The fate of acute myocarditis between spontaneous improvement and evolution to dilated cardiomyopathy: a review.
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Acute Disease↗
Biomedical subjects
G Sinagra
Publications and source records attributed to G Sinagra.
[Changes in medical treatment of heart failure in the light of large clinical trials].
In the last years, the treatment of heart failure has radically changed, as has knowledge of this complex and heterogeneous clinical syndrome. This is largely due to the results of several multicenter clinical trials, which have been undertaken since the late 80's. These trials have not only contributed to the elaboration of present-day treatment protocols, but also to a better understanding of the pathophysiologic mechanisms involved in heart failure. In the past, heart failure was generally interpreted on the basis of pathophysiologic models according to which hemodynamic abnormalities played a very important role in determining the clinical presentation and evolution of the disease. This led to the use of digitalis, diuretics, inotropic drugs and vasodilators for the treatment of heart failure. More recently, improved knowledge of the pathophysiologic mechanisms involved in the progression of this disease has highlighted the central role and the complexity of various neurohormonal mechanisms. Antagonism of these systems has proved to be the only strategy which favorably modifies the natural history of heart failure. The proved effectiveness of ACE-inhibitors and particularly of beta-blockers in patients with heart failure and left ventricular systolic dysfunction was the most convincing demonstration of the validity of this model. However, the evolution and updating of the guidelines on the treatment of heart failure should only be considered as the first step in the development of strategies aimed at extending these principles to daily clinical practice and in particular to the real patient who is different from patients typically enrolled in heart failure trials. Moreover, the development of new effective models for the management of the ever-growing number of patients with heart failure is of utmost urgency.
Clinical Trials as Topic↗
Metoprolol-induced functional benefit in dilated cardiomyopathy is sustained over four years and favorably influences outcome.
BACKGROUND: Beta-blockers improve survival and ventricular function in patients with heart failure. We evaluated the long-term persistence of metoprolol-induced improvement and its impact on prognosis in idiopathic dilated cardiomyopathy. METHODS: Two hundred and four of 586 patients enrolled in a registry on the natural history of idiopathic dilated cardiomyopathy survived 4 years without transplantation; 98 of them were on standard heart failure treatment, whereas 106 took metoprolol in addition. We analyzed the effects of treatment using beta-blockers in terms of changes in left ventricular ejection fraction (LVEF), NYHA functional class and left ventricular end-diastolic diameter index (LVEDDI) after 1, 2 and 4 follow-up years in order to elaborate an improvement score that was related to the subsequent outcome over 60 months after the 4-year follow-up visit. RESULTS: Greater LVEF increases and NYHA functional class and LVEDDI decreases were observed in patients submitted to metoprolol vs standard treatment at all stages of follow-up. Changes (delta vs baseline) for LVEF (p = 0.02), NYHA functional class (p = 0.0001) and LVEDDI (p = 0.004) were maximal during the first year (10 +/- 11 vs 6 +/- 12 units, -0.72 +/- 0.77 vs -0.23 +/- 0.81, -3.5 +/- 5 vs -1.6 +/- 3.5 mm), persisted at 2 (12 +/- 12 vs 8 +/- 12 units, -0.80 +/- 0.70 vs -0.37 +/- 0.87, -4.2 +/- 5 vs -2.3 +/- 4 mm) but showed a trend to decline at 4 years (11 +/- 12 vs 8 +/- 13 units, -0.54 +/- 0.90 vs -0.24 +/- 0.91, -4.3 +/- 5 vs -2.3 +/- 5 mm) of follow-up. Improvement at 4 years was associated with a better transplant-free survival (81 vs 52%, p = 0.0005, odds ratio 0.36, 95% confidence interval 0.18 to 0.74). CONCLUSIONS: In idiopathic dilated cardiomyopathy, the more significant improvement in symptoms and left ventricular function and size, that is observed following treatment using metoprolol, translates into a better outcome. These benefits peak within the first 2 years of start of treatment but may begin to fade thereafter.
Adrenergic beta-Antagonists↗
Incidence and predictors of sudden cardiac death during long-term follow-up in patients with dilated cardiomyopathy on optimal medical therapy.
