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

Angiotensin II has been reported to have both a positive inotropic effect and a coronary constrictor action in the hamster heart. To study the contribution to these responses of phenylalanine in position 8, we assessed the direct cardiac effects of angiotensin-(1-7), which lacks phenylalanine in position 8. Syrian hamsters were used to determine the effects of angiotensin-(1-7) on cardiac performance in the diseased and normal hearts. We used the isolated isovolumic heart preparation perfused either at a constant pressure of 50 mm Hg or at a constant coronary (myocardial) flow rate of 7 ml/min (seven cardiomyopathic hamsters [CMH] and seven normal hamsters [NH] in each subgroup). At constant perfusion pressure, coronary (myocardial) flow rate decreased (p less than 0.01) in both CMH and NH (-31 +/- 8% vs. -39 +/- 4% of baseline, respectively); but the percent decrease in left ventricular pressure and the first derivative of left ventricular pressure over time (LV + dP/dt) was significant only in NH (-8 +/- 1% and -9 +/- 4%) but not in CMH (-14 +/- 5% and -21 +/- 8%). On the other hand, at a constant coronary (myocardial) flow rate, left ventricular pressure and LV + dP/dt tended to increase in both CMH and NH (+10 +/- 3% and +6 +/- 2% of baseline vs. +7 +/- 7% and +7 +/- 5%, respectively) but these changes were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Feb
PMID:Biological activity of angiotensin-(1-7) heptapeptide in the hamster heart. 229 73

A 41-year-old woman had Noonan's syndrome. Her heart was complicated by asymmetric septal hypertrophy, hypertrophy of the left ventricular free wall, severe pulmonary stenosis, and right ventricular hypertension. On autopsy, a quantitative histologic analysis of the heart revealed that the area of disarray was limited both to the ventricular septum and the left ventricular free wall as in a normal heart. This is not typical of hypertrophic cardiomyopathy because the extent of disarray is high in most cases of hypertrophic cardiomyopathy. Some form of hypertrophic cardiomyopathy, however, seemed to be present in this patient because right ventricular pressure overload did not affect the left ventricular free wall. To clarify the relation between hypertrophic cardiomyopathy and Noonan's syndrome, quantitative histologic analysis is necessary.
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PMID:Asymmetric septal hypertrophy in a 41-year-old woman with Noonan's syndrome. 234 36

The prognosis of patients recovering from acute myocardial infarction (MI) depends mainly on their residual left ventricular (LV) function. In patients with asymmetric septal hypertrophy (ASH) who are recovering from MI, a larger functioning myocardial mass may remain. However, the frequency of ASH in these patients has not yet been described. Predischarge echocardiography, radionuclide ventriculography, and treadmill stress tests were performed in 403 consecutive patients who had recovered from acute MI. Eighty-eight patients (22%) had ASH with septal thickness greater than or equal to 1.3, and 32 (8%) had septal thickness greater than or equal to 1.5 cm. One hundred thirty-six patients who had recovered from a first MI and had no ASH served as control subjects. Left ventricular ejection fraction (LVEF) in the group with ASH was significantly higher than in control subjects (61% vs 50%; p = 0.0001). LV end-diastolic diameter (LVD(d] and E point septal separation (EPSS) were smaller in the group with ASH (4.9 cm and 5.4 mm) than in the control group (5.5 cm and 10.5 mm). The frequency of positive treadmill test results, angina pectoris, recurrent MI, heart failure, and death during a 22-month follow-up period was similar in both groups. Fifty subjects in the control group were matched with 50 patients from the group with ASH on the basis of maximal level of creatine phosphokinase, location of infarct, and presence or absence of hypertension, and the difference between the two groups was even more marked (LVEF 48% vs 61%, respectively; p = 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Residual left ventricular function and prognosis of patients with asymmetric septal hypertrophy recovering from acute myocardial infarction. 252 62

