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Biomedical subjects

B Schwartzkopff

Publications and source records attributed to B Schwartzkopff.

At least 73 records · Page 4Linked to original sources
PubMed1992

Prediction of the site and severity of obstruction in hypertrophic cardiomyopathy by color flow mapping and continuous wave Doppler echocardiography.

OBJECTIVE: We investigated whether the site and severity of an obstruction in hypertrophic cardiomyopathy can be accurately predicted by the combined use of color-coded and continuous wave Doppler echocardiography. BACKGROUND: Predicting the site of obstruction by end-systolic cavity shape is not reliable. Therefore, hemodynamic localization of the obstruction is required before surgery is performed. Such localization should be possible with color flow imaging, which provides two-dimensional velocity mapping reflecting the distribution of pressures within the left ventricle. Discrepancies in assessment of the pressure gradient by Doppler echocardiography and cardiac catheterization (which are usually not performed simultaneously) may be due to spontaneous variation of the dynamic obstruction in addition to technical factors related to both methods. METHODS: Twenty consecutive patients with hypertrophic cardiomyopathy were examined 1 day before transseptal left heart catheterization. The obstruction site was defined by color flow mapping. The pressure gradient was determined by continuous wave Doppler echocardiography. Measurements were also performed simultaneously in 10 patients during cardiac catheterization. RESULTS: Midventricular obstruction was correctly identified in 4 patients and subvalvular obstruction in 15 patients. One patient had no obstruction at rest. Invasively and noninvasively determined pressure gradients correlated well (r = 0.89, SEE = 16.3 mm Hg). Multiple single-beat analysis in 10 patients, also simultaneously examined with Doppler echocardiography and catheterization, yielded an excellent correlation (r = 0.97, SEE = 13.1 mm Hg). Comparing the simultaneous (r = 0.96, SEE = 12.5 mm Hg) and nonsimultaneous (r = 0.81, SEE = 23.8 mm Hg) recordings in these patients, we found that the spontaneous variation of the dynamic obstruction mainly accounted for discrepancies (p less than 0.05). CONCLUSION: The combined use of color-coded and continuous wave Doppler echocardiography provides the relevant hemodynamic information required for decision-making in patients with hypertrophic cardiomyopathy who are considered for transaortic myectomy.

Adult↗
PubMed1992

Morphometric investigation of human myocardium in arterial hypertension and valvular aortic stenosis.

UNLABELLED: Both arterial hypertension and aortic stenosis lead to pressure overload of the left ventricle. As intramyocardial vasculature is confronted with pressure overload in hypertension but not in aortic stenosis, structural differences are to be expected in both forms of left ventricular hypertrophy. With the aid of morphometry, we investigated human myocardium from autopsied hearts from six patients with arterial hypertension and 10 controls, as well as myectomy specimens from cardiac surgery from 14 patients with aortic stenosis. Mean left ventricular myocytic diameter was significantly (P less than 0.05) increased compared with controls (12.4 +/- 1.5 microns) during hypertension (+27%) as well as aortic stenosis (+65%) (P less than 0.05). This was combined with a greater volume density of perimyocytic fibrosis (controls = 0.8 +/- 0.4 V upsilon %) during hypertension (+250%) and aortic stenosis (+587%) (P less than 0.05). Walls of intramyocardial arterioles (external diameter 20-40 and 40-80 microns) were thickened to 32% and 44% (P less than 0.05) during hypertension, but not during aortic stenosis. Compared with controls, perivascular fibrosis of these arterioles was increased by +215% and 61% (P less than 0.05), respectively, during hypertension, but not during aortic stenosis. CONCLUSIONS: Myocytic hypertrophy and increased perimyocytic fibrosis accompany intraventricular pressure overload (hypertension and aortic stenosis) in human hearts. Myocardial structure as a result of arterial hypertension, but not aortic stenosis, is also characterized by intramyocardial arteriole wall-thickening and increased perivascular fibrosis. Thus, distinct structural reaction patterns are noted in the cardiac hypertrophy associated with hypertension and aortic stenosis.

