Wall Thinning Rate Research Articles

Echocardiographic features of hypertensive-diabetic heart muscle disease.

Computerized M-mode echocardiography was used to evaluate left ventricular anatomy and function in 20 patients with hypertension and diabetes mellitus, without signs of overt heart disease. A similar study was performed in 20 patients with hypertension of similar severity and duration and in 20 normal subjects. Mean posterior wall thickness and mean septal thickness were increased in hypertensive patients compared to normal (p less than 0.001), but diabetic patients had thicker septa with respect to nondiabetics (p less than 0.05). All hypertensive-diabetic patients had reduced peak lengthening rate and/or peak velocity of posterior wall thinning. Six of them also had reduced peak Vcf and/or peak velocity of posterior wall thickening. Only 9 of the 20 patients with hypertension alone had abnormal diastolic function; 4 out of these 9 also had abnormal systolic function. We conclude that diabetes causes more severe impairment of left ventricular function in patients with a similar degree of hypertension. The more consistent abnormalities are reduced rate of dimension increase during filling and slower wall thinning, suggesting impaired left ventricular relaxation and distensibility.

Effects of long-term treatment with amiodarone on exercise hemodynamics and left ventricular relaxation in patients with hypertrophic cardiomyopathy.

The influence of long-term treatment with amiodarone on exercise hemodynamics and on left ventricular relaxation was studied prospectively in patients with hypertrophic cardiomyopathy. Rest-exercise hemodynamics (n = 9) and echocardiographic relaxation indexes (isovolumic relaxation time, dPW/dt) (n = 11) were measured in control conditions and after 5 weeks of oral amiodarone treatment (600 mg daily first week, 400 mg daily second week, 200 mg daily afterwards). Long-term amiodarone treatment in patients at rest caused a significant drop in heart rate from 80 +/- 11 to 75 +/- 11 beats/min (p less than .05), a rise in mean pulmonary artery pressure from 19 +/- 7 to 25 +/- 10 mm Hg (p less than .02), and a rise in mean pulmonary capillary wedge pressure from 11 +/- 4 to 17 +/- 8 mm Hg (p less than .05). Systemic arterial pressure, cardiac output, and systemic vascular resistance remained unaltered. Exercise tolerance assessed by serial supine bicycle stress testing was reduced in six of nine patients. Amiodarone treatment caused a significant rise in pulmonary capillary wedge pressure from 22 +/- 8 to 37 +/- 9 mm Hg (p less than .001) at the highest identical workloads and from 26 +/- 10 to 37 +/- 9 (p less than .005) at maximal symptom-limited workloads. Similarly, mean pulmonary artery pressure rose from 37 +/- 15 to 51 +/- 18 mm Hg (p less than .01) at highest identical workloads and from 42 +/- 19 to 51 +/- 18 mm Hg (p less than .01) at maximal symptom-limited workloads. There were no significant differences at maximal exercise level in heart rate, systemic arterial pressure, cardiac output, or exercise factor. Echocardiographic studies performed before and during long-term amiodarone treatment revealed no change in isovolumic relaxation time, end-diastolic or end-systolic posterior wall thickness, and peak posterior wall thinning rate. A negative inotropic action of amiodarone could explain the worsened rest and exercise hemodynamics observed during long-term treatment of patients with hypertrophic cardiomyopathy. Echocardiographic relaxation indexes remained unaltered despite the elevated left ventricular filling pressures. This finding could suggest a deleterious effect of amiodarone on myocardial inactivation, possibly similar in mechanism to the depressed myocardial inactivation observed in hypothyroidism.

The mechanism of disappearance of the physiologic third heart sound with age.

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.

U waves in ventricular hypertrophy: possible demonstration of mechano-electrical feedback.

