Mildly dilated congestive cardiomyopathy. Use of prospective diagnostic criteria and description of the clinical course without heart transplantation

Prognosis in classically described dilated congestive cardiomyopathy has been reported to be related to ventricular size. Mildly dilated congestive cardiomyopathy (MDCM) has been defined as end-stage heart failure of unknown etiology (New York Heart Association class IV, left ventricular ejection fraction less than 30%), occurring with neither typical hemodynamic signs of restrictive myopathy nor significant ventricular dilatation (less than 15% above normal range). The present study includes follow-up in 12 nontransplant patients. In the first 4 months after diagnosis, two patients improved and are living, and two showed cardiac dilation and clinical deterioration and died. Six of the remaining eight with persistent MDCM died (four with intractable heart failure and two, sudden deaths) without change in ventricular size before death, despite medical therapy over 20 +/- 8 months. Eight comparable transplanted patients with persistent MDCM demonstrated improved total survival by life table analysis (p less than 0.05). A family history of congestive cardiomyopathy was found in nine of 16 patients (56%) with persistent MDCM. Nontransplant patients were older (p less than 0.02), but other findings were similar in the two groups. Endomyocardial biopsies available in 14 of 16 cases showed little or no myofibrillar loss in spite of severe hemodynamic impairment. The degree of myofibrillar loss did not correlate with hemodynamic parameters but showed good correlation with left ventricular size, that is, five of six patients with no myofibrillar loss had normal ventricular size, whereas all eight patients with mild myofibrillar loss had mild cardiomegaly (p less than 0.002). Our current experience suggests a somewhat variable but negative prognosis after prospective diagnosis of MDCM, with poor survival in patients with persistence of the original diagnostic features during follow-up. Preservation of heart size in MDCM is probably related to lack of significant myofibrillar loss. Thus, irrespective of heart size or myofibrillar preservation on biopsy, heart transplantation should be strongly considered in MDCM if signs of severe cardiac dysfunction persist despite therapy.     

Long-term prognosis of patients with mildly dilated cardiomyopathy.

The long-term prognosis of patients with mildly dilated cardiomyopathy (MDCM) was investigated in 21 patients. MDCM was defined as left ventricular ejection fraction < or = 40% and left ventricular end-diastolic volume < or = 120 ml/m2 by left ventriculography. During a follow-up period of 6.8+/-3.7 years, there were 9 cardiac events (5 heart failure deaths, 2 sudden deaths, and 2 re-hospitalizations for heart failure). Only in the patients without cardiac events was there a significant decrease in left ventricular size (end-diastolic dimension decreased from 58+/-6 mm to 50+/-8 mm, p<0.001) and an improvement in systolic function (fractional shortening increased from 17+/-5% to 26+/-11%, p=0.007). However, left atrial dilation was observed in the patients with an event (from 39+/-5 mm to 43+/-5 mm, p=0.02). Based on proportional hazard analysis, left ventricular end-diastolic pressure and mean pulmonary artery pressure at diagnosis and left atrial dimension at the time of follow-up were significant predictors of poor outcome. A subset of patients with MDCM has impaired hemodynamics at diagnosis, left atrial dilation at follow-up and a poor prognosis, and must be followed carefully even if the left ventricular dilatation is mild.     