Aged↗
PubMed1992

Right ventricular performance in arterial hypertension.

To investigate right ventricular function, 24 patients with arterial hypertension and five normotensive controls underwent equilibrium radionuclide ventriculography with simultaneous right heart catheterization. In normal subjects, left ventricular ejection fraction was 57 +/- 2% at rest and 71 +/- 5% on effort, and right ventricular ejection fraction (RVEF) averaged 51 +/- 5% at rest and 65 +/- 2% during exercise. Pulmonary vessel resistance (PVR) was 56 +/- 37 dyn.s.cm-5 at rest and 46 +/- 10 dyn.s.cm-5 on effort. Hypertensive patients were divided into three groups according to their left ventricular function: group 1 (n = 10) had normal left ventricular ejection fraction (LVEF) at rest and on effort (57 +/- 9%; 65 +/- 6%), in this group, right ventricular systolic reserve was reduced (RVEF 52 +/- 7% at rest, ns; RVEF 57 +/- 7% on effort, P less than 0.01 compared to controls). Pulmonary vessel resistance during exercise averaged 78 +/- 24 dyn.s.cm-5, which was significantly higher compared to controls (P less than 0.01). In group 2, left ventricular contractions were normal at rest (60 +/- 6%, ns) but deteriorated during exercise to 56 +/- 8% (P less than 0.001, compared to controls). These patients also showed a lack of right ventricular augmentation at ejection fraction (54 +/- 8% at rest, ns; 56 +/- 8% under exercise, P less than 0.05). PVR was significantly enhanced during exercise (88 +/- 40 dyn.s.cm-5, P less than 0.05 compared to controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Morphometric investigation of intramyocardial arterioles in right septal endomyocardial biopsy of patients with arterial hypertension and left ventricular hypertrophy.

A reduced maximal coronary vasodilatator capacity is reported in patients with hypertensive heart disease, suggesting structural abnormalities of intramyocardial arterioles. Right septal endomyocardial catheter biopsies (EMCB) of 30 patients with arterial hypertension and of 10 heart donors were investigated morphometrically. In hypertension, the mean external diameter (21.9 +/- 3.0 vs. 17.4 +/- 2.9 microns, p less than or equal to 0.01) of arterioles and the mean arterial wall area (284 +/- 80 vs. 167 +/- 69 microns2, p less than or equal to 0.05) were increased as compared with heart donors. Perivascular fibrosis was markedly increased (260 +/- 183 vs. 41 +/- 30 microns2, p less than or equal to 0.05) as well as volume density of fibrosis (3.0 +/- 1.7 vs. 0.9 +/- 0.8 Vv%, p less than or equal to 0.01) in hypertensive heart disease. There was no significant correlation between echocardiographically determined left ventricular mass index (115 +/- 25 g/m2 for men and 104 +/- 12 g/m2 for women) and mean arteriolar wall area (r = +0.17) or volume density of fibrosis (r = +0.2) in hypertensive heart disease. Our investigations show that in patients with arterial hypertension there is a thickening of intramyocardial arteriolar walls and an increase in fibrosis. Intramyocardial vascular alterations seem to manifest in hypertension independent from left ventricular hypertrophy.

Aged↗
PubMed1992

[Dysplastic intramyocardial arteries with subaortic septum in patients with hypertrophic obstructive cardiomyopathy].

