Search

Background: The classification of heart failure (HF) by phenotypes has a great relevance in clinical practice., Objective: The study aimed to analyze the prevalence, clinical characteristics, and outcomes between HF phenotypes in the primary care setting., Methods: This is an analysis of a cohort study including 560 individuals, aged ≥ 45 years, who were randomly selected in a primary care program. All participants underwent clinical evaluations, b-type natriuretic peptide (BNP) measurements, electrocardiogram, and echocardiography in a single day. HF with left ventricular ejection fraction (LVEF) < 40% was classified as HF with reduced ejection fraction (HFrEF), LVEF 40% to 49% as HF with mid-range ejection fraction (HFmrEF) and LVEF ≥ 50% as HF with preserved ejection fraction (HFpEF). After 5 years, the patients were reassessed as to the occurrence of the composite outcome of death from any cause or hospitalization for cardiovascular disease., Results: Of the 560 patients included, 51 patients had HF (9.1%), 11 of whom had HFrEF (21.6%), 10 had HFmrEF (19.6%) and 30 had HFpEF (58.8%). HFmrEF was similar to HFpEF in BNP levels (p < 0.001), left ventricular mass index (p = 0.037), and left atrial volume index (p < 0.001). The HFmrEF phenotype was similar to HFrEF regarding coronary artery disease (p = 0.009). After 5 years, patients with HFmrEF had a better prognosis when compared to patients with HFpEF and HFrEF (p < 0.001)., Conclusion: The prevalence of ICFEI was similar to that observed in previous studies. ICFEI presented characteristics similar to ICFEP in this study. Our data show that ICFEi had a better prognosis compared to the other two phenotypes.

Background Inspiratory muscle weakness contributes to exercise intolerance and decreased quality of life in patients with heart failure. Studies with inspiratory muscle training show improvement in inspiratory muscle strength, functional capacity and quality of life. However, little is known about the central hemodynamic response (CHR) during inspiratory exercise (IE). Objective To evaluate CHR in a single IE session with different loads (placebo, 30% and 60%) in heart failure. Methods Randomized placebo-controlled clinical trial in patients with heart failure with reduced ejection fraction, functional class II and III. Twenty patients aged 65 ± 11 years completed a single session of inspiratory exercise, in 3 cycles of 15 minutes, with a 1-hour washout, involving loads of 30% (C30), 60% (C60) and placebo, using a linear load resistor (PowerBreathe Light). The noninvasive hemodynamic study was performed by cardiothoracic bioimpedance (Niccomo™ CardioScreen®). Statistical analysis was performed with Student's t-test and Pearson's correlation, and P≤0.05 was considered significant. Results An increase in heart rate (HR) was observed with C30 (64 ± 15 vs 69 ± 15 bpm; p = 0.005) and C60 (67 ± 14 vs 73 ± 14 bpm, p = 0.002). A decrease was observed in systolic volume (SV) with C30 (73 ± 26 vs 64 ± 20 ml; p = 0.004). Cardiac output (CO), on its turn, increased only with C60 (4.6 ± 1.5 vs 5.3 ± 1.7 l/min; p = -0.001). Conclusion When using the 60% load, in a single IE session, changes in CHR were observed. HR and CD increased, as did the Borg scales and subjective sensation of dyspnea. The 30% load reduced the SV. (Arq Bras Cardiol. 2020; 114(4):656-663).

