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

Asymmetric septal hypertrophy (ASH) is the characteristic finding in patients with hypertrophic cardiomyopathy. The purpose of the present study was to examine the effect of chronic pressure overload on left ventricular hypertrophy and ASH in 34 patients with arterial hypertension. 15 patients (Group 1) showed normal blood pressure values (less than 140/90 mm Hg) under antihypertensive treatment but blood pressure remained elevated in 19 patients (Group 2) despite antihypertensive therapy. Left ventricular septal and posterior wall thickness, left ventricular internal diameter and systolic shortening of the internal diameter were measured in all patients by our standard technique. Systolic and diastolic blood pressure were significantly (p less than 0.001) elevated in Group 2 (164/98 mm Hg) as compared to Group 1 (128/84 mm Hg). Septal (1.7 versus 1.1 cm; p less than 0.01) and posterior wall thickness (1.2 versus 1.0 cm; p less than 0.01) as well as the septal/posterior wall ratio (1.4 versus 1.1; p less than 0.001) were significantly increased in Group 2 as compared to Group 1. Left ventricular internal diameter and systolic shortening of the internal diameter did not significantly differ between the two groups. ASH (septal/posterior wall ration greater than or equal to 1.3) was found in 10 patients of Group 2 (55%) and 1 patient of Group 1 (7%). It is concluded that asymmetric septal hypertrophy can be observed in one third of all patients with severe arterial hypertension. Asymmetric septal hypertrophy seems to be dependent on the duration and severity of hypertension and does not appear to be related to hypertrophic cardiomyopathy.
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PMID:[Asymmetric septal hypertrophy in patients with arterial hypertension]. 614 17

M-mode echocardiography was performed on 43 maintenance hemodialysis patients and 3 patients on continuous ambulatory peritoneal dialysis (CAPD). Only seven patients had completely normal echocardiograms. Nine patients (20%) had pericardial effusions and 20 patients (44%) had left ventricular dilatation. Left ventricular hypertrophy was present in 26 patients (57%): in 18 patients this took the form of concentric hypertrophy and in 8 patients there was asymmetric septal hypertrophy. Left ventricular function was depressed in 12 patients (27%). Left ventricular dilatation was more common in patients with multiple vascular accesses, who also tended to have lower hematocrit values. Left ventricular hypertrophy tended to be more common in patients with prolonged hypertension and with excessive inter-dialytic weight gains. Younger patients and those who had been on dialysis for a longer period had less cardiac abnormalities, suggesting that chronic dialysis might reverse these changes. Echocardiography was more sensitive than chest X-ray and ECG in detecting clinically unsuspected abnormalities and provides useful information in the overall evaluation of maintenance dialysis patients.
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PMID:Echocardiographic evaluation of cardiac size and function in dialysis patients. 622 87

Since chronic alcoholics may accompany with asymmetric septal hypertrophy (ASH), the purpose of this study was to find the difference in cardiac function of such cases from the patients with hypertrophic cardiomyopathy. Ninety-seven alcoholic patients (59 non-cirrhotics and 38 cirrhotics) were examined by non-invasive methods including two-dimensional echocardiography and dye dilution method, and these data were compared with those of 16 normal subjects and 26 patients with hypertrophic cardiomyopathy. The results were as follows: Interventricular septal thickness of more than 12 mm was observed in 25.4% of the non-cirrhotics and 28.9% of the cirrhotics. Furthermore, ASH was present in 23.7% of the former and 18.4% of the latter, when ASH was defined as the septal to posterior wall ratio greater than 1.3 with the interventricular septal thickness greater than or equal to 12 mm. In 66.7% of the chronic alcoholics with ASH, hypertrophy was predominantly located in the septum, however 53.8% of the patients with hypertrophic cardiomyopathy had ASH in association with the thickened left ventricular posterior wall. In 21 chronic alcoholics with ASH, ejection indices such as ejection fraction and mean VCF were moderately increased, although scattered widely, as compared with those of the normal subjects. Latent reduced ventricular function compensated by sympathetic overactivity was postulated based on left ventricular performance maintained normally as indicated by a decrease of end-systolic wall stress. Several possible factors including hypertension, catecholamine and metabolic abnormalities were analyzed to explain the genesis of ASH in chronic alcoholics, but the true etiology remained unknown. In conclusion, ASH associated with chronic alcoholism is a type characteristic of alcoholic cardiomyopathy, and seems to belong to a clinical entity different from hypertrophic cardiomyopathy from a standpoint of clinical symptoms, age and the pattern of left ventricular hypertrophy.
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PMID:[Echocardiographic evaluation of cardiac involvement in patients with chronic alcoholism]. 623 96

