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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The haemodynamic shifts during head up and head down tilt were investigated in adult spontaneously hypertensive rats (SHR) and matched normotensive control rats (NCR) under nembutal anaesthesia and autonomic blockage. During head up tilt a greater fall in blood pressure and stroke volume was observed in SHR than in NCR, while the reverse was true when tilted in the opposite direction. This altered cardiac response to venous filling, also observed in patients with essential hypertension, is suggested to be caused by an altered Frank-Starling relationship of the hypertrophied heart in hypertensive individuals.
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PMID:Haemodynamic changes during tilt after autonomic blockade in spontaneously hypertensive rats. 60 71

Central hemodynamics was studied by means of echocardiography in 7 patients suffering from neurocirculatory dystonia with a high cardiac index but normal arterial pressure, and in 41 patients with essential hypertension prior to, and after treatment. Two groups of patients suffering from essential hypertension were distinguished: with a hyperkinetic type of circulation and with a normal cardiac index. In the first group there was a statistically significant increase in the stroke index and the index of diastolic left ventricular diameter with a normal ejection fraction. The increase in the cardiac index in the hyperkinetic type of essential hypertension is caused by an increase in the stroke output according to the Frank--Starling law. The authors believe that the increase in peripheral resistance is the principal pathogenetic mechanism of hypertension with any level of the minute volume.
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PMID:[Hemodynamic types of hypertensive disease according to echocardiographic data]. 72 44

The heart is one of the major target organs that becomes secondarily involved with the unrelenting and progressive vascular disease of essential hypertension. As a result of this increasing afterload that is imposed upon the left ventricle, the ventricular chamber adapts structurally and functionally. Structural changes involve an increase in muscle mass that is achieved through left ventricular hypertrophy (in a manner similar to the arteriolar changes demonstrated by increased thickening). Unless antihypertensive therapy is interdicted in this disease process, left ventricular failure will ensue as the major cardiac hemodynamic consequence. Left ventricular hypertrophy is also associated with a risk that is independent of the pressure overload and hemodynamic risk. Although antihypertensive therapy will reduce from the hemodynamic alterations, only recently have epidemiological findings suggested that the independent risk of LVH may be reduced with pharmacological therapy. There are no data available to indicate just which agents may reduce the risk from LVH; but relatively recent studies seem to indicate that while all agents may reduce LVH with prolonged therapy only certain classes of agents will do so independent of their hemodynamic factors. Some of these agents, however, may impair cardiac function if arterial pressure is increased abruptly following therapeutic reduction of cardiac mass. Other agents may preserve normal function--or even may improve function. Among those classes of antihypertensive agents that reduce cardiac mass at least in part due to nonhemodynamic factors, are the angiotensin converting enzyme inhibitors, the calcium antagonists, and most adrenergic inhibitors. Evidence will be presented demonstrating the hemodynamic/structural dissociation of those pharmacological agents that reduce cardiac mass with short-term treatment in spontaneously hypertensive rats with left ventricular hypertrophy. Although centrally active adrenolytic, angiotensin converting enzyme (ACE) inhibitors, and calcium antagonists all reduce cardiac mass, their structural and cardiac functional effects differ greatly. Even within the ACE inhibitor group their effects vary--improving, impairing, or not changing the Frank-Starling relationships following reduction in left ventricular mass. We postulate great variability of cardiac intramyocytic penetrance of the pharmacological agents and their local intracellular effects on mitogenesis of the ventricular myocyte. The implications on cardiac function and therapy have vast potential. Therefore, current investigative areas involving new concepts of molecular biology of the cardiac myocyte may provide great promise to the quest of unraveling some of the newly postulated questions: What is the role of ionized intracellular calcium? Do the local renin-angiotensin systems in the cardiac and vascular myocyte participate in the development and regression of hypertrophy?(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Left ventricular hypertrophy: dissociation of structural and functional effects by therapy. 183 47

As many as 75 patients with essential hypertension were examined by echocardiography and radiocardiography. The development of hypertrophy was accompanied by the rise of the diastolic dimensions of the left ventricle regardless of the type of the heart overload (by volume or pressure). As left ventricle hypertrophy developed, the myocardial contractility declined and normal hemodynamic function of the heart was maintained due to the Frank-Starling mechanism. The relationship has been established between the intensity of hypertrophy, left ventricle function and the hemodynamic profile of the disease.
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PMID:[Cardiac adaptation in hypertension]. 253 34

