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Peak exercise performance in healthy man is limited not only by pulmonary or skeletal muscle function but also by cardiac function. Thus, abnormalities in cardiac function will have a major impact on exercise performance. Many cardiac diseases affect exercise performance and indeed for some cardiac conditions such as atherosclerotic heart disease, exercise testing is frequently used not only to measure functional capacity but also to make a diagnosis of heart disease, evaluate the efficacy of treatment, and predict prognosis. Early in the course of cardiac diseases, exercise performance will be minimally affected but with disease progression impairment in exercise capacity will become apparent. Ejection fraction, that is, the percent of blood volume ejected with each cardiac cycle is often used as a measure of cardiac performance but frequently there is a dissociation between the ejection fraction and exercise capacity in patients with heart disease. How abnormalities in cardiac function impacts the muscles, vasculature, and lungs to impact exercise performance will here be reviewed. The focus of this work will be on patients with systolic heart failure as the incidence and prevalence of heart failure is reaching epidemic proportions and heart failure is the end result of many other chronic cardiac diseases. The prognostic role of exercise and benefits of exercise training will also be discussed.

Skeletal muscle dysfunction in patients with heart failure (HF) has been linked to impaired growth hormone (GH)/insulin-like growth factor (IGF)-1 signaling. We hypothesized that ventricular assist device (VAD) implantation reverses GH/IGF-1 axis dysfunction and improves muscle metabolism in HF.Blood and rectus abdominis muscle samples were collected during VAD implantation and explantation from patients with HF and controls. Clinical data were obtained from medical records, biomarkers measured by enzyme-linked immunosorbent assay (ELISA), and gene expression analyzed by reverse transcription and real-time polymerase chain reaction (RT-PCR). Grip strength was assessed by dynamometry. Oxidative capacity was measured using oleate oxidation rates. Muscle fiber type and size were assessed by histology.Elevated GH (0.27 ± 0.27 versus 3.6 ± 7.7 ng/ml in HF; p = 0.0002) and lower IGF-1 and insulin-like growth factor binding protein (IGFBP)-3 were found in HF (IGF-1, 144 ± 41 versus 74 ± 45 ng/ml in HF, p 0.05; and IGFBP-3, 3,880 ± 934 versus 1,935 ± 862 ng/ml in HF, p = 0.05). The GH/IGF-1 ratio, a marker of GH resistance, was elevated in HF (0.002 ± 0.002 versus 0.048 ± 0.1 pre-VAD; p 0.0039). After VAD support, skeletal muscle expression of IGF-1 and IGFBP-3 increased (10-fold and 5-fold, respectively; p 0.05) accompanied by enhanced oxidative gene expression (CD36, CPT1, and PGC1α) and increased oxidation rates (+1.37-fold; p 0.05). Further, VAD implantation increased the oxidative muscle fiber proportion (38 versus 54 %, p = 0.031), fiber cross-sectional area (CSA) (1,005 ± 668 versus 1,240 ± 670 μm(2), p 0.001), and Akt phosphorylation state in skeletal muscle. Finally, hand grip strength increased 26.5 ± 27.5 % at 180 days on-VAD (p 0.05 versus baseline).Our data demonstrate that VAD implantation corrects GH/IGF-1 signaling, improves muscle structure and function, and enhances oxidative muscle metabolism in patients with advanced HF.

Background Percutaneous coronary intervention with stent placement for the treatment of patients with cardiac allograft vasculopathy is common, but data regarding stent behavior in this setting is lacking. Objectives We investigated mechanisms and potential differences in stent expansion among transplant patients vs. patients with native coronary artery atherosclerotic disease (“controls”). Methods We compared pre- and poststent intravascular ultrasound in 12 transplant patients (17 lesions) and 33 control patients (34 lesions) matched according to age (60.1 ± 9.2 years), diabetes mellitus, and lesion location. Planar and volumetric analysis was conducted for every 1 mm at the lesion site as well as the first 5 mm proximal and distal to the stent edge. Focal stent expansion was defined as minimum stent area (MSA) divided by mean reference lumen area. Diffuse stent expansion was defined as mean stent area divided by mean reference lumen area. Results Transplant patients had more plaque than “controls” prestenting, but similar MSA and focal and diffuse stent expansion afterwards. The increase in mean lumen area correlated with the increase in mean vessel area in both groups, transplant (R = 0.64, P = 0.008) and controls (R = 0.70, P < 0.0001), but correlated inversely with changes in mean plaque area only in the transplant group (R = 0.55, P = 0.027). There were no differences in calcification between the two groups and no axial plaque distribution from the lesion into the reference segments in either group. Conclusions The mechanism of stent expansion in transplant vasculopathy appears to be similar to de novo atherosclerosis—i.e., mainly vessel expansion to achieve similar acute results. © 2012 Wiley Periodicals, Inc.

Peak oxygen consumption (VO(2) ) during cardiopulmonary exercise testing (CPET) is a powerful predictor of survival, providing an indirect assessment of cardiac output (CO). Noninvasive indices of CO derived from bioreactance methodology would add significantly to peak VO(2) as a means of risk-stratifying patients with heart failure. In this study, 127 patients (53 ± 14 years of age, 66% male) with heart failure and an average ejection fraction of 31% ± 15% underwent symptom-limited CPET using a bicycle ergometer while measuring CO noninvasively by a bioreactance technique. Peak cardiac power was derived from the product of the peak mean arterial blood pressure and CO divided by 451. Follow-up averaged 404 ± 179 days (median, 366 days) to assess endpoints including death (n=3), heart transplant (n=10), or left ventricular assisted device implantation (n=2). Peak VO(2) and peak power had similar areas under the curve (0.77 and 0.76), which increased to 0.83 when combined. Kaplan-Meier cumulative survival curves demonstrated different outcomes in the subgroup with a VO(2)

A prospective, open-label, 3-month study was conducted to evaluate the feasibility and short-term clinical effect of subcutaneous erythropoietin injections in patients with anemia and heart failure with preserved ejection fraction (ejection fraction, 55%+/-2%). Using a dose-adjusted algorithm to effect a rate of rise in hemoglobin not to exceed 0.4 g/dL /wk, hemoglobin (10.8+/-0.3 to 12.2+/-0.3 g/dL) and red blood cell volume (1187+/-55 to 1333+/-38 mL) increased with an average weekly dose of 3926 units. Functional measures increased from baseline (6-minute walk test [289+/-24 to 331+/-22 m], exercise time [432+/-62 to 571+/-51 s], and peak oxygen consumption [8.2+/-0.7 to 9.4+/-0.9 mL/kg/min], all P