Abnormal, dysplastic intramyocardial arteries were reported in autopsied hearts of hypertrophic cardiomyopathy. To elucidate their significance, the operatively-excised myectomy specimens of 24 patients with hypertrophic-obstructive cardiomyopathy (HOCM), of 18 patients with valvular aortic stenosis and of 10 postmortem normal hearts were investigated. Eight patients with HOCM had dysplastic intramyocardial arteries (greater than 100 microns external diameter) as well as dysplastic arterioles (less than 100 microns external diameter). The value of the scores for the thickness and fibroelastosis of the media was nearly doubled, the tunica intima was frequently thickened, and the lumen was relatively reduced in dysplastic vessels. Neither in controls nor in aortic stenosis dysplastic arteries were found. Volume density of patchy fibrosis (scars) was increased in patients with dysplastic arterial vessels (HOCM II) (7.2 +/- 4.4 Vv%) (p less than or equal to 0.05) as compared with HOCM without dysplastic vessels (HOCM I) (0.8 +/- 2.3 Vv%), with aortic stenosis (0.9 +/- 1.6 Vv%) or with controls (0 Vv%), Patients with HOCM II were significantly (p less than or equal to 0.05) younger (30 +/- 13 years) than those with HOCM I (53 +/- 12 years), aortic stenosis (56 +/- 12 years), or controls (63 +/- 21 years). The anterior septum was significantly thicker in HOCM II (29 +/- 7 mm) than in HOCM I (22 +/- 4 mm), in aortic stenosis (19 +/- 3 mm), or in controls (12 +/- 2 mm). Syncopes were complained by about 75% (6/8) of patients in HOCM II, by 54% (9/16) in HOCM I, and by 44% (8/18) in aortic stenosis (not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Effect of extent and distribution of left ventricular hypertrophy on clinical aspects and hemodynamics of patients with hypertrophic obstructive cardiomyopathy].

UNLABELLED: The influence of the extent and distribution of the echocardiographically determined left-ventricular hypertrophy was evaluated in respect to clinical symptoms and hemodynamics at rest and under bicycle-exercise. 49 patients with hypertrophic obstructive cardiomyopathy [HOCM] (34 men, 15 women, mean age 43 years, subvalvular gradient after provocation 10-270 mm Hg, ejection fraction greater than 55%) and 10 controls (seven men, three women, mean age 44 years) were investigated. Enddiastolic left-ventricular diameter and basal thickness of the anterior and posterior septum, and the lateral and posterior wall of the left ventricle were echocardiographically measured. The distribution of basal hypertrophy (for the anterior septum and the posterior wall greater than or equal to 15 mm, for the posterior septum and the lateral wall greater than or equal to 17 mm) was classified as type I (1 segment, n = 17), II (2, n = 14) and III (greater than or equal to 3 segments, n = 18), according to Maron et al. (1981). At rest and during symptom-limited bicycle exercise, cardiac index (CI), stroke volume index (SVI), and mean pulmonary capillary wedge pressure (PCWP) were determined at sinus rhythm by a Swan-Ganz-catheter and by the thermodilution method. RESULTS: With increasing hypertrophy, there was a reduction of the left-ventricular enddiastolic diameter. A NYHA-class greater than II was observed in 18% of patients with type-I hypertrophy, in 29% with type II, but in 61% with type III (p less than or equal to 0.05). Of patients with type III, 44% (p less than or equal to 0.05). In type-III hypertrophy the with type I 6% had suffered syncopes; with type II, 14%, and with type III, 44% (p less than or equal to 0.05). In type-III hypertrophy the maximum exercise level (72 +/- 24 Watt) was significantly (p less than 0.05) lower compared with controls (110 +/- 42 W), in type I (99 +/- 35 W), and in type II (100 +/- 45 W). At maximum stress PCWP was significantly increased in types I, II, and III (type I = 22 +/- 8 mm Hg, II = 24 +/- 12 mm Hg, III = 29 +/- 8 mm Hg) compared with controls (8 +/- 4 mm Hg); SVI was significantly lower in type III (49 +/- 13 ml/m2) than in controls (65 +/- 12 ml/m2) and in type I (60 +/- 11 ml/m2); SVI was 60 +/- 17 ml/m2 in type II. At maximum stress, cardiac index was significantly lower in type III (6.2 +/- 2.1 l/min/m2) than in controls (8.9 +/- 2.1 l/min/m2) and in type I (8.4 +/- 1.7 l/min/m2). CONCLUSIONS: In patients with HOCM, severe left-ventricular hypertrophy type III accompanied by a reduced ventricular cavum is associated with more pronounced clinical symptoms, a reduced working capacity and the occurrence of syncopes. In these patients, despite increased filling pressures, the increase in stroke volume and cardiac index are insufficient at stress. Therefore, echocardiographically evaluated left-ventricular hypertrophy and geometry are helpful to estimate the severity of functional disorder in HOCM.

