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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Left ventricular hypertrophy, a known consequence of hypertension, is associated with an excess mortality independent of other known cardiovascular risk factors. There are multiple mechanisms in which left ventricular hypertrophy may account for this excess mortality including increased incidence of arrhythmias, systolic an diastolic dysfunction, relative ischemia, and associated coronary artery disease. Diastolic dysfunction, manifested by reduced ventricular distensibility of the hypertrophic left ventricle, appears to be an early characteristic of the hypertensive heart since echocardiographic techniques have demonstrated diastolic filling abnormalities in untreated essential hypertensives even before significant left ventricular hypertrophy appears. The presence of left ventricular hypertrophy is difficult to detect by electrocardiography. Echocardiography seems to be the best non-invasive method for the detection of hypertensive heart disease: it shows early abnormalities of left ventricular compliance, frequently left ventricular hypertrophy and late abnormalities of myocardial contractility.
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PMID:[Heart effect of arterial hypertension. Heart hypertrophy as a risk factor. Study technics (electrocardiogram, echocardiography, exercise test and Holter]. 213 76

Epidemiologists have not identified high risk groups nor the entire spectrum of heart disease, especially the subclinical forms underlying nonvalvular atrial fibrillation (NVAF) predisposing to cardioembolic (CE) stroke. We analysed 36 cases of 'isolated' NVAF among 106 consecutive cases of CE stroke after excluding cases of AF associated with valvular disease, myocardial infarcts, ischaemic and other cardio-myopathies (34 cases). This revealed echocardiographic left ventricular hypertrophy (LV mass index 136 +/- 25 g, vs normal 68 +/- 12 g p less than 0.001), enlarged left atria (left atrial area 27.4 +/- 3.6 cm2 vs normal 14.3+/- 1.6 cm2 p less than 0.001), normal systolic function and formed the largest group associated with CE stroke (34%), mean age 72.6 years--Study Group D. Eighty nine per cent had known or undetected hypertension compared to 60% in matched controls (x2 = 8.3 df = 1 p less than 0.01), and hypertension remained the predominant risk factor for left ventricular hypertrophy (LVH). Although all had echocardiographic LVH, 60% had neither electrocardiographic LVH nor cardiomegaly on chest X-ray. Hence usual epidemiologic methods may fail to detect these cases. Hypertensive heart disease is known to predispose to left atrial enlargement and AF. Progressive atrial enlargement is associated with increasing risk of embolic stroke. We conclude that NVAF associated with hypertensive heart disease forms a major component of the spectrum of heart disease associated with NVAF predisposing to CE stroke. Detection and treatment of hypertension to prevent or reverse LVH and atrial enlargement should be an important preventive measure.
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PMID:Nonvalvular atrial fibrillation associated with cardioembolic stroke: the role of hypertensive heart disease. 214 May 6

Cardiac hypertrophy is characterized by marked abnormalities in the contraction/relaxation pattern of the heart. For example, delayed relaxation is a prominent feature, impairing ventricular filling and coronary flow. In intact heart preparations the relative contribution of fibrosis and of the myocardial cell itself to these abnormalities cannot be correctly assessed. Biochemical studies on the mechanisms of impaired contraction and relaxation and hypertensive heart failure are hampered by the fact that 75% of all heart cells are non-myocytes. We therefore established the model of the isolated calcium-tolerant, adult rat cardiomyocyte as a new approach to the investigation of these problems. Contractility was measured using a videomicroscope system with high time resolution (1 ms). Angiotensin II induced a marked relaxation delay in the cardiomyocyte from normotensive rats and showed a moderate positive inotropic effect, whereas isoproterenol had a strong positive inotropic effect but accelerated relaxation. Therefore, angiotensin II is capable of inducing a relaxation delay even in the absence of coronary ischaemia or hypertension. These first results show that the isolated cardiomyocyte model may be a useful approach to investigating the mechanisms of hypertensive heart disease.
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PMID:Isolated myocardial cells: a new tool for the investigation of hypertensive heart disease. 214 54