To investigate the pathophysiological significance of asymmetric septal hypertrophy (ASH), echocardiograms were recorded in 25 patients with hypertension (HT) (12 with ASH, 13 with symmetric hypertrophy (SH), 19 patients with hypertrophic non-obstructive cardiomyopathy (HNCM) (eight with ASH, 11 with SH), and 12 patients with hypertrophic obstructive cardiomyopathy (10 with ASH and two with SH). In eight patients with ASH, 12 patients with SH and eight normal controls, echocardiograms were also recorded during intravenous infusion of 0.02 mu/kg/min of isoproterenol. There were no significant differences in end-diastolic dimension (EDD), end-systolic dimension (ESD), percent fractional shortening (%FS), interventricular septal excursion (IVSE) and posterior wall excursion (PWE) between patients with ASH and patients with SH. Among patients with ASH, interventricular septal thickness (IVST) and its ratio to posterior wall thickness (IVST/PWT) were significantly larger in HOCM than in others. Before isoproterenol infusion, there was no significant difference in the normalized peak rate of change of left ventricular dimension during systole (pVs) between ASH and SH, and between ASH and NC. However, 5 min after isoproterenol infusion, pVs was significantly greater in ASH (7.0 +/- 2.4/sec) than in SH (4.9 +/- 1.3/sec) and in NC (4.5 +/- 1.1/sec) (p less than 0.05 and p less than 0.05, respectively). This study suggests that ASH is related to hyperfunction of the catecholamine-beta receptor system.
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PMID:[Pathophysiology of asymmetric septal hypertrophy with special reference to the response to isoproterenol administration]. 624 May 10

Clinical examinations including echocardiography were performed for 14 acromegalic patients (five men and nine women, whose mean age was 48.6 years). Three of these had hypertension (HT) above 160/95 mmHg, three had diabetes mellitus (DM). Their cardiac sizes and functions were correlated with the durations of disease and plasma growth hormone (GH) levels. The incidences of HT and DM were also evaluated. Three of 14 patients (22%) had increased cardiothoracic ratios (greater than 55%). Electrocardiographic abnormalities were noted in three patients including two with left ventricular hypertrophy (LVH) and one with interventricular conduction defects with abnormal Q waves. By echocardiography (Table 2), nine patients (64%) were judged to be normal. The remaining five patients (36%) had abnormal echocardiograms. These included LVH (sums of the interventricular and posterior wall thicknesses greater than or equal to 25 mm) in two (25 mm in Case 10, 30 mm in Case 11), increased left ventricular end-diastolic dimension (EDD greater than or equal to 55 mm) in one (72 mm in Case 14) and both abnormalities in two patients (Cases 12 and 13). Two patients (Case 13 and 14), whose %FS were 17% and 22%, respectively, had definite evidence of congestive heart failure. Two patients (Case 11 and 13) met the diagnostic criteria for asymmetric septal hypertrophy. One patient with echocardiographic LVH and another who had increased EDD with LVH had histories of HT (Case 11 and 12). Plasma GH levels in patients with LVH were greater than 100 ng/ml (Cases 10 and 11). The left ventricular hypertrophy and/or increased EDD observed in these patients seemed related to the duration of acromegaly but not to the presence of DM. Myocardial biopsy of the right ventricle in two patients with congestive heart failure disclosed myocardial hypertrophy, myocardial fiber disarray, interstitial fibrosis and large nuclei.
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PMID:[The heart in acromegaly: an echocardiographic study]. 624 54

The interventricular septum was studied by biventricular angiography in 52 patients divided into 4 groups: the first group consisted of 14 normal subjects; the second of 10 patients with hypertension (9 cases) or aortic stenosis (1 case); the third, of 19 patients with echocardiographic asymmetric septal hypertrophy, and the fourth, of 9 cases of cardiomyopathy with dilatation. The following parameters were measured: septal thickness at 4 different points and mean septal thickness, the height (long axis) and surface of the septum in diastole and systole. The percentage variation was calculated. There were no significant differences between Group I and II; there was a significant difference (p less than 0,01) in the variations of septal thickness of the upper segments between Group I and III. This difference remained significant (p less than 0,05) for the variations of mean thickness between Group I (-38%) and Group III (-18%). There was also a significant difference (p less than 0,05) in the variation of height between Group I (23%) and Group IV (9%). None of the variations of septal surface reached the threshold of statistical significance between the four groups. Biventricular angiography can therefore demonstrate certain abnormalities of septal motion. In asymmetric septal hypertrophy, the variations in thickness are significantly less pronounced than in normal subjects but the motion in the longitudinal axis does not differ significantly. In cardiomyopathy with dilatation, however, the variation in septal height is the most affected parameter.
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PMID:[Angiographic study of the dynamics of the interventricular septum]. 643 30

