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The article discusses the status and management of heart failure disease in Spain. It states that the Spanish Society of Cardiology issued guidelines on how to manage heart failure in the country. In addition, heart failure is the main cause of hospitalization in older Spanish population. Moreover, drugs for heart failure management may be underused and there were scarcity of the care facilities for older patients.

Background: The alteration of contractile function after tachyarrhythmia ceases is influenced by the type of prior ischemia (acute coronary syndrome or ischemia inherent in a coronary revascularization procedure). We aimed to analyze cardiac dysfunction in an acute experimental model of supraphysiological heart rate preceded by different durations and types of ischemia., Material and Methods: Twenty-four pigs were included in: (S1) series of ventricular pacing; (S2, A and B) series with 10 or 20 min, respectively, of coronary occlusion previous to ventricular pacing; S3 with 20 brief, repeated ischemia/reperfusion processes prior to ventricular pacing and; (S4) control series. Overall cardiac function parameters and regional myocardial contractility at the apex and base of the left ventricle were recorded, as were oxidative stress markers (glutathione and lipid peroxide serum levels). Left ventricular pacing at 60% over baseline heart rate was performed for 2 h followed by 1 h of recovery., Results: High ventricular pacing rates preceded by short, repeated periods of coronary ischemia/reperfusion resulted in worse impairment of overall cardiac and regional function that continued to be altered 1 h after tachycardia ceased. There was significant reduction of stroke volume (26.9 ± 5.3 basal vs. 16 ± 6.2 ml; p<0.05), LVP; dP/dt and LAD flow (13.1 ± 1.5 basal vs. 8.4 ± 1.6 ml/min; p<0.05); the base contractility remained altered when recovering compared to baseline (base SF: 5.6 ± 2.8 vs. 2.2 ± 0.7%; p<0.05); and LPO levels were higher than less aggressive series at the end of recovery., Conclusions: Ischemia and tachycardia accumulate their effects, with increased cardiac involvement depending on the type of ischemia.

Background: High-rate short-duration ventricular pacing induces myocardial hypokinesis that persists once the hemodynamic conditions have been recovered. The aim was to study the factors that determine the persistence of myocardial dysfunction when ventricular tachycardia has ceased and hemodynamic conditions have been restored., Material/methods: An in vivo experimental pig model was used consisting of a ventricular pacing series (n=10), a ventricular pacing and aldosterone blockade (eplerenon) series (n=6), and a control series without ventricular pacing (n=6). Electrical stimulation was performed from the epicardial base of the left ventricle at a frequency 60% above the basal rate for 2 hours followed by a recovery period of 60 minutes. Cardiac and myocardial function parameters were studied. Plasma levels of aldosterone, renin activity, and glutathione were measured., Results: Electrically induced tachycardia produced hemodynamic and myocardial changes that persisted after stimulation had ceased, accompanied by an increase in aldosterone and a coronary flow decrease. These changes were not seen when aldosterone activity was blocked by eplerenon. There was a non-significant elevation in glutathione levels., Conclusions: These data show that although participation of other neurohormones cannot be ruled out, aldosterone blockade (eplerenon) ameliorates myocardial dysfunction persisting after ventricular tachycardia by preventing coronary endothelial dysfunction.

Background: The aim was to assess the effect of trimetazidine (TMZ) on mitochondrial alterations induced in a canine model of brief, repeated episodes of ischemia., Material/methods: Twelve crossbred dogs were analyzed, after double-blind randomization, to a 7-day treatment with either TMZ or placebo. Twenty brief, complete occlusions of the left anterior descending coronary artery were performed. Mitochondrial analysis entailed a qualitative (percentage of mitochondrial damage, merging, pairing, vacuoles, and lipofucsin granules) and a quantitative size analysis (major and minor axes, perimeter, and area) of the mitochondria in the ischemic and control zones., Results: Comparative study of the control zones revealed an increase in lipofucsin granules in the TMZ series and a greater percentage of damaged mitochondria and vacuoles. The control-zone mitochondria treated with TMZ presented a significant increase in the perimeter and major axis and a decrease in the minor axis (p<0.005). No significant differences were found between the series in the qualitative analysis of mitochondrial damage in the ischemic zone. The mitochondria in the TMZ series presented a greater major axis and perimeter than those in the placebo series (p<0.05), which presented a smaller minor axis., Conclusions: TMZ made the mitochondria adopt an elongated, "rod-like" morphology in both the control and ischemic zones. This is interpreted as an increase in the membrane surface. In the non-ischemic zone, TMZ produced an increase in mitochondrial turnover. There were no differences in the myocardium subjected to ischemia in both series in terms of observable mitochondrial damage.

Ventricular extrasystoles and the complex forms of non-malignant ventricular arrhythmias clearly increase in the presence of left ventricular hypertrophy. Left ventricular hypertrophy constitutes a clear sudden death risk factor. The connection between possible malignant arrhythmias, which have also been reported in LVH patients, and an increased incidence of sudden death has not been established. Hypertension, electrical changes in the hypertrophic myocyte, the growth of the collagen matrix and ischaemia (even in the absence of macro-angiographic injuries) are factors present in this group of patients that contribute to the appearance of arrhythmias. The arrhythmogenic substrate of LVH has to do with reentry mechanisms due to fibrillar stretching and anisotropy, as well as with self-sustaining activity triggered by after-potentials that depend on activation of slow calcium channels.