Aims Despite of recent advances in the pharmacological treatment, heart failure (HF) maintains significant morbidity and mortality rates. While serum potassium disorders are common and associated with adverse outcomes, the exact recommended potassium level for patients with HF are not entirely established. We aimed to investigate the prognostic role of potassium levels on a cohort of patients with symptomatic chronic HF. Methods and results Patients with symptomatic chronic HF were identified at the referral to 6 min walking test (6MWT) and were prospectively followed up for cardiovascular events. Clinical and laboratorial data were retrospectively obtained. The primary endpoint was the composite of cardiovascular death, hospitalization due to HF, and heart transplantation. The cohort included 178 patients with HF with the mean age of 51 ± 12.76 years, 39% were female, 85% of non-ischaemic cardiomyopathy, and 38% had New York Heart Association Class III with a relatively high Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) score (12.91 ± 6.6). The mean left ventricular ejection fraction was 39.98 ± 15.79%, and the mean 6MWT distance was 353 ± 136 m. After a median follow-up of 516 days, there were 22 major cardiovascular events (4 cardiovascular deaths, 13 HF admissions, and 5 heart transplants). Patients were stratified according to cut-point level of serum potassium of 4.7 mmol/L to predict combined cardiac events based on receiver operating characteristic analysis. Individuals with higher potassium levels had worse renal function (glomerular filtration rate, K ≤ 4.7: 102.8 ± 32.2 mL/min/1.73 m 2 vs. K > 4.7: 85.42 ± 36.2 mL/min/1.73 m 2 , P = 0.004), higher proportion of New York Heart Association Class III patients (K ≤ 4.7: 28% vs.

Background: Studies have shown significant benefits of exercise therapy in heart failure (HF) with a reduced ejection fraction (HFrEF) and HF with a preserved ejection fraction (HFpEF). The mechanisms responsible for the beneficial effect of exercise in HFrEF and HFpEF are still unclear. We hypothesized that the effect of exercise on myocardial remodeling may explain its beneficial effect. Methods: IMAGING-REHAB-HF is a single-center, randomized, controlled clinical trial using cardiac magnetic resonance imaging, vasomotor endothelial function, cardiac sympathetic activity imaging and serum biomarkers to compare the effect of exercise therapy in HFpEF (LVEF ≥ 45%) and HFrEF (LVEF < 45%). Subjects will be assessed at baseline and after 4 months. The exercise program will consist of three 60-min exercise sessions/week. The primary endpoints are the effect of exercise on myocardial extracellular volume (ECV), left ventricular (LV) systolic function, LV mass, LV mass-to-volume and LV cardiomyocyte volume. Secondary endpoints include the effect of exercise on vasomotor endothelial function, cardiac sympathetic activity and plasmatic biomarkers. Patients will be allocated in a 2:1 fashion to supervised exercise program or usual care. A total sample size of 90 patients, divided into two groups according to LVEF:HFpEF group (45 patients:30 in the intervention arm and 15 in the control arm) and HFrEF group (45 patients:30 in the intervention arm and 15 in the control arm) – will be necessary to achieve adequate power. Conclusion: This will be the first study to evaluate the benefits of a rehabilitation program on cardiac remodeling in HF patients. The unique design of our study may provide unique data to further elucidate the mechanisms involved in reverse cardiac remodeling after exercise in HFpEF and HFrEF patients.

Cardoso et al ASD and PH in professional soccer playerArq Bras Cardiol 2010; 95(2): e38-e39

