovascular disease (CVD) incidence and mortality were compared between patients with LTS hypertension with and without long-term treatment by use of the chi 2 test. Cox proportional hazards regression analysis was used to estimate 10-year risk of death as a function of risk factor levels and treatment. Prevalence of LTS hypertension rose from 138 to 208 per 1000 between the 1950 and 1970 male cohorts (P < .01), while prevalence fell from 253 to 198 per 1000 between the female cohorts (P < .02). Long-term treatment increased 51% between the male cohorts and 45% between the female cohorts (both P < .001). While CVD incidence was similar (26% versus 25%), all-cause mortality was significantly lower among men with long-term treatment (31% versus 43%; P < .05), and CVD mortality was less than half (13% versus 28%; P < .01). Among treated women, all-cause mortality was 21% (versus 34%; P < .01), and CVD mortality was 9% (versus 19%; P < .01). Ten-year risk of CVD death for patients with LTS hypertension with long-term treatment compared with those without was 0.40 (95% CI, 0.27 to 0.60). CONCLUSIONS: This investigation of LTS hypertension, its treatment, and its sequelae in a free-living general population confirms the reduction in CVD mortality demonstrated in more short-term clinical trials of hypertension therapy in select patient groups.

Adult↗
PubMed1996

Epidemiologic assessment of angina before and after myocardial infarction: The Framingham study.

Angina pectoris before and after MI was evaluated in a sample of 729 men and women from a general population in whom MI developed during a 36-year period of follow-up. Relations of AP to subsequent CHD events and mortality after initial MI were analyzed by proportional hazards regression models and were adjusted for covariates (age, sex, blood pressure, serum cholesterol, body mass index, glucose intolerance, cigarette smoking, and antihypertensive medications) obtained from routine biennial examinations preceding the initial MI. Comparisons of the influence of angina were made between pre-MI angina, post-MI angina, and absence of AP. The sample had 484 men and 245 women (mean ages, 63 and 69, respectively) who survived greater than / equal to 30 days after MI. The initial MI was clinically unrecognized in 165 (34%) men and 115 (47%) women. Data on covariates were complete for 622 subjects, among whom 30% had pre-Ml angina, 18% had post-MI angina, and 52% did not have AP. Angina was half as common in persons with unrecognized MIs as in those with clinically recognized MIs. During an average of 8.7 years of follow-up, 57% of subjects developed subsequent CHD events, including recognized and unrecognized MI, coronary insufficiency, and CHD death, and 74% died. Both pre-MI angina (hazard ratio, 1.49; 95% CI, 1.17 to 1.91) and post-MI angina (hazard ratio, 1.43; 95% CI, 1.06 to 1.94) adjusted for accompanying risk factors were associated with increased risk for subsequent CHD events compared with those without AP. Neither pre-MI nor post-MI angina was associated with excess overall mortality.

Age Factors↗
PubMed1996

Effect of weight on cardiovascular disease.

Involuntary weight gains worsen all elements of the cardiovascular risk profile, including dyslipidemia, hypertension, insulin-resistant glucose intolerance, left-ventricular hypertrophy, hyperuricemia, and elevated fibrinogen. On the basis of data from the Framingham Heart Study and from other studies, it can be concluded that the degree of overweight is related to the rate of development of cardiovascular disease. After 26 y of follow-up in the Framingham study, each SD increment in relative weight was associated with 15% and 22% increases in cardiovascular events in men and women, respectively. Avoidance of weight gain after the age of 25 y is advisable to reduce cardiovascular mortality. There is a great potential benefit to weight loss, suggesting that weight control as a means for preventing and lessening cardiovascular disease become a national health priority. The optimal weight for avoidance of cardiovascular disease and prolonging life corresponds to a body mass index of 22.6 for men and 21.1 for women.

Adult↗
PubMed1996

Obesity and coronary heart disease.