Clinical characteristics of cardiomyopathy with mild dilatation

The clinical features of 20 patients with mildly dilated cardiomyopathy (MDCM) were investigated by electrocardiography and echocardiography. MDCM was defined as conditions with: 1) left ventricular end-diastolic dimension between 55 and 65 mm and 2) left ventricular fractional shortening between 10 and 25%. Nine patients (45%) had no histories of congestive heart failure. Eight patients had atrial fibrillation, and the other 12 patients were in regular sinus rhythm. Two patients had supraventricular premature contractions and five patients had ventricular premature contractions. One patient had paroxysmal atrial tachycardia. During the 40-months' span of this echocardiographic study, left ventricular end-diastolic dimension (60.8 +/- 3.8 mm to 57.3 +/- 4.6 mm) and left ventricular fractional shortening (17.2 +/- 4.6% to 22.7 +/- 7.1%) did not change significantly. One patient died suddenly. These results suggest that 1) some patients with MDCM have neither definite histories nor symptoms to suggest heart failure; 2) the hemodynamic conditions of patients with MDCM do not always deteriorate, but rather stabilize, and even improve during follow-up periods; 3) several types of arrhythmias can be observed, even in standard resting electrocardiograms; and 4) patients with MDCM may die suddenly.     

Evolution to dilated cardiomyopathy from acute eosinophilic pancarditis in Churg-Strauss syndrome

Summary We describe the clinical manifestations of a patient with Churg-Strauss syndrome who presented with severe acute cardiac involvement and whose disease evolved to dilated cardiomyopathy (DCM), with special reference to the histopathological findings. Endomyocardial biopsies, conducted sequentially, three times within 10 months, revealed severe eosinophilic endomyocarditis in the acute phase, interstitial fibrosis in the subacute phase, and endocardial thickening with mural thrombi, at 10 months. Although acute inflammation associated with elevation of eosinophil granule proteins subsided with steroid therapy, left ventricular dilatation with reduced contractility progressed. A subgroup of DCM is not considered to be idiopathic but, rather, an aftereffect of hypereosinophilic heart disease.     

Pathogenesis of dilated cardiomyopathy: a study based on comparison of the clinical features with other related conditions

To investigate the pathogenesis and pathophysiology of dilated cardiomyopathy (DCM), we studied 28 patients with DCM by echocardiography and endomyocardial biopsy, and compared their findings with those of 34 patients including eight with myocarditis, seven with alcoholics, 12 with hypertensives and seven patients with hypertrophic cardiomyopathy. All 12 patients in the hypertensive group had congestive heart failure without accompanying high blood pressure, and prominent dilatation and uniform wall motion abnormality of the left ventricle observed echocardiographically on admission. After medical management, both heart failure and the echocardiographic abnormalities gradually resolved. Those in the alcoholic group had larger left ventricles and uniform wall motion abnormality compared to those in the other groups. The myocarditis and hypertrophic cardiomyopathy groups had smaller left ventricles, non-uniform wall motion and larger % myocardial fibrosis. Both ventricles in the hypertrophic cardiomyopathy group were thicker than those of the other three groups. Each patient with DCM had individual echocardiographic abnormalities, which could be categorized as two subsets depending on the degree of left ventricular dilatation and uniformity of the wall motion. The one was characterized by a prominently dilated left ventricle and uniform wall motion abnormality similar to the alcoholic group, and the other had less marked left ventricular dilatation and heterogeneous wall motion abnormality similar to the myocarditis group. From these findings, it was suggested that there are common factors to specific myocardial disease in the pathogenesis and pathophysiology of DCM, and thus, DCM might include many subsets of different etiologies.     

Possibilities of two-dimensional echocardiography in cardiomyopathies

Findings in 20 patients with congestive, in 14 with hypertrophic and in one with restrictive cardiomyopathy are described. In congestive cardiomyopathy, there predominated left ventricular dilatation and diffuse hypokinesis with decreased ejection fraction. The main criteria are reported for differentiating it from advanced diffuse ischaemic heart disease. More detailed characterization is presented of the type of asymmetric septal hypertrophy and of the systolic anterior motion of the mitral apparatus and the possible causes of this finding are discussed. In a patient with restrictive cardiomyopathy there predominated a symmetric thickening of the left ventricle, with diffusely decreased kinetics and increased density of all structures.     

