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

Left ventricular hypertrophy in left ventricular pressure overload occurs in response to excessive work load imposed on the left ventricle by increased impedance to ejection. Right ventricular hypertrophy may occur in patients with these findings, but has been considered to be secondary to pulmonary hypertension. To determine the frequency of right ventricular hypertrophy and its relation to increased left ventricular wall thickness in patients with left ventricular pressure overload, right ventricular wall thickness was measured using M-mode echocardiography with two-dimensional echocardiographic guidance in 65 patients with left ventricular pressure overload; 49 patients had essential hypertension and 16 had aortic valve stenosis. These measurements were compared with data from 13 patients with "thin-walled" dilated cardiomyopathy and 20 normal subjects. Average right ventricular wall thickness in hypertensive patients (7 +/- 2 mm) and patients with aortic stenosis (6 +/- 2 mm) was significantly greater than that in normal subjects (4 +/- 1 mm) and patients with dilated cardiomyopathy (4 +/- 1 mm) who had normal left ventricular wall thickness, even though left ventricular mass was increased in all patient groups. Increased right ventricular wall thickness was present in 40 (80%) of 49 patients with hypertension and 10 (63%) of 16 patients with aortic stenosis. The magnitude of increase in right ventricular wall thickness was linearly correlated (r = 0.76, p less than 0.005) with left ventricular wall thickness, but was not associated with pulmonary hypertension. It is concluded that increased right ventricular wall thickness is common in patients with left ventricular pressure overload, is directly related to increases in left ventricular wall thickness, and is independent of right ventricular hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased right ventricular wall thickness in left ventricular pressure overload: echocardiographic determination of hypertrophic response of the "nonstressed" ventricle. 316 25

Non-inflammatory calcific disease of the mitral valve apparatus is a common finding in elderly patients. This study describes the incidence, clinical findings and location of mitral calcium deposits detected by 2D-echocardiography in an unselected series of patients referred for echocardiography to a general hospital. In addition, valvular function was assessed by Doppler sonography. In 48 out of 217 consecutive patients, 2D-echocardiography showed mitral calcium deposits. The mean age of this patient group was 72 +/- 11 years. Clinical histories and findings in most patients indicated an association between calcium deposits and increased tension of valve structures by left ventricular pressure overload (i.e., hypertension, aortic stenosis), dilatative cardiomyopathy or valve prolapse. Calcific deposits were located predominantly at the posterior mitral ring, but in 48% of our patients calcification of mitral chordae was also seen. Mitral regurgitation was detected by Doppler sonography in 52% of the patient group, in 25% at least moderate mitral regurgitation could be demonstrated. The presence of valve incompetence was not dependent on the location of calcium deposits. Mitral valve area, as assessed by Doppler, ranged from 2.1 to 6.7 cm2.
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PMID:[Calcinosis of the mitral valve system and its effect on valve function. A Doppler echocardiography study]. 319 74

A total of 458 cases (11.5%) with valvular heart diseases in the aged (greater than or equal to 60 years) were found among 4,000 consecutive autopsies. They included 204 cases (45%) of aortic regurgitation (AR), 171 cases (37%) of mitral regurgitation (MR), followed by 45 (10%) of aortic stenosis (AS) and 27 cases (6%) of mitral stenosis (MS). As an etiology of the valvular diseases, degenerative type was found in 195 cases (43%), ischemic origin in 91 cases (20%), followed by inflammatory origin such as syphilitic in 51 and infective endocarditis in three, aortitis in two and rheumatic in 49 (11%). Congenital origin was also found in 18 cases (4%). Among various types of valvular diseases in the aged, degenerative AR was most frequently found in 140 cases, followed by MR due to papillary muscle dysfunction in 91 cases. The clinical characteristics in cases with valvular diseases were as follows: atrial fibrillation was prominent in MS; congestive heart failure was found in 60% of cases except those with degenerative AR; cardiac death was frequent in syphilitic and rheumatic AR; association of hypertension was found in 50% of cases with MR and degenerative AR. In this article the characteristics of the valvular heart disease in the aged and additionally its diagnosis and treatment were discussed.
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PMID:[Valvular heart diseases in the aged]. 327 12