Obesity carries a penalty of an associated adverse cardiovascular risk profile. Largely as a consequence of this, it is associated with an excess occurrence of cardiovascular disease morbidity and mortality. It is concluded on the basis of data from the Framingham study and other large prospective studies that the rate of development of cardiovascular disease rises rapidly in relation to even modest amounts of adiposity. The abdominal pattern of adiposity, and specifically visceral adiposity, appears to be the most hazardous. First identified as a cause of glucose intolerance, abdominal adiposity has been identified as promoting insulin resistance, hypertension and dyslipidemia, as well as CHD. While the impact of epidemic obesity on the health of white Americans is becoming more fully understood, there are important gaps in the knowledge about the nature of influence of adiposity on CHD in large subgroups of the population. The dearth of detailed and long term prospective studies of African-Americans is the most conspicuous shortcoming of the research base. Finally, because there is a great potential benefit of remaining lean or achieving a sustained weight loss when indicated, and given the high prevalence of obesity, research on adiposity prevention and more effective weight reduction methodology are urgently needed.

Adult↗
PubMed1996

The demographics of claudication and the aging of the American population.

Most peripheral artery disease is of ischemic atherosclerotic etiology and manifested as intermittent claudication (IC). Death and disability from atherosclerotic cardiovascular disease (CVD) is a growing problem because of the rapidly increasing elderly segment of the population. By the year 2015 the elderly will constitute 14.8% of Americans. Of the total 255 million, 13.8 million are over age 75 years and 9 million are women. On reaching age 65 years, the average remaining lifetime is 17.4 years. In the USA this 11% of the population accounts for 29% of the health costs and 70% of all deaths are attributable to cardiovascular disease. About 9.6% of cardiovascular events are due to peripheral artery disease manifested as IC requiring 777,000 office visits and 63,000 hospitalizations. Also, 17,400 deaths each year are attributed directly to this cause. The biennial incidence of IC in the Framingham Study was 7.1 per 1000 for men and 3.6% for women, increasing with age in both sexes up to age 75 years. At all ages there is a distinct male predominance. In the 35-64-year age range IC incidence is virtually identical to that of cardiac failure and stroke, but only one-third of CHD incidence. Beyond age 65 years IC incidence is only half that of other atherosclerotic cardiovascular conditions. The incidence of carotid bruits and non-palpable pedal pulses is virtually identical in the two sexes; only femoral bruits are male predominant. At time of diagnosis of IC one in three already have overt evidence of CHD, stroke or congestive heart failure (CHF). In those free of these at outset CHD and strokes occur at two to three times the general population rate and CHF 3.5-4.5 times the rate of persons without IC. Within 10 years of IC onset 43% develop CHD, 21% strokes and 24% cardiac failure. Carotid and femoral bruits are likewise harbingers of other atherosclerotic CVD. As many as 45% of IC victims lose their symptoms for extended periods. Survival following onset of IC is only two-thirds of that general population; after 10 years 60% died. This high mortality is largely attributable to coexistent cardiovascular impairments. A risk profile comprising the major cardiovascular risk factors predicts occurrence of IC even better than CHD. IC risk increases progressively with burden of the risk factors. With an aging population of increased size peripheral artery disease is a problem of increasing dimensions. Attention to comorbid conditions is essential if survival is to be improved. Because IC shares many of the same risk factors, measures to prevent CHD, CHF and strokes should also reduce IC risk.

Aging↗
PubMed1996

Diabetes mellitus and coronary heart disease in the elderly.

Data from epidemiologic studies document the role of clinically manifest diabetes mellitus as a powerful risk determinant for an array of atherosclerotic cardiovascular outcomes including coronary heart disease (CHD), stroke, and peripheral arterial disease, particularly in the elderly. Although dyslipidemias and hypertension are quite prevalent in persons with diabetes mellitus and contribute heavily to the underlying atherosclerotic process, other factors involving alternative pathogenetic mechanisms are necessary to explain for the dramatic acceleration of atherogenesis observed in this condition. Myocardial ischemia may be silent and myocardial infarction (MI) may be either painless or atypical in presentation which further complicates both the diagnostic and therapeutic management of CHD in older diabetic patients. MI, in this context, is confounded by dual prognostic disadvantages of higher risk for MI-related complications attributable to both advanced age and diabetes mellitus. Because available evidence has yet to demonstrate that control of hyperglycemia, either by oral agents or by insulin, effectively forestalls either the development or complications of atherosclerosis, preventive management in older patients with diabetes requires critical attention to correcting coexisting cardiovascular risk factors.