BACKGROUND: In spite of a total mortality reduction in recent years, sudden cardiac death (SD) remains a major problem in patients with idiopathic dilated cardiomyopathy (IDC) and its occurrence is often unpredictable. Furthermore, the risk of SD may change during follow-up because of the natural history of the disease and the effects of therapeutic interventions. In our study, we evaluated the modifications of the risk of SD during follow-up in a cohort of patients with IDC and analyzed the variables predicting SD not only at enrolment but also at the last examination during optimal medical treatment. METHODS: Since 1978, 343 consecutive patients with IDC were enrolled in the Heart Muscle Disease Registry of Trieste (Italy) and submitted to complete invasive and non-invasive study. Patients were re-evaluated usually at intervals of 12 months. RESULTS: After a mean of 68+/-45 months, 125 events (death, heart transplantation or aborted SD) had occurred. The cumulative risk after 5 years was 30%, while after 10 years it almost doubled (54%). During the first 3 months after enrolment, the incidence of SD was high (3%). A plateau, lasting about 3.5 years, followed. A slow but progressive rise in the risk of mortality then occurred (6% at 5 years, 18% at 10 years). No variables evaluated at enrolment were associated with SD at multivariate analysis. On the other hand, the end-diastolic left ventricular diameter (> or = 38 mm/m2) and ejection fraction (< or = 0.30) were predictive of SD if evaluated within 1 year before the event. Beta-blocker treatment was associated with a non-significant reduction of risk. CONCLUSIONS: In patients with IDC the incidence of SD progressively increased during long-term follow-up, especially in those with persistent severe left ventricular dilation and dysfunction who were not on beta-blocker treatment. Serial clinical evaluation may help to select patients at higher risk for SD.
Adult↗
Current perspective new insights into the molecular basis of familial dilated cardiomyopathy.
Genetic disease transmission has been identified in a significant proportion of patients with dilated cardiomyopathy (DCM). Variable clinical characteristics and patterns of inheritance, as well as recent molecular genetic data, indicate the existence of several genes causing the disease. Several distinct subtypes of familial DCM have been identified. Autosomal dominant DCM is the most frequent form (56% of our cases), and several candidate disease loci have been identified by linkage analysis. Three disease genes are presently known: the cardiac actin gene, the desmin gene, and the lamin A/C gene. This latter gene has recently been found to be responsible for both the autosomal dominant form of DCM with subclinical skeletal muscle disease (7.7% of cases) and the familial form with conduction defects (2.6% of cases) or the autosomal dominant variant of Emery-Dreifuss muscular dystrophy. The autosomal recessive form of DCM accounts for 16% of cases and is characterized by a worse prognosis. An X-linked form of DCM (10% of cases) manifests in the adult population and is due to mutations in the dystrophin gene. In the rare infantile form of DCM, mutations in the G4.5 gene have been identified. Finally, some of the rare unclassifiable forms (7.7% of cases) may be due to mitochondrial DNA mutations. Clinical and experimental evidence based on animal models suggest that, in a large number of cases, DCMs are diseases of the cytoskeleton. However, other causes, such as alterations in regulatory elements and in signaling molecules, are possible. Moreover, other genes called modifier genes can influence the severity, penetrance, and expression of the disease, and they will be a main objective of future investigations. Familial DCM is frequent, cannot be predicted on a clinical or morphological basis and requires family screening for identification. The advances in the genetics of familial DCM can allow improved diagnosis, prevention and genetic counseling, and represent the basis for the development of new therapies.
Animals↗
Benefits of beta-blockers in heart failure: a class specific effect?
There is now compelling evidence in favor of the use of beta-adrenergic antagonists for the treatment of chronic heart failure. In clinically stable patients who remain symptomatic despite the fact that they are already receiving an angiotensin-converting enzyme inhibitor, diuretics and digoxin, the addition of a beta-blocker has been shown to produce further improvements in cardiac function and structure as well as in the quality and quantity of life. However, although such benefits can be achieved with a number of beta-blockers, the relevant differences in the ability of inhibiting the adrenergic drive among the various agents in the same class could translate into quantitatively different clinical effects. At present, the question whether all beta-blockers confer equal benefit or not to heart failure patients remains unanswered, since only few studies have prospectively addressed the issue and overall evidence does not permit to draw a conclusion that one agent has to be preferred to another. A large ongoing trial, designed to compare the effects of metoprolol and carvedilol on all-cause mortality in chronic heart failure, will provide much of the information required.
Adrenergic beta-Antagonists↗
Lamin A/C gene mutation associated with dilated cardiomyopathy with variable skeletal muscle involvement.
