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

The systolic motion of the mitral apparatus in patients with hypertensive heart disease and hypertrophic cardiomyopathy was studied in order to quantify the difference. Twelve out of 37 patients with severe systemic hypertension were found to have abnormal systolic anterior motion and had significantly small left ventricular end-systolic dimension (P less than 0.05) and greater ejection fraction and mean velocity of circumferential fibre shortening (P less than 0.01 for each) than the other hypertensive patients without abnormal systolic anterior motion. A comparison between systolic anterior motion in 12 hypertensive patients and mild or moderate systolic anterior motion in 28 patients with hypertrophic cardiomyopathy showed a clear cut difference. 'Pseudo' systole anterior motion reached its peak at end-systole when the posterior wall had contracted fully. 'True' systolic anterior motion, however, reached its peak much earlier than maximum movement of the posterior wall--approximately after two-thirds of systole had been completed. At the time of mitral valve opening, 'pseudo' systolic anterior motion had not yet returned to this initial level, whereas 'true' systolic anterior motion returned prior to the opening of the mitral valve. Anterior chordal motion in hyperdynamic ventricle appears to play a role in the production of 'pseudo' systolic anterior motion.
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PMID:'Pseudo' systolic anterior motion in patients with hypertensive heart disease. 668 23

Due to the multifactorial origin of hypertensive heart disease there are several points of attack for prevention and for non-medicinal therapy. In recent decades prophylactic trials and studies on the therapeutic efficacy of non-medicinal measures in established hypertension have been neglected in favor of drug therapy so that at present only weight reduction and restriction of salt intake show a confirmed action. Further measures are: dietary increase of potassium, physical endurance training and behavior therapy methods. With the low cost of nonmedicinal measures and in view of possible side-effects of a pharmacological hypertension therapy, these should be applied or tested particularly in borderline hypertension.
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PMID:[Prevention and non-medicinal treatment of hypertension (author's transl)]. 679 53

While the current literature contains numerous studies and even more numerous assumptions linking aspects of the work setting, stress, and mortality; no systematic investigation has been made of possible patterns of stress-induced self-destructive behaviors among the work settings per se. This research paper attempts to help fill that gap by reporting on an analysis of data on industry, age and mortality rates for seven stress-related causes of death (suicide, homocide, hypertensive heart disease, cirrhosis of the liver, arteriosclerotic heart disease, ulcer of the stomach, and hypertension). Using available United States' mortality statistics, a consistent pattern is found for all of the stress-related types of deaths by industry and age. A suggested explanation of this pattern is based on status integration theory.
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PMID:Is work conducive to self-destruction? 717 4

Left ventricular hypertrophy in arterial hypertension is characterized by myocyte hypertrophy, myocardial fibrosis, and structural changes of the intramural coronary arteries. Hypertensives with or without left ventricular hypertrophy have a reduced coronary vasodilator reserve due to alterations of the coronary microcirculation. The impairment in coronary vasodilator reserve is likely to initiate a process of malperfusion and malnutrition concomitant with increased metabolic demands. Further, malperfusion is supported by an increase in diastolic filling pressure, which will enhance the extravascular component of coronary resistance. The sum of interactions of these structural alterations of myocardium, interstitium, and coronary vasculature are likely to initiate and maintain a process of myocardial malperfusion and malnutrition, which can provoke functional depression of the myocardial performance, a loss of contractile proteins, an increase in interstitial fibrosis, and, not least, an overall decrease in contractile function in long-standing cardiac hypertrophy. Finally, the reversal of these processes by adequate antihypertensive treatment may contribute to renormalization of cardiac function and to prevention of late cardiac failure in hypertensive heart disease.
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PMID:Systolic ventricular dysfunction and heart failure due to coronary microangiopathy in hypertensive heart disease. 749 18

Myocardial infarction remains the single most common cause of death in patients with essential hypertension. This becomes particularly evident when the hypertension is associated with left ventricular hypertrophy. To combat the continuing high mortality from myocardial infarction in hypertensive heart disease, however, all aspects of the relationship must be studied. Thus, addressing the interface from an epidemiological standpoint as well as from a pathological point is critical and progress in these areas as well as in areas of management are ultimately likely to lead to a fall in morbidity and mortality from ischemic heart disease in patients with hypertension.
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PMID:The interface of hypertension and ischemic heart disease. 749 55