A survey of 1,950 phonocardiograms recorded over a 6-year period revealed 170 (9%) with a distinct aortic ejection sound. All patients were men with a mean age of 61 years (range 29 to 88). Associated clinical features were: aortic stenosis in 28%, history of systemic hypertension in 10%, history of rheumatic fever in 4% and none of these features in 58% of patients. In 141 (83%) of 170 patients the aortic ejection sound occurred simultaneously with or 0.01 second before or after the onset of the rise of the externally recorded carotid pulse. In 37 (66%) of 56 patients who had simultaneous echocardiograms and phonocardiograms recorded, the aortic ejection sound occurred at 0.01 second before or after the maximal opening point of the aortic valve leaflets. Two-dimensional echocardiography was performed in all patients and a bicuspid aortic valve was identified in 38 patients (22%). In 83 patients (49%) 3 cusps were clearly seen. In 49 patients (29%) an accurate determination was not possible. Anatomic examination of 120 consecutive aortic valves at autopsy was performed to identify possible causes of the aortic ejection sound. In 18 (15%) of autopsies fusion of 2 aortic cusps extending greater than or equal to 5 mm from the attachment to the aorta was observed. This abnormality, aortic commissural fusion, may be congenital or acquired. It is concluded that aortic ejection sounds may occur in patients without bicuspid aortic valves and in a variety of clinical conditions. A moderate degree of cuspal fusion may be the cause of the sound.
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PMID:Prevalence and characteristics of the aortic ejection sound in adults. 333 3

Hemodynamic observations were made at different cardiac levels during transient balloon occlusion at the time of aortic or pulmonary valvuloplasty in 37 patients (mean age 8 +/- 9 years); 22 had pulmonary stenosis and 15 had aortic stenosis (6 valvular and 9 discrete subvalvular types). Eighty-two tentative dilatations were performed in patients with pulmonary stenosis and 61 in patients with aortic stenosis. The hemodynamics of the right and left heart were monitored during inflation-deflation time. From selected tracings mean beat-to-beat pressures curves were constructed during occlusion-recovery time. The cycle length (RR interval) did not change significantly during occlusion, except for patients with pulmonary occlusion and patent foramen ovale, where a significant increase in cycle length (p less than 0.01) was observed during recovery time. The mean maximal increase in ventricular pressure reached 95% of basal values for the right ventricle and 58% for the left ventricle. The hypertension was retrogradely transmitted to all cardiac chambers. Angiographic observations during occlusion suggest that the atrioventricular valves and the foramen ovale, when patent, become escape orifices during occlusion, for adapting and relieving intracavitary pressures. The ventricle seems to adapt to sudden occlusion by generating hypertensive and hypokinetic contractions, with atrioventricular regurgitation.
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PMID:Physiopathology of transient ventricular occlusion during balloon valvuloplasty for pulmonic or aortic stenosis. 334 Dec 27

Eight patients, mean age 72 years, with aortic valve stenosis were studied by ultrafast CT 1 day after cardiac catheterization. After injection of radiographic contrast material through a peripheral vein, two contiguous eight-level R wave-triggered cine mode scans in the short axis were acquired, starting above the aortic valve and continuing through the apex of the left ventricle. Seven of eight patients, all with calcified aortic valves, had a detectable central orifice. Catheterization-derived aortic valve areas were within 0.25 cm2 of the CT valve areas in six of seven. LV mass was measured by ultrafast CT in the eight patients with aortic valve stenosis (121.6 +/- 18.2 gm/m2) and was found to be significantly higher (p less than 0.0001) than that in a group of eight subjects with normal LV function, no history of hypertension, and normal ECGs (73.0 +/- 13.1 gm/m2). It is concluded that in selected cases ultrafast CT can contribute to the assessment of severity of calcific aortic stenosis by measurement of LV mass and valve area.
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PMID:Preliminary experience in the use of ultrafast computed tomography to diagnose aortic valve stenosis. 334 62

According to echocardiographic observations, the hypertrophic left ventricle in hypertension and in aortic stenosis is inclined to asymmetric septal hypertrophy. The heart surgeon, after removal of the stenosed aortic valve, is not so rarely forced to resect an additional muscular hump of the basal ventricular septum. These findings contrast with our experiences from autopsy examinations; we see asymmetric septal hypertrophy only in hypertrophic cardiomyopathy (or coronary heart disease). The aim of this study was to demonstrate or refute this impression by measurements of the relevant parameters. In ten hearts with aortic stenosis and in 12 hearts of hypertensive patients there was no evidence of accentuated septal hypertrophy. In some hearts we found a prominent crista supraventricularis, which could explain the echocardiographic feature of a thickened ventricular septum. The muscular hump stenosing the left ventricular outflow tract can easily be explained by concentric hypertrophy. The thickness of the septum corresponded to that of the free wall, but only below the aortic valve did the hypertrophy become functionally relevant. There is no doubt that in certain cases this muscular hump has to be removed. The term asymmetric septal hypertrophy, however, is inadequate.
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PMID:[Asymmetric septum hypertrophy in the pressure-overloaded heart]. 342 9

