Mookadam, Farouk

Decitabine is a pyrimidine analogue of nucleoside cytidine, used for the treatment of myelodysplastic syndromes, chronic myelogenous leukemia, and acute myelogenous leukemia. We present a case of cardiomyopathy associated with decitabine used for secondary acute myelogenous leukemia. The patient presented with new heart failure symptoms and an ejection fraction decline.

Background Data about anticoagulation in pulmonary arterial hypertension (PAH) patients are inconsistent. The objective of this study was to examine the impact of adjunctive oral anticoagulants in patients with PAH through meta-analysis, and to further assess whether response differs by PAH subtype. Methods and Results Cochrane CENTRAL, Medline, and Scopus databases were searched for randomized or nonrandomized studies that assessed the association between anticoagulation and outcomes in patients with PAH. Hazard ratios (HRs) for mortality were pooled using the random effects model. Subgroup analyses were performed for type of PAH and study design. Twelve nonrandomized studies, at moderate risk of bias, were included. These consisted of 2512 patients (1342 receiving anticoagulation and 1170 controls). Anticoagulation significantly reduced mortality in the overall PAH cohort (HR, 0.73 [0.57, 0.93]; P =0.001; I 2 =64%). On subgroup analysis, a significant mortality reduction was seen in idiopathic PAH patients (HR, 0.73 [0.56, 0.95]; P =0.02; I 2 =46%), whereas no significant difference was observed in connective tissue disease–related PAH (HR, 1.16 [0.58, 2.32]; P =0.67; I 2 =71%). Sensitivity analysis specific to scleroderma-associated PAH demonstrated a significant increase in mortality with anticoagulant use (HR, 1.58 [1.08, 2.31]; P =0.02; I 2 =9%). Conclusions This meta-analysis shows that use of anticoagulation may improve survival in idiopathic PAH patients, while increasing mortality when used in scleroderma-associated-PAH patients. Currently, no randomized clinical trials have been published, and until randomized data are available, anticoagulant use in PAH should be tailored to PAH subtype.

ABSTRACT Purpose We assessed resting central/peripheral blood pressure (BP), postexercise BP, and hemodynamic responses (stroke volume, cardiac output, and systemic vascular resistance) after acute exercise and 2 wk of aerobic training in lean and centrally obese men matched for BP. Methods Eight lean (body mass index < 25 kg·m −2 , visceral fat = 279 ± 224 cm 3 ) and eight centrally obese (body mass index > 30 kg·m −2 , visceral fat = 1471 ± 374 cm 3 ) men performed six training sessions (3 d·wk −1 for 40 min at 65%–70% HR max ). Resting BP and hemodynamic measurements were obtained at baseline, after exercise for 60 min, and at 24 h and 48 h after the last training session. Results Postexercise brachial and central systolic BP (SBP) and mean arterial BP decreased 3–4 mm Hg below resting in lean ( P < 0.001) and increased by 3 mm Hg in obese ( P < 0.02). Posttraining resting brachial/central SBP were reduced by 3–4 mm Hg only in lean men ( P < 0.05). Pretraining postexercise hypotension was significantly correlated with the training-induced change in resting brachial SBP at 48 h ( r = 0.58, P = 0.02), but not at 24 h ( r = 0.38, P = 0.15). Similar correlations were observed between acute reductions in central SBP and central SBP at 24 h ( r = 0.43, P = 0.09) and 48 h ( r = 0.54, P = 0.03) posttraining. Conclusions In contrast to the consistent results for lean men, postexercise hypotension was not observed in centrally obese men, and resting SBP was not reduced after a short aerobic training program. Considerable individual variation in postexercise BP response among obese men may have implications for design of exercise interventions to lower BP in these individuals.

Abstract Aims High-intensity interval training (HIIT) improves peak oxygen uptake and left ventricular diastology in patients with heart failure with preserved ejection fraction (HFpEF). However, its effects on myocardial strain in HFpEF remain unknown. We explored the effects of HIIT and moderate-intensity aerobic continuous training (MI-ACT) on left and right ventricular strain parameters in patients with HFpEF. Furthermore, we explored their relationship with peak oxygen uptake (VO2peak). Methods and results Fifteen patients with HFpEF (age = 70 ± 8.3 years) were randomized to either: (i) HIIT (4 × 4 min, 85–90% peak heart rate, interspersed with 3 min of active recovery; n = 9) or (ii) MI-ACT (30 min at 70% peak heart rate; n = 6). Patients were trained 3 days/week for 4 weeks and underwent VO2peak testing and 2D echocardiography at baseline and after completion of the 12 sessions of supervised exercise training. Left ventricular (LV) and right ventricular (RV) average global peak systolic longitudinal strain (GLS) and peak systolic longitudinal strain rate (GSR) were quantified. Paired t-tests were used to examine within-group differences and unpaired t-tests used for between-group differences (α = 0.05). Right ventricular average global peak systolic longitudinal strain improved significantly in the HIIT group after training (pre = −18.4 ± 3.2%, post = −21.4 ± 1.7%; P = 0.02) while RV-GSR, LV-GLS, and LV-GSR did not (P &gt; 0.2). No significant improvements were observed following MI-ACT. No significant between-group differences were observed for any strain measure. ΔLV-GLS and ΔRV-GLS were modestly correlated with ΔVO2peak (r = −0.48 and r = −0.45; P = 0.1, respectively). Conclusions In patients with HFpEF, 4 weeks of HIIT significantly improved RV-GLS.