Background Anthracycline therapy may induce left ventricle (LV) dysfunction. However, few studies investigated how it may affect the right ventricle (RV). Purpose The goal of this study was to assess RV systolic function and biomarkers that may predict early dysfunction in breast cancer patients treated with anthracyclines. Methods Twenty-seven women with breast cancer (51.8±8.9 years), underwent CMR prior, and up to 3-times after doxorubicin with matching measurements of biomarkers: high-sensitive troponin T (TnT), creatinine-kinase MB isoenzyme (CK-MB) and C reactive protein (CRP). Results Before anthracyclines, all subjects had normal LVEF (69.4±3.6%) and RVEF (55.1±9%) and LV and RV EF correlated significantly (ρ=0.42; p=0.031). At 351–700 days after anthracycline, LVEF and LV mass index declined to 58±6% (P<0.001) and 36±6 g/m2 (P<0.001) (table). RVEF also decreased, reaching 46±8% at 231,4 days after (P<0.001), but lost the correlation with LVEF seen at baseline (r=0.22; P=0.068). RVEF showed strong negative association with serum CK-MB (r=−0.4, p=0.004) and no significant correlation with TnT (r=−0.18, p=0.28) or CRP (r=0.03, p=0.932) (figure). In patients with a peak TnT of >10 pg/ml the change of RVEF overtime was significant (Regression Splines coefficients for RVEF: 1.0, p=0.731–peak TnT ≤10pg/ml; 2.51, p<0.001–peak TnT >10 pg/ml). LVEF was not associated with CK-MB (p=ns). Baseline and Follow-Up CMR Findings Median days after anthracycline Pre-DOX (79,146] (146,231] (231,350] (350,700] N 27 16 19 14 16 LVEF, % 69.4±3.6 61.1±7.6† 55.99±5.0† 53.8±8.4† 57.5±6.1† LVEDV index, ml/m2 60.2±9.9 64.3±9.6 66.7±17.7 * 56.9±18.5 59.2±12.6 LVESV index, ml/m2 18.3±4.0 24.7±7.3# 29.0±7.3† 26.2±9.7† 25.3±8.2† LV mass index, g/m2 51.4±8.0 45.3±3.8† 43.2±4.9† 39.9±5.4† 36.0±6.1† RVEF, % 55.1±9.4 51±8.1 48±8.5 46±8.5 50±7.4 RVEDV index, ml/m2 45.07±6.6 46.5±11.31 47.35±9.16 41.14±9.7 46.16±7.3 RVESV index, ml/m2 20.45±5.4 22.31±5.8 24.77±6.6 21.96±6.4 22.24±4.7 Data are presented as mean ± SD. LV: left ventricle; RV: right ventricle; EF: ejection fraction; EDV: end diastolic volume; ESV: end systolic volume (average±SD). *Significantly different from Pre-DOX level (p<0.05 from linear mixed effects model). #Significantly different from Pre-DOX level (p<0.01 from linear mixed effects model). †Significantly different from Pre-DOX level (p<0.001 from linear mixed effects model). RVEF and correlate variables Conclusions RVEF reduction does not follow LVEF changes after anthracyclines and CK-MB may be a more specific biomarker to assess RV dysfunction. A higher peak cTnT could predict a greater change in RVEF during follow-up.

A hipertrofia miocárdica é um achado comum em reposta a estímulos fisiológicos e patológicos, sendo caracterizada pela combinação de hipertrofia celular dos cardiomiócitos e expansão da matriz extracelular no miocárdio, constituída pela fibrose intersticial e pelo acúmulo de colágeno entre os cardiomiócitos. Tanto a fibrose intersticial como a hipertrofia dos cardiomiócitos estão presentes em pacientes com insuficiência cardíaca (IC), sendo que particularmente a fibrose possui associação com a disfunção ventricular, com um prognóstico desfavorável e com uma resposta terapêutica limitada. O exercício isométrico produz o aumento transitório da pressão central da aorta, contribuindo para o desenvolvimento da hipertrofia ventricular esquerda (HVE) concêntrica além de alteração da função diastólica. A investigação do modelo de HVE em atletas de força mostra-se útil para enriquecer o entendimento das alterações precoces que podem estar associadas com o aumento da predisposição para o estabelecimento da IC. Recentemente nosso grupo descreveu e validou nova metodologia para investigação do remodelamento miocárdico a nível celular pela ressonância magnética cardíaca (RMC), com a avaliação da fibrose intersticial e do tamanho dos cardiomiócitos. Neste estudo, pretendemos investigar aspectos do remodelamento miocárdico em modelo de HVE em atletas de força, caracterizando não apenas a fibrose intersticial mas também a hipertrofia dos cardiomiócitos, utilizando técnicas oriundas da RMC.