In the last years, the treatment of heart failure has radically changed, as did the knowledge of this complex and heterogeneous clinical syndrome. The comprehension of the pathophysiologic mechanisms involved in the progression of this disease highlighted the central role of various neurohormonal mechanisms. Antagonism of these systems was demonstrated to be the only strategy which favorably modifies the natural history of heart failure. However, the evolution and updating of guidelines of heart failure treatment should be considered as the first step in the development of strategies aimed at extending these principles to the "real world" and in particular to elderly patients, who are different from patients typically enrolled in heart failure trials. In spite of the relative lack of data on the efficacy of evidence-based treatment in daily clinical practice, the recommendations of heart failure guidelines should also be applied to elderly patients. However, it has to be taken into account the specificity of elderly patients, because of the presence of frequent comorbidities, contraindications, drug intolerance, and potential pharmacologic interactions. The inappropriate prescription, dosage and follow-up in patients treated with digitalis and spironolactone may be associated with a high rate of serious adverse events. Otherwise, in spite of the large amount of evidence about their efficacy, ACE-inhibitors and beta-blockers are largely underprescribed. Low-starting dosages and gradual up-titration may guarantee a good tolerability and long-term efficacy of these drugs also in elderly patients. Diagnosis and treatment of diastolic heart failure remain an unsolved issue. Further researches are needed on the efficacy of treatments in this clinical setting and, in particular, to define simple and reliable diagnostic indexes in elderly patients with preserved systolic function. Finally, the development of new multidisciplinary and effective models for the management of the ever-growing number of patients with heart failure is of utmost urgency.
In recent years, outstanding progress has been made in the diagnosis and treatment of cardiomyopathies. Genetics is emerging as a primary point in the diagnosis and management of these diseases. However, molecular genetic analyses are not yet included in routine clinical practice, mainly because of their elevated costs and execution time. A patient-based and patient-oriented clinical approach, coupled with new imaging techniques such as cardiac magnetic resonance, can be of great help in selecting patients for molecular genetic analysis and is crucial for a better characterisation of these diseases. This article will specifically address clinical, magnetic resonance and genetic aspects of the diagnosis and management of cardiomyopathies.
Background: Peak oxygen consumption (VO2) an old-time classic parameter used to stratify HF patients (pts) was recently combined to VE/VCO2 slope, in order to improve heart transplant selection criteria. The lack of prognostic factors is particularly evident in the subgroup of pts with intermediate grade of risk (i.e. with a peak VO2 between 10 and 18 ml/kg/min).We sought to analyse the predictive role of aerobic indexes obtained during Cardiopulmonary Exercise Testing (CPET) in pts affected by idiopathic dilated cardiomyopathy (IDC) with a peak VO2 between 10 and 18 ml/kg/min. Methods:We analyzed 171 IDC pts enrolled in the Trieste Heart Muscle Disease Registry who underwent CPET from 1997 and 2005. Among these, 97 pts had a peak VO2 between 10 and 18 ml/kg/min (mean age 48±10 yrs, males 71%, NYHA class III-IV 20%, left ventricle ejection fraction (LVEF) 0.30±0.11, peak VO2 14±2 ml/kg/min, ACE-inhibitors 93%, beta-blockers 88%). Combined end-point was considered Cardiovascular Death/Major Ventricular Arrhythmias/Cardiovascular Hospitalizations at 1 year. Results: At univariate analysis, pts who satisfied the end point criteria at one-year, in comparison with those who did not, showed a trend towards more advanced functional NYHA class, lower LVEF and lower circulatory power. The only parameter significantly associated to our combined end-point resulted a higher VE/VCO2 slope (34±7 vs 29±4, p=0.003). At multivariate analysis VE/VCO2 slope was selected as an independent predictor of one-year cardiovascular endpoint (for a 2-unit increase: O.R.1.41, 95% I.C. 1.08-1.85, p=0.012) together with LVEF (for a 5point decrease: O.R.1.71, 95% I.C. 1.08-2.71, p=0.025). At ROC curves VE/VCO2 slope had an AUC of 0.694 for our study end-point with a cut-off value of 28. Conclusions: In pts classified at intermediate risk according to peak VO2, VE/VCO2 slope may add prognostic power to identify pts at higher risk of early heart transplant indication.
