Elissavet Kaldara

The effects of exercise training on the kinetics of oxygen uptake in patients with chronic heart failure.

Background Prolonged oxygen uptake kinetics (O2 kinetics), following the onset of a constant workload of exercise has been associated with a poor prognosis in patients with chronic heart failure. This study aimed to determine both continuous and interval training effects on the different O2-kinetics phases in these patients. Design Twenty-one patients (60 ± 8 years) with stable chronic heart failure participated in a 36-session exercise rehabilitation program (three times weekly). Patients were randomly assigned to interval training (n = 11; 100% of peak work rate for 30 s, alternating with 30s-rest) and to continuous training (n = 10; 50% of peak work rate). Methods Before and after the completion of the program, all patients performed both incremental symptom-limited and constant workload submaximal cardiopulmonary exercise tests. Phase I O2-kinetics was evaluated by time (t), from the start of exercise until the onset of decreased respiratory exchange ratio and phase II by the time constant (τ) of the response from the end of phase I until steady state. Results After training, there was a significant increase in peak oxygen uptake and peak work rate in both continuous (15.3 ± 4.4 vs. 16.6 ± 4.5 ml/kg per min; P=0.03 and 81.8 ± 40.1 vs. 94.7 ± 46.1 W; P=0.03) and interval training groups (14.2 ± 3.1 vs. 15.4 ± 4.2 ml/kg per min; P=0.03 and 82.5 ± 24.1 vs. 93.7 ± 30.1 W; P=0.04). Patients who underwent interval training had a significant decrease in t (39.7 ± 3.7 to 36.1 ± 6.9s; P=0.05), but not τ (59.6 ± 9.4 to 58.9 ± 8.5 s; P=ns), whereas those assigned to continuous training had a significant decrease in both t (40.6 ± 6.1 to 36.4 ± 5.4 s; P=0.01) and τ (63.3 ± 23.6 to 42.5 ± 16.7 s; P=0.03). Conclusions Exercise training improves O2 kinetics in chronic heart failure patients. Both continuous and interval training improve phase I O2-kinetics, but continuous training results in superior improvement of the phase II O2-kinetics, an indirect index of muscle oxidative capacity.

Inotropic Agents Improve the Peripheral Microcirculation of Patients With End-Stage Chronic Heart Failure

BACKGROUND Skeletal muscle microcirculation impairment in patients with chronic heart failure (CHF) seems to correlate with disease severity. We evaluated the microcirculation by near-infrared spectroscopy (NIRS) occlusion technique before and after inotropic infusion. METHODS We evaluated 25 patients with stable CHF, 30 patients with end-stage CHF (ESCHF) receiving treatment with intermittent infusion of inotropic agents, and 12 healthy subjects. Thenar muscle tissue oxygen saturation (StO(2)%) was measured noninvasively by NIRS before, during, and after 3-minute occlusion of the brachial artery (occlusion technique) in all subjects and in patients with ESCHF before and after 6 hours of inotropic infusion (dobutamine and/or levosimendan) or placebo (N = 5). RESULTS Patients with ESCHF or CHF presented significantly lower StO(2)% than healthy subjects (74.5% +/- 7%, 78.6% +/- 6%, and 85% +/- 5%, respectively; P = .0001), lower oxygen consumption rate during occlusion (24.6% +/- 8%/min, 28.6% +/- 10%/min, and 38.1% +/- 11.1%/min, respectively; P = .001), and lower reperfusion rate (327% +/- 141%/min, 410% +/- 106%/min, and 480% +/- 133%/min, respectively; P = .002). After 6 hours of inotropic infusion, patients with ESCHF showed significantly increased StO(2)% (74.5% +/- 7% to 82% +/- 9%, P = .001), oxygen consumption rate (24.6% +/- 8%/min to 29.3% +/- 8%/min, P = .009), and reperfusion rate (327% +/- 141%/min to 467% +/- 151%/min, P = .001). No statistical difference was noted in the placebo group. CONCLUSION Peripheral muscle microcirculation as assessed by NIRS is impaired in patients with CHF. This impairment is partially reversed by infusion of inotropic agents in patients with ESCHF.

Bone mass loss in chronic heart failure is associated with secondary hyperparathyroidism and has prognostic significance

Chronic heart failure (CHF) is associated with increased risk of osteoporosis. We investigated the relationship between severity of CHF and bone loss, underlying pathophysiological mechanisms, and the prognostic significance of bone mass changes in heart failure.

Anemia in heart failure: pathophysiologic insights and treatment options.

Anemia has been recognized as a very common and serious comorbidity in heart failure, with a prevalence ranging from 10 to 79%, depending on diagnostic definition, disease severity and patient characteristics. A clear association of anemia with worse prognosis has been confirmed in multiple heart failure trials. This finding has recently triggered intense scrutiny in order to identify the underlying pathophysiology and the best treatment options. Etiology is multifactorial, with iron deficiency and cytokine activation (anemia of chronic disease) playing the most important roles. Treatment is aimed at not only restoring hemoglobin values back to normal, but also at improving the patients symptoms, functional capacity and hopefully the outcome. Iron supplementation and erythropoietin-stimulating agents have been used for this purpose, either alone or in combination. In this review, the recent advances in elucidating the mechanisms leading to anemia in the setting of heart failure are presented and the evidence supporting the use of different treatment approaches are discussed.

Serum intact parathyroid hormone levels independently predict exercise capacity in stable heart failure patients

[1] McKinney WP, Schiedermayer DL, Lurie N, Simpson DE, Goodman JL, Rich EC. Attitudes of internal medicine faculty and residents toward professional interaction with pharmaceutical sales representatives. JAMA 1990;264:1693–7. [2] Wazana A. Physicians and the pharmaceutical industry: is a gift ever just a gift? JAMA 2000;283:373–80. [3] Zipkin DA, Steinman MA. Interactions between pharmaceutical representatives and doctors in training. A thematic review. J Gen Intern Med 2005;20:777–86. [4] Brett AS, Burr W, Moloo J. Are gifts from pharmaceutical companies ethically problematic? A survey of physicians. Arch Intern Med 2003;163:2213–8. [5] Moubarak G, Martins RP, Zuily S, Mechulan A, Guiot A. [Frequency and type of gifts given by pharmaceutical industry to cardiology residents]. Presse Med 2010;39: e197-204. [6] McCormick BB, Tomlinson G, Brill-Edwards P, Detsky AS. Effect of restricting contact between pharmaceutical company representatives and internal medicine residents on posttraining attitudes and behavior. JAMA 2001;286:1994–9. [7] Schwartz TL, Kuhles II DJ, Wade M, Masand PS. Newly admitted psychiatric patient prescriptions and pharmaceutical sales visits. Ann Clin Psychiatry 2001;13:159–62. [8] Steinman MA, Shlipak MG, McPhee SJ. Of principles and pens: attitudes and practices of medicine housestaff toward pharmaceutical industry promotions. Am J Med 2001;110:551–7. [9] Montague BT, Rosenbaum J. A systematic review of curricula on relationships between residents and the pharmaceutical industry. Med Educ 2008;42:301–8. [10] Coast AJ. Ethics authorship and publishing. Int J Cardiol 2009;131:149–50.