Background: Left ventricular remodeling (LVR) is related to both non-fatal and fatal outcomes., Objective: To describe the geometric patterns of the LV and their associations., Methods: A total of 636 individuals between the ages of 45 and 99 years in Rio de Janeiro, Brazil, were submitted to clinical evaluation, laboratory tests, electrocardiogram, and tissue Doppler echocardiography (TDE). The difference between categories was tested with Kruskall-Wallis with post hoc tests, once all variables studied are non-normally distributed and Pearson's Qui-square (categorical variables). Gross and adjusted ORs were estimated by logistic regression. The level of significance was 5% for all tests. Subjects had LVR characterized as: normal geometry (NG), concentric remodeling (CR), concentric hypertrophy (CH), and eccentric hypertrophy (EH)., Results: The prevalence of altered patterns was 33%. Subjects presented NG (n = 423; 67%); EH (n = 186; 29%); CH (n = 14; 2%); and CR (n = 13; 2%). The variables of gender, age, level of education and albumin/creatinine ratio (A/C), showed a relationship with the chance of EH even after adjustment., Conclusion: Approximately one third of the studied individuals had LVR and were at risk for developing heart failure. Altered A/C in urine was associated with EH, indicating an early relationship between cardiac and renal dysfunction.

Background: Heart rate recovery at one minute of rest (HRR1) is a predictor of mortality in heart failure (HF), but its prognosis has not been assessed at six-minute walk test (6MWT) in these patients., Objective: This study aimed to determine the HRR1 at 6MWT in patients with HF and its correlation with six-minute walk distance (6MWD)., Methods: Cross-sectional, controlled protocol with 161 individuals, 126 patients with stable systolic HF, allocated into 2 groups (G1 and G2) receiving or not β-blocker and 35 volunteers in control group (G3) had HRR1 recorded at the 6MWT., Results: HRR1 and 6MWD were significantly different in the 3 groups. Mean values of HRR1 and 6MWD were: HRR1 = 12 ± 14 beat/min G1; 18 ± 16 beat/min G2 and 21 ± 13 beat/min G3; 6MWD = 423 ± 102 m G1; 396 ± 101 m G2 and 484 ± 96 m G3 (p < 0.05). Results showed a correlation between HRR1 and 6MWD in G1(r = 0.3; p = 0.04) and in G3(r = 0.4; p= 0.03), but not in G2 (r= 0.12; p= 0.48)., Conclusion: HRR1 response was attenuated in patients using βB and showed correlation with 6MWD, reflecting better exercise tolerance. HRR1 after 6MWT seems to represent an alternative when treadmill tests could not be tolerated.

Background: Patients with heart failure (HF) have left ventricular dysfunction and reduced mean arterial pressure (MAP). Increased adrenergic drive causes vasoconstriction and vessel resistance maintaining MAP, while increasing peripheral vascular resistance and conduit vessel stiffness. Increased pulse pressure (PP) reflects a complex interaction of the heart with the arterial and venous systems. Increased PP is an important risk marker in patients with chronic HF (CHF). Non-invasive ventilation (NIV) has been used for acute decompensated HF, to improve congestion and ventilation through both respiratory and hemodynamic effects. However, none of these studies have reported the effect of NIV on PP., Objective: The objective of this study was to determine the acute effects of NIV with CPAP on PP in outpatients with CHF., Methods: Following a double-blind, randomized, cross-over, and placebo-controlled protocol, twenty three patients with CHF (17 males; 60±11 years; BMI 29±5 kg/cm2, NYHA class II, III) underwent CPAP via nasal mask for 30 min in a recumbent position. Mask pressure was 6 cmH2O, whereas placebo was fixed at 0-1 cmH2O. PP and other non invasive hemodynamics variables were assessed before, during and after placebo and CPAP mode., Results: CPAP decreased resting heart rate (Pre: 72±9; vs. Post 5 min: 67±10 bpm; p<0.01) and MAP (CPAP: 87±11; vs. control 96±11 mmHg; p<0.05 post 5 min). CPAP decreased PP (CPAP: 47±20 pre to 38±19 mmHg post; vs. control: 42±12 mmHg, pre to 41±18 post p<0.05 post 5 min)., Conclusion: NIV with CPAP decreased pulse pressure in patients with stable CHF. Future clinical trials should investigate whether this effect is associated with improved clinical outcome.

