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

In selected patients with systemic hypertension it may be difficult to ascertain whether left ventricular (LV) hypertrophy is a secondary end-organ consequence of long-term elevations in blood pressure or, alternatively, a manifestation of a coexistent primary hypertrophic cardiomyopathy. To address this issue and better characterize LV hypertrophy in systemic hypertension, 2-dimensional echocardiography was used to define the patterns of LV hypertrophy in 102 patients with sustained systemic hypertension and marked degrees of wall thickening. Patients ranged in age from 31 to 88 years (mean 61) and were predominantly female (58%); all were black. By selection, each patient had a maximal LV wall thickness of greater than 15 mm (range 16 to 29). Distribution of hypertrophy was judged to be symmetric (i.e., concentric) in most patients (67 of 102, 66%). However, a substantial proportion (35 patients, 34%) demonstrated nonuniform, asymmetric patterns of hypertrophy in which at least 1 segment of the LV wall was at least 1.5 times the thickness of any other. In these 35 patients, the distribution of hypertrophy was similar to that characteristic of the morphologic spectrum of hypertrophic cardiomyopathy, with thickening of portions of both the ventricular septum and free wall in 16 patients, anterior and posterior ventricular septum alone in 11 patients and segmental involvement of only the anterior ventricular septum in 8. Patients with asymmetric patterns of wall thickening did not differ from the patients with symmetric hypertrophy with regard to age, sex or clinical findings. Asymmetric LV hypertrophy appears to represent an important feature of the morphologic spectrum of severe hypertensive heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diversity of patterns of hypertrophy in patients with systemic hypertension and marked left ventricular wall thickening. 213 47

To determine the effects of aging and concentric hypertrophy on the reserve of the left ventricle (LV), 36 patients with hypertension (HT), 22 with hypertrophic cardiomyopathy (HCM) and 25 age-matched normal subjects (N) were studied by isoproterenol (ISP) infusion echocardiography. The end-diastolic LV relative wall thickness (RWT), fractional shortening (FS), peak mitral flow velocity during the rapid filling phase (R) and atrial systole (A), and the A/R ratio were measured. At rest, the RWT and A/R were larger in groups HT and HCM than in group N. There were no significant differences in age, heart rate (HR), and FS among the groups. The A/R of all groups showed a good positive correlation with increasing age. The A/R of the HT group was also positively correlated with RWT. During ISP infusion, the HR, R, A, A/R and FS increased in all groups. The changes in R and FS were smaller in groups HT and HCM than in group N. The change in HR in groups N and HT, and the change in FS in all groups during ISP infusion were all inversely correlated with increasing age. The change in FS during ISP infusion was inversely correlated with RWT in the HT group, but not in HCM. Thus, it was suggested that the impairment of LV reserve in patients with HCM is not only caused by concentric hypertrophy and the aging process, but also by other myocardial factors.
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PMID:Left ventricular reserve of the hypertrophied heart in patients with systemic hypertension and hypertrophic cardiomyopathy--relation to age and left ventricular relative wall thickness. 214 1

To investigate left ventricular (LV) systolic and diastolic function in cardiac hypertrophy, we analysed LV pressure (catheter tip-manometer) and simultaneously performed cineangiography in 24 patients with systemic hypertension (HT), 25 patients with hypertrophic cardiomyopathy (HCM) and 25 normal subjects. We digitized LV cineangiograms frame by frame and computed volume and its derivatives, wall thickness and circumferential wall stress. LV systolic pump function was normal or supernormal in HT and HCM. However, myocardial contractility assessed by end-systolic wall stress-volume relation was depressed in HCM whereas it is normally maintained in HT. LV diastolic function was also impaired in HCM and even in HT despite normal systolic function. The LV hypertrophy group showed significantly prolonged time constant of isovolumic relaxation, increased time from end-systole to the peak filling rate, and upward shift of the diastolic pressure-volume relationship. The characteristic findings of LV diastolic function in LV hypertrophy, therefore, can be summarized as impaired isovolumic relaxation, delayed early diastolic filling and decreased diastolic distensibility. The mechanisms of abnormal systolic and diastolic function may include myocardial ischemia and/or calcium overload in hypertrophied myocardium, but further study will be needed to clarify these problems.
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PMID:Left ventricular systolic and diastolic function in the hypertrophied ventricle. 214 19

