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

This study was designed to ascertain the contribution of hypertension to the early diastolic time intervals in asymmetrical apical hypertrophy (AAH). Eighteen patients with untreated AAH were categorized as those with (n = 13) and without (n = 5) hypertension. Isovolumic relaxation time and early diastolic filling were determined in four groups: normotensive subjects (n = 20), patients with essential hypertension (n = 20), AAH with hypertension, and AAH without hypertension. Early diastolic function was measured by the interval from the aortic closure sound (IIA, phonocardiography) to the opening of the mitral valve (MVO, echocardiography) and the interval from MVO to the O point of the apexcardiogram. The IIA-O interval was also calculated. Peak velocities in the rapid filling phase (R) and atrial contraction phase (A) were measured using two-dimensional Doppler echocardiography in the center of the mitral orifice in diastole. The MVO-O/IIA-MVO and A/R ratios were also calculated. 1. In the AAH with and without hypertension groups, the IIA-O, IIA-MVO, and MVO-O intervals were significantly prolonged. The IIA-O and MVO-O intervals in the AAH without hypertension group were more prolonged than were those in the AAH with hypertension group. In patients with essential hypertension, the IIA-O and the IIA-MVO intervals were prolonged, but there was no prolongation of the MVO-O interval. 2. The MVO-O/IIA-MVO ratio was lower in essential hypertension and in the AAH with hypertension groups, and significantly higher in the AAH without hypertension group. 3. There was no significant change of the R, A, and A/R in each group. These results indicated that prolonged left ventricular relaxation was distinguished in essential hypertension. In AAH with hypertension, the same prolongation was observed, but the disturbance of early diastolic filling was mild. It is suggested that apical hypertrophy has a possible association with hypertension, though it may more properly belong to cardiomyopathy.
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PMID:[Contribution of hypertension to left ventricular diastolic function in patients with asymmetrical apical hypertrophy]. 281 33

The significance of intrauterine growth retardation (IUGR) and the methods currently available for assessment of fetal growth are briefly reviewed. The use of Doppler ultrasound assessment of the flow velocity waveform (FVW) of the uteroplacental waveform at 16-18 weeks of gestation is outlined. A pilot study of 127 pregnancies suggested that the sensitivity of the test was 67% and the specificity 65%. The prediction value of a negative test was 92%. Six of the 14 cases of IUGR had a normal FVW, but 3 of these had asymmetrical morphology. Four of the 8 IUGR cases with an abnormal FVW required delivery by cesarean section. The FVW also appears to be a valuable predictor of pregnancy-induced hypertension and fetal asphyxia.
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PMID:Early diagnosis of intrauterine growth retardation by Doppler ultrasound. 297 Jul 65

Echocardiographic investigation of 110 patients with different forms of stable arterial hypertension demonstrated a moderately close correlation between left-ventricular myocardial weight, and systolic and diastolic arterial blood pressure in patients with essential hypertension and chronic diffuse glomerulonephritis, and a weak correlation between left-ventricular myocardial weight and systolic pressure in patients with renovascular hypertension and chronic unilateral or predominantly unilateral pyelonephritis. Inadequate left-ventricular hypertrophy has similar incidence (15-20%) in patients with different forms of arterial hypertension, whereas excessive hypertrophy only occurs in patients with essential hypertension. The frequency of asymmetrical hypertrophy differs in the two groups.
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PMID:[Characteristics of left ventricular hypertrophy in patients with different forms of arterial hypertension based on echocardiographic data]. 315 74

The effect of hypertension on asymmetrical septal hypertrophy was studied by echocardiography to differentiate idiopathic asymmetrical septal hypertrophy (ASH) from ASH with hypertension. One hundred eight patients with ASH proven by echocardiography were categorized in two groups; 53 patients with hypertension (greater than 160 systolic, greater than 95 diastolic) (hypertensive group: HT) and 55 patients with normal blood pressure (normotensive group: NT). Septal hypertrophy was classified as mid-portion (M-type), diffuse (D-type), and basal (B-type) hypertrophy by the long-axis view, and also diffuse (I-type), anterolateral (II-type), anteroseptal (III-type), and anterior septal (IV-type) by the short-axis view, respectively. Endomyocardial biopsy and left ventriculography were performed in 50 patients (18 hypertensives and 32 normotensives). In the hypertensive group, 45%, 30%, and 25% of cases had diffuse, basal and mid-portion hypertrophy, respectively. There was no case in the basal hypertrophy whose biopsy findings were compatible with hypertrophic cardiomyopathy. In the normotensive group, 78% and 22% of patients had midportion and diffuse hypertrophy, respectively, but none of them had the basal hypertrophy. Type IV was seen in only six patients in the normotensive group.
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PMID:[Effect of hypertension on asymmetrical septal hypertrophy: an echocardiographic study]. 326 13