Echocardiographic findings in myocarditis

This study analyzes morphologic and functional alterations detected by M-mode and 2-dimensional echocardiography in 41 patients with histologically proven myocarditis and different clinical presentations: congestive heart failure (63%), atrioventricular block (17%), chest pain (15%) and supraventricular arrhythmias (5%). Left ventricular dysfunction was common (69%), particularly in patients with congestive heart failure (88%), often without or with minor cavity dilatation. Patients with atrioventricular block or chest pain had usually preserved ventricular function. Right ventricular dysfunction was present in 23%. Additional findings included asynergic ventricular areas (64%), left ventricular "hypertrophy" sometimes reversible (20%), hyperrefractile myocardial areas (23%), ventricular thrombi (15%) and "restrictive" ventricular filling (7%). It is concluded that echocardiographic features of myocarditis are polymorphous and nonspecific. The echocardiographic pattern can simulate alternatively dilated, hypertrophic, restrictive or "right" ventricular cardiomyopathy, as well as coronary artery disease. In an appropriate clinical context, echocardiography can be helpful in the diagnosis of myocarditis and in the selection of patients for endomyocardial biopsy.     

Hypertrophic cardiomyopathy with left ventricular dilatation

There is increasing interest in the notion that some patients with hypertrophic cardiomyopathy (HCM) progress to morphological and functional manifestations similar to those of dilated cardiomyopathy (DCM). From 165 consecutive patients with HCM, 20 patients with left ventricular dilatation (left ventricular end-diastolic diameter greater than or equal to 50 mm) were selected and designated as dilated HCM. The diagnosis of HCM was established in these patients either by detection of the classical form of HCM in family members, with 2-dimensional echocardiographic evidence of asymmetric septal hypertrophy (ASH; septal thickness greater than or equal to 15 mm and a ratio of septal to posterior wall thickness greater than or equal to 1.3); or by demonstrating myocardial fiber disarray in autopsy or biopsy samples. The clinical manifestations of these patients with dilated HCM were then compared with those of other forms of HCM without left ventricular dilatation; 1) 40 patients with hypertrophic obstructive cardiomyopathy (HOCM) who had resting intraventricular pressure gradients of 20 mmHg or more, 2) 80 patients with non-obstructive HCM, each of whom had ASH of the entire ventricular septum (typical ASH), and 3) 25 non-obstructive patients whose hypertrophy was localized to the apical region of the ventricular septum (apical ASH). Patients having apical hypertrophy with a spade-like configuration on the left ventriculogram were excluded from the study. Compared with HOCM and typical ASH groups, the patients with dilated HCM had family histories of significantly more frequent HCM and less frequent hypertension. The patients with dilated HCM also had significantly less fractional shortening (FS), decreased interventricular septal thickness, greater left ventricular end-diastolic pressure (LVEDP), and left ventricular dilatation. During the follow-up period (average: 3.5 years), seven patients (35%) with dilated HCM died; five from congestive heart failure (CHF), one suddenly, and one three days following mitral valve replacement. The other five patients had CHF at the time of their follow-up examination. The patients with apical ASH had clinical features similar to those of dilated HCM; a higher familial frequency, less marked septal hypertrophy, and higher LVEDP. They tended to develop left ventricular dilatation, associated with reduced fractional shortening, although left ventricular diameter at end-diastole did not exceed 50 mm. These findings suggested that dilated HCM is not a rare condition. It is observed in 12% of consecutive patients with HCM.(ABSTRACT TRUNCATED AT 400 WORDS)     

Cyclic changes in pulmonary wedge v waves in dilated cardiomyopathy

Right and left cardiac catheterization was performed in a 29-year-oldmale with dilated cardiomyopathy. During the procedure, prominentv waves appeared spontaneously in the pulmonary capillary wedgepressure recording with a simultaneous decrease in left ventricularsystolic pressure. Left ventricular angiography showed moderateto severe mitral regurgitation and an ejection fraction of 22%.The right ventricular endomyocardial biopsy revealed histologicalfindings consistent with dilated cardiomyopathy. Cardiac catheterization was repeated 9 months later, after aperiod of clinical improvement and a reduction in the rightand left ventricular filling pressures was documented. The cyclicswings in the pulmonary capillary wedge pressure and in theleft ventricular systolic pressure were not observed. Left ventriculographyshowed mild mitral regurgitation with an ejection fraction of37%. Right ventricular endomyocardial biopsy documented a reductionin myofibrillar and nuclear hypertrophy. Thus, cyclic changesin pulmonary wedge v waves may be observed in dilated cardiomyopathy.This finding is consistent with cyclic variations in the degreeof mitral regurgitation. Disappearance of this factor seemsto be related to improvement in left ventricular contractility.     

