34 research outputs found
What Limits Cardiac Performance during Exercise in Normal Subjects and in Healthy Fontan Patients?
Exercise is an important determinant of health but is significantly reduced in the patient with a univentricular circulation. Normal exercise physiology mandates an increase in pulmonary artery pressures which places an increased work demand on the right ventricle (RV). In a biventricular circulation with pathological increases in pulmonary vascular resistance and/or reductions in RV function, exercise-induced augmentation of cardiac output is limited. Left ventricular preload reserve is dependent upon flow through the pulmonary circulation and this requires adequate RV performance. In the Fontan patient, the reasons for exercise intolerance are complex. In those patients with myocardial dysfunction or other pathologies of the circulatory components, it is likely that these abnormalities serve as a limitation to cardiac performance during exercise. However, in the healthy Fontan patient, it may be the absence of a sub-pulmonary pump which limits normal increases in pulmonary pressures, trans-pulmonary flow requirements and cardiac output. If so, performance will be exquisitely dependent on pulmonary vascular resistance. This provides a potential explanation as to why pulmonary vasodilators may improve exercise tolerance. As has recently been demonstrated, these agents may offer an important new treatment strategy which directly addresses the physiological limitations in the Fontan patient
Recommended from our members
Cancer Therapy and Exercise Intolerance: The Heart Is But a Part: JACC: CardioOncology State-of-the-Art Review.
The landscape of cancer therapeutics is continually evolving, with successes in improved survivorship and reduced disease progression for many patients with cancer. Improved cancer outcomes expose competing comorbidities, some of which may be exacerbated by cancer therapies. The leading cause of disability and death for many early-stage cancers is cardiovascular disease (CVD), which is often attributed to direct or indirect cardiac injury from cancer therapy. In this review, the authors propose that toxicities related to conventional and novel cancer therapeutics should be considered beyond the heart. The authors provide a framework using the oxygen pathway to understand the impact of cancer treatment on peak oxygen uptake, a marker of integrative cardiopulmonary function and CVD risk. Peripheral toxicities and the impact on oxygen transport are discussed. Consideration for the broad effects of cancer therapies will improve the prediction and identification of cancer survivors at risk for CVD, functional disability, and premature mortality and those who would benefit from therapeutic intervention, ultimately improving patient outcomes
Lifelong Exercise Patterns and Cardiovascular Health.
OBJECTIVE: To determine the relationship between lifelong exercise dose and the prevalence of cardiovascular morbidity. PATIENTS AND METHODS: From June 1, 2011, through December 31, 2014, 21,266 individuals completed an online questionnaire regarding their lifelong exercise patterns and cardiovascular health status. Cardiovascular disease (CVD) was defined as a diagnosis of myocardial infarction, stroke, or heart failure, and cardiovascular risk factors (CVRFs) were defined as hypertension, hypercholesterolemia, or type 2 diabetes. Lifelong exercise patterns were measured over a median of 32 years for 405 patients with CVD, 1379 patients with CVRFs, and 10,656 controls. Participants were categorized into nonexercisers and quintiles (Q1-Q5) of exercise dose (metabolic equivalent task [MET] minutes per week). RESULTS: The CVD/CVRF prevalence was lower for each exercise quintile compared with nonexercisers (CVD: nonexercisers, 9.6% vs Q1: 4.4%, Q2: 2.8%, Q3: 2.4%, Q4: 3.6%, Q5: 3.9%; P<.001; CVRF: nonexercisers, 24.6% vs Q1: 13.8%, Q2: 10.2%, Q3: 9.0%, Q4: 9.4%, Q5: 12.0%; P<.001). The lowest exercise dose (Q1) significantly reduced CVD and CVRF prevalence, but the largest reductions were found at 764 to 1091 MET-min/wk for CVD (adjusted odds ratio=0.31; 95% CI, 0.20-0.48) and CVRFs (adjusted odds ratio=0.36; 95% CI, 0.28-0.47). The CVD/CVRF prevalence did not further decrease in higher exercise dose groups. Exercise intensity did not influence the relationship between exercise patterns and CVD or CVRFs. CONCLUSION: These findings demonstrate a curvilinear relationship between lifelong exercise patterns and cardiovascular morbidity. Low exercise doses can effectively reduce CVD/CVRF prevalence, but engagement in exercise for 764 to 1091 MET-min/wk is associated with the lowest CVD/CVRF prevalence. Higher exercise doses do not yield additional benefits
What Limits Cardiac Performance during Exercise in Normal Subjects and in Healthy Fontan Patients?
Exercise is an important determinant of health but is significantly reduced in the patient with a univentricular circulation. Normal exercise physiology mandates an increase in pulmonary artery pressures which places an increased work demand on the right ventricle (RV). In a biventricular circulation with pathological increases in pulmonary vascular resistance and/or reductions in RV function, exercise-induced augmentation of cardiac output is limited. Left ventricular preload reserve is dependent upon flow through the pulmonary circulation and this requires adequate RV performance. In the Fontan patient, the reasons for exercise intolerance are complex. In those patients with myocardial dysfunction or other pathologies of the circulatory components, it is likely that these abnormalities serve as a limitation to cardiac performance during exercise. However, in the healthy Fontan patient, it may be the absence of a sub-pulmonary pump which limits normal increases in pulmonary pressures, trans-pulmonary flow requirements and cardiac output. If so, performance will be exquisitely dependent on pulmonary vascular resistance. This provides a potential explanation as to why pulmonary vasodilators may improve exercise tolerance. As has recently been demonstrated, these agents may offer an important new treatment strategy which directly addresses the physiological limitations in the Fontan patient