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Biomedical subjects

W B Kannel

Publications and source records attributed to W B Kannel.

At least 55 records · Page 3Linked to original sources

Intellectual decline after stroke: the Framingham Study.

BACKGROUND AND PURPOSE: The causes and characteristics of cognitive decline after stroke are poorly defined, because most studies have relied on the diagnosis of dementia after stroke, without measurement of prestroke cognitive function. METHODS: The Mini-Mental State Examination (MMSE) was used to assess the cognitive performance of 74 subjects from the Framingham Study cohort who had suffered a stroke during a 13-year period. We compared their poststroke cognitive performance with the prestroke MMSE scores collected during their biennial examinations, and their prestroke/poststroke changes in MMSE score were then compared with those of 74 control subjects matched for age and sex. Cases and controls underwent testing for symptoms of depression using the Center for Epidemiologic Studies of Depression (CES-D) scale, and these findings were correlated with their cognitive performance. Changes in cognitive performance in the cases were correlated with the CT-documented characteristics of the stroke. RESULTS: The cases had a significantly lower mean+/-SE MMSE score at prestroke baseline (27.28+/-0.34) than did the control subjects (28.08+/-0.21), a difference that became more pronounced (23.57+/-0.92 versus 28.31+/-0.25; P<.001) after stroke. The poststroke decline in cognitive function in the cases was correlated only with a large, left-sided stroke on CT. The CES-D scores were significantly higher in the cases, but nondepressed cases had significantly lower MMSE scores than nondepressed controls. CONCLUSIONS: Stroke is followed by a significant decline in cognitive performance when prestroke and poststroke measurements are compared. Although depression is more frequent in the stroke patients, their intellectual decline appears to be independent from the presence of depression.

Aged↗

Cardiovascular risks of hypertension: lessons from observational studies.

Hypertension is an acknowledged major risk factor for cardiovascular disease and death in both men and women. Despite a historical focus by clinicians on the importance of diastolic blood pressure (DBP) risks, epidemiologic data from numerous large-scale studies have clearly demonstrated that both systolic blood pressure (SBP) and DBP are important determinants of cardiovascular risk. Recent analyses have described notable risks associated with isolated and borderline elevations of SBP, which predominate in the elderly, emphasizing the independent contribution of elevated SBP in determining overall risk. Overviews of large-scale treatment trials show that antihypertensive drug treatment confers a favorable net clinical benefit in patients with diastolic and isolated systolic hypertension, and the magnitude of risk reduction is comparable to that expected from the observational data. However, at any level of SBP or DBP, the absolute magnitude of risk varies widely depending on the burden of coexisting risk factors present. Therefore, it is essential that decisions regarding the urgency, risks and benefits of antihypertensive drug treatments be informed by accurate determinations of overall cardiovascular risk.

Adolescent↗

Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study.

BACKGROUND: We attempted to characterize age-related changes in blood pressure in both normotensive and untreated hypertensive subjects in a population-based cohort from the original Framingham Heart Study and to infer underlying hemodynamic mechanisms. METHODS AND RESULTS: A total of 2036 participants were divided into four groups according to their systolic blood pressure (SBP) at biennial examination 10, 11, or 12. After excluding subjects receiving antihypertensive drug therapy, up to 30 years of data on normotensive and untreated hypertensive subjects from biennial examinations 2 through 16 were used. Regressions of blood pressure versus age within individual subjects produced slope and curvature estimates that were compared with the use of ANOVA among the four SBP groups. There was a linear rise in SBP from age 30 through 84 years and concurrent increases in diastolic blood pressure (DBP) and mean arterial pressure (MAP); after age 50 to 60 years, DBP declined, pulse pressure (PP) rose steeply, and MAP reached an asymptote. Neither the fall in DBP nor the rise in PP was influenced significantly by removal of subsequent deaths and subjects with nonfatal myocardial infarction or heart failure. Age-related linear increases in SBP, PP, and MAP, as well as the early rise and late fall in DBP, were greatest for subjects with the highest baseline SBP; this represents a divergent rather than parallel tracking pattern. CONCLUSIONS: The late fall in DBP after age 60 years, associated with a continual rise in SBP, cannot be explained by "burned out" diastolic hypertension or by "selective survivorship" but is consistent with increased large artery stiffness. Higher SBP, left untreated, may accelerate large artery stiffness and thus perpetuate a vicious cycle.