An increase in left ventricular (LV) wall thickness will lead to decreased LV distensibility during both LV passive filling and left atrial contraction. Reduced LV distensibility will change the filling pattern of the left ventricle, and a proportionally smaller part of the stroke volume will be delivered during the passive filling of the preceding diastole and a larger part during late diastole by a more powerful left atrial contraction. With a more pronounced increase in LV wall thickness a reduced distensibility of venous capacitance vessels (functional or structural) will probably help to preserve LV pump function by influencing LV filling and use of the Frank-Starling mechanism. LV wall stress (peak and end-systolic) is high and LV intrinsic contractility is normal or supernormal in early primary hypertension, as judged from the relationship between end-systolic wall stress and different indices of LV function (fractional shortening, mean velocity of circumferential fiber shortening, ejection fraction). Great differences in peak systolic wall stress may be recorded among groups with comparable values for LV end-systolic wall stress, which may be explained by very different degrees of cardiovascular structural changes, with higher values for peak systolic wall stress seen in hypertension caused by high output than those values seen in hypertension caused by high total peripheral resistance. Signs of supernormal LV systolic function are common in high output hypertension, which is also at least partly due to an increase in LV end-diastolic volume and use of the Frank-Starling mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular function in early primary hypertension. Functional consequences of cardiovascular structural changes. 639 89

For clarifying the onset mechanism of essential hypertension, the hemodynamics in 9 mildly hypertensive men, mean age of 39.8 +/- 10.7 (mean +/- SD), was compared with 7 normotensive men, mean age of 39.8 +/- 10.7, by means of exercise echocardiography, and the effects of indenolol (administered 30 mg/day for 7 days orally to both groups) were studied. The interventricular septum and the left ventricular posterior wall were thickened in the mild hypertensives. No significant differences between the both groups were shown in the cardiac performance at rest and the cardiac index during exercise. The total peripheral vascular resistance was higher in the mild hypertensives than the normotensives during exercise. However, during exercise, the normotensives showed significant increases in the left ventricular end-diastolic dimension (LVDd) and the stroke index (SI); these changes were not significant in the mild hypertensives. After administration of indenolol, the significant increases in LVDd and SI during exercise were observed in the mild hypertensives. This study suggests that mild hypertensives with cardiac hypertrophy display a diminished Frank-Starling effect during exercise which may be attributed to the decreased left ventricular compliance due to cardiac hypertrophy and elevated afterload. Indenolol improved the Frank-Starling effect, which decreased in the mild hypertensives.
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PMID:The hemodynamics and hemodynamic effects of indenolol in mild hypertension. 653 Jul 47

The aim of this investigation was to study the coronary pressure-flow relationship in 60 patients with chronic arterial hypertension of diverse aetiologies and in 14 normotensive subjects (control group). The hypertensive cohort included 6 patients with isolated systolic hypertension (ISH), 7 renovascular hypertensive patients with abnormally elevated angiotensin II plasma levels but without electrocardiographic and/or echocardiographic evidence of left ventricular hypertrophy (LVH) and 47 subjects with essential hypertension (EH), 21 of whom had LVH by electrocardiogram and/or echocardiogram. In the hypertensive cohort a Frank-Starling-like curve was found to describe the coronary pressure-flow relationship when the baseline values for coronary sinus blood flow (CBF, intravascular Doppler technique) were plotted against mean aortic pressure (intra-arterial blood pressure). In particular, the descending limb of such a curve represented a critical region where CBF was "inappropriately" low with respect to perfusion pressure. It was thus concluded that this inability of the heart to adapt CBF to its needs might account for the higher propensity to develop myocardial ischaemia encountered in severe essential hypertensive subjects with concomitant LVH and renovascular hypertensive patients.
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PMID:Coronary blood flow and myocardial ischaemia in hypertension. 853 20

The increased susceptibility to infection following splenectomy has been well documented. We report here, a case of brain abscess developed five years after splenectomy in a patient with idiopathic thrombocytopenic purpura (ITP). A 65-year-old woman was admitted to our hospital because of fever, mental disorientation, and weakness in August, 1999. She had been followed with diagnoses of essential hypertension and type 2 diabetes mellitus (DM) since 1988. The patient was diagnosed as having ITP in 1992, and then underwent splenectomy in 1994. Monoclonal gammopathy of undetermined significance (MGUS) of IgG, lambda type was found in February 1999. Though high grade fever persisted after admission, blood cultures were negative. Antibiotics were given without a satisfactory effect. Right hemiparesis and worsening of consciousness developed subsequently. Contrast enhanced cranial computed tomography (CT) disclosed a ringed enhanced low density mass in the left parieto-occipital lobe compatible with a diagnosis of brain abscess. Surgical drainage was performed and 20 ml of pus was obtained. No primary infectious focus of the brain abscess was detected with intensive examinations.
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PMID:[Brain abscess developed five years after splenectomy in a patient with idiopathic thrombocytopenic purpura]. 1128 Sep