Search

Abstract Recent research has demonstrated that cardiovascular deconditioning (i.e., cardiac atrophy and hypovolemia) contributes significantly to the Postural Orthostatic Tachycardia Syndrome (POTS) and its functional disability. Therefore, physical reconditioning with exercise training and volume expansion via increased salt and fluid intake should be initiated early in the course of treatment for patients with POTS if possible. The use of horizontal exercise (e.g., rowing, swimming, recumbent bike, etc.) at the beginning is a critical strategy, allowing patients to exercise while avoiding the upright posture that elicits their POTS symptoms. As patients become increasingly fit, the duration and intensity of exercise should be progressively increased, and upright exercise can be gradually added as tolerated. Supervised training is preferable to maximize functional capacity. Other non-pharmacological interventions, which include: 1) chronic volume expansion via sleeping in the head-up position; 2) reduction in venous pooling during orthostasis by lower body compression garments extending at least to the xiphoid or with an abdominal binder; and 3) physical countermeasure maneuvers, such as squeezing a rubber ball, leg crossing, muscle pumping, squatting, negative-pressure breathing, etc., may also be effective in preventing orthostatic intolerance and managing acute clinical symptoms in POTS patients. However, randomized clinical trials are needed to evaluate the efficacies of these non-pharmacological treatments of POTS. [ABSTRACT FROM AUTHOR]

Objectives The authors sought to determine the relative contributions of baseline coronary artery calcification (CAC), follow-up CAC, and CAC progression on incident cardiovascular disease (CVD). Background Repeat CAC scanning has been proposed as a method to track progression of total atherosclerotic burden. However, whether CAC progression is a useful predictor of future CVD events remains unclear. Methods This was a prospective observational study of 5,933 participants free of CVD who underwent 2 examinations, including CAC scores, and subsequent CVD event assessment. CAC progression was calculated using the square root method. The primary outcome was total CVD events (CVD death, nonfatal myocardial infarction, nonfatal atherosclerotic stroke, coronary artery bypass surgery, percutaneous coronary intervention). Secondary outcomes included hard CVD events, total coronary heart disease (CHD) events, and hard CHD events. Results CAC was detected at baseline in 2,870 individuals (48%). The average time between scans was 3.5 ± 2.0 years. After their second scan, 161 individuals experienced a total CVD event during a mean follow-up of 7.3 years. CAC progression was significantly associated with total CVD events (hazard ratio: 1.14, 95% confidence interval: 1.01 to 1.30 per interquartile range; p = 0.042) in the model including baseline CAC, but the contribution of CAC progression was small relative to baseline CAC (chi-square 4.16 vs. 65.92). Furthermore, CAC progression was not associated with total CVD events in the model including follow-up CAC instead of baseline CAC (hazard ratio: 1.05, 95% confidence interval: 0.92 to 1.21; p = 0.475). A model that included follow-up CAC alone performed as well as the model that included baseline CAC and CAC progression. Conclusions Although CAC progression was independently, but modestly, associated with CVD outcomes, this relationship was no longer significant when including follow-up CAC in the model. These findings imply that if serial CAC scanning is performed, the latest scan should be used for risk assessment, and in this context, CAC progression provides no additional prognostic information. [ABSTRACT FROM AUTHOR]