Adult↗

Blood pressure and cardiovascular morbidity and mortality rates in the elderly.

The influence of blood pressure on the development of cardiovascular disease and mortality rate beyond 75 years of age has been uncertain. A reported inverse relation to mortality rate noted in the very old could reflect poor cardiovascular health. This report examines the impact of blood pressure on cardiovascular morbidity and mortality rates and all-cause mortality rate in those aged 75 to 94 years. For this analysis the data were the Framingham study subjects found free of cardiovascular disease and a second sample of those with cardiovascular disease present on the biennial examinations. Investigation of the relation of systolic and diastolic blood pressures to all causes and cardiovascular morbidity and mortality rates within each 2-year interval for those aged 75 to 94 years was carried out. Over the period of 38 years of follow-up there were increasing cardiovascular morbidity and mortality rates with increasing blood pressure levels for both men and women in the sample free of cardiovascular disease. In those with cardiovascular disease at the biennial examination there was a distinct U-shaped curve of cardiovascular mortality rate in relation to systolic blood pressure in men with a substantial increase in mortality rate below systolic pressures of 120 mm Hg for both men and women. Excess mortality rate reported in elderly persons with low blood pressure appears to be a result of poor cardiovascular health and not from the low pressure itself. The excess mortality rate reported for low blood pressure levels in persons older than 75 years derives from the inclusion of the substantial proportion of this age group who have cardiovascular disease.

Aged↗

Hazards, risks, and threats of heart disease from the early stages to symptomatic coronary heart disease and cardiac failure.

The epidemiologic approach to investigation of atherosclerotic cardiovascular disease has provided many insights into the preclinical and clinical spectrum of the disease. The hazard of developing atherosclerotic cardiovascular disease is substantial with coronary heart disease (CHD), the most common and most lethal feature. The outlook in those who manage to survive the initial episode is also serious, with a 10-year mortality rate of 37% for persons with angina and a 55% rate for those sustaining a myocardial infarction. Fifteen percent of persons developing CHD present with a fatal event, and 38% of infarctions go unrecognized. The presence of atherosclerosis in one vascular territory imposes an increased risk of its appearing in another area at two to six times the general population rate. The major cardiovascular risk factors adversely affect all arterial vascular territories so that correction of risk factors targeted at one particular atherosclerotic outcome may also favorably influence the other risk factors. Coronary disease is the most prevalent lethal hazard of hypertension, dyslipidemia, glucose intolerance, and cigarette smoking. These risk factors cluster and optimal therapy must improve the whole risk profile. Women share the same risk factors for CHD as men. Although women have a lower absolute risk for most risk factors, a high total/HDL cholesterol ratio, left ventricular hypertrophy, and diabetes each tend to eliminate the female advantage. Menopause also promptly escalates risk threefold. Although women tend to have a lower incidence than men, the initial attack is just as highly lethal in women, and their subsequent outlook as survivors is at least as serious as for men. Sudden death is a pre-eminent feature of coronary disease and cardiac failure. Coronary disease increases sudden death risk 3.3-fold and cardiac failure 4.8-fold. Sudden death incidence varies in relation to the same cardiovascular risk factors as coronary heart disease, with no unique risk factors identified. However, multivariate combinations of these in a profile can identify high-risk candidates for sudden death as well as coronary attacks in general. The key to prevention of sudden death is to prevent coronary attacks and cardiac failure. Despite aggressive cardiac revascularization and treatment of hypertension, congestive heart failure (CHF) has not decreased in prevalence, and innovations in the treatments of overt failure have not substantially improved survival. Median survival is only 1.7 years for men and 3.2 years for women. The conditional probability of developing CHF can be estimated using a logistic function comprised of age, systolic pressure, vital capacity, heart rate, ECG-left ventricular hypertrophy (LVH), glucose intolerance, x-ray enlargement, and presence of CHD and heart murmurs. Eighty percent of CHF events occur in persons in the upper quintile of multivariate risk. Continued clinical, metabolic, and epidemiologic research have expanded and refined atherosclerosis risk factors. The lipid connection is now concerned with the apoprotein makeup of the lipids, subfractions of lipids, and Lp(a). The diabetic influence is now focused on insulin resistance. Ambulatory monitoring is being used to evaluate blood pressure and silent ischemia. Fibrinogen and leukocyte counts have emerged as possible indicators of unstable lesions. Prospects for primary and secondary prevention are good if public health measures, health education, and preventive medicine are implemented based on existing knowledge of correctable or avoidable risk factors. The potential for more effective prevention continues to expand, and great advances have already been made in countries where aggressive preventive measures have been implemented to correct the major established risk factors.

