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

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

Right ventricular suction: an important determinant of cardiac performance

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Sudden Cardiac Death in Systemic Sclerosis: Diagnostics to Assess Risk and Inform Management

Cardiac disease is a leading cause of death in systemic sclerosis (SSc) and sudden cardiac death (SCD) is thought to occur more commonly in SSc than in the general population. Diffuse myocardial fibrosis, myocarditis and ischaemic heart disease are all prevalent in SSc and can be reasonably hypothesised to contribute to an increased risk of SCD. Despite this, SCD remains a relatively understudied area of SSc with little understood about SSc-specific risk factors and opportunities for primary prevention. In this review, we present an overview of the possible mechanisms of SCD in SSc and our current understanding of how each of these mechanisms may contribute to cardiac death. This review highlights the need for a future research agenda that addresses the underlying epidemiology of SCD in SSc and identifies opportunities for intervention to modify the disease course of heart disease in SSc