Adult↗
PubMed1991

Ultrastructural abnormalities of mitochondria and deficiency of myocardial cytochrome c oxidase in a patient with ventricular tachycardia.

A 30-year-old woman presented with life-threatening ventricular tachycardia without overt heart disease. Ultrastructural investigation of endomyocardial biopsy disclosed abnormally structured and often enlarged mitochondria. Morphometry revealed the ratio of volume density of mitochondria to myofibrils to be markedly increased to 0.667 as compared with five controls (mean: 0.46; range: 0.445-0.479). Investigation of mitochondrial respiratory chain enzymes revealed a 90% reduction in activity of cytochrome c oxidase. Our data suggest that mitochondrial cardiomyopathy may induce malignant ventricular arrhythmias.

Adult↗
PubMed1991

Coronary circulation in arterial hypertension.

Arterial hypertension is the most common cause of congestive heart failure and an important risk factor in coronary artery disease (CAD). However, even in the absence of CAD, coronary reserve is frequently impaired in hypertensive patients. To study whether the reduced coronary reserve is due to the degree of left ventricular hypertrophy (LVH) or is a consequence of primary vascular alterations, coronary reserve was determined in 31 hypertensive patients (age of 56 +/- 10 years; systolic/diastolic blood pressure of 167 +/- 18/98 +/- 9 mm Hg) with angina pectoris and normal coronary angiogram. Coronary reserve was determined by measuring coronary resistance before and after dipyridamole (0.5 mg/kg of body weight i.v.). Coronary blood flow was measured quantitatively by the gas chromatographic argon method. LV muscle mass was measured by ventriculography. Twelve normotensive patients (age of 52 +/- 8 years) were studied for comparison. Coronary resistance was 20% higher in hypertensive than in normotensive patients, whereas coronary blood flow at rest was not significantly different. The maximal coronary blood flow after dipyridamole was 40% lower in hypertensive than in normotensive patients; accordingly, minimal coronary resistance was significantly increased by 112% in hypertensive patients (p less than 0.0005). Coronary reserve was reduced by 37% (p less than 0.001) in hypertensive patients compared with normotensive patients. Between the impairment in coronary reserve and left ventricular muscle mass, no significant correlation (r = 0.024, n.s.) was found. The impaired coronary vasodilator reserve is reflected by episodes of transient myocardial ischemia during ST-segment monitoring.

Animals↗
PubMed1991

Coronary vascular changes in the progression and regression of hypertensive heart disease.

Coronary hemodynamics (blood flow, coronary reserve, myocardial oxygen consumption) were analyzed in both experimental and clinical hypertension. Significantly reduced coronary reserve was found in hypertensive patients with left ventricular hypertrophy. Medial hypertrophy of small coronary vessels associated with a marked increase in the wall thickness/radius ratio was considered sufficient to explain the impaired coronary flow in hypertensive left ventricular hypertrophy. After long-term pharmacotherapy, there was normalization of both medial hypertrophy and coronary reserve. This small-vessel abnormality correlates well with clinical findings in hypertensive heart disease (angina and electrocardiographic changes despite normal coronary arteriogram). Moreover, this structural adaptation of the small vessels may carry the inherent risk of an impaired oxygen supply to the hypertrophied myocardium. Thus, late cardiac failure of the hypertrophied heart in hypertension may be attributed, in part, to this microcirculation disorder. Conversely, reversal of left ventricular hypertrophy and of hypertrophy of vascular smooth muscle by specific pharmacotherapy can be considered a possible rational approach to the prevention of cardiac failure in hypertensive patients. Controlled clinical trials are needed to confirm these findings with regard to prevention of heart failure, and pharmacotherapeutic studies are necessary to define the optimal drug regimen for reversal of vascular smooth muscle hypertrophy.