Negative U wave is usually observed in ischemic heart disease, left ventricular hypertrophy and in chronic cor pulmonale, sometimes in association with electrolytic imbalance or toxic effects of drugs. We assessed by ECG and echocardiography 559 patients with longstanding arterial hypertension. Negative U wave was significantly more frequent in patients with increased left ventricular mass and/or with congestive heart failure, particularly in the middle-age hypertension group. Negative U wave appears to be an ECG sign closely associated with the anatomical evolution toward hypertensive heart disease with hypertrophy and/or congestive heart failure.
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PMID:[Arterial hypertension: clinical significance of U wave inversion in electrocardiogram]. 214 93

To determine if impairment of left ventricular filling is influenced by acute myocardial infarction in patients with arterial hypertension, left ventricular diastolic function was assessed by pulsed doppler echocardiography in 46 patients (pts) subdivided into four groups (Gr): G.1 (n = 12 pts) with acute myocardial infarction and hypertensive heart disease. G.2 (n = 12 pts) acute myocardial infarction without arterial hypertension. G.3 (n = 10 pts) arterial hypertension without history of coronary artery disease. G.4 (n = 12 pts) healthy subjects. Coronary angiography and left ventricular cineangiogram was performed in 24 pts (G.1 + G.2). Peak mitral flow velocity (cm/s) in early diastole (E), atrial systole (A), A/E and int A/int E ratios were measured by pulsed doppler. Age and heart rate were statistically similar in all groups. No difference was found among G.1 and G.2 in ejection fraction, and left ventricular segmental kinetic. (tables; see text) Conclusion left ventricular filling is impaired in pts with arterial hypertension and in pts with acute myocardial infarction; acute myocardial infarction increase the impairment of left ventricular diastolic function in pts with hypertensive heart disease.
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PMID:[Study of left ventricular diastolic function using pulsed Doppler in myocardial infarct in hypertensive subjects]. 251 Jun 39

The manifestations of cardiac involvement in hypertension include: (1) the development of hypertensive heart disease characterized by left ventricular hypertrophy (LVH), and (2) the consequences of coronary atherosclerosis, as angina pectoris, myocardial infarction, and sudden cardiac death. Whereas the former is directly related to increased blood pressure, the latter are sequelae of atherosclerosis per se, and hypertension acts only as a risk factor in this regard. This can partially explain why antihypertensive treatment is effective in diminishing the incidence of congestive heart failure, which is the final consequence of LVH, but is not very effective in preventing coronary complications. It is generally accepted about LVH that increased arterial pressure is the major stimulus to cardiac hypertrophy in hypertension; however, there are a lot of both quantitative and qualitative events suggesting that other factors beside blood pressure levels can modulate the development of LVH, in particular neurohumoral influences. From a morphological point of view, hypertrophy of the cardiac muscle is defined as an increase in the size of existing myocardial fibers. In most experimental models, myocardial hypertrophy is associated with myosin isoenzymatic changes, consisting in a shift from the faster migrating isoenzyme V1 to V3, a form that migrates more slowly. However these changes do not occur in all animal species and particularly in humans. In the hypertrophied human ventricle, a decreased ATPase activity of myofibrils was observed, probably related to changes in myosin light chains. Presently the changes in ATPase activity and in ventricular contractility do not still have a clear molecular basis in humans.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heart and hypertension. 252 4

The hypertensive damage to the target organ "heart" comprises the sum and interactions of the cardiac organ manifestations of arterial hypertension such as myocardial hypertrophy and disease of large and small coronary arteries. As the prognosis of arterial hypertension is determined, to a considerable extent, by these cardiac complications, the aim of treatment of hypertensive heart disease is reversal of the myocardial hypertrophy in order to prevent later progression to hypertensive failure. A further goal of therapy is reversal of hypertensive small coronary disease in order to improve the coronary reserve. While the evidence that regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, ACE inhibitors, and sympathicolytic substances) is practically conclusive, clinical evidence of reversal of hypertensive small coronary disease has yet to be provided. Moreover, we do not know at present to what extent the prognosis of hypertensive heart disease can be improved by reversal of hypertrophy. Once the stage of hypertensive heart failure is reached, the principles of medical management of heart failure with digitalis, diuretics, and ACE inhibitors apply.
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PMID:[Treatment of myocardial and coronary effects of arterial hypertension]. 253 67