Aged↗
PubMed1996

Need and prospects for prevention of cardiac failure.

Cardiac failure is a lethal end-stage of cardiovascular disease. Survival, once the heart has used up all its reserve and compensatory mechanisms, is little better than for cancer. Once overt failure ensues median survival is only 1.7 years for men and 3.2 years for women, and sudden death is a common mode of exitus. Recent declines in death rates from cardiac disease have not been accompanied by a reduced prevalence or incidence of cardiac failure. A substantial reduction in cardiac failure incidence and mortality requires the detection and correction of presymptomatic left ventricular dysfunction and the risk factors which predispose to its occurrence. Major contributors to the development of cardiac failure have been delineated and quantified. Methods for efficiently identifying presymptomatic candidates for cardiac failure for preventive measures have been developed. High-risk candidates can now be cost-effectively targeted for treatment to delay failure. Independent predictors of heart failure have been identified by epidemiologic research which enable construction of multivariable risk profiles that efficiently predict congestive heart failure (CHF). The conditional probability of an event can be estimated over a wide range using a logistic function including the variables of age, systolic blood pressure, vital capacity, heart rate, ECG-LVH, X-ray cardiac enlargement, glucose intolerance, and coronary heart disease or valvular deformity. In this way it is possible to identify high-risk candidates for CHF. Some 80% of CHF events occur in persons in the upper quintile of multivariate risk. These persons at high risk yield a high prevalence of persons with echocardiographic evidence of impaired cardiac function likely to benefit from vigorous preventive management including angiotensin-converting enzyme (ACE) inhibitors.

Adult↗
PubMed1995

Clinical misconceptions dispelled by epidemiological research.

The epidemiological approach to investigation of cardiovascular disease was innovated in 1948 by Ancel Keys' Seven Countries Study and T.R. Dawber's Framingham Heart Study. Conducted in representative samples of the general population, these investigations provided an undistorted perception of the clinical spectrum of cardiovascular disease, its incidence and prognosis, the lifestyles and personal attributes that predispose to cardiovascular disease, and clues to pathogenesis. The many insights gained corrected numerous widely held misconceptions derived from clinical studies. It was learned, for example, that the adverse consequences of hypertension do not derive chiefly from the diastolic pressure, left ventricular hypertrophy was not an incidental compensatory phenomenon, and small amounts of proteinuria were more than orthostatic trivia. Exercise was considered dangerous for cardiovascular disease candidates; smoking, cholesterol, and a fatty diet were regarded as questionable promoters of atherosclerosis. The entities of sudden death and unrecognized myocardial infarction were not widely appreciated as prominent features of coronary disease, and the disabling and lethal nature of cardiac failure and atrial fibrillation was underestimated. It took epidemiological research to coin the term "risk factor" and dispel the notion that cardiovascular disease must have a single origin. Epidemiological investigation provided health professionals with multifactorial risk profiles to more efficiently target candidates for cardiovascular disease for preventive measures. Clinicians now look to epidemiological research to provide definitive information about possible predisposing factors for cardiovascular disease and preventive measures that are justified. As a result, clinicians are less inclined to regard usual or average values as acceptable and are more inclined to regard optimal values as "normal." Cardiovascular events are coming to be regarded as a medical failure rather than the first indication of treatment.

Aged↗
PubMed1995

Range of serum cholesterol values in the population developing coronary artery disease.