Pulmonary arterial hypertension in aortic stenosis (AS) is considered uncommon, and the possible mechanisms involved in its insorgence are only speculative. We analyzed a group of 95 patients with severe AS (mean systolic gradient greater than or equal to 50 mmHg and/or aortic valve area less than or equal to 0.7 cm2) studied by standard hemodynamic techniques. In the study group the incidence of pulmonary hypertension was 50.5%. We divided the overall population in: Group I (47 patients), with systolic pulmonary artery pressure (PAP) less than or equal to 30 mmHg; Group II (33 patients), with moderate hypertension (PAP 31-50 mmHg); Group III (15 patients), with severe hypertension (PAP greater than 50 mmHg). Subjects with pulmonary hypertension were slightly older, and had more severe obstruction to left ventricular (LV) outflow. Impairment of LV diastolic function in the presence of pulmonary hypertension was expressed by a highly significant increase of LV end-diastolic pressure (p less than .001); reduced ejection performance was represented by a significant decrease of ejection fraction (p less than .01). Pulmonary vascular resistances also appeared to be increased. The correlation between variables showed PAP to be strongly correlated in a positive way to the LV end-diastolic pressure, and in an inverse way to the LV systolic performance (p less than .001 for both). Less striking was the correlation of pulmonary vascular resistances to LV diastolic and systolic function: a reactive and reversible vasoconstriction seemed likely. Surgery was not performed in 8 of the 95 patients: 5 of them died shortly after diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary hypertension in severe aortic stenosis. Incidence, mechanisms, clinical and surgical implications. 369 68

In order to clarify the pathogenetic mechanism of stenosis in the intramural coronary branch, morphological changes were examined by postmortem coronary angiography and determination of the Coronary Stenosis Index of the Myocardium (CSIM) were made in hearts obtained by autopsy from 10 patients with hypertension, 15 with normotensive myocardial infarction, 25 with hypertensive myocardial infarction, 6 with mitral valvular disease, 7 with aortic stenosis and 14 control subjects. CSIM was significantly higher in patients with hypertension, infarction with hypertension and aortic stenosis than in other three groups, indicating higher incidence of stenosis in those with a left ventricular pressure load. There was no specific correlation between the degree of stenosis of the epicardial coronary artery and that of the intramural coronary branches supplied by the former in any groups examined. Major pathological changes of the intramural coronary branches were muscular hypertrophy of media and proliferation of internal elastic lamella, both observed with a high incidence in vessels with high CSIM values. These findings suggest that intramural pressure which exerted extravascular pressure played an important role in the pathogenetic mechanisms of stenotic changes in the intramural coronary branches.
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PMID:Pathogenetic mechanism of stenosis in the intramural coronary artery. 380 29

Among 509 patients referred to our Institute for Holter monitoring, between 1st September, 1982-30th October, 1983, 28 patients aged 65-90 (mean 76) were referred for dizziness and syncope. There were 17 men and 11 women. Seven patients had a M.I. in their past, 4 angina pectoris, 5 hypertension, 4 aortic stenosis or aortic insufficiency or both, hemodynamically significant, one had mitral valve prolapse (MVP) and one transient ischemic attacks (TIA). In our series 16 out of 28 patients received digoxin and antiarrhythmic drugs (quinidine, propranolol, procainamide, Neo-gilurythmal, amiodarone), 2 of them digoxin and quinidine in full doses and one digoxin and amiodarone. Other drugs administered to our patients included Aldomin, Isordil, Lasix, aminophylin, cromoglycate etc. In 10 patients (35.7%) we found complex ventricular arrhythmias (7 with M.I., 3 patients of 4 with significant aortic valve lesion, 2 patients of 2 with left anterior hemiblock (LAH), 1 patient with MVP, 1 patient with TIA). In another 5 patients (17.8%) we found atrial fibrillation, fast rhythm (2 with chronic obstructive lung disease, 2 with hypertension and 1 in post M.I.) which explained their symptomatology. From our data we conclude that the pluripathology found in old age as well as the multimedication administered, cause a plurietiology of syncope, arrhythmias playing an important role in its determination, in this particular age group.
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PMID:Holter monitoring for dizziness and syncope in old age. 387 98


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