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

To clarify clinically the pathogenesis of septal hypertrophy in terms of its morphology and wall dynamics, simultaneous biventricular cineangiography (BVG) and endomyocardial biopsy of the left ventricle were performed for patients with left ventricular hypertrophy. The patients were categorized in four groups according to their clinical and BVG findings; 1) 24 normal control subjects (C), 2) 39 patients with hypertension and symmetrical septal hypertrophy (SH-HT), 3) 17 patients with hypertension and asymmetrical septal hypertrophy characterized by the ratio (IVS/PW) greater than or equal to 1.3 by BVG, and 4) 25 patients with hypertrophic cardiomyopathy (HCM). The BVG's configuration of the septum in SH-HT showed a normal form of septal hypertrophy (NH form) essentially similar to that of the control subjects (N form), except for septal thickness increases of more than 10 mm. In HCM, a triangle or shell (TS) form or spindle (S) form of the septum was demonstrated by BVG. The TS form was characterized by straight or convex thickening of the septum from its center to its base toward the left ventricle. The S form was characterized by convex thickening localized to the central part and a relatively thin base. However, the configuration in ASH-HT was either the NH form (7 cases) or the TS or S form (10 cases). The configuration in ASH-HT with the NH form was not distinguishable from that of SH-HT, nor was the configuration in ASH-HT with the TS or S form distinguishable from that of HCM. Systolic thickening (%) of the septum and systolic shortening (%) of the septal length decreased significantly in this order: C, SH-HT, ASH-HT with the NH form, and ASH-HT with the TS or S form. Those of HCM were similar to those of ASH-HT with the TS or S form. In the cases of the N or NH form, there was a negative correlation between systolic thickening (%) and thickness of the septum in diastole. In cases with the TS or S form, systolic thickening (%) was not affected by the thickness of the septum in diastole, and a lower value was observed in all cases. Histological studies of endomyocardial biopsies revealed a positive correlation between the transverse diameters of the myocytes and the total systemic peripheral resistance (TSPR) in 25 patients with SH-HT. In 12 patients with HCM, there was no correlation, and severe hypertrophy of the myocytes was observed despite a lower TSPR.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Evaluation of septal hypertrophy and wall dynamics by biventricular cineangiography and endomyocardial biopsy]. 654 88

HNCM tends to have more diffuse or generalized hypertrophy than HOCM, although these two types are not fundamentally different in aetiology (genetic). Extreme ASH is primarily related to a hereditary factor while HNCM, including apical hypertrophy, seems to be based on an abnormal disposition to produce myocardial hypertrophy in response to endogenous or exogenous stimulation such as catecholamines, chronic anoxia, hypertension or even aging. Hypertension by itself, however, can not be a cause of apical hypertrophy. The configuration of left ventricular hypertrophy in HCM can be divided roughly into several patterns: ASH, apical, postero-inferior, generalized or diffuse types, etc. ASH is not an essential morphology for HNCM. Apical hypertrophy is the only specific hypertrophic pattern which shows characteristic ECG abnormalities (giant negative T waves and high QRS voltage in left precordial leads). Inverted T waves combined with high QRS voltage tends to be a reflection of a localized hypertrophic portion in the left ventricular free wall. Abnormal Q waves associated with left axis deviation usually suggest marked septal hypertrophy. They seem to be related to conduction disturbances in myopathic septum.
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PMID:Electrocardiographic, echocardiographic and ventriculographic characterization of hypertrophic non-obstructive cardiomyopathy. 668 26

To assess the prevalence of asymmetric septal hypertrophy (ASH) in hypertensive patients, 613 echocardiographic examinations performed over a period of one year were reviewed. Asymmetric septal hypertrophy (defined by an echocardiographic interventricular septum to left ventricular free wall thickness ratio of greater than or equal to 1.3 and by the presence of suggestive two-dimensional echocardiographic abnormalities) was found in 28 patients (5%). Clinical characteristics of asymmetric septal hypertrophy were assessed in 101 patients who underwent a complete evaluation. Patients with asymmetric septal hypertrophy (n = 9) were compared with patients with echocardiographic symmetrical left ventricle hypertrophy (n = 38) and without left ventricular hypertrophy (n = 54). Our results indicate that neither the severity of hypertension, nor the renin-angiotensin system nor sympathetic nerve activity appear to be the primary determinants in the development of asymmetric septal hypertrophy.
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PMID:Prevalence and significance of asymmetric septal hypertrophy in hypertension: an echocardiographic and clinical study. 668 50


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