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Cardiovascular disease is a competing cause of death in patients with cancer with early-stage disease. This elevated cardiovascular disease risk is thought to derive from both the direct effects of cancer therapies and the accumulation of risk factors such as hypertension, weight gain, cigarette smoking, and loss of cardiorespiratory fitness. Effective and viable strategies are needed to mitigate cardiovascular disease risk in this population; a multimodal model such as cardiac rehabilitation may be a potential solution. This statement from the American Heart Association provides an overview of the existing knowledge and rationale for the use of cardiac rehabilitation to provide structured exercise and ancillary services to cancer patients and survivors. This document introduces the concept of cardio-oncology rehabilitation, which includes identification of patients with cancer at high risk for cardiac dysfunction and a description of the cardiac rehabilitation infrastructure needed to address the unique exposures and complications related to cancer care. In this statement, we also discuss the need for future research to fully implement a multimodal model of cardiac rehabilitation for patients with cancer and to determine whether reimbursement of these services is clinically warranted.

Exercise and competitive sports should be associated with a wide range of health benefits with the potential to inspire a positive community health legacy. However, the reputation of sports is being threatened by an ever-expanding armamentarium of agents with real or perceived benefits in performance enhancement. In addition to the injustice of unfair advantage for dishonest athletes, significant potential health risks are associated with performance-enhancing drugs. Performance-enhancing drugs may have an effect on the cardiovascular system by means of directly altering the myocardium, vasculature, and metabolism. However, less frequently considered is the potential for indirect effects caused through enabling athletes to push beyond normal physiological limits with the potential consequence of exercise-induced arrhythmias. This review will summarize the known health effects of PEDs but will also focus on the potentially greater health threat posed by the covert search for performance-enhancing agents that have yet to be recognized by the World Anti-Doping Agency. History has taught us that athletes are subjected to unmonitored trials with experimental drugs that have little or no established efficacy or safety data. One approach to decrease drug abuse in sports would be to accept that there is a delay from when athletes start experimenting with novel agents to the time when authorities become aware of these drugs. This provides a window of opportunity for athletes to exploit with relative immunity. It could be argued that all off-label use of any agent should be deemed illegal.

We were delighted to read the article by Bohm et al1 addressing the potential deleterious impact of exercise on right ventricular (RV) function. This field definitely needs further study. The work was carried out by a renowned group. However, we were surprised by their conclusion “that the hypothesis of an exercise-induced ARVC needs to be questioned,”1 not only because the small study is underpowered but mainly because the conclusion is not supported by the findings. The authors summed up 4 criteria by which to test the hypothesis. The first concerned the ratio of left ventricular end-diastolic volume/right ventricular end-diastolic volume (LVEDV/RVEDV). This test is indirect at best, only …

Introduction: Due to the absence of a sub-pulmonary ventricle, the Fontan circulation is sensitive to respiration-induced changes in intrathoracic pressure. However, the importance of a ‘respiratory pump’ in creating forward flow remains controversial. We aim to investigate the effects and mechanisms of respiration on ventricular filling at rest and exercise using clinical data and computational modeling. Hypothesis: We assess the hypotheses that (1) changes in intrathoracic pressure due to respiration would aid ventricular filling and output and (2) this effect would be maintained or enhanced during incremental exercise. Methods: Ten Fontan patients (6 male, 20±4 years) underwent ungated cardiac magnetic resonance imaging at rest and during supine bicycle exercise (3 incremental intensities) to evaluate systemic ventricular volumes. Patient-specific computational simulations using a lumped-parameter network model of Fontan exercise elucidated resting and exercise physiology in details for each patient at each metabolic state tested. Results: Compared to expiration, inspiration increased EDVi (98±16 to 103±15 mL/m2;P=0.001), SVi (55±9 to 59±9 mL/m2;P=0.001) and cardiac index (3.9±0.7 to 4.2±0.8 L/min/m2;P=0.002), but did not affect ESVi (P=0.096). Respiratory-dependent SVi did not change significantly during incremental exercise (3±2% to 5±3%; P=0.084). Computational modeling showed highest caval vein flow return during end-inspiration, and peak SV during expiration, exposing a phased time-delay mechanism at work. Removal of respiration in simulations corresponded to decreases in cardiac index of 0.39±0.037 L/min/m2. Conclusions: Inspiration increased ventricular filling at rest and exercise by similar amounts. A phased time-delay between highest caval vein flow and highest SV suggests an indirect mechanism where respiration aids ventricular filling via pulmonary compliance.