In recent years, there has been increased recognition of the relative importance of abnormalities of diastolic function in patients with essential hypertension. Indeed, diastolic dysfunction may be the earliest indicator of hypertensive heart disease. In this article, the mechanisms governing normal ventricular relaxation and the factors that may cause diastolic dysfunction are reviewed. Noninvasive clinical methods, particularly Doppler echocardiography and radionuclide angiography, for determination of diastolic function are outlined, and the limited experience in the management of hypertensive patients with abnormalities of diastolic function is discussed. When congestive heart failure develops in a patient with hypertension, it is especially important to determine whether it is due primarily to systolic or to diastolic left ventricular dysfunction.
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PMID:Hypertension and left ventricular diastolic function. 257 61

The aim of this study was to evaluate left ventricular anatomy and diastolic function in borderline essential hypertension. To this aim, 16 borderline hypertensive patients underwent echocardiographic and pulsed-wave Doppler evaluation. As control groups, 20 normotensive controls and 20 patients with established hypertension were evaluated by the same procedure. By the Doppler assessment of transmitral blood flow, the following indices of left ventricular diastolic function were obtained: early (E) and late (A) peak flow velocity, late to early velocity ratio (A/E), early filling fraction (EFF) and acceleration and deceleration times of early and late flow peaks. Borderline hypertensives had an interventricular septum and posterior wall thickness significantly higher than normotensives and lower than established hypertensives. As regards the diastolic indexes, borderline hypertensive patients had significantly higher A peaks (P less than .02) and A/E ratios (P = .05) and lower EFF (P less than .02) as compared to normotensive controls. No significant differences were on the other hand observed with established hypertensive patients. This resultant diastolic pattern was independent of age, as indicated by the analysis of age-matched subgroups. The presence of diastolic function changes in borderline hypertension confirms the early appearance of this kind of abnormality in hypertensive heart disease. On the other hand, the finding of increased left ventricular wall thickness in borderline hypertensives does not allow us to conclude that, as suggested by other authors, diastolic function changes in the early stage of hypertension are independent on anatomical modifications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Echo-Doppler assessment of left ventricular filling in borderline hypertension. 261 Sep 93

Despite recent declines in mortality from coronary heart disease (CHD), it remains the major cause of death in the United States for blacks and whites. Although the prevalence of the ischemic syndromes in blacks and whites is similar, cardiac mortality and sudden cardiac death rate are higher in blacks. Recent attempts to explain the excess mortality in blacks have focused on barriers to health care and on sociocultural differences in perceptions of and responses to symptoms of CHD. However, the anatomic substrates of ischemia and sudden cardiac death are also different in blacks and whites. Obstructive coronary artery disease tends to be more severe in whites, while blacks have a greater prevalence of hypertensive heart disease. A body of evidence has recently emerged showing that the presence of left ventricular hypertrophy (LVH) is an important, potent predictor for subsequent cardiac death and that the mortality risk of LVH may be particularly high when underlying coronary disease is present. The greater prevalence and severity of hypertension and LVH in blacks may explain the higher cardiac mortality in blacks, even in the presence of less severe coronary disease. The reason why mortality risk is increased in the presence of LVH has not been established. Evidence suggests that it may be due to the increased predisposition to malignant arrhythmias and the increased frequency of potentially lethal silent ischemic events that occur in hypertensive individuals, particularly those with LVH.
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PMID:Anatomic substrate differences between black and white victims of sudden cardiac death: hypertension, coronary artery disease, or both? 262 Apr 68


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