Chronic mechanical stress of the heart by arterial hypertension is a primary cause of left ventricular hypertrophy. The cardiac renin-angiotensin system is often found activated in conditions of increased afterload or mechanical stress of myocytes. Cardiac expression of angiotensinogen and angiotensin-converting enzyme (ACE) is increased resulting in elevated cardiac angiotensin II formation. This has been demonstrated in stretched cardiac myocytes in vitro as well as in animal models of pressure overload hypertrophy (supravalvular aortic stenosis and spontaneously hypertensive rats) and in human pressure overload hypertrophy (aortic stenosis). Functional consequences of elevated angiotensin II levels may be vasoconstriction of the coronary vasculature and a deterioration of diastolic function of the hypertrophied heart. Local formation of angiotensin II may also have proliferative effects on cardiac myocytes and connective tissue cells. Angiotensin II may, thus, be an important factor causing development and progression of left ventricular hypertrophy by itself. Blockade of the renin-angiotensin system has been found to be an effective treatment of hypertensive heart disease, probably better than any other antihypertensive medication. Regression of left ventricular hypertrophy has been achieved by blockade of the angiotensin II pathway either by administration of an angiotensin-converting enzyme inhibitor or an angiotensin II type 1-receptor blocker. The animal model of supravalvular aortic stenosis has been used to show beneficial effects of blockade of the renin-angiotensin system on hypertrophy and survival. In this rat model regression of left ventricular hypertrophy by ACE-inhibition or angiotensin II type 1-receptor blockade could be demonstrated by serial echocardiographic analyses while afterload of the left ventricle was still elevated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of the cardiac renin-angiotensin system in hypertensive heart disease]. 749 79

Based on the epidemiologic data of the Framingham heart study, arterial hypertension and coronary artery disease are the most frequent etiologic factors for the development of heart failure. In the pressure overloaded heart, hypertrophic growth of the myocardium includes the enlargement of cardiac myocytes stimulated by ventricular loading. Non-myocyte cell growth involving cardiac fibroblasts may also occur but is not primarily regulated by the hemodynamic load. Cardiac fibroblast activation is responsible for the accumulation of fibrillar type I and type III collagens within the interstitium while vascular smooth muscle cell growth accounts for the medial thickening of resistance vessels. This remodeling of the cardiac interstitium represents a major determinant of pathological hypertrophy in that it accounts for abnormal myocardial stiffness and impaired coronary vasodilator reserve, leading to ventricular diastolic and systolic dysfunction and ultimately to the appearance of symptomatic heart failure. Several lines of evidence suggest that the renin-angiotensin-aldosterone system is involved in regulating the structural remodeling of the nonmyocyte compartment, including the cardioprotective effects of angiotensin converting enzyme (ACE) inhibition that was found to prevent myocardial fibrosis in the rat with renovascular hypertension. In rats with genetic hypertension, established left ventricular hypertrophy, abnormal diastolic stiffness due to interstitial fibrosis, and reduced coronary vasodilator reserve associated with medial wall thickening of intramyocardial resistance vessels, the ACE inhibitor lisinopril was able to restore myocardial structure and function to normal. These cardioreparative properties of ACE inhibition may be valuable in reversing left ventricular dysfunction in hypertensive heart disease.
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PMID:[Cardiac structure-function relationship and the renin-angiotensin-aldosterone system in hypertensive heart disease]. 749 80

