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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension and obesity frequently coexist in the same patient. However, the two disorders disparately affect cardiovascular function and structure. The presence of obesity significantly affects hypertensive target organ involvement. On one hand, obesity may tend to mitigate the harmful effects of a chronically elevated total peripheral and renal vascular resistance and lessen end-organ damage such as nephrosclerosis in essential hypertension. However, since both obesity and hypertension increase cardiac workload, although by different mechanisms, their presence in the same patient results in a double burden to the left ventricle. Congestive heart failure, sudden death, and coronary heart disease are common sequelae of obesity hypertension. Weight loss reduces arterial pressure by a decrease in intravascular volume and cardiac output associated with a fall in sympathetic activity. Intervention in obesity hypertension diminishes the dual hemodynamic burden imposed on the heart and becomes therefore a major objective in the prevention and treatment of heart disease.
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PMID:Obesity in hypertension: how innocent a bystander? 623 45

This study analyzes and compares systemic and coronary hemodynamics in patients with essential hypertension in relation to hypertrophic heart disease of nonhypertensive origin. Left ventricular function (as assessed from the cardiac index, stroke volume index, ejection fraction, mean velocity of circumferential fiber shortening, mean normalized systolic ejection rate, and isovolumic indexes) may be normal in patients with hypertensive hypertrophy, even with a large increase in muscle mass and in the presence of concomitant coronary artery disease. Left ventricular function is impaired when regional contraction abnormalities or ventricular dilatation, or both, occur and is inversely related to both cardiac size and systolic wall stress. Coronary blood flow (+ 18%), coronary resistance (+ 38%), and myocardial oxygen consumption (MVO2) (+ 21%) are increased in essential hypertension. Coronary reserve is reduced even in hypertensive hypertrophy without evidence of coronary artery disease. MVO2 per mass unit was directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. Coronary reserve may remain normal in both moderate and excessive hypertrophy, provided systolic wall stress and hence the myocardial oxygen consumption are not increased. It is concluded that the appropriateness of left ventricular hypertrophy, as a result of mass-to-volume ratio and stress, is a major determinant of left ventricular performance, of coronary blood flow, and of myocardial oxygen consumption.
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PMID:The coronary circulation in hypertensive heart disease. 624 Apr 56

In this overview of the achievements of the National Heart, Lung, and Blood Institute (NHLBI), the major developments in each major form of heart disease since the birth of the Institute 35 years ago are reviewed. In the case of congenital heart disease, it has become possible to establish an accurate diagnosis, often by noninvasive methods, and to correct by surgical treatment almost all congenital cardiac malformations. The major challenge now is to eliminate these disorders; this will require an understanding of the fundamental molecular basis of these lesions. Acquired valvular heart disease can also now be characterized by hemodynamic, angiographic, as well as noninvasive techniques, principally echocardiography. Surgical treatment is usually successful, but improvement in the durability of valves without thromboembolic potential remains an important challenge. While essential hypertension can now be managed pharmacologically in almost every patient and while such management reduces the excess mortality resulting from this condition, current research focuses on elucidating the underlying basis of this disorder. Atherosclerosis remains the most common cause of cardiac and vascular disease. Although its cause has not been defined, several abnormalities in lipid metabolism that play an etiologic role in many patients with atherosclerosis have been identified. The treatment of these disorders with cholesterol-binding resins, which increase the number of cellular receptors for low-density lipoprotein, and with inhibitors of the enzyme required for cholesterol biosynthesis holds considerable promise. Noninvasive techniques will be used increasingly for detection of atherosclerosis in asymptomatic persons and for determining the efficacy of therapy. The mortality resulting from acute myocardial infarction has been reduced in half by the development of coronary care units and the prompt treatment of potentially fatal ventricular tachyarrhythmias. Current research is focused on preventing pump failure by limiting infarct size; lysis of coronary thrombi now appears to be the most promising method of accomplishing this. Chronic angina pectoris can be relieved by the judicious use of three classes of drugs--organic nitrates, beta-adrenergic blockers, and calcium antagonists, and two mechanical approaches--percutaneous transluminal coronary angioplasty and coronary artery bypass grafting--are usually successful in relieving angina in patients who do not respond adequately to medical management. Whether or not any of these approaches prolong life is not yet settled.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thirty-five years of progress in cardiovascular research. 638 25

