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

Two-dimensional echocardiography is superior to M-mode echocardiography for estimation of left ventricular mass when left ventricular shape is markedly abnormal. Left ventricular mass measurement by two-dimensional echocardiography depends on careful experimental calibration of the echocardiographic instrument using either a standard phantom or actual heart slices, and appropriate geometric algorithm, and short axis images to determine myocardial cross-sectional area. Several well-validated algorithms are available, of which the short-axis area-length technique is the simplest. In hypertensive heart disease, in which left ventricular shape is usually close to normal, two-dimensional echocardiography may offer a smaller standard error than M-mode, but this issue requires further evaluation. Further, it is uncertain whether the incremental accuracy of two-dimensional echocardiography in hypertensive heart disease would offset its increased cost and complexity relative to M-mode echocardiography.
Hypertension 1987 Feb
PMID:Standardization in the measurement of left ventricular wall mass. Two-dimensional echocardiography. 380 96

The heart may play an active, passive, or incidental role in the pathogenesis of hypertension. Echocardiography probably contributes little to understanding of active mechanisms, although it may provide important information relative to structural and functional adaptive changes associated with development of left ventricular hypertrophy. Moreover, because other clinical conditions frequently coexist with hypertensive heart disease, echocardiography may provide another dimension in the assessment of obesity, coronary heart disease, mitral valve prolapse, idiopathic hypertrophic subaortic stenosis, and asymmetric septal hypertrophy in the overall problem. Critical in this understanding are the subtle changes that occur in the individual patient, reflecting the natural history of the disease or response to its treatment. Since technical problems preclude echocardiographic evaluation in all patients with hypertension, particular care must be exercised in making epidemiologic generalizations.
Hypertension 1987 Feb
PMID:Future directions in the use of echocardiography. 380 1

Early detection and prevention of cardiac dysfunction is an important goal in the management of hypertensive patients. In this study, Doppler echocardiography was used to evaluate the pattern of left ventricular diastolic filling in 38 subjects: 18 treated hypertensive patients (blood pressure 141 +/- 17/83 +/- 10 mm Hg, mean +/- SD) without other coronary risk factors and 20 risk-free normotensive subjects of similar age (47 +/- 10 and 49 +/- 13 years, respectively). Peak velocity of late left ventricular filling due to the atrial contraction was greater in hypertensive compared with normotensive subjects (69 +/- 14 versus 52 +/- 13 cm/s; p less than 0.001). Peak velocity of late filling was significantly greater in hypertensive versus normotensive subjects in those aged 50 years or younger and those older than age 50 (65 +/- 12 versus 50 +/- 11; p less than 0.01 and 75 +/- 15 versus 56 +/- 15 cm/s; p less than 0.05, respectively). In hypertensive subjects, peak velocity of late filling did not correlate with routine indexes of hypertensive heart disease (including posterior wall thickness and left ventricular mass), systolic and diastolic blood pressure or duration of hypertension. These results indicate that increased velocity of late left ventricular filling may be independent of left ventricular hypertrophy and persist despite effective blood pressure control.
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PMID:Doppler echocardiographic analysis of left ventricular filling in treated hypertensive patients. 380 21

The normal heart has the capacity to either augment or reduce its mass in relation to long-term alterations in hemodynamic and metabolic demands. However, once cardiac hypertrophy is established, as in hypertensive heart disease, it is less clear whether the augmented mass can revert to normal with control of arterial pressure. In experimental models in which systemic hypertension is induced in genetically normotensive animals, left ventricular weight generally returns toward normal with the removal of the inciting stimulus for the hypertension. However, when arterial pressure control is achieved by pharmacologic therapy, and the inciting stimulus (mechanical or genetic) is intact, the results of pressure reduction on ventricular weight are much more variable than that observed with the removal of a mechanical stimulus for hypertension. It is hypothesized that pharmacologic pressure reduction elicits secondary adjustments in cardiorenal and neurohumoral function which have important influences on ventricular hypertrophy.
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PMID:Pharmacologic regression of cardiac hypertrophy in experimental hypertension. 608 41

Management of patients with concomitant hypertension and angina pectoris mandates that the physician pay attention to the underlying pathophysiology. The heart, when exposed to years of hypertension, becomes "remodeled." Overall mass is enlarged, the walls are thickened, and initial cavity volume remains normal or relatively small. Left ventricular end-diastolic pressure rises in the setting of a hypertrophic noncompliant ventricle; coronary resistance and coronary perfusion pressure are increased; and coronary vascular reserve, even with widely patent coronary arteries, is decreased. Long-standing hypertension--a risk factor for coronary atherosclerosis--is often accompanied by epicardial coronary stenoses that aggravate these coronary abnormalities. In managing the patient with hypertension and angina pectoris, it is important to determine whether the angina occurs in the setting of hypertensive hypertrophic disease alone or coexists with coronary arterial stenoses. Also important to therapy is whether the ventricle is of normal size with good function or decompensated with dilatation and diminished function. The latter two anatomic considerations, namely, epicardial coronary patency and left ventricular cavity size, will influence the choice of an anti-ischemic regimen. For example, diuretic and nitrate therapy can be hazardous, and digitalis unnecessary, in the setting of a nondilated hypertrophic ventricle with hyperdynamic function. On the other hand, the combined use of beta blocking agents plus calcium antagonists is particularly effective in lowering blood pressure and in improving coronary blood flow. Finally, this combination has been shown to be rapidly effective and to have prolonged benefit in this setting. The choice of these latter agents is also affected by the underlying state of the ventricle. Calcium channel blocking agents without significant negative inotropic effect, such as nifedipine and nitrendipine, would be suitable in patients with decompensated ventricular function and dilated left ventricular cavities. Both of these drugs have been shown to increase cardiac output and contractility via a reflex effect and to have little or no direct negative inotropic effect. In contrast, verapamil has a direct negative inotropic effect. The final choice of agents must be tailored to the needs of the individual patient, and the physician also has to determine the role of specific agents in the natural history of hypertensive heart disease.
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PMID:Management of patients with hypertension and angina pectoris. 614 86