MR-tomography of the heart in cardiomegaly caused by dilated cardiomyopathy and ischemic heart disease]

The paper deals with the results of magnetic resonance cardiac tomography in 19 patients with dilated cardiomyopathy and 10 patients with coronary heart disease who had severe cardiomegaly and congestive heart failure symptoms. Magnetic resonance tomography showed that the patients with dilated cardiomyopathy exhibited profound dilatation of all the 4 cardiac cavities and a chaotic pattern of impaired segmental left ventricular contractility, whereas those with coronary heart disease had predominant dilatation of the left cavity and local myocardial dysfunctions. Magnetic resonance may be one of the non-invasive tools which make the genesis of cardiomegaly clear in patients with heart failure.     

Clinico-pathological evaluation of restrictive cardiomyopathy (endomyocardial fibrosis and idiopathic restrictive cardiomyopathy) in India

BACKGROUND: Restrictive heart disease is characterized by impairment of ventricular filling during diastole with preserved systolic function. The clinical and histopathological profile on endomyocardial biopsy of a cohort of patients with restrictive cardiomyopathy (RCM) is presented. METHODOLOGY: The medical records of patients presenting with heart failure with systemic congestion, subsequently diagnosed as restrictive heart disease after evaluation including cardiac catheterisation, were studied retrospectively to determine the clinical spectrum of restrictive cardiomyopathy. The diagnosis of RCM was made, based on systemic congestion with dilated atria and near normal ventricular size and function. Only patients who had an endomyocardial biopsy were included in the study. Patients with chronic constrictive pericarditis and secondary restrictive heart disease mainly amyloidosis were excluded from the study. RESULTS: All 52 patients had heart failure with normal or near normal left ventricular size and function. Based on right and left ventricle angiography, patients were classified into two groups. Group I with findings suggestive of EMF (n=30) and Group II no evidence of EMF on angiography i.e. 'idiopathic RCM' (IRCM) (n=22). Baseline characteristics were similar in the two groups. Echocardiography revealed typical features of endomyocardial fibrosis in Group I patients, with apical obliteration of right and left ventricular apices. Group II patients had no apex obliteration (except in four patients, who were misclassified and in whom angiography did not show apex obliteration). The Group II patients had features of IRCM in the form of normal left and right ventricular size and function with restrictive features of doppler filling along with dilated left and right atria. Angiocardiography in EMF patients showed isolated RV involvement in only two patients. In the remaining 28 patients, the obliterative changes were biventricular with RV involvement more severe than LV involvement. Angiographic findings in Group II (IRCM) patients were unremarkable with preservation of normal trabecular pattern and absence of obliterative changes. Mild atrioventricular regurgitation was present in 10/22 patients. Histopathological examination revealed that endocardial thickening was more common (77% vs. 23%) in EMF patients. The presence of myocyte hypertrophy (70-80%), myocytolysis (40-50%) and interstitial fibrosis (46-56%) were similar in both groups. CONCLUSIONS: The majority of our patients had biventricular EMF. A significant number of patients had clinical hemodynamic features of restrictive heart disease but no evidence of EMF on angiography. These IRCM patients had similar clinical profiles to EMF but on endomyocardial biopsy the endocardial thickening was minimal and seen in few patients (5/22).     