In order to understand the mechanism of development of asymmetric septal hypertrophy (ASH) in hypertension, 290 patients with essential hypertension (HT) were examined echocardiographically. Out of them 84 cases of advanced left ventricular hypertrophy (LVH) [37 cases of symmetric hypertrophy (HT-SH group) and 47 cases of ASH (HT-ASH group)] were compared in their clinical and echocardiographic findings with hypertrophic cardiomyopathy (HCM). In the 290 HT cases, the highest systolic pressure in each patient's history was found to correlate with left ventricular (LV) posterior wall thickness (PWT), but not with the septal wall thickness (IVST). There were no differences in LV thickness (IVST + PWT) among patients in the HT-ASH, HT-SH and HCM groups. While the HCM group patients showed no significant differences in IVST and PWT from those in the HT-ASH group, they did have greater IVST and smaller PWT than HT-SH group patients. The rapid filling rate (RFR) was also not much different in the HCM and HT-ASH groups, but was significantly lower in the HCM group than in the HT-SH group. Furthermore, HT-ASH group patients has a milder degree of hypertension and a higher incidence of familial occurrence of HCM than did those in the HT-SH group. After treatment for HT, the HT-SH group showed a significant decrease in wall thickness during long-term observation, while the HT-ASH and HCM groups, failed to exhibit such changes. Moreover, the degree of myocardial disarrangement in the HT-ASH group did not differ significantly from that in the HCM group. These results suggested that LVH in HT is related not only to pressure load but also to genetic factors similar to that in HCM.
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PMID:Mechanism of development of asymmetric septal hypertrophy in patients with essential systemic hypertension. 253 75

Left adrenal pheochromocytoma and mesenteric paraganglioma were diagnosed in a 52-year-old female with diabetes mellitus (fasting blood glucose 14.5 mmol/l), hypertension and myocardial asymmetric septal hypertrophy (septal/left ventricular free wall thickness 1.31). Carbohydrate metabolism and cardiac disease returned to normal after the resection of both tumors (fasting blood glucose 5.2 mmol/l, septal/left ventricular free wall thickness 1.10). This is the first patient reported in the Spanish literature in whom asymmetric septal hypertrophy has been correlated with the hypersecretion of catecholamines.
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PMID:[Asymmetric septal myocardial hypertrophy associated with pheochromocytoma: reversibility of cardiopathy after extirpation of chromaffin tumor]. 275 42

Cardiac enlargement and dysfunction are common in patients with acromegaly. Whether these changes are a direct consequence of growth hormone excess is obscured by the high frequency of hypertension, diabetes mellitus, or atherosclerosis in acromegalic patients. In this study, the effects of chronic elevations of growth hormone (GH) upon the heart were studied in rats with GH-producing tumours implanted subcutaneously for 4 weeks. Geometric measurements and histology were employed to detect the presence of cardiac changes. Increased mass was observed in the tumour-bearing animals. When compared with controls, in tumour-bearing rats there were significantly greater (P less than 0.05) right (0.17 +/- 0.03 v. 0.13 +/- 0.01 g) and left (0.62 +/- 0.05 v. 0.50 +/- 0.04 g) ventricular weights, external cardiac dimensions, and myocardial fibre diameters (9.4 +/- 0.6 v. 8.3 +/- 0.4 micron). However, these increases were linearly-related to increased body mass in the tumour-bearing group so that the ratios of ventricular weights to body weight were similar in both groups. Furthermore, no pathologic changes such as myocardial fibrosis or asymmetric septal hypertrophy were present in the tumour-bearing rats. Thus, under the conditions of this study, growth hormone excess induced cardiac growth, which appeared to represent a manifestation of generalized body growth rather than a distinct pathologic process.
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PMID:Cardiac morphology in rats with growth hormone-producing tumours. 293 34

We report a case of idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. A 64-year-old woman was admitted because of dyspnea. There was no past history of hypertension or heart disease and no family history of hypertrophic cardiomyopathy. Laboratory examinations revealed general inflammatory changes and mild elevation of serum CK and GOT. The clinical course was fulminant and the patient died of heart failure one day after admission. On autopsy, asymmetric septal hypertrophy was revealed and the pathohistological examination revealed panmyocarditis with mononuclear cell infiltration, interstitial edema, necrosis of myocytes, and giant cells. The inflammatory changes were most severe in the ventricular septum with asymmetric septal hypertrophy. The extent of myocardial fibers with disarray was within normal limits. Thus, the asymmetric septal hypertrophy appeared to be due to marked interstitial edema and inflammatory cell infiltration in the septum. This case suggests that myocardial inflammation and edema may cause thickening of the ventricular wall during the course of acute myocarditis.
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PMID:Idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. 295 39

