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 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Development or progression of left ventricular hypertrophy has recently been described in children with hypertrophic cardiomyopathy. To determine whether similar changes in magnitude and distribution of left ventricular hypertrophy may also occur in adult patients with this disease, serial assessment of left ventricular wall thickness was obtained with M-mode and two-dimensional echocardiography in 65 patients with hypertrophic cardiomyopathy who were 23 to 50 years of age. The follow-up period was 3 to 6 years (mean 4). None of the 65 patients showed a substantial increase (greater than or equal to 5 mm) in left ventricular wall thickness; however, 9 (14%) demonstrated a substantial decrease (5 to 9 mm). Wall thinning most commonly involved the anterior ventricular septum (seven patients), but was also identified in the posterior septum (six patients), lateral free wall (two patients) and posterior free wall (one patient). In the nine patients with wall thinning, left ventricular end-diastolic diameter increased significantly (from 44 +/- 6 to 51 +/- 6 mm; p less than 0.001); however, in seven of the nine, absolute cavity size remained within normal limits (less than or equal to 52 mm) at the most recent evaluation. Eight of the nine patients with left ventricular wall thinning and relative cavity enlargement were severely symptomatic and one was mildly symptomatic. In conclusion, substantial progression of left ventricular hypertrophy was not identified in any of the study patients. Hence, if such progression occurs in adults with hypertrophic cardiomyopathy, it is probably rare. Conversely, an important minority of adult patients with hypertrophic cardiomyopathy may show progressive left ventricular wall thinning and relative cavity enlargement, which are usually associated with severe cardiac symptoms.
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PMID:Absence of progression of left ventricular hypertrophy in adult patients with hypertrophic cardiomyopathy. 295

The relative sensitivities of and interrelations between different measurements of diastolic function were studied in 50 patients with left ventricular hypertrophy diagnosed on anatomical grounds. Isovolumic relaxation time, the interval from minimum cavity dimension to mitral valve opening and relative dimension increase during this period, and the peak rate of dimension increase and wall thinning during rapid ventricular filling were measured by digitised M mode echocardiography. The relative heights of peak early diastolic and atrial velocities (a/E) and the time for decline of early diastolic velocity to half its peak value (velocity half time) were measured on continuous wave and pulsed Doppler and the relative height of the "a" wave was measured by apexcardiogram. All sets of values except those of the interval from minimum dimension to mitral opening were unimodally distributed, and all differed significantly from those in 20 age matched controls. The relative height of the "a" wave on the apexcardiogram (90% values were abnormal) was the most sensitive method of studying left ventricular diastolic function and peak rate of dimension increase was the least sensitive. Though none of the correlations was high, there were individual associations between peak rate of dimension increase, a/E, peak wall thinning rate, and velocity half time, and independently between delay in mitral valve opening and dimension change during this period. Other values seemed to be independent of one another, suggesting a different physiological basis. It is concluded that these various abnormal values do not reflect a single underlying disturbance of diastolic function. There are at least four possible discrete abnormalities: prolongation of isovolumic relaxation; incoordination during isovolumic relaxation; reduced rate of rapid filling; and an increase in the relative amplitude of the "a" wave probably caused by increased passive stiffness. These may be present singly or in combination in any patient.
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PMID:Patterns of diastolic dysfunction in left ventricular hypertrophy. 296 87

We investigated the natural course of 59 patients with hypertrophic cardiomyopathy (HCM) in follow-up periods of one to 13 years and analyzed the clinical, hemodynamic and echocardiographic parameters to determine the factors influencing the prognosis. Among these patients, 44 (75%) remained stable in a compensated condition with or without medications. Five patients died suddenly and two died of congestive heart failure. Heart failure developed in another eight. At the initial evaluation, these 15 patients had high left ventricular end-diastolic pressure (mean: 22 +/- 8 mmHg) significantly higher than that of 44 compensated patients (mean: 13 +/- 6 mmHg, p less than 0.001). There were no differences in age at the initial evaluation between compensated and end stage groups. Atrial fibrillation occurred persistently in three and transiently in two among ten patients with heart failure during follow-up periods. Ventricular dimensions and systolic function did not statistically differ between the two groups. However, six patients with heart failure had cavity dilatation and deteriolated ventricular contractile function at the initial evaluation. Four of them did not show any change in left ventricular hypertrophy, but the regional thinning of the wall was observed in the remaining two. There were no characteristic features to predict sudden death in the clinical, hemodynamic or echocardiographic parameters. Thus, increased left ventricular end-diastolic pressure, atrial fibrillation, left ventricular dilatation and the regional thinning of the left ventricular wall are useful predictive markers for poor prognosis in HCM.
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PMID:[Natural course of hypertrophic cardiomyopathy: clinical, hemodynamic and echocardiographic features in the end stage]. 297 74