Familial cardiomyopathy with different clinical features in individual members

The mother and three children of a family whose parents were consanguineous, each had cardiomyopathy with various patterns of hypertrophy and dilatation. All members had asymmetrical septal hypertrophy (ASH), and three of them were characterized as hypertrophic cardiomyopathy (HCM). Another one had ventricular dilatation mimicking dilated cardiomyopathy (DCM). Case 1: The 57-year-old mother had a typical ASH pattern; her septal/posterior wall thickness ratio (IVST/LVPWT) was 2.5. Case 2: The 37-year-old daughter had basal septal hypertrophy. Case 3: The 32-year-old elder son had typical concentric hypertrophy. Case 4: The 30-year-old younger son had an episode of congestive heart failure, and showed DCM-like features with considerable dilatation and impaired wall motion of the left ventricle. The hypertrophic pattern in cardiomyopathies is thought to depend partially on the ages of the onset, or its evolution with aging.     

Relation between myocardial contractility,hypertrophy and pump performance in patients with chronic aortic regurgitation: an echocardiographic study

The aim of this study was to establish prognostic indices and to detect irreversible left ventricular dysfunction before aortic valve replacement in patients with chronic aortic regurgitation. Therefore, we determined the left ventricular pump/contractility relation (expressed as a ratio between ejection fraction and peak systolic pressure/end-systolic volume), afterload mismatch (the relation between the ejection fraction and mean systolic wall stress) and the left ventricular end-diastolic radius/posterior wall thickness ratio in 52 patients with chronic aortic regurgitation by means of M-mode echocardiography. These indices were also calculated in 14 patients with idiopathic dilated cardiomyopathy and in 20 normal controls. The indices allowed separation of normals and patients with mild to moderate aortic insufficiency from patients with idiopathic dilated cardiomyopathy indicating that these indices could distinguish between patients with a reversible afterload mismatch and those with irreversible impaired muscle function. The 38 patients with severe aortic insufficiency showed a large overlap between normal and abnormal indices. Twelve of these patients had a pump/contractility index and a ratio between ejection fraction and wall stress similar to that found in patients with idiopathic dilated cardiomyopathy. All these patients, however, had a left ventricular end-diastolic radius/thickness ratio > 4 indicating “inadequate hypertrophy”. Of these, 3 patients died perioperatively and 4 developed congestive heart failure within 12 months postoperatively.We conclude that an end-diastolic radius/thickness ratio > 4 is a sensitive but not a specific preoperative indicator of irreversible left ventricular damage in patients with chronic aortic regurgitation. This index is readily obtained preoperatively by M-mode echocardiography.     

Structure and function of contractile proteins in human dilated cardiomyopathy

The pathogenesis of reduced systolic left ventricular function in dilated cardiomyopathy is yet unclear. To analyze a possible involvement of contractile protein, function and structure of left ventricular myofibrils were examined in hearts of patients with advanced cardiomyopathy undergoing heart transplantation and in normal control hearts (from renal transplant donors). Myosin and actin content of the left ventricular myocardium was slightly reduced in cardiomyopathic hearts. Myofibrillar polypeptide composition was determined using two-dimensional electrophoresis and immunoblotting. No differences in constituting polypeptides were apparent, including Z-line proteins and proteins of the endosarcomeric lattice. M-line-bound creatine kinase was identical in both groups. Further, basal and maximal myofibrillar adenosine triphosphatase (ATPase) activities were unaltered in dilated cardiomyopathy. The structure of purified myosin was identical in both groups by the following criteria: electrophoretic mobility of native myosin, identical pattern of light chains after isoelectric focusing, identical cleavage peptides of myosin's heavy chain, and identical patterns after immunoblotting of heavy chain cleavage peptides using polyclonal antibodies generated against myosin from normal and cardiomyopathic ventricles. Ca2+-activated, K+-EDTA-activated and actin-activated myosin ATPase activities were identical in control and cardiomyopathic hearts. A structural alteration or functional defect of myofibrils does not seem to be primarily involved in the pathogenesis of reduced myocardial contractility in dilated cardiomyopathy.     

