Gerardina Lardieri

Metoprolol in dilated cardiomyopathy: Is it possible toidentify factors predictive of improvement?

Background: Some controlled clinical trials showed a beneficial effect of beta-blockers on symptoms, exercise tolerance, and left ventricular function in dilated cardiomyopathy. The purpose of this study was to investigate if there are clinical variables at baseline that could predict a favorable response to long-term metoprolol therapy.

Nonpredictive value of fibrosis in dilated cardiomyopathy treated with metoprolol

Therapy with β-adrenergic blocking agents has been advocated as a potential useful approach in heart failure. Recent studies suggest that histologic parameters may be helpful in assessing the effectiveness of β-blocker treatment in dilated cardiomyopathy (DCM). In order to predict the response to β-blockers in DCM, fibrous tissue was evaluated at endomyocardial biopsy (EMB) in 45 patients (pts) with a mean left ventricular ejection fraction of 0.28 ± 0.07, who were successively long-term treated with metoprolol (M) (mean dosage 138 ±26 mg/die). EMB was performed from left (n = 32) or right (n = 13) ventricle by means of a Kings bioptome or the Cordis adaptation of this instrument. Quantification of fibrous tissue was performed at 9 × magnification and with a computerized morphometric system. Qualitative evaluation at light microscopy distinguished four types of fibrosis: pericellular, perivascular, focal, and endocardial. Volume fraction of fibrous tissue ranged from 1.3 to 35.5% (mean 12.1 ± 9.3%) and was not significantly correlated with any clinical variable considered. After 24 ± 12 months of treatment, 25 pts were considered improved (group A), whereas the remaining 20 pts were considered not improved (group B), according to criteria based on ejection fraction, left ventricular end-diastolic diameter, filling pattern at Doppler-Echocardiography, cardiothoracic ratio, NYHA functional class, and exercise duration at ergometric test. Volume fraction of fibrous tissue did not differ significantly between the two groups (group A = 12.1 ± 9.1%; group B = 11.3 ± 9.6%;p = NS). Dominant pericellular type of fibrosis was equally distributed between the two groups (group A = 9 25 pts, 36%; group B = 10 20 pts, 50%), whereas a perivascular and/or focal replacement fibrosis was more frequent in group A (group A = 10 20 pts, 50%; group B = 2 20 pts, 10%; p = .05, OR 5.55 at univariate analysis). At multivariate analysis mean aortic blood pressure was the only variable discriminating the two groups; the type of fibrosis, although not statistically significant, maintained a high value of odds-ratio (5.23). In conclusion, extent of total fibrosis assessed by EMB may range widely in patients with DCM, is not correlated with the most important clinical variables, and is not predictive of long-term response to β-blocker treatment. Otherwise, prevalent perivascular and/or focal replacement fibrosis could be associated with a higher probability of improvement after long-term β-blocker treatment.

Natural History of Idiopathic Dilated Cardiomyopathy

Idiopathic dilated cardiomyopathy (IDC) continues to be an etiological and pathogenetic enigma. Many possible causes have been considered and are being studied at present. Genetic factors, virus infections, autoimmunity alcohol, pregnancy, and slight hypertension may play a role. However the etiology continues to be unknown in a large percentage of patients. The possibility of different etiological factors and of various pathogenetic mechanisms may explain the heterogeneity of clinical presentation, functional status, complications, and characteristics of evolution and response to therapy of the disease [22].

Clinical management of dilated cardiomyopathy: current knowledge and future perspectives

ABSTRACT Dilated cardiomyopathy (DCM) is a primary heart muscle disease characterized by a progressive dilation and dysfunction of either the left or both ventricles. The management of DCM is currently challenging for clinicians. The persistent lack of knowledge about the etiology and pathophysiology of this disease continues to determine important fields of uncertainty in managing this condition. Molecular cardiology and genetics currently represent the most crucial horizon of increasing knowledge. Understanding the mechanisms underlying the disease allows clinicians to treat this disease more effectively and to further improve outcomes of DCM patients through advancements in etiologic characterization, prognostic stratification and individualized therapy. Left ventricular reverse remodeling predicts a lower rate of major cardiac adverse events independently from other factors. Optimized medical treatment and device implantation are pivotal in inducing left ventricular reverse remodeling. Newly identified targets, such as angiotensin–neprilysin inhibition, phosphodiesterase inhibition and calcium sensitizing are important in improving prognosis in patients affected by DCM.

Management of Bradyarrhythmias in Emergency

The sudden appearance in patients of changes in heart rhythm is a situation that requires rapid diagnosis and treatment in emergency departments and intensive care units. The slowdown and block of cardiac impulse conduction form the basis of symptomatic bradycardia.

ACE-Inhibitors, β-Blockers, Spironolactone: Do We Need Many More Drugs to Treat Chronic Heart Failure?

Over the last two decades, considerable insights into the pathophysiology of chronic congestive heart failure (HF) have been gained to suggest that the overstimulation of biologically active pathways - primarily the reninangiotensin-aldosterone and sympathoadrenergic systems - may play a key role in determining the progression of the syndrome [1]. Supporting this concept, a large body of evidence has been accumulated to show that drugs possessing the ability to counteract these up-regulated neuroendocrine mechanisms may represent an effective therapeutic strategy to improve the course of the disease [2-7].