SummaryBackgroundAcute decompensation heart failure (ADHF) remains a cause of hospitalization in patients with end-stage congestive HF. The administration of levosimendan in comparison with a standard therapy in CHF patients admitted for ADHF was analysed.Material/MethodsConsecutive patients admitted for ADHF (NYHA class III–IV) were treated with levosimendan infusion 0.1 μg/kg/min or with furosemide infusion 100–160 mg per day for 48 hours (control group). All subjects underwent determination of brain natriuretic peptide (BNP), non-invasive cardiac output (CO), and echocardiogram at baseline, at the end of therapy and 1 week after therapy.ResultsSeven patients admitted for 20 treatments in 16 months (age 66 years; mean admission/year 5.4) were treated with levosimendan and compared with 7 patients admitted for 15 treatments (age 69.1 years; mean admission/year 6.1). At the end of levosimendan therapy, BNP decreased (from 679.7±512.1 pg/ml to 554.2±407.6 pg/ml p=0.03), and 6MWT and LVEF improved (from 217.6±97.7 m to 372.2±90.4 m p=0.0001; from 22.8±9.1% to 25.4±9.8% p=0.05). Deceleration time, E/A, E/E’, TAPSE, pulmonary pressure and CO did not change significantly after levosimendan therapy and after 1 week. At follow-up, only 6-min WT and NYHA class showed a significant improvement (p=0.0001, p=0.001 respectively). The furosemide infusion reduced NYHA class and body weight (from 3.4±0.6 to 2.3±0.5 p=0.001; from 77.5±8.6 kg to 76±6.6 kg p=0.04), but impaired renal function (clearances from 56.3±21.9 ml/min to 41.2±10.1 ml/min p=0.04).ConclusionsTreating end-stage CHF patients with levosimendan improved BNP and LVEF, but this effect disappeared after 1 week. The amelioration of 6MWT and NYHA class lasted longer after levosimendan infusion.
Post-myocardial infarction left ventricular remodelling should be considered an important therapeutic target in patients after an acute myocardial infarction, considering the heavy prognostic implication. The therapies used in these patients should reduce the progression of the left ventricular dysfunction to refractory heart failure. In order to prevent post-myocardial infarction cardiac remodelling, different therapies have been tested, and for ACE-inhibitors and beta-blockers a clear demonstration of efficacy has been obtained. Losartan and valsartan, two widely used angiotensin receptor blockers, demonstrated to be safe and equally useful compared to ACEI. The addition of spironolactone to the standard therapy for heart failure has a clear beneficial effect but the clinical use has been refrained by the risk of iperkaliemia. Aerobic physical training improves the left ventricular ejection fraction in patients with systolic dysfunction, reducing the progressive enlargement after myocardial infarction. The positive effect of aerobic training on cardiac remodelling might be related to the positive effect on neurhormonal assessment, to he improvement of microcirculatory myocardial perfusion and of endothelial function.
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