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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on the prevalence of chronic heart failure (CHF) in a random sample of a population (aged 20-64 years) from the Veneto region in northern Italy. The relationship between CHF and hypertension and obesity was also investigated. These data were collected during an international research project coordinated by the World Health Organization. The overall prevalence of CHF was 2.0% both in the male and female population. The prevalence of CHF increased significantly with age and was positively correlated with body mass index in both sexes. Patients with borderline hypertension showed a 3.5-fold increased prevalence of CHF. The prevalence of CHF was 4.9-fold higher in hypertensive than in the normotensive subjects. Patients treated with hypotensive drugs had a significantly higher prevalence of CHF than untreated patients.
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PMID:[Heart failure in the population: prevalence data]. 129 74

A health risk appraisal function has been developed for the prediction of stroke using the Framingham Study cohort. The stroke risk factors included in the profile are age, systolic blood pressure, the use of antihypertensive therapy, diabetes mellitus, cigarette smoking, prior cardiovascular disease (coronary heart disease, cardiac failure, or intermittent claudication), atrial fibrillation, and left ventricular hypertrophy by electrocardiogram. Based on 472 stroke events occurring during 10 years' follow-up from biennial examinations 9 and 14, stroke probabilities were computed using the Cox proportional hazards model for each sex based on a point system. On the basis of the risk factors in the profile, which can be readily determined on routine physical examination in a physician's office, stroke risk can be estimated. An individual's risk can be related to the average risk of stroke for persons of the same age and sex. The information that one's risk of stroke is several times higher than average may provide the impetus for risk factor modification. It may also help to identify persons at substantially increased stroke risk resulting from borderline levels of multiple risk factors such as those with mild or borderline hypertension and facilitate multifactorial risk factor modification.
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PMID:Probability of stroke: a risk profile from the Framingham Study. 200 1

Cardiac arrhythmias were studied in patients with essential hypertension in relation to their myocardial function. It was found that the arrhythmias occurring in the early period of the disease (borderline hypertension, Stage I hypertension) were primarily functional and affected the course of the disease and hemodynamics to a small degree. The life-threatening arrhythmias recorded in early hypertension were more commonly caused by mitral prolapse. The duration and severity of hypertension, development of left ventricular myocardial hypertrophy, myocardial fiber distension in relative heart failure play a decisive role in the development of cardiac arrhythmias in patients with Stage II hypertensive disease. It is essential to make comprehensive clinical and instrumental studies to clarify the genesis of the arrhythmic syndrome and to correctly choose the management policy in these patients.
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PMID:[Clinical significance of arrhythmia in patients with hypertension]. 206 87

Studies of cardiac performance in hypertension have often been restricted to cardiac output determinations, although the latter alone are inadequate for that purpose. To define the range of cardiac performance in hypertension, the response of left ventricular filling pressure to increased workload (static exercise) was determined in 39 subjects--eight normotensive (NT) volunteers, seven patients with borderline hypertension (BLH), and 24 essential hypertensives (EH), of age-matched groups. A rise of mean pulmonary wedge pressure (PWP) by 5 mm Hg or more during maximum handgrip (HG) was considered "abnormal" for a workload (SBP x HR x 10(-3)) increase of greater than or equal to 25%. All NT subjects and all patients with BLH as well as 16 of the 24 EH (EH-I) showed normal cardiac performance by this definition. In contrast, PWP increased greater than or equal to 5 mm Hg during HG in eight patients with EH (EH-II). The calculated increase in cardiac workload was not significantly different among the four groups (+5, 5.8, 5.4 and 5.5 respectively). Beta blockade (propranolol, 10 mg i.v.) slowed heart rate in all subjects and reduced SBP x HR product in all groups both at rest and during HG. Responses of PWP to HG were widely divergent in the different patients. However, as a group those patients with "impaired cardiac performance" before propranolol (EH-II) had a greater reduction in performance following propranolol than EH-I or NT. This study suggests that adrenergic support of cardiac performance might be important in some hypertensive patients with no evidence of heart failure.
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PMID:Sympathetic contribution to the cardiac response to stress in hypertension. 684 61