To study left ventricular diastolic function in Chagas's disease, simultaneous echocardiograms, phonocardiograms, and apexcardiograms were recorded in 20 asymptomatic patients with positive Chagas's serology and no signs of heart disease (group 1), 12 with Chagas's heart disease and symptoms of ventricular arrhythmia but no heart failure (group 2), 20 normal subjects (group 3), and 12 patients with left ventricular hypertrophy (group 4). The recordings were digitised to determine left ventricular isovolumic relaxation time and the rate and duration of left ventricular cavity dimension increase and wall thinning. In groups 1 and 2 (a) aortic valve closure (A2) and mitral valve opening were significantly delayed relative to minimum dimension and were associated with prolonged isovolumic relaxation, (b) left ventricular cavity size was abnormally increased during isovolumic relaxation and abnormally reduced during isovolumic contraction, and (c) peak rate of posterior wall thinning and dimension increase were significantly reduced and duration of posterior wall thinning was significantly prolonged; both of these abnormalities occurred at the onset of diastolic filling. These abnormalities were more pronounced in group 2 and were accompanied by an increase in the height of the apexcardiogram "a" wave, an indication of pronounced atrial systole secondary to end diastolic filling impairment due to reduced left ventricular distensibility. Group 4, which had an established pattern of diastolic abnormalities, showed changes similar to those in group 2; however, the delay in aortic valve closure (A2) and in mitral valve opening and the degree of dimension change were greater in the latter group. Thus early isovolumic relaxation and left ventricular abnormalities were pronounced in the patients with Chagas's heart disease and may precede systolic compromise, which may become apparent in later stages of the disease. The digitised method is valuable in the early detection of myocardial damage.
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PMID:Echocardiographic features of impaired left ventricular diastolic function in Chagas's heart disease. 315 54

Left ventricular hypertrophy due to aortic stenosis, hypertension and other forms of heart disease is associated with abnormalities of diastolic function. It is uncertain whether these changes are an inherent consequence of the hypertrophic process or represent additional pathologic factors. To investigate this issue, echocardiographic indexes of left ventricular early diastolic function in highly trained athletes were compared with those in age-matched normal control subjects. Athletes were equally classified into two groups: 11 swimmers who had a pattern of myocardial hypertrophy with normal wall thickness to dimension ratio and 11 power lifters whose wall thickness to dimension ratio was increased. The peak rates of left ventricular dimension increase and wall thinning in swimmers and power lifters were greater than in control subjects despite significantly higher left ventricular wall thickness and left ventricular mass index in the athletes. This increase in diastolic function indexes was associated with greater ventricular size and systolic performance. Normalization of the peak rate of dimension increase for end-diastolic dimension and adjustment of the peak rate of wall thinning for the fractional systolic thickening resolved any differences between groups. Thus, after the effects of ventricular size and systolic function were taken into consideration, diastolic function was normal in these subjects with considerable physiologic hypertrophy. This is in contrast to the findings in patients with hypertrophy associated with left ventricular pressure or volume overload, and suggests that abnormalities of diastolic function seen in pathologic hypertrophy are due to factors other than cardiac hypertrophy itself.
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PMID:Left ventricular diastolic function in elite athletes with physiologic cardiac hypertrophy. 316 24

