Secondary Left Ventricular Hypertrophy Research Articles

Clinical and echocardiographic correlates of mitral E-wave transmission inside the left ventricle: Potential insights into left ventricular diastolic function

The mitral inflow wave is initially directed to the left ventricular apex and then turns around facing the left ventricular outflow tract. The E and A waves are transmitted to the left ventricular outflow tract where they are registered as Er and Ar waves, respectively. We hypothesized that the E-wave transit time to the left ventricular outflow tract recorded as the E-Er interval may depend on left ventricular early diastolic performance such as relaxation. This hypothesis was tested in clinical settings known to have abnormal left ventricular relaxation. Mitral E and left ventricular outflow tract Er waves were recorded with pulsed wave Doppler technique in 63 subjects: 25 healthy subjects, 18 patients with secondary left ventricular hypertrophy, and 20 patients with hypertrophic cardiomyopathy. The E-Er interval was measured from the onset of E wave to the onset of Er wave timed to the R wave of the electrocardiogram. The E-Er interval ranged from 45 to 300 msec: 96 ± 28 msec in the controls, 127 ± 46 msec in patients with left ventricular hypertrophy ( p = 0.0091 versus controls), and 179 ± 57 msec in patients with hypertrophic cardiomyopathy ( p < 0.0001 versus controls). It correlated with left ventricular free wall thickness ( r = 0.42, p = 0.0006), thickness of the ventricular septum ( r = 0.43, p = 0.0004), left ventricular end-diastolic diameter ( r = –0.38, p = 0.0022), left ventricular end-systolic diameter ( r = –0.55, p < 0.0001), left ventricular isovolumic relaxation time ( r = 0.39, p = 0.0063), RR interval ( r = 0.28, p = 0.045), mitral E/A velocity ratio ( r = –0.33, p = 0.010), and E-wave deceleration time ( r = 0.38, p < 0.0044) but not with age. Multivariate analysis with all the previously mentioned variables and the group the patient belonged to as the dichotomous variable showed that the grouping variable was the sole independent determinant of the E-Er interval (multiple r = 0.74). The E-Er interval is an easily measurable Doppler parameter which is increased in left ventricular hypertrophy and hypertrophic cardiomyopathy. It is related to left ventricular wall thickness, left ventricular isovolumic relaxation time, mitral E/A velocity ratio, and E-wave deceleration time and may provide useful insight into left ventricular early diastolic performance—possibly the relaxation process. (J Am Soc Echocardiogr 1997;10:532-9.)

Coronary artery dimensions in primary and secondary left ventricular hypertrophy

Background. Coronary artery enlargment has been previously described in left ventricular hypertrophy.Objectives. We sought to assess coronary artery dimensions and their relation to left ventricular muscle mass in primary and secondary hyperthropy.Methods. Cross-sectional area of the left and right coronary arteries was determined by quantitative coronary angiography in 52 patients: 12 control subjects and 40 patients (13 with hypertrophic cardiomyopathy, 12 with dilated cardiomyopathy and 15 with aortic valve disease). As a measure of left ventricular hypertrophy, angiographic left ventricular mass and equatorial cross-sectional muscle area were determined.Results. Cross-sectional area of both the left and right coronary arteries is increased in left ventricular hypertrophy (p < 0.05 vs. values in control subjects). There is a curvilinear relation between left coronary artery size and left ventricular muscle mass (r = 0.76) or cross-sectional muscle area (r = 0.75). However, normalization of coronary cross-sectional area for left ventricular muscle mass or muscle area shows insufficient enlargement of the coronary arteries in both primary and secondary hypertrophy.Conclusions. 1) Coronary artery size increases as left ventricular mass increases in both primary and secondary hypertrophy. 2) The enlargement of left coronary cross-sectional area is independent of the cause of the increase in left ventricular mass. 3) The size of the coronary arteries is inappropriate with regard to left ventricular hypertrophy. Thus, the stimulus for growth of the coronary arteries is not influenced by the underlying disease but appears to depend on the degree of left ventricular hypertrophy.

Coronary Artery Dimensions in Primary and Secondary Left Ventricular Hypertrophy

Coronary Artery Dimensions in Primary and Secondary Left Ventricular Hypertrophy

Synthesis and distribution of atrial natriuretic peptide (ANP) in hearts from normal dogs and those with cardiac abnormalities

The cardiac distribution of immunoreactive atrial natriuretic peptide (IR-ANP) and ANP-specific mRNA was studied in 35 normal dogs and 44 dogs with primary and secondary heart abnormalities. According to clinical and pathological findings the dogs were assigned to seven groups: Group 1, normal young dogs (< 12 months); Group 2, normal adult dogs (> 12 months); Group 3, low to moderate hypertrophy; Group 4, severe hypertrophy; Group 5, dilated cardiomyopathy; Group 6, renal failure with secondary left ventricular hypertrophy; and Group 7, other heart abnormalities. In comparison with hearts of normal dogs, the amount of IR-ANP and ANP-specific mRNA was reduced in the atria and increased in the ventricles of dogs with hypertrophy and cardiomyopathy. The immunoreactivity in normal canine atria was far lower than in control rats and hamsters. The pattern of ventricular immunoreactivity was faint and patchy. Only in a few ventricular localizations of three dogs of Group 5 and one dog of Group 6 was there a granular pattern suggesting the presence of secretory granules. A state of intense secretory stimulation in cardiomyopathy was indicated by electron microscopy. Due to its low concentration and localized pattern, however, IR-ANP does not seem to be a reliable marker for the presence of hypertrophic or cardiomyopathic changes in dogs.