Age Factors↗

The occurrence of Raynaud's phenomenon in a general population: the Framingham Study.

The prevalence and predisposing conditions for primary and secondary Raynaud's phenomenon (RP) were examined in The Framingham Study based on 16 years of follow-up of a cohort of 4182 men and women. The association with atypical chest pain and migraine headache was also investigated. Over the 16 years of follow-up there were 130 men and 171 women who developed primary RP. The prevalence in women (9.6%) was somewhat higher than in men (8.1%) and 81.4% of the RP was primary. Secondary RP was equally prevalent in men (18.6%) and women (19.7%). The most common causes of secondary RP were beta-blocker use (34.2%), carpal tunnel syndrome (10.5%) and rheumatoid arthritis (7.2%). Primary RP cases differed from noncases by having lower systolic blood pressure (p < or = 0.001) and diastolic blood pressure (p < 0.0001), and more coronary disease (p = 0.009), smoking (p < or = 0.01) and higher blood sugars (p < or = 0.009). Atypical chest pain was present more often than noted previously in The Framingham Study general population survey, and was equally prevalent in primary and secondary RP and in the two sexes. Associated migraine was more prevalent in women (14.4%) than men (5.0%). Vibrating tool use with associated RP occurred in 14.6%.

Adrenergic beta-Antagonists↗

Influence of fibrinogen on cardiovascular disease.

Results from prevalence, case-control, angiographic and echocardiographic investigations incriminate elevated fibrinogen levels as a strong independent risk factor for the occurrence of initial and recurrent cardiovascular events. Average fibrinogen levels are higher in women and persons with other risk factors including hypertension, diabetes, cigarette smoking, obesity, elevated haematocrit value and dyslipidaemia. Fibrinogen tends to cluster with most of these major atherogenic cardiovascular risk factors and further enhances their risk. Prospective data indicate a relationship between fibrinogen and the subsequent development of all the major atherosclerotic cardiovascular events including coronary heart disease, stroke and peripheral artery disease. Fibrinogen adds to the multivariate risk of cardiovascular events, especially in the high risk subset of the population. In the Framingham Heart Study, a comparison of risk gradients, exemplified by their regression coefficients, was similar for all outcomes (coronary heart disease, stroke, peripheral artery disease and cardiovascular disease) in men, whereas, in women, the risk gradient for fibrinogen appeared weakest for stroke. Fibrinogen exerts an independent influence on the frequency of cardiovascular disease in general, and coronary heart disease in particular. For example, in both men and women, each standard deviation increase in fibrinogen level (about 0.56 g/L) within the range of usual values is associated with about a 20% age- and risk factor-adjusted increase in the incidence of an initial cardiovascular event. Fibrinogen should be added to the list of major atherogenic cardiovascular risk factors; in addition, there is a need for intervention trials designed to test the efficacy of lowering fibrinogen in individuals at high risk for cardiovascular disease.

Cardiovascular Diseases↗

Cardiovascular risk factors in the older adult.

The potential benefits of correcting identified cardiovascular risk factors in the elderly are substantial. Treatment of hypertension has been shown to reduce morbidity and mortality, and correction of dyslipidemia prevents recurrent coronary events. Other measures (e.g., lowering fibrinogen and homocysteine levels, weight reduction) whose efficacy in the elderly has not been established are nevertheless recommended.