Observations from pediatric epidemiology studies over the past 20 years document that atherosclerosis and essential hypertension begin in childhood. Evidence of coronary artery disease and hypertensive cardiovascular renal disease is found and relates strongly to clinical cardiovascular risk factors. Obesity, especially central obesity, and hyperinsulinemia are commonly found, and these cluster with other risk factors. Lifestyles, such as poor eating behavior and tobacco usage, also begin early and influence cardiovascular risk. The implication from these pediatric observations is that intervention should begin early to prevent unhealthy lifestyles and encourage adoption of healthy behaviors. Where adult heart diseases pervade the major part of the United States population and other industrialized cultures, various epidemiologic strategies of prevention are needed. A high-risk, clinical approach can be applied to individuals with heart disease or to individuals with underlying risk factors and their families. Primary and secondary prevention are both important and should be implemented by primary care physicians. A population approach is also needed because of the widespread occurrence of heart disease. A public health approach to prevention can occur through health education and health promotion programs. Physicians should play a role in encouraging prevention for the general population. The future direction of Preventive Cardiology for our nation rests on educating children to adopt and maintain healthy lifestyles. The Bogalusa Heart Study has made a major contribution in providing the background information for that direction.
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PMID:Preventive cardiology and its potential influence on the early natural history of adult heart diseases: the Bogalusa Heart Study and the Heart Smart Program. 750 17

Patients with mild to moderate essential hypertension were treated mainly with an ACE inhibitor (delapril, n = 980) or a Ca antagonist (n = 956) for 12 months, and the incidence of cerebrovascular and cardiovascular events as well as drug-related side effects were compared between the two groups. There were no significant differences between the clinical backgrounds of the two groups. In both groups, the blood pressure was decreased significantly from 1 month of treatment onwards, with the degree of reduction being greater in the Ca antagonist group throughout the study period (p < 0.001). Cerebrovascular or cardiovascular events occurred in 11 out of 980 patients in the delapril group and 18 out of 956 patients in the Ca antagonist group (p = NS). Cerebrovascular disease developed in 5 delapril-treated patients and 11 Ca antagonist-treated patients, and heart disease developed in 5 and 7 patients, respectively (both p = NS). Discontinuation of treatment due to side effects was significantly more common in the delapril group than in the Ca antagonist group (p < 0.001). There was no significant difference in the incidence of cerebrovascular and cardiovascular events between the two groups, and the results suggested that blood pressure reduction per se did not necessarily lead to a parallel decrease in cerebrovascular and cardiovascular complications.
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PMID:A 12-month comparison of ACE inhibitor and CA antagonist therapy in mild to moderate essential hypertension--The GLANT Study. Study Group on Long-term Antihypertensive Therapy. 758 34

This article provides an in-depth overview of the relationship between primary hypertension and adult obstructive sleep apnea syndrome. The background data and research are taken from the English-language literature through 1993. Primary hypertension is a common cause of major medical illnesses, including stroke, heart disease, and renal failure, in middle-aged males. Its prevalence in the United States is around 20%, with the rate of newly diagnosed hypertensive patients being about 3% per year. Sleep apnea syndrome is common in the same population. It is estimated that up to 2% of women and 4% of men in the working population meet criteria for sleep apnea syndrome. The prevalence may be much higher in older, non-working men. Many of the factors predisposing to hypertension in middle age, such as obesity and the male sex, are also associated with sleep apnea. Recent publications describe a 30% prevalence of occult sleep apnea among middle-aged males with so called "primary hypertension." Is this association fortuitous, related to a high prevalence of both diseases in the same population, or is it caused by a factor common to both diseases, such as obesity? Should the diagnosis of apnea be actively sought with sleep studies in hypertensive populations? If a diagnosis of "asymptomatic" sleep apnea is made in a hypertensive person, should the apnea be treated? Current research data provide only partial answers to these and other questions regarding the association of apnea and hypertension. Logic dictates that clinically symptomatic patients in hypertensive clinics should receive appropriate evaluation for apnea, but broad populations of hypertensive individuals should not be referred for sleep studies.
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PMID:The relationship between systemic hypertension and obstructive sleep apnea: facts and theory. 784 28

Heart disease, stroke, and kidney failure are leading causes of death. Essential hypertension is the major predisposing risk factor of cardiovascular disease. Yet, after several decades of intensive investigation, the initiating causative mechanism of essential hypertension is still unknown. However, investigators in the field generally agree that an increased total peripheral resistance (TPR) is the fundamental hemodynamic disorder in essential hypertension. This review addresses the hypothesis that the increased TPR of essential hypertension is due to a defective mechanism in the contractility of arterial smooth muscle. Force-velocity and length-tension studies have shown that both caudal arterial muscle and mesenteric resistance arterial muscle from spontaneously hypertensive rats (SHR) can shorten more and faster than muscle from normotensive control Wistar-Kyoto rats (WKY). In addition, the SHR muscle relaxation rate is slower compared with the WKY muscle. These alterations in mechanical behavior of SHR arterial muscle appear to be primary to the high blood pressure since MK-421 (enalapril maleate)-treated SHR arterial muscle shows the same increased velocity of shortening, increased shortening ability, and decreased relaxation rate as the untreated SHR muscle. MK-421 is an angiotensin-converting enzyme blocker. SHR maintained on MK-421 treatment have normal blood pressures in spite of being of the genetically hypertensive strain. While these findings are encouraging, several other important issues supporting the hypothesis require resolution and warrant review. Firstly, structural alterations of blood vessel walls in hypertension cause the walls to thicken and encroach on the vessel lumens contributing to the increased TPR. Whether such wall thickening is the cause or consequence of high blood pressure has been controversial in the literature. In this report, data are presented from a study in which MK-421-treated SHR were utilized as a model of prehypertensive SHR. Light micrograph observations and morphometric analyses were made of cross-sections of mesenteric resistance arteries from SHR, MK-421-treated SHR, and WKY. Results show that the MK-421-treated SHR resistance arteries had media thicknesses and a number of smooth muscle cell layers that were significantly less than in the untreated SHR and not different from the WKY. Secondly, velocity of shortening is dependent on actomyosin ATPase activity, and, since maximum velocity of shortening has been shown to be increased in SHR arterial muscle, it became necessary to know whether or not an increased actomyosin ATPase activity might be responsible. Therefore, data from a study of SHR and WKY caudal arterial myofibrillar ATPase activities are compared.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in arterial smooth muscle contractility, contractile proteins, and arterial wall structure in spontaneous hypertension. 793 46