Calcium antagonists are now widely used for the treatment of clinical hypertension and angina pectoris. They are efficacious for the treatment of vasospastic, fixed atherosclerotic and mixed angina; they reduce the incidence of silent ischemia; and they have been shown to reduce postmyocardial infarct angina. Experimental data suggest that they may have certain cardioprotective properties in cases of acute myocardial ischemia and infarction, stunned myocardium, diastolic dysfunction, left ventricular hypertrophy and atherosclerosis. Moreover, they have been shown to improve exercise performance, as well as the diastolic abnormalities in patients with hypertrophic cardiomyopathy. In animals, they may delay or reduce the extent of myocardial necrosis after coronary occlusion or coronary occlusion followed by reperfusion, and in low doses that do not alter the hemodynamic profile, they have been shown to enhance the return of ventricular function in animals with stunned myocardium. However, the early first-generation calcium antagonists (nifedipine, verapamil, diltiazem) have not been shown to reduce myocardial infarct size or to enhance survival in patients with acute myocardial infarction. There now are clinical studies that suggest that, unlike beta blockers or nitrates, nifedipine may slow the development of atherosclerotic progression in humans over a 2-year period, and it seems likely that in the 1990s there will be further expansion of the use of calcium antagonists for not only angina and hypertension but also for aspects of cardioprotection. That calcium antagonists may delay, prevent or possibly regress atherosclerotic lesions is an exciting possibility.
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PMID:Progress in cardioprotection: the role of calcium antagonists. 214 58

Abnormalities in the diastolic function of the left ventricular pump are the common determinant and, above all, the earliest manifestation of all forms of chronic left ventricular failure, whether or not the left ventricular systolic function is abnormal. Congestive signs, in particular, are directly related to abnormalities of ventricular filling. Primary diastolic dysfunction is the cause of left ventricular failure in about 40 p. 100 of the cases, but it may also be observed in almost all cardiopathies. In myocardial ischaemia the pressure-volume relation is displaced upwards owing to a slowed down, inhomogeneous and incomplete relaxation. Left ventricular hypertrophy, whether it is due to excessive pressure (arterial hypertension, aortic stenosis) or reflects a primary hypertrophic cardiomyopathy, is associated with a slowing down of ventricular relaxation and a reduction of left ventricular diastolic distensibility, even though the ventricular pump systolic function remains normal for a long time. Outside alterations in the distensibility of the ventricular muscle, ventricular dilatation alters ventricular filling by forcing the ventricle to function on the vertical part of its diastolic pressure-volume relation. Nowadays, the aged hearts is the most frequent cause of heart failure with normal systolic function. In all cases dysrhythmias and atrioventricular desynchronization act as aggravating factors. Treatment is often difficult since positively inotropic drugs or arterial vasodilators frequently have a modest or even deleterious effect.
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PMID:[Disorders of diastolic function in chronic left ventricular insufficiency]. 214 34

Diastolic filling can be measured by radionuclide ventriculography with use of several techniques including those based on gated and list-mode acquisitions, the first-pass method, and the nuclear probe. Radionuclide ventriculography specifically assesses volumes, rates of volume change, and intervals during ventricular filling. Normal values for diastolic filling measurement vary depending on the individual radionuclide methods used and the age of the patient. Comparative studies of the radionuclide method with contrast angiographic and Doppler echocardiographic techniques for measuring diastole are discussed, and the advantages and disadvantages of the radionuclide techniques are explored. The role of radionuclide assessment of diastolic function in specific clinical examples of hypertrophic cardiomyopathy, hypertension, anthracycline-induced cardiomyopathy, and coronary artery disease is reviewed. Radionuclide ventriculography is an accurate and easily applicable procedure for studying left ventricular volume changes in diastole.
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PMID:Determination of diastolic function by radionuclide ventriculography. 219 92