This study was designed to assess left ventricular contractility in hypertensive patients with normal coronary angiography and anginal pain. An abnormally high percentage of hypertensive patients (approximately 30%) undergoing cardiac catheterization because of anginal pain and/or exercise-induced ST-segment depressions has angiographically normal coronary arteries. Possible reasons for these signs of ischemia include a microvasculopathy, metabolic abnormalities and an increased oxygen consumption as a result of left ventricular hypercontractility which was studied here. Left ventricular volumes and ejection fraction were determined in 50 patients with arterial hypertension (23 men, 27 women, age 60 +/- 8 years, RR 154 +/- 24/91 +/- 12 mm Hg) by cardiac catheterization and computerized analysis of laevocardiographies. The control group were 50 normotensives (30 men, 20 women, age 57 +/- 12 years, RR 128 +/- 12/76 +/- 8 mm Hg) without coronary artery disease. The angiographical data were correlated with age, sex. ECG, echocardiography, laboratory findings, medication and duration of hypertension. The left ventricular ejection fraction was significantly increased in the group of hypertensives (75.8 +/- 6.3 vs. 67.7 +/- 5.0%, p < 0.001). This difference was mainly due to a significantly reduced endsystolic left ventricular volume (37.1 +/- 15.3 vs. 47.7 +/- 10.8 ml, p < 0.001); enddiastolic left ventricular volume was not significantly different (140.5 +/- 26.8 vs. 149.0 +/- 27.5 ml, p > 0.1). A hyposystolic form of hypertensive heart disease was not observed in this group of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular hypercontractility in hypertensive patients with anginal pain and normal coronary angiograms. 757 66

We report two cases presented with a clinical picture of acute myocardial ischemia, chest pain and giant negative T waves on electrocardiogram (absent in previous tracings). The echocardiogram B-Mode showed in both cases an asymmetric left ventricular hypertrophy caused, respectively, by hypertrophic cardiomyopathy and hypertensive heart disease. Short-term electrocardiographic evolution to complete normalization was observed in both cases. The echo-dipyridamole test did not show dissynergias and this fact suggested the absence of coronary artery disease; this hypothesis was confirmed by a normal coronary angiography. We suppose that in both patients a few factors contributed to the ischemic events: respectively an acute anemia due to gastric bleeding and high blood pressure values. This clinical presentation is an example of a difficult differential diagnostic problem between left ventricular hypertrophy and acute myocardial ischemia, as it shows that giant negative T waves in hypertrophic cardiomyopathy do not necessarily depend on left myocardial hypertrophy involving the apex or other segments but may be associated to an acute myocardial ischemia related or not to a coronary artery disease. A correct evaluation of these clinical cases is important for clinical, therapeutic and prognostic implications.
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PMID:[Acute ischemia in myocardial hypertrophy: a report of 2 clinical cases]. 764 41

The measurement of wall stress allows study of morphological adaptation of the left ventricle, especially in conditions associated with symmetric hypertrophy (hypertension, aortic stenosis). The calculation is performed in hypertensive heart disease but not in aortic stenosis because of the ventriculo-aortic pressure gradient. In a preliminary study, the authors validated the peak systolic left ventricular pressure calculated by adding the systolic brachial artery pressure to the maximal transvalvular pressure gradient by comparing the value with that obtained by catheterization in 21 patients with aortic stenosis. The second phase of the study was to measure meridian and circumferential wall stress prospectively in 35 patients with aortic stenosis (29 symptomatic, 6 asymptomatic) and to compare the results with those observed in 21 normal subjects. In the latter group, the values were 151 +/- 22 and 311 +/- 37 10(3) dynes/cm2 respectively, whereas in asymptomatic aortic stenosis the stresses were 136 +/- 28 and 303 +/- 41 10(3) dynes/cm2 respectively (NS) and in symptomatic aortic stenosis 210 +/- 55 and 437 +/- 94 10(3) dynes/cm2 respectively (p < 0.0001). None of the cases of asymptomatic aortic stenosis had raised wall stress values whereas only 6 symptomatic aortic stenosis patients had normal wall stress. The values of wall stress obtained using the method proposed were comparable to those reported by other authors with invasive investigations. Non-invasive measurement of wall stress by Doppler echocardiography may be proposed as a method of evaluation of left ventricular adaptation, especially in severe stenosis and in patients with a patent geometric abnormality (abnormal dilatation or even an inadequately hypertrophied wall).
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PMID:[Doppler echocardiographic evaluation of left ventricular wall stress in aortic stenosis]. 764 49


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