The sympathetic nervous system (SNS) plays an important role in the regulation of cardiac performance and peripheral circulation. Changes in SNS activity measured as catecholamines in plasma or organ spillover have been implicated in the pathogenesis of hypertension. Recent studies using microneurography to directly assess peripheral sympathetic nerve activity have demonstrated an increase in sympathetic activity in patients with borderline hypertension at rest and during hypoxia. We have recently shown that resting muscle sympathetic nerve activity is comparable in offspring of hypertensive and normotensive parents. However, during mental arithmetic the increase in muscle sympathetic nerve activity and blood pressure was significantly more pronounced in offspring of hypertensive than in offspring of normotensive parents, but resting blood pressure was in the normotensive range and comparable in both groups. These data indicate that the response to mental stress results in a more pronounced activation of SNS in normotensive subjects with a genetic background of hypertension. In other cardiovascular disease states such as acute myocardial infarction and heart failure activity of the SNS may determine prognosis significantly. Some calcium antagonists which are successfully used to treat patients with hypertension and stable angina pectoris may have unfavourable effects in patients with impaired left ventricular function. This could be due in part to baroreceptor-mediated activation of the SNS, an effect which seems to be related to pharmacokinetics and pharmacodynamics of the drugs. In contrast, angiotensin converting enzyme inhibitors seem to directly decrease sympathetic nerve activity. This may explain at least in part their beneficial effects in patients with impaired left ventricular function. Thus, the SNS as a regulator of the cardiovascular system also plays an important role in the pathophysiology of cardiovascular diseases such as hypertension, myocardial infarction and heart failure. Furthermore, drug therapy could have a significant impact on the activity of the SNS.
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PMID:Role of sympathetic nervous system in hypertension and effects of cardiovascular drugs. 965 33

The body's vasculature plays a critical role in the development of functional and structural alterations responsible for tissue and organ damage in laboratory animals and human subjects during illness and senescence, and in response to stress. Components of the vasculature, namely, major arteries such as the aorta, smaller arteries, arterioles, capillaries, post-capillary venules, and collecting central veins, all serve as conduits through which vital substrates are delivered to cellular masses and/or waste products are removed. A number of physical and neurohumoral agents known to be responsive to stress stimuli exert functional control over the vasculature. Both physical and emotional stress have been found to cause significant hemodynamic alterations. Large artery rigidity, for instance, develops rapidly following stress-induced activation of the autonomic nervous system. Associated with this process is increased release into the circulation of catecholamines and angiotensin-II. At the same time, insulin resistance develops, accompanied by nitric oxide release and changes in the immune system. The response of large arterial conduits to stress is characterized by increased pulse pressure, which in turn affects the endothelium of the arterial vessels responsible for determining total peripheral resistance. Microcirculation networks, where a large fraction of the blood volume is contained, are affected as well, and the blood in them is subject to redistribution into adjacent interstitial fluid compartments. Changes in endothelial permeability, secondary to variations in pulse pressure, can lead to interstitial edema and changes in the physicochemical properties of interstitial compartments. These changes give rise to alterations in the traffic of substrates and waste products between blood and cells. This sequence of events also takes place in the vasa vasorum microcirculation that nourishes large arteries, and likely contributes to remodeling of the vascular wall and to atherogenesis. The contribution of large artery rigidity to the morbidity and mortality associated with arterial hypertension, diabetes mellitus, heart failure, and terminal uremia, is relatively well established in human populations. In addition, it appears that aortic rigidity precedes the development of arterial hypertension in the spontaneously hypertensive rat (SHR) model, as well as in individuals with borderline hypertension. The fact that some of the functional and structural vascular alterations produced by stress are reversible reinforces the importance of developing behavioral techniques and pharmacologic agents that can successfully interrupt this pathological sequence of events.
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PMID:Vascular response to stress in health and disease. 1204 May 37