Eisenmenger syndrome complicated by pulmonary artery dissection.
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Aortic Dissection↗
Biomedical subjects
Lorenzo Monti
Publications and source records attributed to Lorenzo Monti.
The current therapeutic approach to chronic heart failure.
In the past 20 years, enormous progress has been made in the understanding of the pathophysiology and treatment of the complex clinical syndrome of heart failure. It has been a bidirectional process, with improvements in the understanding of the pathophysiology suggesting new therapeutic approaches and the success and failures of clinical trials refining our hypotheses or even suggesting the involvement of new pathophysiological mechanisms. In the past, heart failure was interpreted on the basis of a pathophysiological model according to which the hemodynamic abnormalities played a key role in determining the clinical presentation and the evolution of the disease. Therefore, the objective of pharmacological treatment was to improve these hemodynamic abnormalities. At the beginning of the '90s it became clear that the activation of the reninangiotensin-aldosterone system and of the sympathetic system caused by the abnormality in cardiac function had deleterious clinical effects in the long term. Heart failure was therefore considered as a "neurohormonal" disorder and the objective of pharmacological treatment was to improve survival by antagonizing this reflex activation. More recently, even the so-called "neurohormonal" hypothesis has itself evolved in several ways. In the present review the efficacy of each class of drug will be discussed in the light of the results of the most important clinical trials. In fact, from a practical point of view, since we learned so much from the published trials, it is very important that we know how these have been structured to evaluate the applicability of pharmacological treatments to individual patients.
Chronic Disease↗
Clinicopathological correlates can predict acute myocarditis in patients with recent-onset heart failure: preliminary data.
BACKGROUND: The aim of this study was to verify whether or not the clinical profile could be helpful in diagnosing myocarditis in patients with recent-onset (< 6 months) heart failure, suspected myocarditis and a biopsy-proven diagnosis. METHODS: From March 1998 to December 2000, 118 patients underwent a complete clinical, hemodynamic, echocardiographic and laboratory examination and a diagnostic endomyocardial biopsy in our Department; among them, 28 patients were admitted with clinically suspected myocarditis; in 9, the diagnosis was confirmed by the histopathologic findings. RESULTS: At the time of presentation, patients with biopsy-proven myocarditis showed early in-hospital admission (median 6 vs 69 days) with fever, a higher sinus rate and a significantly lower systolic blood pressure. Left ventricular dilation was observed in the non-myocarditis group only (left ventricular end-diastolic diameter 65.0 +/- 8.9 vs 52.6 +/- 5.8 mm); right ventricular function, as assessed by evaluation of the tricuspid annulus plane systolic excursion (TAPSE) and the right ventricular ejection fraction (RVEF) were found to be significantly lower in the myocarditis group (TAPSE 14.2 +/- 3.6 vs 20.3 +/- 7.0 mm; RVEF 21.3 +/- 11.1 vs 30.3 +/- 11.5%). Only patients with biopsy-proven myocarditis had an increase in serum creatine kinase and inflammatory markers (erythrocyte sedimentation rate and white blood cell count). Three cases had a clinical presentation of fulminant myocarditis showing marked increases in the serum levels of creatine kinase and inflammatory markers, and severely compromised right ventricular function and cardiac index. CONCLUSIONS: At univariate analysis, an early onset, fever, tachycardia, hypotension, a reduced right ventricular function, increased creatine kinase, erythrocyte sedimentation rate and white blood cell count were predictive of myocarditis. In patients with recent-onset heart failure, the clinical, laboratory and echocardiographic profiles can suggest, but not prove, a diagnosis of myocarditis.
Acute Disease↗
[Levosimendan in heart failure].
Clinical trials investigating traditional inotropic agents in patients with heart failure demonstrated an increased mortality rate (odds ratio 1.50; IC=0.51-3.92), high incidence of discontinuation of infusion therapy (odds ratio 0.46; IC=0.083-2.29) due to major side effects and, most of all, a limited clinical benefit (odds ratio 0.75; IC=1.42-0.08). On this background a new class of inotropic drugs, the calcium-sensitisers, have been developed. The safety and efficacy of levosimendan (Simdax) has been recently demonstrated in trials (LIDO e RUSSLAN) in patients with heart failure due to ischemic and not ischemic disease. Twenty-six patients with decompensated heart failure of different etiology have been treated with 24 hour infusion of levosimendan. In this experience the levosimendan improved the clinical status and the left ventricular ejection fraction.
Calcium Channel Agonists↗