Acromegaly involves cardiovascular complications mostly due to the presence of hypertension, diabetes and atherosclerosis. However the appearance of cardiac decompensation and arrhythmias in the absence of predisposing factors tends to support the hypothesis of a specific myocardiopathy caused by excess GH. In order to assess the existence and course of subclinical cardiac alterations, 8 acromegaly patients were examined: 4 males and 4 females aged 31-56 with GH levels of 24-70 ng/ml (M + CD X 47 +/- 16) and no cardiovascular symptoms. One of the patients had moderate hypertension and 2 reduced glucose tolerance. The basal ECG showed sporadic ventricular extrasystoles in 2 cases and alterations compatible with left ventricular hypertrophy in another, while the effort ECG produced an asymptomatic depression of the ST segment in the hypertensive patient. The chest X-ray was normal in all cases. The echocardiography study investigated: the thickness of the interventricular septum (IVS = 13.9 +/- 2.8 mm), the thickness of the posterior wall of the left ventricle (LPW = 10.6 +/- 2.9 mm), the septum/posterior wall ratio (IVS/LPW = 1.3 +/- 0.2 the diastolic diameter (DD = 15.4 +/- 11.4 mm), the fraction of shortening (FS = 39.1 +/- 14.5%), the ejection fraction (EF = 64.1 +/- 18.4%) and revealed asymmetrical septal hypertrophy in 3 cases, concentric hypertrophy in another two. In two cases the DD and EF were distinctly altered. The patients were re-examined 2-4 years after surgical or radiation treatment. GH levels (M +/- SD = 10.3 +/- 10.1 ng/ml) were normal in 4 cases and still high, though lower in another two. The remaining two patients had borderline GH levels with high Sm-C. The ECG and chest X-ray were unchanged while echocardiography revealed a significant deterioration in heart function as far as DD (56.4 +/- 10.8 mm, p less than 0.05) were concerned with frankly pathological results in 4 and 3 cases respectively. These data confirm the view that most acromegalic patients present subclinical abnormalities in cardiac function and that the evolution of these is slightly influenced by the reduction in GH and Sm-C. levels. In fact, while the persistence of high GH and Sm-C. levels may explain the progression of cardiac alterations in some cases, it does not in others. It is also emphasised that echocardiography appears to be the most sensitive non-invasive technique for the diagnosis and follow-up of cardiac involvement in acromegaly.
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PMID:[Cardiological findings in acromegaly]. 343 27

This is a report of a patient with mitral valve prolapse (MVP) and myocardial abnormalities on endomyocardial biopsy in whose relatives hypertrophic cardiomyopathy (HCM) was identified. A 19-year-old woman was admitted to our hospital for evaluation of a heart murmur. A systolic ejection murmur was audible in the third intercostal space at the left sternal border, and a standard 12-lead electrocardiogram showed ST-T wave changes in leads II, III and aVF. Echocardiography revealed prolapse of the anterior leaflet of the mitral valve, but no left ventricular hypertrophy. Endomyocardial biopsy disclosed mild hypertrophy and disarrangement of the myocardium. The family study revealed asymmetrical septal hypertrophy in her mother, who had no history of hypertension. Her younger sister had mild hypertrophy of the interventricular septum on echocardiography, and her histopathological findings suggested a diagnosis of HCM. This case was clinically regarded as MVP, but development of left ventricular hypertrophy as noted in her mother may occur in the future.
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PMID:[Mitral valve prolapse with myocardial disarrangement and familial hypertrophic cardiomyopathy: a case report]. 378 85

Angiotensin II is a potent vasoconstrictor and has profound effects on autonomic neural mechanisms in experimental animals. Human carotid baroreflex control of arterial pressure and heart period was examined before and after acutely decreasing angiotensin II levels by administering 50 mg of oral captopril, an angiotensin converting enzyme inhibitor. Carotid baroreceptor stimuli were delivered by a neck chamber worn by 14 normotensive volunteers. Four subjects received placebo. Arterial pressure responses to carotid distention and tachycardia in response to carotid compression were not changed in captopril or placebo groups; however, there was an augmented bradycardic response to carotid stretch in captopril-treated subjects. These results indicate that captopril has an asymmetrical effect on carotid baroreflex function and suggest that enhanced baroreflex mediated bradycardia is due to a reduction in central nervous system angiotensin II levels by captopril, which augments vagal-cardiac responses to carotid stimuli.
Hypertension
PMID:Captopril potentiates chronotropic baroreflex responses to carotid stimuli in humans. 389 17