Functional differentiation of various types of cardiomyopathies by echocardiography.

Echocardiography was used to compare the left ventricular function in 35 cases of congestive cardiomyopathy (COCM), 16 cases of obstructive and 28 cases of non-obstructive asymmetric septal hypertrophy, 43 cases of scleroderma heart disease, 21 cases of ischaemic cardiomyopathy (ICM), 2 cases of restrictive cardiomyopathy, and one case of cardiac amyloidosis. COCM was characterized by left ventricular dilatation, decreased contractility and signs of elevated end-diastolic pressure. In asymmetric septal hypertrophy there was a decreased distensibility of the obstructed left ventricle, both in early and end-diastole, but the pump function remained normal. In scleroderma and amyloid heart disease both the contractility and distensibility of the small, stiff heart were reduced. In restrictive cardiomyopathy the only abnormality was the impaired end-diastolic distensibility. Reduced contractility confined primarily to the interventricular septum and impaired early diastolic distensibility are the characteristic features distinguishing ischaemic cardiomyopathy from COCM. However, echocardiography is not suitable for individual differentiation of ICM and COCM. The COCM can be differentiated from left ventricular aneurysm by M-mode sector scanning technique.     

Mechanism of Mitral Regurgitation in Dilated Cardiomyopathy

Dilated cardiomyopathy is a condition characterized by chamber dilatation and impaired systolic function, resulting in the clinical manifestations of congestive heart failure. Mitral regurgitation occurs with varying frequency in dilated cardiomyopathy, and its detection depends on the diagnostic modality utilized. The presence of mitral regurgitation imposes an additional burden on the failing ventricle, and appears to be an independent prognostic indicator of mortality. The mechanism of mitral regurgitation in dilated cardiomyopathy is complex, controversial, and incompletely understood. The mitral apparatus consists of the left atrial wall, mitral annulus, mitral leaflets, chordae tendineae, papillary muscles, and left ventricular wall, and each of these components and the intimate interrelationship between these structures may contribute to the development of mitral regurgitation. Left atrial enlargement, reduced left atrial contractility, mitral leaflet retraction, abnormal vector of chordal tendineae pull, papillary muscle dysfunction (either asynergic contraction or malalignment), mitral annular dilatation, and changes in the size, shape, and function of the left ventricle have been suggested as possible mechanisms for the development of mitral regurgitation in dilated cardiomyopathy. The primary event in the development of mitral regurgitation appears to be left ventricular dilatation and dysfunction. Controversy persists as to whether the associated mechanism is annular dilatation, papillary muscle or free left ventricular wall dysfunction, or a combination of all, but recent echo-Doppler studies reviewed in this article support the notion that annular dilatation is the predominant mechanism. Improved understanding of the mechanism of mitral regurgitation in dilated cardiomyopathy may lead to a more aggressive approach with regard to pharmacological therapy, thus impacting on survival in this group of patients. (ECHOCARDIOGRAPHY, Volume 8, March 1991)     

