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Query: UMLS:C0020538 (hypertension)
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Myocardial hypertrophy, with high morbidity and mortality, is a natural outcome of hypertensive heart disease. The increase in myocardial mass is associated with a cellular and subcellular reorganization of the myocytes. The following study uses rapid myothermal techniques to assess the contribution of the major intracellular changes to the adaptive hypertrophic process in various heart models. Pressure overload and thyrotoxic hypertrophy were produced in the rabbit. In the rat, hypertrophy was produced by constricting the renal artery (Goldblatt hypertensive rat) or by using the spontaneously hypertensive rat strain. Atrophy was produced by administration of propylthiouracil in the drinking water. The V1/V3 myosin isoenzyme ratio was decreased in the pressure overload, Goldblatt, and propylthiouracil animals. This was associated with a decrease in total activity-related heat, initial heat, and tension-dependent heat per tension time integral. The tension-independent heat was decreased in the pressure overload, while the time to peak tension was increased. The economy of the metabolic recovery process was unchanged in the pressure overload and Goldblatt preparations. In the propylthiouracil preparation the recovery processes became uneconomical. The spontaneously hypertensive rat exhibited mild cardiac hypertrophy but in all other respects the heart was unchanged from the normal animals. The thyrotoxic hearts had a high V1/V3 myosin isoenzyme ratio, which was associated with a high total activity-related heat, initial heat, and tension-dependent heat per tension time integral. The tension-independent heat was reduced in the thyrotoxic preparations. The appropriateness of each of the intracellular changes is evaluated in terms of the demands made on the heart.
Hypertension
PMID:The inhomogeneity and appropriateness of the myocardial response to stress. 624 Apr 54

With the purpose to study the haemodynamic changes that occur with myocardial ischaemia induced by atrial pacing (AP) in hypertensive heart disease, we studied 7 patients with such condition, all of them with a long time history of systemic hypertension, electrocardiographic signs at rest of left ventricular hypertrophy and ST-segment depression, at least of 0.5 mm. All the patients showed normal coronary arteries in angiocardiogram. AP was started 10 beats above the basal heart rate with increments of 10 beats every 2 minutes until a ST-segment depression at least of 2 mm was obtained which occurred in all the cases studied. After every 2 minutes of AP a simultaneous 12-leads electrocardiogram recording and left ventricular and aortic pull-back pressure were obtained. At the desired end point the AP was abruptly stopped and the same parameters were registered at 3, 5, 10 and 15 minutes until recovery. During AP the left ventricular systolic pressure (LVSP) did not show any significant change, with the exception of a patient who experienced angor pectoris during the proceeding. The left ventricular end-diastolic pressure (LVEDP) increased in 3.4 +/- 1.7 mmHg, change that was statistically significant (p less than or equal to 0.01) but not hemodynamically important since only in one patient it increased above the normal levels (from 13 mmHg basal to 17 mmHg during AP). In contrast, LVEDP markedly rose above normal when AP was stopped. It is concluded that neither LVEDP nor LVSP play an important role in the genesis of the ST segment depression seen in these patients. It is showed that, similar as in patients with obstructive coronariopathy, these cases work on a depressed Starling curve during AP and its recovery for what is thought that the functional meaning of ischaemia for both entities is similar no matter that their pathogenetic mechanisms are different.
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PMID:[Hemodynamic study in hypertensive cardiopathy under ischemia induced by atrial stimulation in the absence of fixed coronary obstructions]. 624 59

Numerous epidemiologic and experimental studies have shown that increased arterial pressure accelerates atherosclerotic disease including coronary heart disease. Left ventricular hypertrophy also develops along with the development of hypertension. In uncomplicated stages of hypertension, left ventricular hypertrophy may enable the heart to maintain its performance against an increased afterload. Development of coronary heart disease in hypertensive heart disease could be one of the factors that impairs cardiac function in later stages of the disease so that the function of the heart can no longer match the increased afterload. It can also be argued that atherosclerotic disease commonly contributes to an increase in systolic blood pressure. Short-term increases in arterial pressure due to angina pectoris or other stressful events may trigger permanent hypertension; this is an interesting alternative that is yet to be investigated. Thus, it is possible that a cause/consequence relationship is involved between hypertension and coronary heart disease as opposed to a simple association. Furthermore, this cause/consequence relationship could sometimes be bidirectional.
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PMID:Hypertension and coronary heart disease: cause and consequence or associated diseases? 636 50

