Ventricular Wall Hypertrophy Research Articles

Fetal cardiovascular hemodynamics in the presence of complete atrioventricular block

OBJECTIVE: Our purpose was to follow serially the hemodynamic adaptation to a congenital complete heart block in a human fetus. STUDY DESIGN: Longitudinal and serial M-mode and Doppler echocardiography over a 10-week span were performed on a fetus affected by complete heart block. Ventricular fractional shortening, size, and flow across the atrioventricular valves and outflow tracts were determined starting at 20 weeks up to the time of delivery. Neonatal Doppler follow-up was performed at 2 days of life after implantation of a temporary pacemaker. RESULTS: The right and left ventricles were able to adapt to sustained bradycardia by increasing their size. This ventricular dilatation was also associated with an increase in fractional shortening, which was associated with ventricular free wall hypertrophy. When ventricular heart rate decreased to 38 beats/min, fractional shortening decreased, this was associated with the rapid onset of ascites and pericardial effusion. CONCLUSION: In the presence of sustained bradycardia ventricular output can increase, because this fetus was able to increase ventricular size and fractional shortening and wall thickness. (AM J OBSTET GYNECOL 1994;170:1258-62.)

Fetal cardiovascular hemodynamics in the presence of complete atrioventricular block

<b>OBJECTIVE</b> Our purpose was to follow serially the hemodynamic adaptation to a congenital complete heart block in a human fetus. <b>STUDY DESIGN:</b> Longitudinal and serial M-mode and Doppler echocardiography over a 10-week span were performed on a fetus affected by complete heart block. Ventricular fractional shortening, size, and flow across the atrioventricular valves and outflow tracts were determined starting at 20 weeks up to the time of delivery. Neonatal Doppler follow-up was performed at 2 days of life after implantation of a temporary pacemaker. <b>RESULTS:</b> The right and left ventricles were able to adapt to sustained bradycardia by increasing their size. This ventricular dilatation was also asspciated with an increase in fractional shortening, which was associated with ventricular free wall hypertrophy. When ventricular heart rate decreased to 38 beats/min, fractional shortening decreased, this was associated with the rapid onset of ascites and pericardial effusion. <b>CONCLUSION:</b> In the presence of sustained bradycardia ventricular output can increase, because this fetus was able to increase ventricular size and fractional shortening and wall thickness.

The effect of recombinant human erythropoietin (r-HuEPO) on left ventricular mass and left ventricular hemodynamics in hemodialysis patients.

The purpose of this study was to examine the effect of recombinant human erythropoietin (r-HuEPO) on left ventricular mass. Twenty-seven hemodialysis patients (13 men and 14 women) were given r-HuEPO for renal anemia. Blood pressure and heart rate were measured before and after the 16-week course of r-HuEPO, and at the same time echocardiography was performed to measure left ventricular dimensions and wall thickness. These measurements were used to calculate left ventricular volume, cardiac output (CO), and left ventricular mass (LVmass). Diastolic blood pressure (DBP) increased after administration of r-HuEPO (from 75.8 +/- 10.8 mmHg to 85.6 +/- 12.7 mmHg), but there was no change in systolic blood pressure (SBP) or heart rate. LVmass increased significantly in seven cases (from 194.7 +/- 40.0 g to 240.3 +/- 47.3 g). These cases, Group I, showed no decline in stroke volume (SV) or CO, and showed significant increases in SBP. In the remaining 20 cases, Group II, LVmass decreased or was unchanged. In this group SV and CO decreased, but there was no increase in SBP. We conclude that increases in LVmass may be associated with elevated systolic blood pressure and hypertrophy of the left ventricular wall, when hemodialysis patients with severe renal anemia are given r-HuEPO.

Left ventricular wall thickness and disease duration in systemic sclerosis.