卡维地洛治疗扩张型心肌病心力衰竭疗效观察

目的　评价第三代 β受体阻滞剂卡维地洛治疗扩张型心肌病 (DCM)心力衰竭的临床疗效。方法　 6 2例 DCM心力衰竭患者在接受常规治疗 (洋地黄、利尿剂、血管紧张素转换酶抑制剂 )病情稳定后 ,随机分为卡维地洛组和美多心安组。均从小剂量 (卡维地洛组 ,2 .5 m g bid;美多心安组 ,6 .2 5 m g bid)缓慢递增。检测治疗前后 DCM患者左心室功能和结构的变化以及血液中内皮素 - 1(ET- 1)、心钠素 (ANP)和血管紧张素 (Ang )的改变。结果　治疗 6个月后 ,两组心脏功能分级均明显改善 ,左心室射血分数 (L VEF)、短轴缩短率 (FS)、左心室射血前期与射血时间比(PEP/ L VET)、舒张早期峰值血流速度 (PFVE)、舒张早期峰值血流速度与舒张晚期峰值血流速度比 (PFVE/ PF-VA)均明显增加 ,卡维地洛组较美多心安组 L VEF增加更为明显。两组左心房内径 (L AD)、左心室收缩末期内径(L VSD)、左心室舒张末期内径 (L VDD)明显减小 ,卡维地洛组 L VSD减小较美多心安组更明显。治疗后血浆中ET- 1、ANP和 Ang 均明显降低。结论　卡维地洛和美多心安都能够改善 DCM心力衰竭患者左心室收缩和舒张功能 ,逆转左心室重构 ,卡维地洛较美多心安疗效更佳。     

A case of biopsy-proven myocarditis progressing to autopsy-proven dilated cardiomyopathy

A 22-year-old man presented with congestive heart failure following flulike symptoms. The diagnosis of acute myocarditis was confirmed by endomyocardial biopsy, which revealed mild infiltration of inflammatory cells. A favorable response to beta-adrenergic receptor blockade was seen, and the patient was discharged without symptoms. Five months later, however, congestive heart failure recurred, and intracardiac thrombi were demonstrated. The patient died after two months. Postmortem examination revealed left ventricular dilatation with slight interstitial fibrosis; the diagnosis was dilated cardiomyopathy. Thus, progression of biopsy-proven myocarditis to dilated cardiomyopathy 10 months after the onset of disease was documented.     

Assessments of left ventricular function during exercise in patients with dilated cardiomyopathy: comparison with ischemic cardiomyopathy

Responses to supine bicycle ergometer exercise were assessed in a study population consisting of 26 patients with dilated cardiomyopathy (DCM) and 23 patients with ischemic cardiomyopathy (ICM). Left ventricular ejection fraction (LVEF) and regional wall motion were analyzed at rest and during supine bicycle ergometer exercise with radionuclide ventriculography. Although the same degree of LVEF between DCM (23 +/- 8%) and ICM (26 +/- 4%) occurred at rest, the left ventricular regional wall motion abnormality was more prominent in DCM. LVEF during the peak exercise stage in DCM was almost unchanged (24 +/- 8%), but in ICM it decreased significantly (22 +/- 5%). Exercise-induced regional wall motion abnormalities were detected in nine patients (35%) in DCM and 13 patients (57%) in ICM. Although patients with DCM are believed to have diffuse hypokinesis of the left ventricle, severe regional wall motion abnormalities (akinesis or dyskinesis) were frequently observed. During the follow-up period of up to six years, eight patients with DCM died of congestive heart failure. In eight patients with DCM who showed decreased LVEF during exercise, five patients died. However, only three of 18 patients without decreased LVEF during exercise died. Exercise-induced left ventricular dysfunction in DCM seems to be a poor prognostic sign.     

Haemodynamic effects of acute beta-adrenergic receptor blockade in congestive cardiomyopathy.

Acebutolol ('Sectral'), a cardioselective beta-blocking drug, was administered intravenously in a dose of 25 mg to 10 patients with congestive cardiomyopathy. All of them were in a stable condition on antifailure regimens. The drug resulted in a statistically significant decline in left ventricular contractility as judged by peak left ventricular dP/dT and the contractility index. The mean aortic blood pressure also fell. There was a significant increase in end-diastolic and end-systolic left ventricular volumes. Mean values for heart rate, ejection fraction, left ventricular stroke work index, and cardiac output also fell, but the results were not statistically significant. Left ventricular distensibility as judged by the slope of the diastolic pressure-volume relation also improved significantly. A reduction in myocardial energy requirements, improved compliance, and lowering of arterial pressure would be haemodynamically advantageous. However, further cardiac dilatation and reduction contractility--the basic defects in congestive cardiomyopathy--could lead to further deterioration.