Blood lipids have been established as fundamental to atherogenesis, and there is a better understanding of the pathogenesis of atherosclerosis and of the various pharmacologic agents available to counter the mechanisms involved. However, more optimal lipid levels must be established for treatment of both the healthy population and persons already with coronary artery disease (CAD). In the Framingham Study cohort, those with elevated serum total cholesterol (> 275 mg/dl) had an increased risk of adverse outcomes whether healthy or with CAD. Compared with persons with cholesterol levels < 200 mg/dl (< 5.17 mmol/liter), the risk ratios for patients with elevated cholesterol levels were 3.8 for reinfarction, 2.6 for CAD mortality, and 1.9 for overall mortality. The prevalence of cholesterol levels > or = 240 mg/dl (> or = 6.21 mmol/liter) in persons who had sustained myocardial infarction was 35-52% in men and 66% in women, but 20% of myocardial infarctions occurred in people who had cholesterol levels < 200 mg/dl (< 5.17 mmol/liter). The average levels of serum total cholesterol and low density lipoprotein (LDL) cholesterol (225 mg/dl [5.82 mmol/liter] and 150 mg/dl [3.88 mmol/liter], respectively) at which CAD events occurred in men were below the levels recommended for treatment according to the guidelines of the National Cholesterol Education Program. In women, these levels were only slightly above the guideline levels. The average cholesterol levels at which CAD events occurred were substantially higher in women and decreased with age. Also, a steady decline in the average cholesterol levels of patients over the decades reflected chiefly the aging of the cohort.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Alcohol intake and bone mineral density in elderly men and women. The Framingham Study.

Alcohol consumption has multiple effects on bone, and alcoholic men have a high risk of osteoporotic fracture. The objective of this study was to assess the association between alcohol consumption and bone mineral density in elders. The authors evaluated 1,154 members of the Framingham Heart Study Cohort at biennial examination 20 (1988-1989). Subjects ranged in age from 68 to 96 years. Bone density was assessed at the radius (ultradistal and shaft) and at the proximal femur and spine. Alcohol consumption, assessed every 2 years from examination 12 (1967-1969) through examination 20, was averaged. The association of alcohol intake with bone density was examined after adjustment for age, weight, height, smoking, and, in women, age at menopause and years of estrogen use. Women who drank at least 7 oz (206.99 ml)/week of alcohol had higher bone densities at most sites (4.2-13.0% range with 7.7% average differences across all sites) than women in the lightest category of intake (< 1 oz (29.57 ml)/week). Men who were heavy drinkers (> or = 14 oz (414 ml)/week) also had higher bone densities than light drinkers, but the difference was less than in women (3.9% average across all sites). Lesser amounts of intake did not affect bone density. The authors conclude that alcohol intake of at least 7 oz (206.99 ml)/week is associated with high bone density in postmenopausal women, an effect possibly related to the augmentation of endogenous estrogen levels by alcohol.

Age Distribution↗
PubMed1995

Role of smoking in the U-shaped relation of cholesterol to mortality in men. The Framingham Study.

Elevated mortality has been reported at extremes of the serum total cholesterol distribution, with increased coronary mortality reported at high total cholesterol levels and increased cancer and non-cardiovascular/non-cancer mortality at low total cholesterol levels. The authors used data collected on 1,959 males aged 35-69 years from the fourth Framingham Study examination to analyze the relations between total serum cholesterol levels and 409 coronary deaths, 325 cancer deaths, and 534 other deaths for a 32-year follow-up. Age- and risk factor-adjusted Cox regressions were computed. Nonlinear (U-shaped) relations were investigated with the use of quadratic regression and with dummy variables using the 160-199 mg/dl group as the comparison group. Subset analyses investigated the relation in smokers and men who drank > or = 14 alcoholic drinks per week. All analyses were repeated removing those with existing cardiovascular disease and cancer and those who died during the first 5 years of follow-up. A significant U-shaped relation with all-cause mortality was noted, as were an inverse relation to cancer mortality and a monotonic increasing relation with coronary disease mortality. In subset analyses, the association of low serum cholesterol (< 160 mg/dl) with cancer mortality was observed in men who smoked cigarettes. Compared with the 160-199 mg/dl group, the relative risk was 3.72 (p = 0.0001, 95% confidence interval 1.91-7.25). Studies of the relation of low total serum cholesterol levels, cigarette smoking, and cancer are needed.

Adult↗
PubMed1995

Risk factors that attenuate the female coronary disease advantage.