Myocardial thickness, left ventricular functions, and right heart overloading were investigated in 80 patients with systemic sclerosis by echocardiography. Based on the left ventricular wall thickness, three groups were formed. Fifteen patients with asymmetrical left ventricular wall hypertrophy (Group 1) showed shorter mean disease duration with marked diastolic and mild systolic left ventricular functional impairment. The 25 patients with wall thinning (Group 3) had a slight increase in left ventricular diameters, impaired systolic functions and longer disease duration. Group 2 with wall thickness exhibited mixed changes. Patients with increased wall thickness tended to have a shorter disease duration than patients with wall thinning. Patients with systemic sclerosis showed systolic and diastolic function impairment as compared to the 18 control healthy individuals. Pericardial disease was found in 23 cases (28.7%).

Echocardiographic left ventricular wall thickness: A poor predictor of the severity of aortic valve stenosis

Echocardiographic left ventricular hypertrophy is thought to be helpful in grading the severity of aortic stenosis. This study compared M-mode echocardiographic left ventricular wall dimensions with Gorlin aortic valve area. Good quality echocardiograms were obtained in 294 patients with aortic stenosis who also underwent cardiac catheterization. Patients with grade 3 or 4 aortic regurgitation were excluded. The correlation was calculated between the aortic valve area and the left ventricular wall dimensions. Correlation coefficients were poor; r = 0.13 for the septum, r = 0.15 for the posterior wall, and r = 0.17 for the mean wall dimension. Correlation was not improved significantly if patients with poor left ventricular function or systemic hypertension were excluded. Correlation with other hemodynamic parameters was better, peak left ventricular systolic pressure having r values of 0.36 and 0.30 for posterior wall and septum. Mean and peak aortic valve gradient had r values approaching 0.30 for both dimensions. If the peak gradient was included in multivariate analysis, the wall dimensions then had no predictive power for severity of aortic stenosis. This study demonstrates that the degree of left ventricular wall hypertrophy is not related to the severity of aortic outflow obstruction and therefore cannot be used to grade the severity of aortic stenosis.

Asymmetric Septal Hypertrophy in a 41-Year-old Woman with Noonan’s Syndrome

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.

An autopsy case of hypertrophic cardiomyopathy showing dilated cardiomyopathy-like features by serial ventriculography.

An autopsy case of hypertrophic obstructive cardiomyopathy (HOCM), in which the clinical features of dilated cardiomyopathy (DCM) developed after 10 years is described. Three serial left ventriculograms (LVG) and bi-ventriculograms (BVG) were performed during the 10-year follow-up. At the time of the first observation, the ECG revealed a giant negative T wave (GNT) in V5 (-1.5mV) and high voltage (SV1 + RV5 = 8.1mV). The LVG and BVG showed concentric left ventricular wall hypertrophy and a pressure gradient in the left ventricular out-flow tract. However, follow-up studies disclosed resolution of the GNT with decreased high voltage. All wall thicknesses and the ejection fraction were significantly decreased and the wall motion was reduced serially. These findings were consistent with the clinical profile of DCM. At autopsy, the heart weighed 610 g and showed dilated change of the left ventricular cavity. Significant myocardial fibrosis, bizarre myocardial hypertrophy with disorganization (BMHD) and severe narrowing of the intramural small arteries due to intimal thickening were found in the left ventricular wall, especially in the anterior and interventricular septal wall. This autopsy case suggests that some cases of HCM, with serial disappearance of the deep negative T wave and high voltage, deteriorate to the clinical profile of DCM.

Tetralogy of Fallot: MR findings.

Surgical treatment of patients with tetralogy of Fallot requires accurate definition of all anatomic structures, particularly the central pulmonary arteries. Magnetic resonance (MR) images of 22 patients with tetralogy of Fallot were studied to assess their usefulness in providing information regarding the spectrum of anatomic abnormalities in this condition. MR findings were compared with information obtained at catheterization (in 16 patients) and at surgery (in nine patients), both of which were performed within 3 months of MR imaging. Ventricular chamber enlargement and wall hypertrophy were clearly delineated in most of the 17 patients who were examined before definitive surgical repair, and ventricular septal defects were visualized in all 17. Palliative systemic-to-pulmonary shunts were visualized in 11 patients and could be evaluated for patency. Most important, the morphology and size of the right ventricular outflow tract and central pulmonary arteries could be accurately assessed. Pulmonary artery measurements obtained from MR images demonstrated excellent correlation with angiographic measurements. In six patients examined after complete surgical repair, MR images accurately reflected changes in pulmonary artery outflow tract morphology and complications, such as residual pulmonary artery stenosis and thrombosis. The findings suggest that MR imaging can complement or obviate catheterization in the evaluation of tetralogy of Fallot with regard to suitability for definitive surgical repair.