Common functional polymorphisms in β-adrenergic receptor (βAR) genes have been associated with heart failure (HF) phenotypes and pharmacogenetic interactions with βAR blockers. This study evaluated the association between βAR polymorphisms and carvedilol drug response and prognosis in patients with HF. In this prospective cohort controlled study, 326 volunteers were enrolled [146 HF patients (ejection fraction (EF)<50% by Simpson) and 180 healthy controls]. Drug response was evaluated by echocardiography and outcomes were mortality and hospitalization. DNA was extracted from peripheral blood leukocytes, fragments were amplified by the polymerase reaction and genotyped by restriction fragment length polymorphism (RFLP) for Ser49Gly and Arg389Gly βAR-1 polymorphisms and Gln27Glu and Arg16Gly βAR-2 polymorphisms. The study population was in Hardy‑Weinberg equilibrium. The survival rate was adjusted using the Kaplan-Meier method. HF patients showed the following characteristics: EF 35±9%, 69.9% male, age 59±13 years, 50.7% self-identified as black, 46% had ischemic etiology. The mean follow-up of 23 months showed 18 mortalities and 46 hospitalizations. The genotypes Glu27Glu (24.7 vs. 6.1%, p=0.0004) and Arg16Arg (72.6 vs. 22.8, p<0.0001) of βAR2 polymorphisms and Gly49Gly (33.6 vs. 4.3%, p<0.0001) of the βAR1 polymorphism were higher in HF patients compared with controls. Patients with hospital admission showed a significantly higher Gly389 allelic frequency (54.9 vs. 42.1%, p=0.039), and the trend prevailed among patients who succumbed to the disease (61.1%, p=0.047). Black patients with the Ser49Ser genotype showed a reduced survival compared with the Gly49Gly or Ser49Gly genotypes (p=0.028). There was no association between improved LVEF >20% and βAR polymorphisms. HF patients with β-blocker therapy and the Gly389 allele have reduced event-free survival compared to those carrying the Arg389 allele. Additionally, systolic HF outpatients undergoing β-blocker therapy, self‑identified as black and homozygous for Ser49Ser may have reduced event-free survival, while Glu27Glu, Arg16Arg and Gly49Gly genotypes may be associated with risk for HF.

Brazilian population has a multi-ethnical profile and the prevalence of endothelial nitric oxide synthase enzyme (eNOS) polymorphism in heart failure (HF) has not been previously studied. Therefore the present study assessed the association of eNOS Glu298Asp polymorphism in patients with HF and controls. In a crossover study, was analysed the distribution of the Glu298Asp in 100 outpatients with HF, and 103 healthy controls. Self-reported race were analyzed. Left atria and left ventricle diameters and ejection fraction were evaluated in patients group. Glu298Asp was analysed by polymerase chain reaction and restriction fragment length polymorphism. The patient's average age was 59 years, 66% males, 49% Afro-descendants. The allelic frequency in patient group was Glu298=72%/Asp298=28% and the genotype frequency (GF) was Glu298Glu:49%; Glu298Asp:47%; Asp298Asp:4%. In control group, 60% Glu298 and 40% Asp298; 35% Glu298Glu, 49.5% Glu298Asp and 15.5% Asp298Asp. The prevalence of allele Glu298 was significantly higher in patients (p=0.009) as genotype Glu298Glu (p=0.03). The Glu298 in Afro-Brazilians (79%) and white patients (67%) were similar, although there was significant difference (p=0.03) in GF Glu298Glu between Afro-Brazilians and whites. There was an increased prevalence of hypertension and increased atria in Glu298Glu patients comparing with combined genotype Glu298Asp and Asp298Asp. This study suggests a regional variation in the distribution of Glu298Asp. The comparison of this distribution in African-Brazilian suggests a synergistic effect of African-descendent, Glu298Glu genotype and HF. Also demonstrated an increased frequency of Glu298 and Glu298Glu, suggesting interaction of them with HF. In HF patients, the clinical, echocardiograph and genotype analysis suggests an association of Glu298 allele and hypertension., (Copyright 2010 Elsevier Inc. All rights reserved.)