Introduction: Right ventricular dysfunction (RVD) is a marker of adverse outcome in HFpEF patients. While RVD in HFpEF has been demonstrated using dobutamine stress and invasive hemodynamic studies, detailed assessment of RV and pulmonary vascular (PV) function using simultaneous exercise cardiac MRI and invasive hemodynamic measurements has never been performed. Methods In a prospective study, we performed CPET to determine maximal power output (Pmax) in patients with HFpEF (n=11, age 73±9 years) and in healthy controls (n=8, age 53±7 years). We also investigated asymptomatic subjects with echocardiographic evidence of LV concentric remodeling (LVCR) and impaired relaxation (n=4, age 63±7 years). All participants then performed a three-stage supine bicycle exercise test during real-time CMR imaging (at 25%, 50% and 66% of Pmax) with continuous recording of pulmonary arterial pressures using fluid-filled catheters. We determined the ratio of mPAP relative to cardiac output (mPAP/CO slope) as a measure of PV reserve and the change in RV end-systolic pressure volume ratio (dRVESPR) as a measure for RV contractile reserve. Results At rest, there was no difference in LV or RV ejection fraction (EF) between HFpEF patients and controls (p=NS). However, during exercise, HFpEF patients showed a decline in RVEF (-3.9±1.7%), contrasting with a marked increase in RVEF in the control group (+12.49±2.33%, p Conclusion In patients with HFpEF, RV functional reserve and pulmonary pressure-flow relationships are markedly impaired. These data suggest an important role for cardiac exercise MRI in phenotyping heart failure patients and guiding RV or pulmonary vasculature targeted therapy.

2This has led to considerable confusion in discussions of the health benefits of high-level exercise. Until we devise some standard reference of exercise quantification, we will continue to lump recreational exer cise enthusiasts and professional athletes under nonspecific umbrella terms when the amount of exercise, extent of cardiac remodeling, and related health consequences may be quite different. In the words of Paracelsus referred to by Scott and Haykowsky, we cannot attempt to discriminate between the “the right dose [which] differentiates a poison and a remedy” if we do not even know how to measure the dose. We would support a peer group discussion aimed at establishing clearer definitions of exercise quantification so that we can approach this expanding field of scientific discovery with greater clarity. Dr Mohlenkamp and colleagues highlight another interaction between intense exercise and cardiac health that we did not address. We thank them for highlighting the fact that intense exercise can serve as a trigger of cardiac events in persons with underlying atherosclerotic coronary disease. In our article, 1 we discussed the controversial and unproven causal relationship between exercise-induced cardiac remodeling and predisposition to arrhythmias such as atrial fibrillation and ventricular arrhythmias. As a very important but different clinical question, Mohlenkamp et al investigated subclinical coronary vessel disease in middle-aged exercise enthusiasts who had relatively recently taken up marathon running. They studied 108 subjects who were >50 years of age (mean age, 57 years) and had started marathon training within the preceding decade.3 More than half of the subjects were previous smokers, their body mass indexes were in the upper end of the healthy range, and their exercise training volume was relatively modest compared with that proposed to cause cardiac remodeling. Therefore, it was perhaps not surprising that Mohlenkamp et al identified an incidence of coronary vessel disease approximating that of the general population. For reasons that remain unexplained, they also found more prevalent myocardial fibrosis. Their study design does not address the causal question, that is, whether intense exercise prevents or promotes atherosclerotic heart disease. This would

Introduction: Ventricular arrhythmias in endurance athletes (EAs) frequently originate from a mildly dysfunctional right ventricle (RV). We evaluated whether RV dysfunction in EAs with ventricular arrhythmias of RV origin (EA-VAs) becomes more apparent during exercise than at rest. Methods: Ten healthy EAs, 7 healthy non-athletes (NAs) and 17 EA-VAs (8 with ICD) first underwent cardiopulmonary exercise testing to determine maximal power (Pmax). Then, exercise echocardiography was performed at 25%, 50% and 66% of Pmax to measure the RV end-systolic pressure-area ratio (ESPAR), a surrogate of RV contractility, which was calculated as systolic pulmonary artery pressure/RV end-systolic area. Finally, all subjects without ICD underwent cardiac MRI during supine bicycle exercise at similar workloads with simultaneous invasive pulmonary artery pressure measurement to determine the RV end-systolic pressure-volume ratio (SP/ESV). Results: At rest, RV ESPAR was similar in EA-VAs relative to NAs (P=0.1), although slightly lower than in NAs (P=0.02). During exercise, EA-VAs had an impaired increase in RV ESPAR compared to both EAs and NAs (interaction P2 had a sensitivity of 77% and 79% and specificity of 80% and 100%, respectively, to identify EA-VAs. Conclusion: EA-VAs have impaired RV contractility which is evident during exercise but hardly at rest. This strengthens the association between RV arrhythmias and functional impairment. Our data suggest that exercise echocardiography is sufficiently accurate to determine RV contractile reserve in a non-invasive manner and may assist in risk stratification of RV remodeling in EAs.