Echocardiographie Features of Myotonic Dystrophy

Thirty adult patients with myotonic dystrophy from a defined population in northern Sweden were examined by echocardiography. The patients were subdivided into three groups according to the severity of the disease. Abnormal echocardiograms were found in 1 of 7 (14%) patients with mild disease, 7 of 13 (54%) patients with moderate disease, and 6 of 10 (60%) patients with severe disease. Two main types of échocardiographie changes occurred, namely left ventricular dilatation which was found in 6 (20%) of 30 patients and left ventricular wall hypertrophy which was found in 4 (13%) of 30 patients. Half of the patients with dilated left ventricle had coincident impaired left ventricular systolic function measured as ejection fraction. We found no greater prevalence of mitral valve prolapse in this series than would be expected in the normal population. This study shows that there is a myocardial disease associated with myotonic dystrophy which may take two disparate forms, left ventricular dilatation or left ventricular hypertrophy. This myocardial disease seems to be progressive and can be detected by echocardiography in patients with moderate and severe neurological disability.

Left ventricular wall stress and contractile function in transposition of the great arteries after the Rastelli operation

Left ventricular wall stress and contractile function were determined by echocardiographic methods in 11 patients studied 0.7 to 13.8 years (mean +/- standard error of the mean = 5.6 +/- 1.2 years) after undergoing the Rastelli operation for transposition of the great arteries associated with ventricular septal defect and left ventricular outflow tract obstruction. Age at operation ranged from 4.6 to 11.3 years (mean +/- standard error of the mean = 7.4 +/- 0.7 years). Data were compared with data of 24 normal subjects of similar age and heart rate. Left ventricular end-diastolic dimension and end-diastolic volume were significantly higher than normal, averaging 134% +/- 8% of normal dimension (p less than 0.004) and 106 +/- 13 ml/m2 versus a normal volume of 60 +/- 3 ml/m2) (p less than 0.007). In addition left ventricular wall mass was 215 +/- 40 gm/m2 versus a normal value of 72 + 6 gm/m2 (p less than 0.004). Both meridional and circumferential end-systolic and peak systolic stress values were not significantly different between normal subjects and Rastelli patients. Estimates of ventricular pump function including shortening fraction, rate-corrected velocity of circumferential fiber shortening, and ejection fraction were all depressed when compared with normal values. Velocity of fiber shortening, evaluated as a function of end-systolic stress, demonstrated abnormal contractile function in eight of 11 (73%) patients. These data indicate that left ventricular function is usually abnormal and residual left ventricular dilation and wall hypertrophy remain despite successful use of the Rastelli operation for repair in patients with transposition of the great arteries, ventricular septal defect, and left ventricular outflow tract obstruction.

Pharmacodynamic properties of felodipine.

This overview presents the pharmacodynamic properties of felodipine as studied in animal experiments with emphasis on results from our laboratory. Felodipine is 100-fold more potent in causing inhibition of spontaneously active vascular smooth muscle than myocardium in vitro. This vascular selectivity is significantly greater than that of nifedipine (potency ratio 15). Verapamil, D-600, La3+ and reduction of [Ca2+]o lack selectivity. The cellular mechanisms underlying this variable selectivity are not clear at present. In conscious spontaneously hypertensive rats (SHR), the plasma concentration required for 20% reduction of mean arterial pressure is approximately 10 nmol. Mean arterial pressure is lowered dose-dependently as a result of reduced peripheral vascular resistance accompanied by increased cardiac output due to transient tachycardia and increased stroke volume. There was rapid resetting of the baroreflex set point but unaltered sensitivity after felodipine and hydralazine in SHR. Therefore, the reflexogenic increase in heart rate and plasma renin activity subsided within 3 to 5 hours of continuous felodipine administration in SHR. In addition, there was a uniform dilatation of the peripheral vascular beds after felodipine administration. During long term treatment of SHR with felodipine, progression of left ventricular and vascular wall hypertrophy was prevented. Within the 'therapeutic dose range', the only primary effect observed in addition to arterial vasodilation is diuresis/natriuresis caused by a renal tubular action.