BACKGROUND: Dilated cardiomyopathy is a form of heart muscle disease characterized by impaired systolic function and ventricular dilation. Familial transmission of the disease is frequently observed, and genetic heterogeneity is indicated by clinical and morphological variability in the disease phenotype. In the family MDDC1 reported here, the disease phenotype is severe and characterized by an autosomal dominant pattern of transmission. In addition, the majority of affected family members show signs of mild skeletal muscle involvement. METHODS AND RESULTS: On the basis of the clinical observation of both cardiac and skeletal muscle abnormalities in the MDDC1 family, the lamin A/C gene was examined in this kindred. Coding regions were polymerase chain reaction-amplified from genomic DNA and sequenced. A single nucleotide deletion was identified within exon 6, and all affected individuals were found to be heterozygous for this deletion. CONCLUSIONS: Heterozygosity for a single nucleotide deletion in exon 6 of lamin A/C segregates with both the cardiac and skeletal abnormalities observed in the MDDC1 family.
Adolescent↗
Clinical relevance of right ventricular dysplasia/cardiomyopathy.
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Arrhythmogenic Right Ventricular Dysplasia↗
[Heart failure due to diastolic dysfunction: the treatment principles].
The clinical relevance of diastolic dysfunction in heart failure has recently been emphasized. In fact, the presence of signs of heart failure does not imply a depressed left ventricular systolic function; moreover, the severity of heart failure and effort tolerance are more closely related to diastolic than to systolic indexes. However, the principal trials about the treatment of heart failure were mainly addressed to patients with significant left ventricular systolic dysfunction, whereas the optimal therapy for diastolic dysfunction is not well known. The aim of this review was to assess the rationale and the therapeutic options in heart failure due to diastolic dysfunction. A diastolic dysfunction can be exclusive or associated with systolic dysfunction, as in dilated cardiomyopathy. It has to be noted that in this disease an improvement of diastolic function was demonstrated for most of the drugs currently employed in the treatment of heart failure, such as vasodilators, ACE inhibitors, beta-blockers, digitalis, and other inotropic drugs. Moreover, the favorable effect of the treatment on diastolic parameters (reduction of left ventricular filling pressure, regression of restrictive filling pattern) is associated with a positive prognostic impact. The main objective of the treatment of heart failure with preserved left ventricular systolic function is to control the symptoms by means of lowering high left ventricular filling pressure without significantly lowering cardiac output. According to the therapeutic guidelines of the American College of Cardiology/American Heart Association Task Force, the drugs indicated to treat symptomatic patients with heart failure and preserved left ventricular systolic function are diuretics and nitrates. Potentially useful, but with insufficiently proven efficacy are beta-blockers, calcium antagonists and ACE inhibitors, whereas direct vasodilators and inotropic drugs were considered inadvisable. It is important to remember that the treatment might possibly be oriented to the cause and also to the possible precipitating factors of the heart failure syndrome (i.e. ischemia, tachycardia, arrhythmias, hypertension). In conclusion, considering the relatively common incidence of heart failure due to prevalent diastolic dysfunction, and the few available data about the therapeutic options in these patients, large multicenter trials devoted to the treatment of this syndrome are needed.
Cardiovascular Agents↗
[Echocardiographic follow-up of patients with heart failure. Which parameters should be measured? How often?].
The echocardiographic evaluation keeps a relevant place in the evaluation of patients with heart failure and left ventricular systolic dysfunction, not only for its contribution to the diagnosis, prognostic stratification and comprehension of pathogenetic mechanisms, but also for the analysis of the evolution of the disease and the response to optimal medical therapy. On the other hand, the role of echocardiography in the follow-up of patients with diastolic dysfunction is still unclear. In patients with heart failure and left ventricular systolic dysfunction the analysis of changes in left ventricular function and dimension during follow-up is particularly relevant to recognize the potential benefit of optimal medical therapy with ACE-inhibitors and beta-blockers and their prognostic significance. The echo-Doppler hemodynamic evaluation is also of clinical and prognostic value particularly for the recognition of the persistence or (re)appearance of restrictive filling pattern during follow-up. Moreover, in patients with persistent severe left ventricular systolic dysfunction, the evaluation of right ventricular function may allow for the identification of a subset of patients at high risk for cardiovascular events. A practical flow-chart of echocardiographic assessment of patients with heart failure and left ventricular systolic dysfunction includes the following steps: 1) after 3 to 6 months on optimal therapy, to detect the persistence of restrictive filling pattern, if present at diagnosis; 2) after 12 to 24 months, to analyze the response of left ventricular function and dimension to optimal medical treatment; 3) serial examinations, according to the stage of the disease or to the episodes of worsening heart failure, to identify echocardiographic indicators of disease progression, such as worsening of left ventricular and/or right ventricular function or (re)appearance of restrictive filling pattern. The changes in these parameters seem to have a relevant prognostic significance to define the risk profile of patients with heart failure and left ventricular systolic dysfunction.