Recent advances in echocardiography have revealed that hypertension causes several types of cardiac hypertrophy. We classified hypertensive patients by type of cardiac hypertrophy, and evaluated left ventricular function and the severity of hypertension. The subjects consisted of 257 hypertensive patients, 13 patients with cardiac hypertrophy, and 95 normotensive controls. The hypertensives were classified in four groups: no hypertrophy, concentric hypertrophy, asymmetrical septal hypertrophy (ASH), and asymmetrical apical hypertrophy (AAH). The normotensive patients with cardiac hypertrophy included nine with ASH and four with AAH. Cardiac functions in these patients were determined by echocardiography, RI-angiocardiography and cardiac catheterization. The results were as follows: Among 257 hypertensive patients, the incidence of concentric hypertrophy, ASH, and AAH was 53%, 10%, and 4%, respectively. In patients with AAH and hypertension, the hypertensive blood pressure levels and hypertensive organ involvements were mild. The blood pressures of most of these patients fell to the normal range after admission. The cardiac index and left ventricular systolic function (FS, mVCF, and ejection fraction) were significantly higher in AAH with hypertension than in the other hypertensive groups or in the normotensive controls. The hypertensive patients showed lower E-F slopes and higher A/E ratios than the normotensive controls, as well as the normotensive patients with ASH or AAH. Cardiac function did not differ appreciably between normotensive AAH and hypertensive AAH. Left ventricular dimension and left ventricular end-diastolic volume index were larger in AAH with hypertension. The total peripheral resistance of the hypertensive AAH was significantly lower than that of the hypertensives with concentric hypertrophy (p less than 0.01), though it was higher than that of the normotensive AAH (p less than 0.01). It was, therefore, concluded that mild hypertension observed in patients with AAH may be the result of regulatory mechanisms in the hyperkinetic states.
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PMID:[The role of hypertension in apical hypertrophy]. 406 56

To clarify the pathogenesis of apical hypertrophy with asymmetrical septal hypertrophy (ASH), left ventriculography in the right anterior oblique projection (LVG), biventriculography (BVG), and endomyocardial biopsy of the right ventricle were performed for patients with ASH. The patients were categorized in four groups according to ECG, LVG and BVG. Patients with hypertrophic cardiomyopathy (HCM) were divided into two subsets; (A) Apical hypertrophy group (AH: nine patients), with ECG showing left ventricular hypertrophy (LVH) and giant negative T waves (GNT), and with LV configurations showing the S or SR form at end-diastole on LVG. (B) Non-apical hypertrophy group (non-AH: 12 patients), with ECG showing LVH without GNT and LV configuration showing R form at end-diastole on LVG (cf: Fig. 1). Patients with ASH and hypertension (ASH-HT) were also divided into two subsets; (A) AH: seven patients. (B) non-AH: nine patients. Analysis of LVG and BVG: In HCM, the septal configuration showed the TS X S form in both two subset groups. The septal configuration in ASH-HT was divided into the NH form, which was clearly distinguishable from the septal configuration in HCM, and the TS X S form as in cases with HCM. In both HCM and ASH-HT, the diastolic thickness of the anterior apical wall was significantly thicker in all patients with AH than that in non AH. In HCM, the diastolic thickness of the septum and the percent systolic thickening did not significantly differ between AH and non-AH groups. In ASH-HT, the NH form showed similar diastolic thickness of the septum and % systolic thickening in AH and non-AH groups. On the other hand, the TS X S form in non-AH group showed greater thickness and lower % systolic thickening similar to those of HCM. Histological analysis of endomyocardial biopsy; In HCM, the transverse diameters of the myocytes and the biopsy scores did not differ significantly between AH and non-AH groups. In ASH-HT, the TS X S form in non-AH group had longer diameters and higher biopsy scores similar to those of HCM compared to the NH form in AH group. In conclusion, both HCM and ASH-HT may have apical hypertrophy manifested by giant negative T waves in the EKG and spade like form of left ventriculogram. In addition, apical hypertrophy in ASH-HT with the NH form of septal configuration seemed to be caused by hypertension.
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PMID:[Biventriculographic and clinicopathologic evaluation of apical hypertrophy: with reference to asymmetrical septal hypertrophy with hypertension]. 409 18

The mode of right ventricular hypertrophy was assessed by two-dimensional echocardiography (2DE) for 24 patients with hypertrophic cardiomyopathy (HCM), and the results were compared with those of 51 patients with hypertension (HT). The patients with HT were categorized in four groups depending on the thickness of the interventricular septum (IVST) and left ventricular posterior wall (PWT): HT-ASH with both left ventricular hypertrophy (LVH) (IVST greater than or equal to 13 mm) and asymmetric septal hypertrophy (ASH) (IVST/PWT greater than or equal to 1.3), severe HT with LVH and without ASH, and mild HT without LVH and ASH. Anterior wall thickness (AWT), posterior wall thickness (PWT), and diaphragmatic wall thickness (DWT) of the right ventricle were obtained from 2DE in the parasternal long-axis view, the short-axis view and subxiphoid view, respectively. These were recorded on video tape, and the measurements were made on the stop frames. Right ventricular hypertrophy (RVH) was estimated by the maximal right ventricular wall thickness (max RVWT), and the ratio of the maximal and minimal thickness (max RVWT/min RVWT) was calculated to evaluate asymmetrical hypertrophy (AH) of the right ventricle (RV). The incidence of RVH (Max RVWT greater than or equal to 5 mm) and asymmetrical hypertrophy (AH) (max RVWT/min RVWT greater than or equal to 1.3) of the RV in HCM, HT-ASH and mild HT were 67% and 41%, 57% and 45%, and 15% and 11%, respectively. The incidence of RVH with AH was more frequent in patients with HCM as well as HT with ASH than in patients with HT without ASH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Regional right ventricular hypertrophy in hypertrophic cardiomyopathy and hypertension]. 409 19


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