Morphological Observations following “Anatomical Correction” for Abnormal Ventriculo-arterial Connection

Seven postmortem hearts from children who underwent anatomical correction for complete transposition (6 cases) and double outlet right ventricle (1 case) were examined in order to gain a better understanding of the pathological morphology in relation to the surgical procedure. Associated malformations were ventricular septal defect in all, patient arterial duct in 4 and aortic coarctation in 3. In all hearts the coronary arteries arose from the facing aortic sinuses and were relocated into the facing sinuses of the pulmonary trunk with minimal displacement. The orifices of the coronary arteries were reduced in caliber in one case. The sinus node artery arising from a lateral atrial artery was transected in one case. The Lecompte maneuver was performed in 4 cases and tension on the pulmonary trunk was observed in 2 cases. Potential right ventricular outflow tract obstruction was evident in all (including one in which it had been resected during surgery). The substrates of obstruction were anomalous parietal insertion of the outlet septum (2 cases), anomalous muscular trabeculation (1 case), rightward displacement of the outlet septum (1 case), parietal insertion of the outlet septum (1 case) and restrictive muscular infundibulum (1 case--DORV). In addition, all the complete transposition cases had hypertrophy of the parietal right ventricular wall. This study highlighted the anatomical features which could lead to poor results in the anatomical correction procedure. Some of the potential problems could be avoided by minor modifications to the technique.

Nuclear magnetic resonance in hypertrophic cardiomyopathy.

The large differences in the spin lattice relaxation times (T1) of blood and myocardium (measured by nuclear magnetic resonance) allow the heart to be visualised without the use of contrast media. The findings using nuclear magnetic resonance in 11 unselected patients with hypertrophic cardiomyopathy were compared with those in equal numbers of normal subjects and patients with electrocardiographic features of left ventricular hypertrophy. In patients with hypertrophic cardiomyopathy characteristic septal hypertrophy was noted together with variable and sometimes pronounced hypertrophy of the left ventricular free wall, which is consistent with the heterogeneous nature of this disease. The mean (SD) ratio of septal to free wall thickness was 1.5(0.8) for patients with hypertrophic cardiomyopathy, 0.8(0.2) for those with left ventricular hypertrophy, and 0.9(0.2) for normal subjects. Although septal measurements by nuclear magnetic resonance were greater than those obtained by echocardiography there was a significant correlation between the two. Septal and free wall area were significantly smaller in normal subjects. There were no differences in septal or free wall T1 values between the three groups. Non-gated nuclear magnetic resonance can detect septal and free wall hypertrophy. With the addition of multiple slice acquisition, rapid estimation of myocardial mass will be possible allowing the potentially important assessment of progression or regression of myocardial hypertrophy.

Microvascular spasm as a cause of cardiomyopathies and the calcium-blocking agent verapamil as potential primary therapy

The origin of cardiomyopathies, a major cause of cardiac disability and death, has been largely unexplained. Pathologic features, common to all cardiomyopathies independent of origin, include ventricular hypertrophy and diffuse scarring with variable amounts of ventricular dilatation. This problem was studied experimentally in 2 models of congestive cardiomyopathy: the hereditary cardiomyopathic Syrian hamster and the hypertensive-diabetic rat. In both the genetic and the acquired disease models, there is focal myocytolytic necrosis followed by healing with focal scars, ventricular wall hypertrophy, ventricular dilatation with congestive heart failure and, ultimately, death. In view of the heterogeneous pathologic features of both diseases, silicone rubber perfusions have been used to study the microcirculation of the heart in these animals; microvascular spasm has been demonstrated early in the disease associated with small areas of myocytolytic necrosis that undergo subsequent fibrosis. Reactive hypertrophy then ensues as a compensatory response to this myocellular necrosis; it is the combination of cell loss and slowly decreasing contractility resulting from the reactive hypertrophy, which culminates in a cardiomyopathy. Administration of verapamil or prazosin to the cardiomyopathic Syrian hamster prevents microvascular spasm and development of cardiomyopathic changes in the myocardium. In view of these and other findings related to the anatomy and hyperreactivity of microcirculation, it is concluded that hypertrophic congestive cardiomyopathies may be caused by focal cell loss due to microvascular spasm and reperfusion injury, with the subsequent development of focal fibrosis and reactive hypertrophy in response to the myocardial necrosis. Myocytes in the cardiomyopathic heart may also be abnormal so that they are unable to tolerate transient focal ischemia without becoming necrotic. A suggestion is made that the ultimate therapy of cardiomyopathies may involve the early treatment of the microvascular spastic lesion in order to prevent further myocardial cell loss. Support of myocardial contractility and treatment of peripheral circulatory defects late in the process of this disease can then only be viewed as largely palliative.