Follow-Up Studies↗
Potential risk of beta-blockade withdrawal in congestive heart failure due to abrupt autonomic changes.
Beta-Blockers reduce mortality in patients with congestive heart failure and a proposed mechanism has been changes of autonomic tone. Heart rate variability is a non-invasive tool to estimate cardiac autonomic tone. The aim was to study changes of heart rate variability in patients with congestive heart failure on placebo, on the beta1-selective antagonist metoprolol or 24 h after metoprolol withdrawal. Forty-five patients with congestive heart failure were studied with Holter recordings. Heart rate variability measurements were performed before, after 6-12 months of treatment with 150 mg metoprolol/placebo, or 24 h after discontinued metoprolol. After treatment, patients on beta-blockade had a significantly longer mean RR interval and changes of heart rate variability, suggesting elevated vagal tone. Patients monitored in the rebound phase of beta-blocker withdrawal had a significant vagal reduction to the level of the placebo group. There was also a nonsignificant trend towards increased sympathetic tone (LF/HF over 24 h), compared with the beta-blockade group. Heart rate variability indicates an elevated vagal tone during treatment with metoprolol but beta-blockade withdrawal shifts the autonomic balance towards lower vagal and higher sympathetic tone within 24 h. These results could imply a potential risk when abruptly discontinuing beta-blockade medication in these patients.
Adolescent↗
Long-term effects of carvedilol in idiopathic dilated cardiomyopathy with persistent left ventricular dysfunction despite chronic metoprolol. The Heart-Muscle Disease Study Group.
OBJECTIVES: The purpose of this study was to analyze whether long-term treatment with the nonselective beta-adrenergic blocking agent carvedilol may have beneficial effects in patients with dilated cardiomyopathy (DCM), who are poor responders in terms of left ventricular (LV) function and exercise tolerance to chronic treatment with the selective beta-blocker metoprolol. BACKGROUND: Although metoprolol has been proven to be beneficial in the majority of patients with heart failure, a subset of the remaining patients shows long-term survival without satisfactory clinical improvement. METHODS: Thirty consecutive DCM patients with persistent LV dysfunction (ejection fraction < or =40%) and reduced exercise tolerance (peak oxygen consumption <25 ml/kg/min) despite chronic (>1 year) tailored treatment with metoprolol and angiotensin-converting enzyme inhibitors were enrolled in a 12-month, open-label, parallel trial and were randomized either to continue on metoprolol (n = 16, mean dosage 142+/-44 mg/day) or to cross over to maximum tolerated dosage of carvedilol (n = 14, mean dosage 74+/-23 mg/day). RESULTS: At 12 months, patients on carvedilol, compared with those continuing on metoprolol, showed a decrease in LV dimensions (end-diastolic volume -8+/-7 vs. +7+/-6 ml/m2, p = 0.053; end-systolic volume -7+/-5 vs. +6+/-4 ml/m2, p = 0.047), an improvement in LV ejection fraction (+7+/-3% vs. -1+/-2%, p = 0.045), a reduction in ventricular ectopic beats (-12+/-9 vs. +62+/-50 n/h, p = 0.05) and couplets (-0.5+/-0.4 vs. +1.5+/-0.6 n/h, p = 0.048), no significant benefit on symptoms and quality of life and a negative effect on peak oxygen consumption (-0.6+/-0.6 vs. +1.3+/-0.5 ml/kg/min, p = 0.03). CONCLUSIONS: In DCM patients who were poor responders to chronic metoprolol, carvedilol treatment was associated with favorable effects on LV systolic function and remodeling as well as on ventricular arrhythmias, whereas it had a negative effect on peak oxygen consumption.
Adrenergic beta-Antagonists↗
Familial dilated cardiomyopathy: evidence for genetic and phenotypic heterogeneity. Heart Muscle Disease Study Group.