The clinical differentiation of hypertensive heart disease from hypertrophic cardiomyopathy usually presents no problem but it is less clear whether an echocardiographic distinction can always be made and, if so, what those echocardiographic criteria of difference are. It can be inferred from recent publications that when echocardiographic criteria for hypertrophic cardiomyopathy are met in hypertensive subjects, both diagnoses may be made. This may be unjustified, and in order to clarify this problem that M-mode echocardiographic features of 37 patients with severe systemic hypertension were compared with those of 70 patients with hypertrophoic cardiomyopathy and normal blood pressure. Systolic anterior movement of the mitral valve and/or mid-systolic closure of the aortic valve were found in 82 per cent of patients with obstructive and 35 per cent of patients with non-obstructive hypertrophic cardiomyopathy. These features were not seen in patients with hypertension. The conventional echocardiographic features of left ventricular hypertrophy and function did not permit distinction between hypertensive heart disease and hypertrophic cardiomyopathy. The echocardiographic diagnosis of hypertensive heart disease from hypertrophic cardiomyopathy is, therefore, difficult unless systolic anterior movement of the mitral valve and/or mid-systolic closure of the aortic valve can be shown.
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PMID:Echocardiographic differentiation of hypertensive heart disease and hypertrophic cardiomyopathy. 644 11

After indications to the great epidemiologic importance of hypertensive heart disease and its relationship with the ischaemic heart disease several results are reported collected during the past 10 years by examinations of more than 500 patients for early diagnosis of cardiac insufficiency in hypertension. The methods of microcatheterization of the pulmonary artery and radiography have been used (even under ergometrical exercise) as well as the calibrated apex cardiography and the echocardiography. For the practising physician a classification of hypertensive heart disease with 4 phases or forms is proposed. The paper ends with a demonstration of the close relationship between prevention and treatment of hypertension as well as between hypertensive and ischaemic heart disease at the same time in a sense of the integrative role of heart insufficiency.
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PMID:[The heart in hypertension]. 645 89

To analyze changes in left ventricular diastolic properties in hypertensive heart disease, the atrial emptying index was used to assess the rapid phase of diastolic filling of the left ventricle. Ten normal subjects (Group 1), 11 hypertensive patients without evidence of cardiac involvement (Group 2) and 10 hypertensive patients with echocardiographic evidence of left ventricular hypertrophy (Group 3) were compared using M mode echocardiography and systemic hemodynamic data. Whereas cardiac index (dye-dilution method) and rate of circumferential fiber shortening (echocardiogram) were normal in all three groups, there was a progressive increase in left atrial index (p less than 0.001, Group 1 versus Group 2 and versus Group 3) and a progressive decrease in the atrial emptying index (p less than 0.001, Group 1 versus Group 2 and versus Group 3). No correlation existed between the atrial emptying index and the left atrial index, mean arterial pressure or total peripheral resistance in any of the three groups. These data suggest that rapid filling of the left ventricle is reduced early in hypertension, even before electrocardiographic or systolic echocardiographic abnormalities are detectable. The atrial emptying index therefore appears to be an early indicator of abnormalities of left ventricular diastolic compliance in uncomplicated hypertension.
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PMID:Echocardiographic diastolic ventricular abnormality in hypertensive heart disease: atrial emptying index. 645 11