OBJECTIVE: To compare the coronary disease experience of men and women in a community setting. DESIGN AND SETTING: Prospective cohort study. PATIENTS: Long-term follow-up of a population-based sample of 5209 men and women. RESULTS: Women outlive men and experience fewer cardiovascular events. By middle age, women lag 20 years behind men in the incidence of myocardial infarction, but the gap closes in the elderly, when cardiovascular disease becomes the leading cause of death in women as well as in men. Menopause promptly escalates coronary disease risk threefold and greatly erodes the advantage over men. Women and men share the same major risk factors for coronary disease, although women experience a lower absolute risk. However, high ratios of total/high-density lipoprotein cholesterol level ratios, left ventricular hypertrophy, and diabetes tend to eliminate the female advantage. CONCLUSION: Coronary disease is not a minor problem in women. Consequently, women should take vigorous preventive measures. There is a need for particular attention to glucose tolerance and blood lipid levels and a greater sense of urgency when hypertension progresses to left ventricular hypertrophy.

Adult↗
PubMed1995

An update on coronary risk factors.

Epidemiologic research continues to produce additional independent risk factors, including small dense LDL, Lp(a), isolated systolic hypertension, the insulin-resistance syndrome, leucocyte count, plasma fibrinogen, homocystinemia, and sleep disturbance. Alcohol in moderation appears protective. Because the hazard posed by any particular risk factor is markedly influenced by other metabolically linked risk factors with which it tends to cluster, multivariate risk assessment provides a substantially better risk estimate than that based on single risk factors.

Aged↗
PubMed1995

Concept of bridging the gap from youth to adulthood.

Clinical atherosclerotic cardiovascular disease reaches substantial incidence beginning at age 45 years in men and age 55 years in women but has its onset in childhood. Lesions progress in relation to exposure to identified risk factors and, once initiated, tend to be self-perpetuating. Because predisposing factors are often initiated in childhood, interventions beginning early in life are optimal for prevention of adult disease. Even genetically predisposed people usually require an unfavorable lifestyle for the atherogenic trait to be expressed. No combination of risk factors entirely accounts for the increase in clinical atherosclerotic events with advancing age. This may be a reflection of longer exposure to risk factors or impaired ability to cope with them in advanced age. The declining risk factor risk ratios with advancing age may be a consequence of the selective early removal of those most susceptible from the population at risk. Risk of major cardiovascular events increases about 2.5-fold with each 10 years of age, even in people without major risk factors who are considered at low risk for atherosclerotic cardiovascular events. However, at any age vulnerability to cardiovascular events is strongly influenced by the burden of risk factors. Decreased risk ratios with advanced age are offset by a greater absolute risk. The female advantage over men erodes with age, with the menopause and with acquisition of an unfavorable lipid profile and glucose intolerance.

Adult↗
PubMed1995

Framingham study insights into hypertensive risk of cardiovascular disease.

Elevated blood pressure is a common and powerful predisposing factor for stroke, coronary disease, cardiac failure and peripheral artery disease imposing a 2-3 fold increased risk of one or more of these atherosclerotic sequelae. The risk ratio imposed by hypertension is greatest for cardiac failure and stroke, but in Western countries coronary disease is the most common and lethal hazard. In hypertensive men and women respectively, 35% and 45% of myocardial infarctions are silent or unrecognized necessitating routine periodic ECG examination for its detection. Comparison of the impacts of systolic and diastolic blood pressure gives no indication of a greater impact of diastolic pressure and isolated systolic hypertension is distinctly hazardous. Over-reliance on diastolic pressure to assess risk can be misleading, particularly in advanced age. Attributable risk estimates suggest that 78% of hypertension in men and 65% in women is directly attributable to adiposity, making weight control of paramount importance for primary prevention of hypertension. The likelihood of development of cardiovascular disease in the hypertensive patient is greatly enhanced by the presence of metabolically-linked risk factors and already existent cardiovascular conditions. These influence the urgency and choice of therapy. Rational and efficient assessment of the hypertensive candidate for cardiovascular disease requires use of a cardiovascular risk profile evaluating the joint effect of multiple risk factors and effective treatment improves multivariate risk.

Adult↗