OBJECTIVES: This study was performed to evaluate the characteristics, mode of inheritance and etiology of familial dilated cardiomyopathy (FDC). BACKGROUND: A genetic form of disease transmission has been identified in a relevant proportion of patients with dilated cardiomyopathy (DCM). Variable clinical characteristics and patterns of inheritance, and an increased frequency of cardiac antibodies have been reported. An analysis of FDC may improve the understanding of the disease and the management of patients. METHODS: Of 350 consecutive patients with idiopathic DCM, 281 relatives from 60 families were examined. Family studies included clinical examination, electrocardiography, echocardiography and blood sampling. Of the 60 DCM index patients examined, 39 were attributable to FDC and 21 were due to sporadic DCM. Clinical features, histology, mode of inheritance and autoimmune serology were examined, molecular genetic studies were undertaken and the difference between familial and sporadic forms was analyzed. RESULTS: Only a younger age (p = 0.0005) and a higher ejection fraction (p = 0.03) could clinically distinguish FDC patients from those with sporadic DCM. However, a number of distinct subtypes of FDC were identified: 1) autosomal dominant, the most frequent form (56%); 2) autosomal recessive (16%), characterized by worse prognosis; 3) X-linked FDC (10%), with different mutations of the dystrophin gene; 4) a novel form of autosomal dominant DCM with subclinical skeletal muscle disease (7.7%); 5) FDC with conduction defects (2.6%), and 6) rare unclassifiable forms (7.7%). The forms with skeletal muscle involvement were characterized by a restrictive filling pattern; the forms with isolated cardiomyopathy had an increased frequency of organ-specific cardiac autoantibodies. Histologic signs of myocarditis were frequent and nonspecific. CONCLUSIONS: Familial dilated cardiomyopathy is frequent, cannot be predicted on a clinical or morphologic basis and requires family screening for identification. The phenotypic heterogeneity, different patterns of transmission, different frequencies of cardiac autoantibodies and the initial molecular genetic data indicate that multiple genes and pathogenetic mechanisms can lead to FDC.
Adolescent↗
[Classification of cardiomyopathies].
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Adult↗
[Improvement of prognosis in idiopathic dilated cardiomyopathy: role of early diagnosis and optimized medical treatment. Study Group on Heart Muscle Diseases].
BACKGROUND: The aim of this study was to assess the extent to which a more widespread use of new effective treatments for heart failure associated with earlier detection of the disease may have contributed to enhancing the prognosis of idiopathic dilated cardiomyopathy (IDC) patients over the past 20 years. METHODS: Heart transplant-free survival curves were analyzed in 343 IDC patients, prospectively enrolled from January 1, 1978 to June 30, 1997 in the Heart Muscle Disease Registry of the Cardiology Department in Trieste (94 enrolled between 1978 and 1987, Group 1; 249 between 1988 and 1997, Group 2). At enrollment, 91 patients had no heart failure symptoms (NoHF), whereas the remaining 252 showed HF of recent (HF < or = 6 months, n = 132) or non-recent (HF > 6 months, n = 120) onset. RESULTS: In comparison to Group 1, Group 2 was treated more frequently with ACE-inhibitors and beta-blockers (p < 0.0001) and showed a better long-term survival (p = 0.0034), resulting from a reduction of death for refractory HF or need for heart transplant (p = 0.011). Conversely, the risk of sudden death did not significantly differ between the two groups. NoHF, HF > 6 months and HF < or = 6 months groups were similarly treated with ACE-inhibitors and beta-blockers. Long-term survival was better in patients without HF than in those with overt HF (p = 0.0015). As compared to Group HF > 6 months, Group HF < or = 6 months had a poorer one-year prognosis (p = 0.045), related to the presence of a subgroup of patients with refractory HF and need for heart transplant, but showed a better survival rate over the following years (p = 0.015). Over the two subsequent decades of enrollment, a significant improvement in patient survival was observed within Groups NoHF (p = 0.03) and HF > 6 months (p = 0.01), but not in Group HF < or = 6 months. CONCLUSIONS: Over the past 20 years, the increasing use of ACE-inhibitors and beta-blockers in IDC was associated with a significant improvement in long-term survival, resulting from a reduction in mortality for refractory heart failure or need for heart transplant. In addition, early diagnosis may have contributed significantly to enhancing the prognosis of IDC, since the benefits of medical therapy were lower in patients identified and treated in advanced stages of the disease. Moreover, early diagnosis was shown to be useful in recognizing patients with recent onset of heart failure who are not responders to aggressive medical treatments and urgently need heart transplant.
Cardiomyopathy, Dilated↗
Cardiac tamponade: an unusual, fatal complication of infective endocarditis.