Adult↗
PubMed1990

Coronary microangiopathy and cardiac hypertrophy.

Even in the absence of coronary heart disease, coronary vasodilator reserve is frequently impaired in hypertensive patients. To study, whether the reduced coronary reserve is due to the degree of left ventricular hypertrophy or is a consequence of primary vascular alterations, coronary reserve was determined in 54 hypertensive patients with angina pectoris and angiographically normal coronary arteries. Twelve normotensive persons were studied for control purposes. Coronary blood flow was measured quantitatively by the gas chromatographic argon method. Coronary reserve was determined by measuring coronary resistance before and after dipyridamole (0.5 mg (kg body weight)-1 i.v.). Left ventricular muscle mass was determined by ventriculography. In hypertensive patients, minimal coronary resistance was markedly increased by 124% and coronary reserve significantly reduced by about 38% compared with healthy normotensives. Hypertensives and normotensives did not differ with respect to myocardial oxygen consumption per unit weight myocardium (11.9 +/- 2.3 vs 11.4 +/- 2.4 ml O2 100g-1 min, n.s.) and resting coronary flow (92.1 +/- 20.8 vs 91.4 +/- 18.9 ml min-1. 100 g, n.s.). No significant correlation was found between minimal coronary resistance and coronary reserve and left ventricular muscle mass and between coronary reserve and diastolic wall stress. Accordingly, the reduced coronary regulation capacity in hypertensives does not parallel the degree of left ventricular hypertrophy and is not due to an increased myocardial oxygen consumption under resting conditions. Consequently, the impaired coronary reserve in hypertensive patients seems to be the consequence of primary microvascular lesions, which are independent of the process of left ventricular hypertrophy.

Angina Pectoris↗
PubMed1988

Regression of cardiac hypertrophy: morphometric and biochemical studies in rat heart after swimming training.

There is currently little information about the morphological changes of the myocardium accompanying the reversal of cardiac hypertrophy. In this study the hypothesis was tested that myocardial alterations induced by exercise will regress within a short interval after the end of training. Rat hearts were examined using morphometric and biochemical methods at the end of a 9-week period of endurance training and also 7, 10 and 14 days after its termination. At the end of the training period the heart weight had increased by 65% but the weight ratio of the right and left ventricular wall remained unchanged. A decline in the DNA content by 27% as well as a decrease in the volume density of the interstitial space by 14% and in the number of interstitial cell nuclei by 32% against controls, are explained by a 30% increase in the width of myofibres. The capillary density was reduced by 22% but the volume density of capillaries remained nearly constant as a result of widening of the capillary diameter by 27%. The surface density of capillaries was diminished by 10%. Ultrastructurally an increase in the ratio of mitochondrial to myofibrillar volume density was observed in the myocytes of hypertrophied hearts as compared to controls (0.54 and 0.63, respectively). Fourteen days after termination of training, 80% of the increment in heart weight had regressed. At this time the width of the myofibres and the volume density of the interstitial space had nearly normalized, while the capillary to fibre ratio had significantly increased. The ratio of mitochondrial and myofibrillar volume density became nearly normal, and a confluence of intermyofibrillar mitochondria resulted in significantly longer organelles. The increased DNA content 10 days after the training, as compared to controls, is attributable to the genesis of non-myocardial cells during the hypertrophic growth and their persistence during regression. The study has shown that cardiac hypertrophy induced by physical training nearly completely regresses within 14 days after termination of conditioning. The increased capillary to fibre ratio indicates neoformation of transversely oriented capillary branches in hypertrophy which particularly becomes apparent in two-dimensional estimation in the regression period. In comparison with myofibres, regression of capillaries seems to be delayed. The decline of heart weight and a significantly diminished RNA content during the regression of hypertrophy suggest that reduced synthesis is responsible for the decrease in heart weight.