In view of the paucity of reports describing symptoms of increased degree, and deterioration of left ventricular systolic function in patients with apical hypertrophic cardiomyopathy (apical HCM), two cases with congestive heart failure and progressive thinning of previously hypertrophied apical portions of the left ventricle are reported. These were among 13 patients observed from eight to 10 years. Case 1: A 56-year-old man was diagnosed as having apical HCM at the age of 49 years. Severe left ventricular hypertrophy and prominent ST-T changes were observed on ECG during his first admission. His left ventricular end-diastolic pressure (LVEDP) was 24 mmHg and a left ventriculo-gram revealed a decrease in the left ventricular cavity in the apex and marked hypertrophy of the apical wall. Moderate interstitial fibrosis without hypertrophy or disarray of myocytes was observed in a left ventricular endomyocardial biopsy specimen. In two episodes of cardiac arrest he was successfully resuscitated at the age of 50 years. At the age of 55 years, two-dimensional echocardiography revealed thinning and abnormal motion in the apical wall, and a defect in 201T1 accumulation was observed in the same region by perfusion scintigraphy. This patient was readmitted with a diagnosis of cerebral embolism at the age of 56 years. Cardiac catheterization revealed normal LVEDP (8 mmHg), and a left ventriculogram revealed an aneurysm in the left ventricular apex with normal major epicardial coronary arteries. He has been under treatment with antiarrhythmic medications, calcium antagonists and anticoagulants, and has become relatively asymptomatic. Case 2: A 69-year-old-man was diagnosed as having apical HCM after a complete evaluation, including cardiac catheterization, at the age of 59 years. His LVEDP was elevated (17 mmHg), and a left ventricular angiogram revealed marked hypertrophy localized to the apex. Ejection fraction was 64%. A left ventricular endomyocardial biopsy revealed interstitial fibrosis without hypertrophy of myocytes. Thereafter, he has been followed as a New York Heart Association functional class III to IV with occasional elevation of cardiac enzymes but without chest pain or acute changes in his ECGs. However, atrial fibrillation with complete right bundle branch block developed at the age of 60 years. Apical wall thinning and dyskinesis were diagnosed by 2D echocardiography and a defect in the 201T1 accumulation was observed at about 65 years of age. He was readmitted in severe cardiac failure at the age of 69 years, and he was diagnosed as having cardiac asthma with pulmonary capillary wedge pressure of 35 mmHg.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Advanced sequelae of apical hypertrophic cardiomyopathy: report of two cases with wall motion abnormalities]. 322 16

The prognosis of patients with acute myocardial infarction is related to the infarction size. We evaluated the ability of a clinical technique, two-dimensional echocardiography, to assess infarct size based on the extent of regional contraction abnormalities. Conscious closed-chest dogs with preplaced coronary snares underwent permanent coronary occlusion. The animals were studied by two-dimensional echo 20 min and 2 days after occlusion. The extent of myocardial contraction abnormalities (systolic wall thinning instead of normal systolic thickening) was correlated with the infarct size determined pathologically. Some dogs had pressure-induced left ventricular hypertrophy. Extent of regional contraction abnormalities demonstrated by two-dimensional echo correlated well with infarct size both early (20 min) (r = 0.92) and late (2 days) (r = 0.94) after permanent coronary occlusion. Dyskinesis extent modestly overestimated the infarct size. The relationship between dyskinesis and infarct size were similar in both normal and left ventricular hypertrophied hearts. We then undertook a study to assess the effects of coronary reperfusion on dyskinesis-infarct size relationships. Conscious, closed-chest dogs underwent 1-2 h of coronary occlusion followed by 2-10 days of coronary reperfusion. Significant regional dyskinesis was present after 1-2 h of occlusion and decreased by 50-60% of the occlusion value after 2 days of reperfusion without further change in extent of dyskinesis between 2 and 10 days of reperfusion. Of importance, however, was that there was no significant correlation between infarct size and extent of regional dyskinesis by two-dimensional echo after reperfusion, either after 2 days (r = 0.09) or 10 days (r = 0.29) of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Late effects of coronary reperfusion on regional left ventricular function. Can infarct size be estimated noninvasively? 353 3