Using computerized M-mode echocardiography we have investigated 58 hypertensive subjects in order to assess whether a correlation could be demonstrated between left ventricular changes induced by hypertension and age of the patients, the duration and severity of hypertension, and damage to other target organs. Various morphological changes of the left ventricle were detected: 14 patients (24%) had concentric hypertrophy of the left ventricle, 12 (20%) had asymmetric septal hypertrophy, 5 (8%) had dilated left ventricle without hypertrophy. Left ventricular mass was increased, when compared to normal controls in 24 patients (41%). With respect to functional abnormalities, the peak lengthening rate of left ventricular dimension in diastole was decreased (+dD/dt less than s-1) in 25 patients (43%). Eight of these patients (14%) also had depressed peak shortening rate of left ventricular diameter in systole (-dD/dt less than 1.9 s-1). Hypertensive retinopathy was present in 23 patients (39%) and impairment of renal function in 8 (14%). Left ventricular mass and systolic and diastolic parameters of left ventricular function did not correlate significantly either with the age of the patients, or with the duration and severity of hypertension, or with the damage present in target organs other than the heart. Left ventricular mass was inversely correlated with the index of left ventricular relaxation (r = -0.53; P less than 0.001), whereas neither the latter nor left ventricular mass were correlated with peak systolic stress. Instead, peak systolic stress was inversely correlated with peak shortening rate of left ventricular diameter, an index of systolic function (r = -0.50; P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Functional anatomy of the left ventricle in hypertensive subjects. Correlations with the clinical severity of hypertension]. 297 24

M-mode echocardiography was used to study cardiac involvement in 78 patients with acromegaly. Proportionate concentric or eccentric left ventricular hypertrophy (LVH) was a common finding. Calculated left ventricular mass (LVM) was increased significantly in a hormonally active disease group compared to an inactive disease group or a control group (153 +/- 7 vs. 96 +/- 8 and 89 +/- 3 g/m2 resp.; p less than 0.001 for both). The increase of LVM in hormonally active disease is due to predominantly LV dilatation, whereas associated hypertension, if present, aggravates the LVH exclusively due to thickening of the LV wall. Hypocorticalism, if present, does not influence the degree of LVH. Asymmetric septal hypertrophy was not found to be specific for acromegaly and was seen in only 7.7% of patients. There was no correlation between LVM and both the plasma levels of growth hormone and duration of disease. On the basis of a retrospective analysis of LVM in successfully treated patients the authors conclude that specific heart muscle disease in acromegaly, manifesting itself as LVH, is slowly reversible after cessation of the growth hormone hyperproduction.
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PMID:The nature of cardiac hypertrophy in acromegaly: an echocardiographic study. 316 77

There is increasing interest in the notion that some patients with hypertrophic cardiomyopathy (HCM) progress to morphological and functional manifestations similar to those of dilated cardiomyopathy (DCM). From 165 consecutive patients with HCM, 20 patients with left ventricular dilatation (left ventricular end-diastolic diameter greater than or equal to 50 mm) were selected and designated as dilated HCM. The diagnosis of HCM was established in these patients either by detection of the classical form of HCM in family members, with 2-dimensional echocardiographic evidence of asymmetric septal hypertrophy (ASH; septal thickness greater than or equal to 15 mm and a ratio of septal to posterior wall thickness greater than or equal to 1.3); or by demonstrating myocardial fiber disarray in autopsy or biopsy samples. The clinical manifestations of these patients with dilated HCM were then compared with those of other forms of HCM without left ventricular dilatation; 1) 40 patients with hypertrophic obstructive cardiomyopathy (HOCM) who had resting intraventricular pressure gradients of 20 mmHg or more, 2) 80 patients with non-obstructive HCM, each of whom had ASH of the entire ventricular septum (typical ASH), and 3) 25 non-obstructive patients whose hypertrophy was localized to the apical region of the ventricular septum (apical ASH). Patients having apical hypertrophy with a spade-like configuration on the left ventriculogram were excluded from the study. Compared with HOCM and typical ASH groups, the patients with dilated HCM had family histories of significantly more frequent HCM and less frequent hypertension. The patients with dilated HCM also had significantly less fractional shortening (FS), decreased interventricular septal thickness, greater left ventricular end-diastolic pressure (LVEDP), and left ventricular dilatation. During the follow-up period (average: 3.5 years), seven patients (35%) with dilated HCM died; five from congestive heart failure (CHF), one suddenly, and one three days following mitral valve replacement. The other five patients had CHF at the time of their follow-up examination. The patients with apical ASH had clinical features similar to those of dilated HCM; a higher familial frequency, less marked septal hypertrophy, and higher LVEDP. They tended to develop left ventricular dilatation, associated with reduced fractional shortening, although left ventricular diameter at end-diastole did not exceed 50 mm. These findings suggested that dilated HCM is not a rare condition. It is observed in 12% of consecutive patients with HCM.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Hypertrophic cardiomyopathy with left ventricular dilatation]. 324 61


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