The relation between ventricular function and electrocardiographic evidence of hypertrophy (by voltage criteria, "strain", and U wave inversion) was examined by means of M mode echocardiography and apex cardiography in 73 patients with diseases associated with left ventricular hypertrophy and 10 normal volunteers. In patients with disease, left ventricular cavity dimension and fractional shortening were unrelated to electrocardiographic findings, but left ventricular posterior wall thickness was greater in those with strain or U wave inversion. Without U wave inversion, hypertrophy and strain were weakly related to diastolic abnormalities, but the addition of U wave inversion was strongly associated with a reduced rate of early diastolic posterior wall thinning, prolonged isovolumic relaxation time, delayed mitral valve opening after minimum cavity dimension, and a pronounced increase in transverse dimension during the isovolumic period suggesting incoordinate relaxation. It is concluded that, whereas a negative U wave frequently occurs in association with the pattern of left ventricular hypertrophy or strain, it alone is strongly related to abnormalities of isovolumic relaxation. The close relation between incoordinate relaxation and U wave inversion, events which occur virtually simultaneously during the isovolumic period, suggests a mechanical influence on U wave genesis.

Echocardiographic evaluation of verapamil in Friedreich's ataxia.

Nine patients with hypertrophic cardiomyopathy associated with Friedreich's ataxia were treated with the calcium antagonist verapamil, which is known to reduce myocardial hypertrophy and improve diastolic function in patients with idiopathic hypertrophic cardiomyopathy. Daily oral doses of 7 mg/kg were given for a mean (SD) of 24 (8) months. M mode echocardiography performed at the start of the study and at the end of follow up showed no significant difference between the treated group and an untreated control group of nine patients. Verapamil produced no changes in left ventricular wall thickness, mass index, left ventricular internal diameter, fractional shortening, peak normalised lengthening rate, peak rate of septal and posterior wall thinning, and time from minimum ventricular cavity dimension to mitral valve opening. Myocardial calcium overload has been suggested as a cause of cardiac disease in Friedreich's ataxia; however, verapamil had no beneficial effect on these patients with established myocardial hypertrophy.

Left ventricular diastolic function in elite athletes with physiologic cardiac hypertrophy

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.

Early diastolic left ventricular function in children and adults with aortic stenosis

Pressure overload hypertrophy of the left ventricle is associated with abnormal left ventricular early diastolic filling. The roles of the extent of cardiac hypertrophy, depressed left ventricular systolic function and aging in the pathogenesis of left ventricular diastolic dysfunction have not, however, been fully defined. To determine the relative importance of these factors in the pathogenesis of diastolic dysfunction in pressure overload hypertrophy, 16 children and 25 adults with aortic stenosis were compared with 48 normal children and adults, using rates of left ventricular early diastolic filling and wall thinning derived from M-mode echocardiography. Left ventricular early diastolic filling and wall thinning rates were significantly depressed in both children and adults with aortic stenosis as compared with values in normal subjects. Filling and thinning rates correlated negatively with age, left ventricular peak systolic pressure and wall thickness in all subjects. Furthermore, the effect of age on diastolic function appeared to be mediated by age-related increases in systolic pressure and wall thickness. In adults with aortic stenosis, early diastolic filling and wall thinning rates were depressed to a similar extent in subjects with normal and abnormal systolic function; thus, diastolic dysfunction does not appear to be a manifestation of abnormal systolic loading and ejection performance. These results suggest that extent of hypertrophy itself plays a dominant role in the mechanism of impaired left ventricular early diastolic filling in pressure overload due to aortic stenosis.