The purpose of the study was to investigate the possible role of autoantibodies in the development and type of left-ventricular hypertrophy (LVH). Three groups of subjects were studied: (a) 15 patients with hypertrophic cardiomyopathy (HCM; 11 males, 4 females; mean age 50.0 +/- 16.3 years); (b) 15 patients with essential hypertension (10 males, 5 females; mean age 56.8 +/- 13.5 years) with normal renal function and serum electrolytes and (c) 15 male athletes (mean age 20.8 +/- 5.9 years). The control group consisted of 15 normal subjects with no sign of heart disease. The following indices of cardiac performance were determined by means of echocardiography: end-diastolic and end-systolic diameters, interventricular septum thickness, left-ventricular (LV) wall thickness, LV mass and LV mass index. The immunologic parameters studied included autoantibodies against (a) specific (anticardiac cell; ACA) and (b) nonspecific (antimitochondrial cell; AMA) autoantigens according to a conventional indirect immunofluorescence technique. (1) Higher values for LV mass and LV mass index were observed in HCM. (2) The incidence of specific and non-specific autoantibodies in hypertensive patients and in patients with HCM was significantly higher compared to athletes and controls. All ACA-positive individuals (5 with HCM, 3 with hypertension and 1 athlete) were AMA positive as well, while all ACA-negative individuals were also AMA negative. The ACA-positive individuals had higher C3c and C4 levels compared to the ACA-negative individuals. An autoantibody-mediated immunopathogenic role is discussed in the development and type of myocardial hypertrophy.
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PMID:A possible role for autoantibodies in left ventricular hypertrophy. 818 13

To assess racial difference in cardiac responses to elevated blood pressure, we compared echocardiographic measurements of left ventricular (LV) mass and the wall thickness to chamber dimension ratio (relative wall thickness) in 380 white and 47 black patients with uncomplicated essential hypertension consecutively enrolled in echocardiographic research studies at The New York Hospital Hypertension Center. Diastolic blood pressure and weight were slightly greater in black as compared with white subjects (104 +/- 18 v 98 +/- 11 mm Hg; P = .014 and 82 +/- 17 v 77 +/- 15 kg; P = .037, respectively), however the groups were similar with respect to age, duration of hypertension, cholesterol level, cigarette smoking, past use of antihypertensive therapy, family history of heart disease, and height. On average, LV mass indexed for body surface area and relative wall thickness were significantly greater in blacks than whites (119 v 105 g/m2; P = .02 and 0.46 v 0.39; P = .003) and blacks had twice the prevalence of LV hypertrophy (41% v 19%; P < .001) or concentric remodeling (21% v 12%; P < .05). The magnitude of increased LV mass and relative wall thickness in blacks was similar in men (132 v 110 g/m2; P = .01 and 0.44 v 0.39; P = .04) and in women (107 v 94 g/m2; P = .11 and 0.48 v 0.39; P = .02). In multivariate analyses, systolic blood pressure, age, and race were consistently predictors of increased LV mass and abnormal cardiac geometry. Cholesterol level was not independently associated with increased LV mass but was weakly associated with increased relative wall thickness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of left ventricular mass and geometry in black and white patients with essential hypertension. 826 36

In the past 10 years, cardiomyopathy has been diagnosed in 16 athletes, out of them in 13 this abnormality has been ascertained for the first time when they were examined or they were in the outpatient department. The paper provides clinical and instrumental findings of 13 patients with hypertrophic cardiopathy and 3 with dilated cardiomyopathy whose diagnosis was established by making a differential diagnosis of congenital and acquired heart diseases, coronary heart disease, essential hypertension and athletic heart. Most athletes with hypertrophic cardiomyopathy has an asymptomatic or mild natural history.
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PMID:[Cardiomyopathies in the practice of sports medicine]. 830 77


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