Seven elderly patients with hypertrophic obstructive cardiomyopathy (HOCM), who had the three following characteristics on echocardiograms 1) extremely thickened septum, 2) systolic anterior motion of the mitral valve, 3) mid systolic semi-closure of the aortic valve, were clinically evaluated. Ages ranged from 73 to 86 years old (average 78.9% yr.) and all were women. None had not a family history of hypertrophic cardiomyopathy but they had mild hypertension. Six patients showed a significant high voltage on the ST-segment and T-wave abnormalities ("strain" pattern). The left ventricular posterior wall as well as the septum was thickened in 5 and the remaining 2 showed asymmetrical septal hypertrophy (ASH) on echocardiograms. The left ventricular cavity was narrowed due to left ventricular hypertrophy and the shape of the left ventricular cavity was ovoid in all patients. The aorto-septal angles in these 7 patients were 80 degrees to 120 degrees. In addition, proximal septal bulge in all and anterior displacement of the mitral posterior leaflet due to the mitral ring calcification (MRC) in some patients contributed to the narrowing of the left ventricular outflow tract, and the mitral valve was pulled up toward the septum because of the good left ventricular systolic function (ejection fraction: 70 to 94% by echocardiography) and blood was ejected at a high velocity through a narrowed outflow tract (Venturi effect). Pressure gradients in the left ventricular outflow tract was 38 to 146 mmHg in 5 examined by cardiac catheterization. Biopsy specimens were obtained from 2 patients, showing hypertrophic myocytes (diameter: 20 to 30 micron) in 2 and mild disarray in 1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A clinical study of hypertrophic obstructive cardiomyopathy in the elderly]. 226 18

Single-photon emission computed tomography was performed in 29 patients with hypertrophic cardiomyopathy (HCM) using 123I-metaiodobenzylguanidine (MIBG). Segmental myocardial uptake of MIBG and 201T1 was calculated in 21 patients with primary HCM without history of hypertension. Septal thickness was measured by echocardiography and the relationship to septal MIBG uptake was studied. Initial MIBG uptake and 201T1 uptake showed positive correlation with the septal thickness (R = 0.581, p = 0.0058 and R = 0.677, p = 0.0007). When the septal MIBG uptake was divided by the corresponding 201T1 uptake (MIBG/T1), both the early and delayed MIBG/T1 showed negative correlation with the septal thickness (R = -0.485, p = 0.0255 and R = -0.535, p = 0.0125). Significant positive correlation was observed between septal MIBG clearance and the thickness (R = 0.510, p = 0.0182). In patients with severe septal hypertrophy (greater than 20 mm), the MIBG clearance was significantly higher compared with less hypertrophic (less than or equal to 20 mm) group (13.4 +/- 8.0%/hr vs. 3.2 +/- 4.7%/hr, p = 0.0028). Thus, MIBG was useful for the evaluation of sympathetic innervation and activity in HCM. The MIBG clearance and uptake in conjunction with 201T1 study seemed to reflect the severity of hypertrophy in HCM.
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PMID:[Evaluation of hypertrophic cardiomyopathy with 123I-metaiodobenzylguanidine]. 233 65

Nineteen patients with LBBB were studied by clinical, electrocardiographic (ECG), echocardiographic, electrophysiological and coronary angiographic examination. The commonest etiology of LBBB observed was idiopathic/degenerative in 10 (52.6%), followed by atherosclerotic coronary artery disease in 6 (31.5%) and hypertrophic cardiomyopathy, dilated cardiomyopathy and systemic hypertension in 1 case each (15.7%). In all patients with coronary artery disease (CAD), significant lesion of the left anterior descending artery was observed. On ECG, presence of Q in I, aVL, V5 or V6 was most helpful in predicting the presence of CAD while primary T-wave changes were least helpful. The degree of QRS axis was not helpful in predicting the presence as well as severity of CAD. Altered septal/regional wall motion abnormalities were commonly encountered on echocardiography and left ventriculography. Although infrahisian conduction delay was frequently observed and 11 (61.1%) had prolonged HV interval, in 2 of these there was additional suprahisian conduction delay. All patients with prolonged PR interval (more than or equal to 200 msec) or wide QRS duration (more than 140 msec) had infrahisian block with or without associated suprahisian block. Hence, hemodynamic evaluation, coronary angiographic studies and electrophysiological evaluation is essential in patients with LBBB.
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PMID:Noninvasive and invasive evaluation of left bundle branch block (LBBB). 233 87

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


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