Apical left ventricular asynergy in chronic aortic regurgitation

Apical left ventricular (LV) wall motion abnormalities have been described in chronic volume overload. To evaluate if these abnormalities are due to an actual hypokinesia we analyzed the percent shortening of apical LV radiants (PS%) by an angiographic computerized method and the endocardial systolic movement (ESM) and thickening (%Th) of the same region using M-mode echocardiographic technique in 11 patients affected by pure aortic regurgitation (AR). In these patients mean apical radii shortening was reduced with respect to normal values. Both %Th and ESM were significantly reduced in AR when compared to normal subjects (24.5 +/- 31.7% vs. 63.8 +/- 35.8%, p less than 0.01 and 4 +/- 7 vs. 10 +/- 3 mm, p less than 0.01, respectively). In addition, %Th and ESM directly correlated with PS% (r = 0.79, p less than 0.01 and r = 0.77, p less than 0.01, respectively). PS% correlated positively with systolic eccentricity and inversely with end-systolic volume index (r = 0.64, p less than 0.05 and r = 0.57, p less than 0.05, respectively). Finally, in AR %Th was related to a normalized peak rate of systolic wall thickening (r = 0.85, p less than 0.01) and to a normalized peak rate of diastolic wall thinning (r = 0.68, p less than 0.05). These results showed that in AR a reduced apical radii percent shortening was associated with a reduced normalized peak rate of systolic wall thickening and of diastolic wall thinning, thus indicating an actual hypokinesis and an impaired contractility. Moreover, the observed abnormalities correlated with an altered LV dynamic geometry linked to chronic volume overload.

Echocardiographic features of impaired left ventricular diastolic function in Chagas's heart disease.

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.

Relation between electrocardiographic repolarisation changes and mechanical events in left ventricular hypertrophy.

The relation between ventricular function and the presence of electrocardiographic "strain" in patients with left ventricular hypertrophy was examined using digitised M mode echocardiography and 12 lead electrocardiograms in 64 patients with pressure overload, 21 with hypertrophic cardiomyopathy, and 14 athletes. Although all had increased left ventricular mass, those with strain had a prolonged interval from minimum cavity dimension to mitral valve opening and a reduced rate of early diastolic posterior wall thinning and dimension increase compared with those with normal ST segments and T waves. Both groups had normal systolic function (fractional shortening and peak velocity of circumferential fibre shortening), and the time between the termination of the T wave and minimum dimension was similar. In athletes, however, electromechanical systole was shorter than normal, and the end of the T wave and minimum cavity dimension were synchronous. It is concluded that abnormal electrical recovery in left ventricular hypertrophy is closely related to impaired early relaxation and may be dissociated from impaired systolic function, cavity dimension, interventricular conduction delay, and the presence of increased mass alone. The normal relation between electrical and mechanical systole is preserved even when the polarity of repolarisation is reversed.

Relation of regional echo amplitude to left ventricular function and the electrocardiogram in left ventricular hypertrophy.

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.

Left ventricular hypertrophy. Relation of structure to diastolic function in hypertension.

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.

A Prospective Study of Heart Disease in Diabetes Mellitus

Six hundred and twenty-five patients with diabetes mellitus were studied by standardised clinical methods, resting and exercise electrocardiography (ECG) and digitised echocardiography to determine the prevalence of coronary and non-coronary heart disease. Clinical evidence of coronary artery disease (angina and infarction) was present in 110 (18 per cent) normotensive patients. Hypertension (blood pressure greater than 165/95 mmHg) was present in 172 (27 per cent) of whom 32 had cardiac symptoms. Heart failure or left ventricular dilatation was seen in 18 of whom 11 had either hypertension or coronary artery disease and six asymptomatic patients had unexplained ventricular hypertrophy. Echocardiograms in 245 of 290 asymptomatic patients with normal ECG showed that relaxation was prolonged (p less than 0.001) and mitral valve opening delayed (p less than 0.001) from normal especially in those with severe microangiopathy (proliferative retinopathy and/or heavy proteinuria). The peak rates of cavity dimension increase and posterior wall thinning were reduced from normal (both p less than 0.001) and patients with severe microangiopathy had the most marked changes. Redivision of these 245 diabetics by abnormalities of left ventricular function showed that 147 had normal function in whom only one of 23 (random 15 per cent sample) had a positive exercise ECG. Prolonged relaxation or delayed mitral valve opening alone (a nonspecific abnormality) was present in 41 and only three of 28 had a positive exercise ECG. Thirty-one had delayed mitral valve opening with inco-ordinate relaxation (abnormalities very suggestive of coronary artery disease) of whom 20 of 29 had a positive exercise ECG. Twenty-six had delayed mitral valve opening with slow cavity dimension increase or wall thinning (without hypertrophy) of whom 21 of 25 had a negative exercise ECG. This is a relatively specific abnormality similar to that found in left ventricular hypertrophy. Coronary artery disease is common in symptomatic and asymptomatic forms in diabetes mellitus. Non-coronary left ventricular diseases, such as dilation and hypertrophy, are probably no more common in diabetics than non-diabetics. A small number of diabetics with severe microangiopathy had abnormal relaxation and reduced peak rate of dimension increase or wall thinning which may represent left ventricular disease due to microangiopathy.

Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: Altered left ventricular loading or improved muscle inactivation?

The calcium channel blocking agent, nifedipine, has been shown to improve indexes of left ventricular relaxation, diastolic filling and compliance in patients with hypertrophic cardiomyopathy. The mechanism of action of nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy is unclear and could result from an improvement in myocardial inactivation or from systemic vasodilation and left ventricular unloading. To distinguish between these mechanisms, the effects of nifedipine and the vasodilator nitroprusside on left ventricular diastolic properties were compared in 10 patients with nonobstructive hypertrophic cardiomyopathy using simultaneous micromanometer left ventricular pressure and echocardiographic measurements. Left ventricular peak systolic pressure was comparable during nitroprusside infusion (132 +/- 38 mm Hg) and after nifedipine (132 +/- 32 mm Hg). During nitroprusside infusion, the decrease in left ventricular end-diastolic pressure (22 +/- 11 to 17 +/- 11 mm Hg, p less than 0.05) was associated with a decrease in left ventricular end-diastolic dimension. In contrast, the decrease in left ventricular end-diastolic pressure after nifedipine (22 +/- 11 to 18 +/- 10 mm Hg, p less than 0.05) was associated with no reduction of left ventricular end-diastolic dimensions, suggesting an increase in left ventricular distensibility. Compared with nitroprusside, nifedipine was associated with less prolongation of the left ventricular isovolumic relaxation time and less depression of the peak left ventricular posterior wall thinning rate and peak left ventricular internal dimension filling rate. These data suggest that the effects of the calcium channel blocker, nifedipine, on diastolic mechanics in hypertrophic cardiomyopathy result not only from systemic vasodilation but also from improved cardiac muscle inactivation.

Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.

The left ventricular diastolic pressure-volume relationship shifts upward during angina, but why this happens is not known. To assess regional myocardial stiffness, we studied 12 patients who had coronary artery disease using simultaneous left ventricular micromanometer pressure recording and M-mode echocardiography before and during angina induced by pacing tachycardia. All patients had two- or three-vessel coronary artery disease that involved the posterior left ventricular wall circulation and had positive pacing stress tests, i.e., development of angina and a postpacing rise in left ventricular end-diastolic pressure (15 +/- 3 to 31 +/- 6 mm Hg, p less than 0.001). A marked upward shift in the relationship between the diastolic left ventricular pressure and the posterior wall thickness (h) occurred after pacing tachycardia, but the change in left ventricular posterior wall end-diastolic thickness was minimal (8.9 +/- 2.1 to 9.2 +/- 2.1 mm, NS). After pacing, the peak rate of left ventricular posterior wall thinning decreased (82 +/- 37 to 48 +/- 27 mm/sec, p less than 0.005) and the time constant of relaxation derived from the best exponential fit to the isovolumic left ventricular pressure decay increased (49 +/- 5 to 58 +/- 7 msec, p less than 0.001). Diastolic active left ventricular pressure decay, extrapolated from the exponential fit, was subtracted from the measured left ventricular pressure (which is equal in magnitude but opposite in sign to the radial stress at the endocardium) to calculate residual left ventricular pressure (PR) and hence residual stress (sigma R = -PR). A radial stiffness modulus (ER) was determined by the slope of the PR vs log h plots before and after pacing. Over the same range of residual radial stress (sigma R), ER was always higher during pacing-induced angina, indicating increased residual myocardial stiffness. Increased myocardial stiffness in addition to a decreased rate of wall thinning and slow active pressure decay contribute to the upward shift in left ventricular pressure-wall thickness and pressure-volume relationships during pacing-induced angina.