Animals↗
PubMed1988

Ultrastructural findings in endomyocardial biopsy of patients with Kearns-Sayre syndrome.

Kearns-Sayre syndrome is clinically defined by progressive external ophthalmoplegia, atypical retinitis pigmentosa and the potential occurrence of complete atrioventricular (AV) block. Right septal endomyocardial biopsy specimens from nine patients (four men and five women with a mean [+/- SD] [corrected] age of 36.3 +/- 14.4 years) with chronic progressive external ophthalmoplegia and mitochondrial skeletal myopathy were studied. Three patients had atypical retinal pigmentation. An atrioventricular or intraventricular conduction defect was observed in five patients. A pacemaker was prophylactically implanted in one patient because of abnormal conduction distal to the His bundle. Ultrastructural investigations revealed mitochondriosis in many heart muscle cells and an increased variability of mitochondrial form and size in all patients. In seven patients, 0.4 to 2.1% of all examined myocytes contained exclusively abnormal mitochondria. Three main types were observed: huge, mainly round mitochondria with concentric cristae; large, round or oval mitochondria with transverse or curved cristae; and small, vacuolated mitochondria. The volume density of myofibrils was reduced (41.9 +/- 11.1 compared with the normal value of 56.5 +/- 2.5 volume density [in percent], p less than 0.01) in these myocytes. Increasing numbers of vacuolated mitochondria correlated significantly with a reduction of myofibrils (r = -0.64, p less than 0.01). The data suggest that the ventricular myocardium of most patients with complete and even incomplete Kearns-Sayre syndrome is affected by disseminated mitochondrial cytopathy.

Adolescent↗
PubMed1988

[Alcohol and the cardiovascular system].

Because of the high frequency of cardiovascular diseases and a steadily increasing consumption of alcohol the potentially causal relationship between alcohol and cardiovascular diseases gains great interest for public health policy. Alcohol and its metabolites induce a toxic damage of myocardial metabolism with an injury of electromechanic coupling. As a consequence of acute alcoholic intake cardiac arrhythmias and a reduced contractility of the myocardium are found not only for chronic alcoholics but also in healthy non-drinkers. Chronic abuse of alcoholic beverages for many years can be the cause of alcoholic cardiomyopathy in a small percentage of patients, who have a bad prognosis. Atria and ventricles are dilated, light and electron microscopic changes of the myocardium are unspecific. The pathogenesis of alcoholic cardiomyopathy is unknown, modulations of cardiomyocytic membranes are discussed in the course of a toxic damage. In the genesis of atherosclerosis alcohol can approach from different sites: Changings on thrombocytes and an increase of HDL-cholesterin can be protective, however an increase in blood pressure support the process of atherosclerosis. In numerous investigations a smaller degree of atherosclerosis was found for little or moderate alcohol intake, while in chronic heavy abuse of alcohol a higher extent of atherosclerosis was observed. As the amount of alcohol, assumed to be protective against the development of atherosclerosis, is consumed already by the majority of the population, there is no reason to propagate a regulate consume of moderate amount of alcoholic beverages.

Alcoholism↗
PubMed1987

Morphologic criteria of progression and regression of cardiac hypertrophy.

The heart is able to adapt itself to a demanded load by increasing (hypertrophy) or decreasing (regression of hypertrophy) its muscular mass within a wide range. Overstressing of the ability of adaptation is accompanied by degenerative changes of myocytes. Semiquantitative investigations of endomyocardial biopsies (EMCBs) of patients with dilative cardiomyopathy (DCM) and hypertrophic nonobstructive cardiomyopathy (HNCM) show a fibrosis of the interstitial space, as well as almost similar changes of myofibrils and mitochondria. A reduced number of myocytes in hearts with DCM could explain the decreased functional capacity. Quantitative investigations of endomyocardial biopsies and myectomy specimens in patients with hypertrophic obstructive cardiomyopathy have revealed that hypertrophy and, to a certain extent, hyperplasia of muscle fibers cause asymmetrical thickening of the septum. Experimental investigations of the regression of training-induced hypertrophy in rats have shown that nearly all parameters (cardiac weight, thickness of muscle fibers, myofibrillar mass, interstitial space, and capillary width) returned to the values of controls 14 days after termination of a swimming training regimen. A significantly higher density of capillaries after regression of muscle fiber hypertrophy compared to controls points to a temporal dissociation in the regression of myocyte size and capillary network. Decrease in RNA concentration and an increased number of autophagic vacuoles give evidence for decreased anabolism and increased catabolism may occur during regression. In humans, fibrosis of the myocardium and scar formation explain the irreversibility of cardiac hypertrophy, as observed in some patients with valvular heart disease, despite valve replacement.