To study the mechanism of disappearance of the physiologic third heart sound (S3) with advancing age, combined phonoechocardiographic and phonomechanocardiographic recordings from 165 normal subjects between 6 and 62 years old were quantitatively analyzed. Nearly all individuals under 40 years old had a recordable S3. Although recordable in 38.6% of the 44 subjects over 40 years old, the physiologic S3 found in adults was less intense and occurred later in diastole when compared with that in children and adolescents. Marked changes in left ventricular filling hemodynamics were observed with aging, including an increase in left ventricular wall thickness and mass, a prolongation of the left ventricular isovolumetric relaxation period, a decrease in left ventricular early diastolic filling and wall thinning rates, and a reduction in the height and steepness of the rapid filling wave measured on the calibrated left apexcardiogram (linear correlation with age significant at p less than .001 for all parameters). Although less pronounced, these changes were very similar to the diastolic abnormalities found in patients with pressure overload left ventricular hypertrophy. Therefore, the higher pressure load imposed on the left ventricular wall due to the well-known gradual increase in blood pressure that occurs during normal growth and adulthood appears to be the most likely explanation for the observed changes in diastolic filling. It is concluded that the later occurrence, the diminishing amplitude, and the eventual complete disappearance of the physiologic S3 with age results from a decrease in early diastolic left ventricular filling and subsequent deceleration of inflow caused by the development of relative left ventricular hypertrophy in adulthood as compared with childhood.
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PMID:The mechanism of disappearance of the physiologic third heart sound with age. 369 32

Digitised M mode echocardiography was used to determine the relation between the degree of left ventricular hypertrophy and abnormalities of isovolumic relaxation and diastolic function. Fifty six patients with varying severity of non-malignant systemic hypertension without evidence of ischaemic heart disease, left ventricular dilation, or clinical heart failure were studied. In addition, 10 athletes with hypertrophy and 20 normal subjects were studied. Athletes and patients with moderate (systolic blood pressure 175 to 200 mm Hg) and severe hypertension (greater than 200 mm Hg) had a significant increase in left ventricular mass. Cavity dimensions were normal in hypertensive patients and increased in athletes. Systolic function was normal in all groups. Regardless of the degree of hypertrophy patients with hypertension had a prolonged isovolumic relaxation period and delayed mitral valve opening. Patients with hypertrophy also had a reduced rate and prolonged duration of rapid early diastolic dimension increase and posterior wall thinning. Athletes, however, who had an equivalent degree of hypertrophy to patients with moderate or severe hypertension had entirely normal function. Measurements of diastolic function were significantly correlated with wall thickness and left ventricular mass. These indices of hypertrophy, particularly posterior wall thickness and the sum of posterior wall and septal thickness, were positively correlated with the duration of isovolumic relaxation and delay in mitral opening and negatively with the peak rate of early diastolic dimension increase and wall thinning. Thus in hypertensive patients with non-dilated left ventricular hypertrophy there appears to be a relation between the degree of wall thickening and abnormalities of diastolic function.
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PMID:Left ventricular hypertrophy. Relation of structure to diastolic function in hypertension. 623 10

In order to determine the relation between three manifestations of left ventricular hypertrophy--ST-T wave changes on the electrocardiogram, diastolic disturbances, and increased myocardial echo intensity--M mode and cross sectional echocardiograms were recorded in 12 normal subjects, 15 athletes, 16 patients with hypertrophic cardiomyopathy, and 42 patients with secondary left ventricular hypertrophy due to aortic stenosis (20), severe essential hypertension (8), coarctation (7), or subaortic stenosis (7). M mode echocardiograms were digitised and cross sectional echocardiograms were analysed for regional echo intensity. In patients with hypertrophy regional echo amplitude was significantly increased in mid and basal septum and posterior left ventricular wall. Patients with increased echo amplitude in any region showed a higher incidence of ST-T wave abnormalities than those without and of diastolic abnormalities--including prolongation of isovolumic relaxation time, delay in mitral valve opening with respect to minimum cavity dimension, and a reduction in peak rate of posterior wall thinning and dimension increase. There was a significant rank order correlation between median pixel count and these diastolic abnormalities. No significant differences were demonstrable in these relations between the diagnostic groups. By contrast, electrocardiographic findings, diastolic function, and pixel count were uniformly normal in athletes, although the increase in left ventricular mass was similar to that in the patients. Thus an increase in left ventricular mass alone is not responsible for repolarisation or wall motion abnormalities occurring in pathological left ventricular hypertrophy. These latter changes are, however, strongly associated with the change in myocardial properties detected as an increase in echo intensity and may be due to increased interstitial fibrosis.
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PMID:Relation of regional echo amplitude to left ventricular function and the electrocardiogram in left ventricular hypertrophy. 623 8


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