To assess patterns of left ventricular adaptation, 38 patients with borderline and 38 with sustained mild essential hypertension, all lacking electrocardiographic and roentgenographic criteria for left ventricular hypertrophy, were compared using systemic hemodynamic values and M-mode echocardiograms. All patients had normal left ventricular function and measurements of wall thickness. Those with borderline hypertension showed no asymmetric increase in the ratio of septal to posterior wall thickness. The ratio of the left ventricular radius to wall thickness remained normal in both groups, indicating no disproportionate hypertrophy or dilatation of chambers during the phase of normal left ventricular function. Neither finding substantiates asymmetric septal hypertrophy in early hypertension. Those with mild essential hypertension demonstrated an augmented mean circumferential fiber shortening rate compared to those with borderline hypertension (P less than 0.005), suggesting an early stage of left ventricular hyperfunction in the development and elaboration of hypertensive heart disease.
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PMID:Patterns of left ventricular adaptation in borderline and mild essential hypertension. Echocardiographic findings. 645 32

The biracial population of New Orleans has a high overall mortality rate, high coronary heart disease (CHD) mortality rate, and high autopsy rate. In the New Orleans Community Pathology Study we investigated atherosclerosis and CHD in all deceased males aged 25 to 44 years, with major focus on the 52% of subjects from whom heart and arterial specimens were collected and evaluated according to standardized procedures. Morphologic correlates of CHD are the same in young black and white males. CHD mortality and mortality from cerebral hemorrhage, hypertensive heart disease, chronic renal disease, and diabetes are greater in young black males than young white males. Age, serum cholesterol, and hypertension were identified as important associated factors in the atherosclerotic process, as well as in CHD. The extent of coronary lesions seems to have decreased between 1960-1964 and 1969-1978 in young white males but not in blacks. Racial differences in coronary lesion involvement in non-CHD deaths are smaller than in our earlier studies.
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PMID:Coronary heart disease in young black and white males in New Orleans: Community Pathology Study. 647 44

To investigate the usefulness of stress testing for the evaluation of hypertensive heart disease, 40 subjects, 28 men and 12 women (mean age 30.8 +/- 6.2 years), with mild or moderate hypertension, without ST segment or T wave abnormalities in their resting ECG, were examined. 13 patients (32.5%) showed exercise-induced ST segment depression. The heart rate at rest was significantly higher in the patients with a positive response; 6 of the 7 subjects with electrocardiographic signs of left ventricular hypertrophy (summed SV1 + maximum R V5/V6 voltage of 45 mm or more) had a positive exercise electrocardiographic test. There were no significant differences between positive and negative cases in age, sex, systolic and diastolic blood pressure, or the double product (heart rate X systolic pressure) at rest or during exercise. After resting blood pressure values had been significantly decreased by giving methyldopa with or without diuretics for at least 6 months, there were a regression of left ventricular hypertrophy in the resting ECG and an impressive reduction in the prevalence of exercise-positive responses (to 17.5%). In the 7 patients with positive exercise electrocardiographic tests even after antihypertensive treatment, no significant reduction in blood pressure values during exercise was obtained.
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PMID:Usefulness of stress testing for the evaluation of hypertensive heart disease in young hypertensive subjects. 648 27

Scanning 3000 cases admitted for rehabilitation after cerebrovascular accident over a 20 year period produced a sample of 1369 subjects, without age restrictions, admitted within six months of a first stroke of thrombotic etiology. In this sample, survival rates showed no significant difference between men and women. Age at onset, however, clearly influenced survival changes; the expected mean survival was 6 years at 40 and 2 at age 80; average loss of life was 14 years for the whole sample, meaning a vital prognosis two to three times worse than that of the general population. At least 86% of the sample presented one or more of five etiological antecedents to stroke: hypertensive heart disease, peripheral vascular disease, diabetes mellitus, myocardial infarction and atrial fibrillation. In 87% of those, HHD and/or PVD were present. Presence of hypertension significantly lowered life expectancy and so did PVD; their influence is felt from the earliest stages. In contrast, diabetes mellitus, the next most common factor, has a late influence, starting about the fifth year after stroke. MI and AF were present in relatively fewer patients, but they contributed towards a considerable decrease in life expectancy, evident from the first stages, the more drastic reduction being observed in the AF group.
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PMID:Hemiplegics after a first stroke: late survival and risk factors. 665 53


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