ISSN:0268-4705    

出版商:OVID    

年代:1994

数据来源: OVID

ISSN:0268-4705    

出版商:OVID    

年代:1994

数据来源: OVID

ISSN:0268-4705    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

For more than 30 years there has been general agreement that in the established phase of essential hypertension, the cardinal hemodynamic disturbance is an increased total peripheral resistance with cardiac output normal during rest, but subnormal during exercise. However, there are still different opinions about the hemodynamics in the starting phase of essential hypertension. Several studies from 1993—mainly performed in the offspring of hypertensive parents—reported high as well as low cardiac index values, depending on the patient selection and the methods used. Irrespective of whether the early phase of essential hypertension is caused primarily by increased cardiac output or increased total peripheral resistance, an increased sympathetic activity is usually held responsible for either hemodynamic disturbance. Simultaneous recordings of central and regional hemodynamics and sympathetic nerve traffic in young subjects with mild hypertension did show increased cardiac output, reduced calf blood flow, and increased nerve traffic as the characteristic features. However, recent studies in subjects with borderline hypertension have shown that if the subjects were aware of having hypertension, they showed higher blood pressure and higher reactivity to mental stress and cold-pressor tests than uninformed subjects with similar blood pressures. With respect to regional circulation, studies have shown that the coronary reserve is reduced in early hypertension, and also in subjects without left ventricular hypertrophy. The role of the endothelium in the regulation of blood flow has attracted great interest. Abnormalities in the production of vasoconstricting and vasodilating substances from the endothelial cells may be at least partially responsible for the increased vascular resistance characteristic of essential hypertension.

ISSN:0268-4705    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

The capacity of the myocardium to grow depends mainly on the capacity of myocardial cells to synthesize proteins. The capacity for protein synthesis is determined by the quantity of ribosomes present. The rate of ribosome formation is the major factor controlling ribosome content and is limited by the rate of ribosomal DNA transcription. Therefore, hypertensive myocardial growth can be considered as a process of stimulation of gene transcription and protein synthesis in myocardial cells found in animals and humans with elevated blood pressure Current work in the cell biology of hypertensive left ventricular hypertrophy is directed toward the characterization of the initiating stimuli and the coupling mechanisms that activate the myocardial gene program that, in turn, leads to the acquisition of the left ventricular hypertrophic phenotype. In addition, investigations are being made to define the involvement of changes in myocardial composition and structure in the functional abnormalities of hypertrophied myocardium.

ISSN:0268-4705    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

The therapeutic benefits of angiotensin-converting enzyme inhibitors in the treatment of hypertension, congestive heart failure, and atherosclerotic heart disease are undeniable. Recent studies, however, suggest that the cardioprotective effect produced by these drugs is complex and may not be solely related to inhibition of the generation of angiotensin II. An alternative pathway for the generation of angiotensin II from angiotensin I has been proposed, following the recent identification of a chymotrypsin-like protease (chymase) that may contribute to the formation of angiotensin II in human heart tissue. The enzyme is present in cardiac mast cells and displays unusual substrate specificity for the conversion of angiotensin I to angiotensin II. While biochemical studies have provided convincing evidence for a chymase-dependent production of angiotensin II, the contribution of this enzyme to the physiologic or pathological regulation of arterial pressure and cardiac function remains undetermined.

ISSN:0268-4705    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Despite the advances in antihypertensive therapy, the majority of patients who develop heart failure have antecedent hypertension, left ventricular hypertrophy, and a poor prognosis. Studies in animals and humans have shown that equipotent antihypertensive agents variously effect the regression of cardiac hypertrophy, one of the reasons for which may be the differences in their effects on vascular load and structure. Recent advances in instrumentation (micromanometers, applanation tonometers, ultrasonic probes, and so forth) have permitted the noninvasive measurement of pressure contours, vessel diameters, and pulse-wave velocity. This new technology has allowed the evaluation of the effects of antihypertensive agents on arterial compliance and structure in relation to the agent's ability to regress left ventricular hypertrophy.

ISSN:0268-4705    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Left ventricular hypertrophy is associated with an increased risk of coronary heart disease and all-cause mortality. Electrocardiographic criteria for left ventricular hypertrophy have high specificity but low sensitivity. Recent advances in methodology have improved the sensitivity of the electrocardiogram for detecting left ventricular hypertrophy. Criteria for left ventricular hypertrophy have been developed from epidemiologic studies using M-mode echocardio-graphy. The prevalence of left ventricular hypertrophy is influenced by blood pressure, age, sex, and obesity. Recent studies have shown that waist-to-hip ratio, hyperinsulinemia, a dominant late systolic peak in the arterial pressure waveform, and a decrease in nocturnal blood pressure decline are also determinants of left ventricular mass. Left ventricular hypertrophy is associated with an increased incidence of ventricular arrhythmias and with an impairment in coronary flow reserve. Newer imaging techniques, such as two- and three-dimensional echocardiography, magnetic resonance imaging, and ultra-fast computed tomography are more accurate and reproducible than M-mode echocardiography, but these methodologies are expensive and not readily available for assessment of left ventricular mass.

ISSN:0268-4705    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Patients with essential hypertension are at an increased risk for sudden cardiac death. As is the case with other complications of hypertension, this increased risk reflects the interplay between a higher prevalence of coronary artery disease and the pathophysiologic consequences of left ventricular hypertrophy. The presence of coronary artery disease is the most important factor, but left ventricular hypertrophy also results in changes in the coronary circulation that predispose to myocardial ischemia, and is also associated with an increased frequency of ventricular arrhythmias. Hypertension itself is associated with changes in the autonomic nervous system that may predispose to sudden death. It is therefore likely that the mechanisms responsible for sudden death are multifactorial, but it is also clear that effective antihypertensive therapy will prevent or mitigate these predisposing factors and will reduce the incidence of this and other cardiac complications.

ISSN:0268-4705    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Abnormalities of left ventricular diastolic function in hypertension are multifactorial in origin. Of importance is the demonstration that abnormalities of left ventricular filling in hypertension may be accompanied by deleterious cardiovascular neurodynamic regulations. However, the left ventricular filling rate can be normalized during medical treatment of hypertension. In particular, regression of left ventricular hypertrophy is almost always associated with or followed by improvement of left ventricular filling. The effects of this normalization on cardiovascular dynamics and the outcome of hypertensive heart disease are yet to be demonstrated.

ISSN:0268-4705    

出版商:OVID    

年代:1994

数据来源: OVID