Obstructive Left Ventricular Hypertrophy. Reversibility of Outflow Tract Obstruction by Drug Therapy

We report the cases of four patients with secondary left ventricular hypertrophy (three due to hypertension and one to aortic stenosis) in whom Doppler echocardiography showed dynamic left ventricular outflow tract obstruction and marked impairment of diastolic filling. Each patient derived marked symptomatic benefit from treatment with either a beta-blocker (atenolol) or calcium antagonist (verapamil). Repeat Doppler studies in three patients revealed a substantial improvement in systolic and diastolic flow abnormalities. Ventricular outflow tract obstruction should be recognized as occurring in a subgroup of patients with secondary left ventricular hypertrophy, and its presence should be sought by Doppler echocardiography before embarking on therapy. Negatively inotropic or positively lusitropic agents such as beta-blockers and rate-limiting calcium antagonists appear to be logical therapy for this condition.

Quantitative effects of speckle reduction on cross sectional echocardiographic images.

Speckle is prominent on all cross sectional echocardiograms. In order to assess its effects on image quantification, frames from a sector scanner with a six bit grey scale were stored and processed off line to identify and smooth the speckle by means of an adaptive filter based on fully developed speckle. In 14 controls, 12 patients with hypertrophic cardiomyopathy, and 12 with secondary left ventricular hypertrophy, filtering significantly reduced the standard deviation of echo intensity, which was used as a measure of the scatter of pixel amplitude, in all three groups (by 52%, 46%, and 46% respectively). The mean value of back-scattered echo intensity itself, however, was reduced by only 7%, 5%, and 8% respectively, and median values were not affected at all. Mean (SD) left ventricular cavity areas on the apical four chamber view were significantly increased from 26 (15) to 30 (17) cm2. The valve dimensions in the parasternal minor axis in 10 patients with mitral stenosis were significantly increased by 11% laterally, but were unaffected anteroposteriorly. Subjective image quality was appreciably modified: endocardial boundaries in apical views were enhanced and the septal "ground glass" appearance was lost in hypertrophic cardiomyopathy. Speckle reduction therefore greatly reduced the scatter of pixel values, with little effect on the mean regional back scattered echo amplitude. It also modified the perceived image texture. Improved boundary definition consistently increased the area estimates, particularly when these depended on lateral rather than range resolution.

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.

Pathophysiology of the hypertrophied heart in man.

Increase in sympathetic drive, the Frank-Starling effect and myocardial hypertrophy represent the three compensatory mechanisms in chronic mechanical overloading of the heart. Chronic pressure overload is associated with concentric and chronic volume overload with eccentric hypertrophy. The changes in ventricular geometry have an important influence on the ejection dynamics of the heart; the magnitude of fiber shortening is the predominant mechanism for systolic reduction of cavity size in eccentric hypertrophy whereas in concentric hypertrophy the contribution of systolic wall thickening to ejection becomes very important. The main abnormality of diastolic function in patients with left ventricular (LV) hypertrophy is the increase of chamber stiffness indicated by the steepened slope of the diastolic pressure-volume relationship. In contrast LV diastolic myocardial stiffness as evaluated from the stress-strain relationship remains relatively unaltered in hypertrophy unless there is massive admixture of fibrosis in the LV wall (congestive cardiomyopathy). Finally LV relaxation (rate of pressure decay) is often impaired in hypertrophied states although the relationship of abnormalities of relaxation to alterations of systolic function remains to be established. There has been considerable debate whether in secondary LV hypertrophy from chronic pressure or volume overload myocardial contractility is normal or depressed. We have recently shown that in patients with myocardial hypertrophy from aortic stenosis ejection phase indexes of contractility are correlated inversely to peak systolic wall stress and that this relationship is modulated according to the actual inotropic state. The patients on the downward shifted curve (depressed contractile state) had a significantly increased LV angiographic mass. Thus advanced LV hypertrophy in chronic pressure overload appears to be associated with compromised contractile state. The structural and metabolic abnormalities which may be ultimately responsible for the depression of contractility of the hypertrophied human myocardium encompass the following findings: reduced intracellular volume fraction of myofibrils; massive increase of the average fiber diameter and increased variability of the thickness of the individual fibers and reduced activity of the myofibrillar ATPase.

Echocardiographic features of secondary left ventricular hypertrophy.

Echocardiographic features of secondary left ventricular hypertrophy.