Background: Diuretics such as torasemide are commonly used to treat chronic heart failure (CHF). Aims: The objective of the TOrasemide In Congestive Heart Failure (TORIC) Study was to investigate the safety, tolerability and efficacy of torasemide in CHF patients compared to furosemide or other diuretics in an open-label, non-randomised, post-marketing surveillance trial.Methods: The present analysis shows the findings of 1377 patients with New York Heart Association (NYHA) class II-III CHF who received diuretic therapy with torasemide 10 mgyday orally (ns778) vs. patients who received furosemide 40 mgyday orally (ns527) or other diuretics (ns72) on top of their existing standard CHF therapy for 12 months. Besides safety and tolerability, efficacy was assessed by documentation of mortality, morbidity, functional class and serum potassium levels every 3 months. Results: TORIC confirmed the safety and tolerability of torasemide in CHF patients. Mortality was significantly lower in the torasemide (ns17, 2.2%) than in the furosemideyother diuretics group (ns27, 4.5%) (P-0.05). Functional improvement as assessed by NYHA class was observed in more patients who received furosemide torasemide (ns356, 45.8%) than those who received furosemideyother diuretics (ns223, 37.2%) (Ps0.00017). At the end of the study abnormally low serum potassium levels were observed in fewer torasemide (ns95, 12.9%) than furosemideyother diuretics patients (ns102, 17.9%) (Ps0.013). Conclusion: Torasemide is safe and well tolerated in CHF patients. Although not designed as a mortality study, TORIC suggests a lower mortality amongst CHF patients treated with torasemide compared to furosemideyother diuretics. A functional improvement and a lower incidence of abnormal serum potassium levels were also observed in patients receiving torasemide as compared to those receiving furosemideyother diuretics.

In this real-life study, 32% of patients received an inappropriate dose of DOAC. Several clinical factors can identify patients at risk of this situation.

The effects of left ventricular diastolic pressure changes on the values of the time constant (T) of isovolumic pressure fall are controversial. Normally, T is calculated either by linear regression of 1n left ventricular pressure (LVP) vs. time (TL) or by using an exponential model with asymptote (PB, extrapolated base-line pressure to which LVP would fall if decay continued indefinitely). This study, in intact dogs, has been designed to revise the effects that drugs that alter load (angiotensin and nitroprusside, without and with autonomic blockade) and inotropism (isoproterenol and propranolol) might have on the relaxation rate using different numerical methods. We found that 1) the upward or downward translation of the LVP curve had an important effect on the value of TL calculated by the semilogarithmic method; 2) when a model with asymptote was used, the simultaneous changes of T and PB, were not related to the dose of the drug; 3) the values of TL and the -dP/dt values extrapolated to 15 mmHg from a model with PB, were much more sensitive to beta-agonist or antagonist drugs than to others whose action was through load alteration. We feel that some of the earlier studies on relaxation rate determinants should be revised as possibly some of the conclusions have been based on artifacts introduced by the method chosen for the computation of the relaxation parameters.

In two thirds of a group of patients with vascular disease, 200 to 300 mg ASA was insufficient to block platelet reactivity in the presence of erythrocytes despite abolishing thromboxane A2 synthesis. Platelet activation in the presence of erythrocytes can induce the release reaction and generate biologically active products that recruit additional platelets into a developing thrombus. Insufficient blockade of this proaggregatory property of erythrocytes can lead to development of additional ischemic complications.