Differentiation of constrictive pericarditis and restrictive cardiomyopathy using digitized echocardiography

Constrictive pericarditis and restrictive cardiomyopathy are difficult to distinguish at the bedside and occasionally at routine cardiac catheterization. Left ventricular diastolic function was studied by computer analysis of digitized M-mode echocardiograms in four patients with constrictive disease and three with restrictive disease, and the data were compared with those of normal subjects. The respective distinguishing echographic features of constrictive pericarditis and restrictive cardiomyopathy were as follows: the major filling period of the left ventricle was 78 +/- 9% of normal versus 128 +/- 4% (p less than 0.01), minimal left ventricular dimension to peak filling interval was 50 +/- 10 versus 110 ms (p less than 0.05) and the maximal rate of left ventricular posterior wall thinning was -4.9 versus -2.3 seconds-1 (p less than 0.05). This preliminary study suggests that it may be possible to accurately diagnose the two disease entities using this technique at the bedside and to avoid cardiac catheterization.

Effects of short-term administration of verapamil on left ventricular relaxation and filling dynamics measured by a combined hemodynamic-ultrasonic technique in patients with hypertrophic cardiomyopathy.

The effects of short-term administration of verapamil on left ventricular isovolumetric relaxation and early and late diastolic filling dynamics were studied in 10 patients with hypertrophic cardiomyopathy by a combined hemodynamic-ultrasonic technique. Left ventricular pressures (recorded with high-fidelity micromanometers) were determined simultaneously with M mode echocardiography. After 10 mg of verapamil was given intravenously (2 mg/min), left ventricular contractility and systolic pressure dropped significantly (p less than .05). Left ventricular dP/dt fell from 1947 +/- 544 to 1489 +/- 334 mm Hg/sec, maximal velocity of the contractile element at zero load fell from 50 +/- 17 to 42 +/- 15 1/sec, peak velocity contraction of the contractile element fell from 37 +/- 10 1/sec to 29 +/- 10 1/sec (p less than .05), and left ventricular systolic pressure fell from 149 +/- 30 to 127 +/- 22 mm Hg. Left ventricular negative dP/dt increased from 1770 +/- 479 to 1477 +/- 377 mm Hg/sec (p less than .05), and the time constant of isovolumetric pressure decay was prolonged from 48 +/- 9 to 64 +/- 15 msec (p less than .05). Left ventricular end-diastolic pressure rose from 21 +/- 7 to 23 +/- 6 mm Hg (p less than .05). The time constant of isovolumetric pressure decay was calculated in three different ways, but none of these measurements was influenced by verapamil. Time of isovolumetric relaxation, duration of rapid ventricular filling, and peak rate of left ventricular lengthening were not significantly influenced by verapamil and remained highly abnormal. In contrast, peak rate of left ventricular posterior wall thinning declined further after verapamil from 2.9 +/- 1.2 to 2.4 +/- 1.4 1/sec (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of age related changes in chamber size, wall thickness, and heart rate on left ventricular function in normal children.