The spontaneously hypertensive rat (SHR) exhibits both a compensated phase of cardiac hypertrophy in which forward output is maintained despite persistently elevated systemic arterial pressures and a decompensated phase in which cardiac performance has deteriorated in spite of further hypertrophic growth. To determine whether chronic antihypertensive therapy prevents the development of heart failure and the progression of cardiac hypertrophy in SHR with advanced hypertension, captopril (2 g/l of drinking water), a converting enzyme inhibitor, was administered to 14 month old female SHR and normotensive American Wistar rats (NWR) for 10 months. The severe left ventricular hypertrophy of the 24 month old untreated SHR (4.37 +/- 0.2 mg/g v. 2.50 +/- 0.06 mg/g, untreated NWR) was markedly reduced (P less than 0.02) by captopril (3.01 +/- 0.1 mg/g). Chronic therapy prevented the reduction of both baseline and maximal cardiac indices in SHR, but did not alter blood flow in NWR. Left ventricular dilatation was present in 24 month old SHR and, as peak stroke volume index was diminished, the ejection fraction index of the SHR was reduced. Captopril restored this index in SHR to normal. The relation of ejection fraction index and afterload (peak systolic wall stress) was depressed in untreated SHR, but was normal in treated SHR. Thus, chronic therapy with captopril prevented the development of severe cardiac dysfunction and produced a marked regression of cardiac hypertrophy in SHR with advanced hypertensive heart disease.
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PMID:Prevention of the development of heart failure and the regression of cardiac hypertrophy by captopril in the spontaneously hypertensive rat. 622 Aug 93

Sixty four patients with essential hypertension were studied by phonocardiographic systolic time intervals. Prolongation of the pre-ejection period (PEP) at expense of the isovolume contraction time and of the true isovolume contraction time, which suggests myocardial contractile depression due to the increase in after-load. The significant increase, in rise of mean velocity of ventricular pressure suggests that the Anrep phemomena is used by the human heart as a compensatory mechanism in systemic hypertension. Ejection fraction in hypertensives was significantly lower (P less than 0.001) than that of normal controls, which indicates subclinical depression of ventricular function in the former. Myocardial hypertrophy can be considered as a compensatory mechanism which appears late in systemic hypertension and helps normalize ventricular performance and MVO2. It is clinically detected by an s-4 (registered by phonocardiographic tracings) and by an increase in the "A" index and the apexcardiogram (14.5 +/- 8%). The authors conclude that hypertensive heart disease can be identified early through the functional adaptations wich produce detrimental physiopathological reactions to the heart compensated initially by homeometric autorregulation and latter by myocardial hypertrophy.
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PMID:[Hypertensive cardiopathy. Phonomechanocardiographic study and review of its physiopathological mechanisms]. 622 4

Massive cardiomegaly (heart weight above 400 g in females and 450 g in males) was studied in 26 Zambians examined post mortem. The aetiologies found were: hypertensive heart disease alone in six cases; hypertensive and alcoholic heart disease in two cases; alcoholic heart disease alone in five; alcoholic and pulmonary heart disease in one; alcohol with possible hypertensive heart disease in one. Eleven cases were classified as being idiopathic mainly due to lack of data and in five of these hypertension was suspected as being the cause. The series qualitatively represented the spectrum of non-rheumatic heart disease seen in patients admitted to the Central Hospital, Ndola, Zambia. Hypertension had a central role in the causation of massive cardiomegaly. Follow-up of several patients enabled observations on the cardiac effects of hypertension and alcoholism operating simultaneously and on the relationship between hypertension and congestive cardiomyopathy.
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PMID:Cardiomegaly in Northern Zambia: clinico-pathological observations. 622 32

Left ventricular hypertrophy (LVH) is both a target organ response to hypertensive vascular disease and a factor that might be responsible for other cardiovascular events. Therefore we studied by means of echocardiography 41 patients with untreated hypertension classified into 4 groups according to electrocardiographic and chest X-ray LVH criteria. The patients in group IV had in addition a history of coronary disease. Thirty-seven patients (92%) presented concentric LVH and 4 patients combined LVH and dilatation. Five patients from group IV presented impairment of interventricular septum or posterior wall motion. Thirty-seven patients (92%) had increased left ventricular mass (p less than 0.01). Ejection fraction was normal in groups I, II and III but significantly decreased (p less than 0.001) in group IV. We conclude that LVH is part of the natural evolution of hypertensive vascular disease. Echocardiography proved to be the most indicated method for the assessment of cardiac dimensions and function in hypertensive heart disease.
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PMID:M-mode echocardiography in hypertensive heart disease. 624 Jan 11

In essential hypertension ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by the organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). Digitalis glycosides, together with antihypertensive measures, are indicated for the dilated hypertensive heart; beta-receptor blockers are sound medication for the compensated hypertensive heart both with and without coronary stenoses. The following discussion includes classification of hypertensive heart disease based on the cardiac complications following hypertension.
Hypertension
PMID:Functional dynamics of the left ventricle in hypertensive hypertrophy and failure. 624 Apr 52


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