Infective endocarditis still occurs in Western countries and so far, it has been an important medical problem. The spectrum of infective endocarditis complications may be extremely wide. We report two unusual cases of infective endocarditis complicated with heart rupture and pericardial effusion. In one case, the infective process spread from the aortic valve developing a sinus of Valsalva aneurysm with subsequent aortic perforation. The perforation reached the right auricular epicardial region with subsequent epicardial rupture and hemopericardium. In the other patient, an infective process of the aortic cusps induced the formation of multiple abscesses in the left ventricle and in the right atrium. An annular abscess of the tricuspid valve was found. From the right atrium, an infected fistula spread through the atrial wall and perforated the epicardial surface of the right auricle. Aside from the rare occurrence of these complications in patients affected with infective endocarditis, these cases are of clinical interest because they raise the problem of the need of greater sensitivity to the diagnosis of endocarditis and proper diagnostic approach.
Aged↗
Polypoid osteosarcoma of the left atrium: report of a new case with autopsy confirmation and review of the literature.
We describe a new case of heart osteosarcoma manifesting as a large polypoid mass of the left atrium. Clinically, the lesion presented with dyspnea, syncopal attacks, and fever. Ultrasound scans of the heart were suggestive of a cardiac myxoma, although some imaging features could retrospectively indicate a malignant neoplasm. In particular, the lesion was relatively immobile, did not show the characteristic myxoma motion during the heart cycle, and extended into the left pulmonary veins. Exploratory thoracotomy showed a nonresectable polypoid mass of the left atrium widely infiltrating the myocardium and the epicardium, histological features of a polymorphic sarcoma. The patient died 5 months after presentation with diffuse metastases. At autopsy, a 5-cm polypoid tumor was seen protruding into the left atrium. Neoplastic infiltration of the atrial myocardium, pericardium, and pulmonary veins was evident. Extensive metastatic deposits were observed in numerous sites, including the skin, lung, liver, and brain. Microscopically, a spindle cell sarcoma forming malignant osteoid was seen, admixed with areas indistinguishable from myxoid and pleomorphic malignant fibrous histiocytoma. This case provides further evidence that although rare, osteosarcoma of the heart usually presents as a polypoid mass of the left atrium and is histologically characterized by conspicuous polymorphism. It is associated with a poor prognosis and rapid appearance of distant metastases. Although at echocardiography it may mimic a myxoma, subtle features such as tumor extension into pulmonary veins and main origin from nonseptal atrial walls suggest the presence of a nonmyxomatous tumor and a preoperatory diagnosis of aggressive malignant disease.
Adult↗
Long-term survival effect of metoprolol in dilated cardiomyopathy. The SPIC (Italian Multicentre Cardiomyopathy Study) Group.
OBJECTIVE: To evaluate the additive effect of metoprolol treatment on long-term incidence of fatal and non-fatal cardiac events in idiopathic dilated cardiomyopathy. DESIGN: 586 patients with idiopathic dilated cardiomyopathy were prospectively enrolled in a multicentre registry and followed up for a mean (SD) of 52 (32) months. Metoprolol, carefully titrated to the maximum tolerated dose, was added to conventional heart failure treatment in 175 patients. RESULTS: Survival and transplant-free survival at seven years were significantly higher in the 175 metoprolol treated patients than in the remaining 411 on standard treatment (81% v 60%, p < 0.001, and 69% v 49%, p < 0.001, respectively). By multivariate analysis, metoprolol independently predicted survival and transplant-free survival (relative risk reduction values for all cause mortality and combined mortality or transplantation 51% (95% confidence interval 21% to 69%), p = 0.002, and 34% (5% to 53%), p = 0.01, respectively). New York Heart Association class, left ventricular end diastolic diameter, and pulmonary wedge pressure were also predictive. Seven year survival (80% v 62%, p = 0.004) and transplant-free survival (68% v 51%, p = 0.005) were significantly higher in 127 metoprolol treated cases than in 127 controls selected from the entire control cohort and appropriately matched. Metoprolol was associated with a 30% reduction in all cause mortality (7% to 48%, p = 0.015) and a 26% reduction in mortality or transplantation (7% to 41%, p = 0.009). CONCLUSIONS: The addition of metoprolol to standard heart failure treatment, including angiotensin converting enzyme inhibitors, was effective in the long-term, reducing both all cause mortality and transplantation in patients with idiopathic dilated cardiomyopathy.
Adrenergic beta-Antagonists↗