We assessed the effects of age related changes in chamber size, wall thickness, and heart rate of left ventricular function in 78 normal children, aged 1 1/2 to 12 1/2 years, using computer analysis of their left ventricular echocardiograms. Left ventricular cavity size and wall thickness increased linearly with age. Left ventricular fractional shortening, percentage of wall thickening, and the ratio of end-diastolic wall thickness to cavity radius (H/R ratio) did not change with age. Peak Vcf correlated with heart rate and the decrease in heart rate with age resulted in the progressive fall in peak Vcf, while peak rate of left ventricular was thickening remained constant. The peak rate of increase in left ventricular cavity dimension in early diastole varied inversely with heart rate, but independently of cavity size, increasing throughout childhood. The peak rate of wall thinning also increased with age, correlating with wall thickness and not heart rate. Thus, age related increases in left ventricular cavity dimension and wall thickness during the rapid growth period of childhood occurred in such a way that left ventricular architecture (H/R ratio) remained unchanged. This may account for the constancy of regional and cavity systolic function. The greater dependence of diastolic cavity function on heart rate may be explained by the disproportionately greater effect of cardiac cycle length on the duration of diastole and systole.

Echocardiographic features of impaired ventricular function in diabetes mellitus.

In order to study left ventricular diastolic function in diabetes mellitus, simultaneous echo- and phonocardiograms were recorded in 142 diabetics (free from heart disease), 20 normal subjects, and 16 patients with coronary artery disease. The resultant traces were digitised, and left ventricular relaxation and the rate and duration of cavity dimension increase and wall thinning were determined. Diastolic variables of left ventricular function were normal in 12 young diabetics with no complications. Significantly delayed mitral valve opening relative to minimum dimension and aortic valve closure was found in all other groups of diabetics. Forty-four diabetics with severe microvascular complications had significantly reduced peak rate and prolonged duration of wall thinning and dimension increase. The abnormalities were unlike those found in subjects with coronary artery disease. The extent of microvascular complications was significantly correlated to most variables of diastolic function. This relation was maintained in 31 diabetics with significant cavity dimension increase during isovolumic relaxation (incoordinate relaxation). In 42 juvenile onset patients there was good correlation between the duration of diabetes and most variables of diastolic function. These studies show that the primary cardiac abnormality in diabetic micro-angiography is a prolonged duration and reduced rate of posterior wall thinning with impaired left ventricular dimension increase, reflecting abnormal myocardial properties.

Modification of abnormal left ventricular diastolic properties by nifedipine in patients with hypertrophic cardiomyopathy.

The effect of nifedipine on left ventricular isovolumic relaxation and diastolic filling properties and systemic and left ventricular hemodynamics was studied in 15 patients with hypertrophic cardiomyopathy. After nidefipine (10 mg sublingually), the prolonged left ventricular isovolumic relaxation time assessed by echocardiography decreased from 112 +/- 26 to 83 +/- 23 msec (p less than 0.0001), and the left ventricular pressure decay as measured by time constant T improved from 63 +/- 20 to 49 +/- 11 msec (p less than 0.05). Left ventricular filling dynamics also improved as assessed by a return toward normal in the depressed peak rate of left ventricular diastolic filling (dimension change 72 +/- 37 to 101 +/- 39 mm/sec, p less than 0.01) and the peak rate of posterior wall thinning (47 +/- 31 to 68 +/- 36 mm/sec, p less than 0.001). These changes were accompanied by hemodynamic evidence of improved diastolic function shown as a decrease in left ventricular end-diastolic pressure and a downward shift in the left ventricular diastolic pressure-dimension relationship, suggesting improved left ventricular distensibility. After nifedipine, there was a slight increase in heart rate and a decrease in systemic ventricular distensibility. After nifedipine, there was a slight increase in heart rate and a decrease in systemic arterial blood pressure, and no depression of the left ventricular percent fractional shortening or cardiac index. These data indicate that abnormal left ventricular relaxation and diastolic filling rates in hypertrophic cardiomyopathy are dynamic and favorably modified by nifedipine, and that this effect is not related to a depression of left ventricular systolic function.