Heart failure with normal ejection fraction (HFNEF) is a complex syndrome that has been broadly studied since the last decade. It is caused by diastolic ventricular dysfunction demonstrated by complementary methods, such as hemodynamic study or echocardiogram, in the presence of a normal ejection fraction (EF). It affects primarily elderly individuals with comorbidities, such as systemic arterial hypertension, coronary failure and obesity. The physiopathological mechanisms are complex and multifactorial, involving the myocardial passive stiffness, the ventricular geometry, the pericardial restraint and the interaction between the ventricles. The main objectives of the treatment were to decrease the pulmonary venous congestion and the heart rate and control the comorbidities. There is no strong evidence that the use of specific medications, such as the angiotensin-converting enzyme inhibitors or beta-blockers can influence mortality. The poorer prognostic factors include advanced age, presence of kidney dysfunction, diabetes, functional class III and IV (NYHA) and advanced-stage diastolic dysfunction, with a restrictive pattern of ventricular filling. Another aspect that has been increasingly cited in the literature is the analysis of the role of the systolic function in HFNEF cases. All these aspects are analyzed in detail in the present review.

Background: There are few data on the factors decreasing quality of life (QoL) in patients with coronary artery disease (CAD) before a percutaneous coronary intervention (PCI).

The objective of this study is to evaluate the role of pentoxifylline (P) in heart remodeling induced by exposure to tobacco smoke (ETS).MethodsWistar rats were allocated in 4 groups: C (control); S (smoke); P (diet with P 100mg/kg) SP (smoke + diet with P100mg/kg). After 2 months, animals were submitted to echocardiography, isolated heart study, and oxidative stress evaluation. Two way anova and Holm Sidak tests were performed.ResultsETS leaded to an increase in left atrium area (p=0,04) and in left ventricle weight (p=0,04) and to impairment of ventricle function that was improved by pentoxifylline as observed in maximum positive derivative (C=3851±245; P=3500±400; S=2725±310; SP=3950± 310) (p=0,01). ETS increased oxidative stress that was attenuated by pentoxifylline: lipoperoxides (C=133,4±14,7; S=175,8±11,5; P=100,0±14,5; SP=128,3±11,9) (p<0,001), Glutathione peroxidases (C=37,4±4,8; S=17,519±3,9; P=33,6±6,4; SP=37,2±5,3) (p<0,001), superoxide dismutase (C=19,4±1,9; S=11,2±0,89; P=16,4±1,6; SP=21,7±2,9) (p<0,001).ConclusionIt is possible that pentoxifylline attenuates cardiac remodeling induced by ETS, in part due to reduction of oxidative stress.

Background: Aortic regurgitation (AR) is a valvulopathy that causes volume overload to the heart leading to left ventricle dilation and eccentric hypertrophy. A common co-morbidity associated with cardiovascular disease is depression. We have previously shown that paroxetine, a selective serotonin re-uptake inhibitor widely prescribed as antidepressant, improves cardiac contractility by preserving fractional shortening (FS) of AR rat hearts.In failing hearts, decrease of the ability of the myocardium to generate an effective shortness velocity is well correlated with the shift of myosin isoform distribution from α to β-MyHC expression. In order to understand the molecular mechanism involved in the improvement of FS after paroxetine treatment, we verified the expression of genes involved in heart contractility and hypertrophy.Methods and Findings: Male Wistar rats were submitted to AR surgery, by retrograde puncture of the aortic valves leaflets, or sham surgery. Morphofunctional variables of the hearts were analyzed by echocardiograms at weeks 4 and 8 after the induction of AR.At week 8 the animals were euthanized for tissue collection and posterior analysis of gene expression by RTq-PCR. Paroxetine treatment for 4 weeks in AR rats reduced the gene expression of β-MyHC and its myomiRs (miR-208 and miR-499). BNP, a molecular biomarker of hypertrophy, also showed their gene expression reduction after paroxetine treatment. Conclusion:These results suggest that paroxetine treatment improves FS in AR hearts through reductions in the expression of several genes involved with cardiac contractility and hypertrophy.

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