Adult↗

Epidemiologic assessment of the role of blood pressure in stroke: the Framingham Study. 1970.

Control of hypertension, labile or fixed, systolic or diastolic, at any age, in either sex appears to be central to prevention of atherothrombotic brain infarction (ABI). Prospectively, hypertension proved the most common and potent precursor of ABI's. Its contribution was direct and could not be attributed to factors related both to stroke and hypertension. Asymptomatic, causal "hypertension" was associated with a risk of ABI about four times that of normotensives. The probability of occurrence of an ABI was predicted no better with both blood pressure measurements or the mean arterial pressure than with systolic alone. Since there was no diminishing impact of systolic pressure with advancing age, the concept that systolic elevations are, even in the aged, innocuous is premature. Comparing normotensives and hypertensives in each sex, women did not tolerate hypertension better than men.

Adult↗

Use of vital capacity for cardiac failure risk estimation in persons with coronary disease and left ventricular hypertrophy.

Cardiac failure is a common lethal outcome of coronary heart disease and left ventricular hypertrophy. The efficacy of forced vital capacity (FVC), measured biennially, in predicting the onset of cardiac failure was explored in 818 Framingham Study subjects with those predisposing conditions, among 324 developed cardiac failure. Among the men and women who had coronary disease or left ventricular hypertrophy, those with FVCs in the lower quartile were at substantially increased risk of developing cardiac failure. For men, comparing the lowest quartile with men whose FVCs were in the highest quartile (<2.7 L vs >5.6 L), the risk ratio was 1.8; for women with FVCs <1.7 L, the risk was 2.3 times those with FVCs of > or = 3.5L. The excess risk of cardiac failure imposed by a low FVC was similar in those with coronary disease and left ventricular hypertrophy. The simple FVC is an inexpensive and robust predictor of cardiac failure in persons predisposed by coronary disease or left ventricular hypertrophy. FVC determination should help identify candidates for cardiac failure needing echocardiographic examination for ventricular dysfunction.

Aged↗

Alcohol and coronary heart disease: the evidence for a protective effect.

There is a considerable body of evidence indicating that moderate alcohol intake is associated with a reduced incidence of, and mortality from, coronary heart disease (CHD). There is also substantial evidence that problem drinking (well beyond two drinks per day) is associated with increased cardiovascular mortality. However, the frequently reported harmful effect of alcohol abuse on CHD mortality rates could be a result of mislabelling as CHD conditions such as alcohol-induced dilated cardiomyopathy, dysrhythmias, and hypertensive cardiovascular disease. The combination of protective and harmful influences of alcohol consumption results in a U-shaped mortality curve. A true protective effect of moderate intake of alcohol is likely, because of consistent findings in many large, well-conducted studies of diverse population samples and the apparent specificity of the protective effect for CHD and possibly atherosclerotic-thrombotic brain infarction. There are also biologically plausible mechanisms whereby the protection might be conferred. Alcohol has been shown convincingly to raise HDL subfractions which have been found to be protective against CHD, and it may also provide protection by an antithrombotic effect. There is a suggestion that wine, and red wine in particular, may be more protective than other alcoholic beverages. However, it is difficult to control adequately for confounding factors, since persons who prefer wine have been found to have a more advantageous lifestyle, a better cardiovascular risk profile, are better educated, and smoke less. The evidence for a protective effect of moderate alcohol intake includes population studies of alcohol and CHD mortality in 20 countries, case-control studies, prospective cohort studies, arteriographic studies, and animal experiments. Nevertheless, because there are no controlled trial data, it is possible that some other factor may be responsible for the apparent protective effect of alcohol. The inclusion of former drinkers or sick individuals in the non-drinker category, and lack of control for cigarette smoking and other risk factors, have been excluded as reasons for higher CHD rates among individuals who do not consume alcohol. No alternative explanation for the protective effect has surfaced after two decades of investigation of the alcohol-CHD relationship, yet, the penalties of heavy alcohol consumption are too large to ignore. Until we can be sure that advice that encourages the public to drink to avoid coronary heart disease does not increase abuse, we must be cautious in making general recommendations.

Alcohol Drinking↗