Adult↗
PubMed1987

Evidence for muscle fiber hyperplasia in the septum of patients with hypertrophic obstructive cardiomyopathy (HOCM). Quantitative examination of endomyocardial biopsies (EMCB) and myectomy specimens.

Asymmetric thickening of the septum is one of the hallmarks of hypertrophic obstructive cardiomyopathy (HOCM). Endomyocardial biopsies (EMCB) from the right side of the septum and myectomy specimens from its left part were morphometrically investigated to determine the size of septal myocytes, as well as the volume density of the interstitium and fibrous tissue, and to estimate the number of transseptal muscle fiber layers. EMCBs of seven patients with normally shaped hearts, taken as controls (N), EMCBs of seven consecutively examined patients with HOCM (HOCM 1), and of seven HOCM patients with additionally available myectomy specimens (HOCM 2) were evaluated. In myectomy specimens muscle fiber thickness and volume density of the interstitium and fibrous tissue were significantly increased, as compared with the findings in the EMCBs. The echocardiographically determined septal thickness was increased by 93% in HOCM 1 and by 150% in HOCM 2 compared with controls; however, the increase in muscle fiber thickness and volume density of the interstitium did not give a sufficient explanation for the increased septal thickness in both groups of HOCM. Based on EMCB data, the estimated number of septal muscle fiber layers was 715 +/- 93 in group N, 1242 +/- 149 in HOCM 1, and 1119 +/- 177 in HOCM 2, while 810 +/- 232 layers were estimated according to the findings from myectomy specimens. Taking into account that EMBC represent only 1 mm of septal thickness, and myectomy specimens up to 15 mm, an increase in the septal muscle cell layers of about 30% can be estimated in HOCM hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗
PubMed1987

Variability and reproducibility of morphologic findings in endomyocardial biopsies of patients with hypertrophic obstructive cardiomyopathy.

Morphometric investigations of endomyocardial catheter biopsies (EMCB) promise to give more insight in the morphologic-functional relationship in patients with hypertrophic obstructive cardiomyopathy (HOCM), and may disclose the morphologic course of the disease. Variability and reproducibility of morphologic findings in EMCB of patients with HOCM are still undefined. We investigated 112 right ventricular biopsies of 25 patients with HOCM of a mean age of 38.3 +/- 15.2 years (six women, 19 men). Mean EMCB size was 0.755 +/- 0.567 mm2. 28.6% of EMCB were not suitable for morphometric investigation. Variability of morphologic findings was investigated by analysis of variance and described by the coefficient of variation (CV). Sampling variabilities of muscle fiber diameter (CV = 5%), volume density of interstitium (CV = 9%) and fibrous tissue (CV = 17%) differed. Reproducibility in terms of intra- and interobserver variations for these variables reached a comparable level, diminishing observed differences between biopsies from the same heart, which became non-significant. Sampling variability of endocardial thickness (CV = 79%) and muscle fiber disarray (CV = 100%) were higher than intra- and interobserver variations. For an estimate of muscle fiber size, one EMCB specimen is sufficient, three for volume density of interstitium and nine for fibrous tissue. High sampling variability of endocardial thickness and muscle fiber disarray demand numerous biopsies; here the greatest measured value from a few biopsies may be of more clinical relevance. From our data, five EMBC are desirable, and give the most information at an acceptable strain.

Adult↗