Echocardiographic and Holter findings in 321 uremic patients on maintenance hemodialysis.

Cardiac manifestations in 321 patients on chronic hemodialysis (dialysis duration of from 0.1 to 11.3 years) were examined with non-invasive technique. In contrast to the previous assumption that cardiac dilatation and pericardial effusion are common in patients on chronic hemodialysis, interventricular septal hypertrophy (51.3%) and left ventricular posterior wall hypertrophy (47.1%) on echocardiography and left ventricular hypertrophy (47.0%) on ECG were the most frequent abnormalities in these patients. Although premature beats on routine ECG were found in a limited number of patients (4.7%), ventricular premature beats were recognized in 45.7% and high grade arrhythmias in 27.2% of 92 patients examined with 24-hour Holter ECG monitoring. There were no high grade arrhythmias and the frequency of ventricular premature beats was 19.4% in 31 age-matched healthy subjects studied. Furthermore, the PQ interval was progressively prolonged in relation to the duration of hemodialysis. This finding may suggest that long-term hemodialysis is associated with disturbances of the conduction system. These results indicate that myocardial hypertrophy and high grade arrhythmias are the prominent findings in uremic patients maintained on hemodialysis. We consider that such high grade arrhythmias could be responsible for a high incidence of cardiac death in these patients.

Reversal of left ventricular hypertrophy and improvement of cardiac function in man by nifedipine.

The effects of long-term (mean 3.9 months) pharmacotherapy of hypertensive and normotensive hypertrophy (hypertensive heart disease, hypertrophic non-obstructive cardiomyopathy) as well as of advanced cardiac disease due to coronary artery disease and dilatative cardiomyopathy by large doses of nifedipine (mean 120 mg/day-1) were analyzed with regard to systolic blood pressure, to left ventricular function and to the hypertrophy degree of the ventricle. Nifedipine, in addition to conventional and maintained antihypertensive and cardiac therapy, lowers blood pressure in hypertensive patients, whereas hypotensive effects in the normotensive patients were absent. Nifedipine enhances left ventricular function in all patient groups significantly, i.e. in normotensive hypertrophic non-obstructive cardiomyopathy, in hypertensive heart disease and especially in heart disease due to coronary artery disease and dilatative cardiomyopathy. Significant regression of septal and of global hypertrophy was found in hypertrophic non-obstructive cardiomyopathy and in hypertensive heart disease. These results indicate, that long-term nifedipine treatment may be beneficial for left ventricular function in all patient groups and for hypertrophy regression in established left ventricular hypertrophy due to hypertrophic, non-obstructive cardiomyopathy and due to hypertensive left ventricular hypertrophy. It is concluded that long-term nifedipine treatment improves left ventricular function and leads to regression of established ventricular wall hypertrophy in hypertrophic non-obstructive cardiomyopathy and in hypertensive heart disease.

Anatomical and Physiological Aspects of Cardiovascular Function in Wistar—Kyoto and Spontaneously Hypertensive Rats at Birth

1. The present study was designated to determine whether there are any detectable differences in cardiovascular anatomy or physiology between Wistar-Kyoto (WKY) and spontaneously hypertensive rat (SHR) pups at birth. 2. It was found that mean arterial pressures were significantly higher, heart rates were slightly higher, and heart weight/body weight ratios were higher in SHR. 3. Vascular dimensions were determined in a small sample of those rats, and the data there also indicate hypertrophy to some degree: the ratio of wall thickness/lumen radius was higher in SHR, tangential wall tension and number of cell layers in the media were increased. 4. It is concluded that some of the concomitant features of hypertension, such as left ventricular wall hypertrophy and arterial wall hypertrophy, may be genetically determined to some extent in SHR.

Pulmonary atresia and intact ventricular septum: a revised classification.

The dismal outlook for patients with pulmonary atresia with intact ventricular septum may be related to associated right ventricular hypoplasia. Study of 32 autopsy specimens and 46 angiocardiograms of neonates with this lesion suggested that the cavitary hypoplasia was related to massive hypertrophy of the right ventricular wall. This hypertrophy was sufficient to obliterate the trabecular and/or infundibular portion of the ventricular cavity entirely in one-third of the cases; this observation forms the basis for a revised classification of these hearts. Three autopsies and 14 angiograms of neonates with critical pulmonary stenosis were examined. Hearts with obliterated infundibular and trabecular cavities had thicker walls and smaller tricuspid valves, as estimated angiographically or at autopsy, than those in which the normal three portions of the ventricular cavity were represented.

Effects of renal transplantation on left ventricular size and function.

Thirteen patients with chronic renal failure and uraemia were investigated by echocardiography preoperatively before and after haemodialysis and again after a successful renal transplantation to evaluate the cardiac changes caused by renal transplantation. After renal transplantation, the left ventricular end-diastolic and end-systolic diameters, as well as the cardiac index, decreased, probably because of the decreased left ventricular filling pressure. The left ventricular wall thickness and mass decreased, apparently as a result of the decrease of the left ventricular preload and also of the decrease of the afterload, because the systolic blood pressure decreased. The left atrial diameter decreased in response to the decreased left ventricular preload and wall hypertrophy. The changes in the indices of left ventricular function as a result of haemodialysis appeared to predict the changes seen after renal transplantation. Renal transplantation appears to have a tendency to result in normal left ventricular and left atrial volumes, as well as to lessen left ventricular hypertrophy, without significantly improving left ventricular function.

Hypertrophic cardiomyopathy with unusual locations of left ventricular hypertrophy undetectable by M-mode echocardiography. Identification by wide-angle two-dimensional echocardiography.

Twenty-one patients without evidence of hypertrophy by M-mode echocardiography were studied by wide-angle two-dimensional echocardiography to determine if they had a form of hypertrophic cardiomyopathy that could not be detected by conventional M-mode echocardiography. Each patient was suspected clinically of having hypertrophic cardiomyopathy because of a distinctly abnormal ECG and either a family history of hypertrophic cardiomyopathy or cardiac symptoms. Patients were 5-49 years old (mean 16 years) and 16 of the 21 had no functional limitation. The most common electrocardiographic abnormalities were deep Q waves, T-wave inversion and right ventricular hypertrophy. Using wide-angle two-dimensional echocardiography to reconstruct the geometry of the left ventricular wall, 16 of the 21 patients (76%) were shown to have prominent but unusually located regions of left ventricular wall hypertrophy. In each instance, the hypertrophy involved regions of the left ventricular wall through which the M-mode ultrasound beam does not usually pass, i.e., posterior ventricular septum (seven patients), anterior or lateral left ventricular free wall (seven patients) and ventricular septum near the apex (two patients). There was no echocardiographic or hemodynamic evidence of left ventricular outflow tract obstruction in any patient. Hence, some patients with hypertrophic cardiomyopathy may have substantial hypertrophy present in unusual locations of the left ventricular wall. Although electrocardiographic abnormalities suggested the presence of myocardial disease, conventional M-mode echocardiography (performed from standard parasternal positions) did not reliably identify such sites of hypertrophy, which were limited to regions of the left ventricle not accessible to the M-mode beam. Only wide-angle two-dimensional echocardiography permits definitive identification of these unusually located regions of cardiac hypertrophy and confirmation of the diagnosis of hypertrophic cardiomyopathy.