Background: Postural orthostatic tachycardia syndrome (POTS) affects primarily young women and impairs quality of life. We found that in a research setting, exercise training along with lifestyle intervention is effective as a nondrug therapy for POTS.Objective: To evaluate the efficacy of our exercise training/lifestyle intervention in POTS patients in a community environment.Methods: We established a POTS registry and enrolled 251 patients (86% women, aged 26 ± 11 [SD] years) through their physicians. A 3-month program involving mild- to moderate-intensity endurance training (progressing from semirecumbent to upright, 3-5 times/wk, 30-45 min/session) plus strength training was implemented along with increasing salt/water intake. The program was delivered to the physicians, who oversaw training in their patients. A 10-minute stand test was performed at the physician's office and patient quality of life was assessed using the 36-Item Short Form Health Survey.Results: One hundred and three patients completed the program. Of those that completed, 71% no longer qualified for POTS and were thus in remission. The increase in heart rate from supine to 10-minute stand was markedly lower (23 ± 14 vs. 46 ± 17 beats/min before intervention; P < .001), while patient quality of life was improved dramatically after intervention (P < .001). Of those who were followed for 6-12 months (n = 31), the effect was persistent.Conclusions: A training/lifestyle intervention program can be implemented in a community setting with physician supervision and is effective in the treatment of POTS. It remains to be determined whether exercise can be an effective long-term treatment strategy for this condition, though patients are encouraged to maintain an active lifestyle indefinitely. [ABSTRACT FROM AUTHOR]

Summary We have developed a Drosophila lung cancer model by targeting Ras1 G12V —alone or in combination with PTEN knockdown—to the Drosophila tracheal system. This led to overproliferation of tracheal tissue, formation of tumor-like growths, and animal lethality. Screening a library of FDA-approved drugs identified several that improved overall animal survival. We explored two hits: the MEK inhibitor trametinib and the HMG-CoA reductase inhibitor fluvastatin. Oral administration of these drugs inhibited Ras and PI3K pathway activity, respectively; in addition, fluvastatin inhibited protein prenylation downstream of HMG-CoA reductase to promote survival. Combining drugs led to synergistic suppression of tumor formation and rescue lethality; similar synergy was observed in human A549 lung adenocarcinoma cells. Notably, fluvastatin acted both within transformed cells and also to reduce whole-body trametinib toxicity in flies. Our work supports and provides further context for exploring the potential of combining statins with MAPK inhibitors such as trametinib to improve overall therapeutic index. [ABSTRACT FROM AUTHOR]

The article discusses research that reviewed the basic principles of exercise physiology, cardiovascular adaptations unique to the cardiovascular system of athletes, and exercise testing in athletes. Topics covered include the ability of the cardiovascular system to meet the increased metabolic demand for oxygen by the working muscles, the "athlete's heart" phenomenon that involves physiologic hypertrophy and resting sinus bradycardia, and exercise testing for evaluating sports performance.

Patients with the Postural Orthostatic Tachycardia Syndrome (POTS) have orthostatic intolerance, as well as exercise intolerance. Peak oxygen uptake (VO 2peak ) is generally lower in these patients compared with healthy sedentary individuals, suggesting a lower physical fitness level. During acute exercise, POTS patients have an excessive increase in heart rate and reduced stroke volume for each level of absolute workload; however, when expressed at relative workload (%VO 2peak ), there is no difference in the heart rate response between patients and healthy individuals. The relationship between cardiac output and VO 2 is similar between POTS patients and healthy individuals. Short-term (i.e., 3 months) exercise training increases cardiac size and mass, blood volume, and VO 2peak in POTS patients. Exercise performance is improved after training. Specifically, stroke volume is greater and heart rate is lower at any given VO 2 during exercise after training versus before training. Peak heart rate is the same but peak stroke volume and cardiac output are greater after training. Heart rate recovery from peak exercise is significantly faster after training, indicating an improvement in autonomic circulatory control. These results suggest that patients with POTS have no intrinsic abnormality of heart rate regulation during exercise. The tachycardia in POTS is due to a reduced stroke volume. Cardiac remodeling and blood volume expansion associated with exercise training increase physical fitness and improve exercise performance in these patients. [ABSTRACT FROM AUTHOR]

Physical activity (PA) and cardiorespiratory fitness (CRF) both have inverse relationships to cardiovascular (CV) morbidity and mortality. Recent position papers and guidelines have identified the important role of both of these factors in CV health. The benefits of PA and CRF in the prevention of CV disease and risk factors are reviewed. In addition, assessment methodology and utilization in the research and clinical arenas are discussed. Finally, the benefits, methodology, and utilization are compared and contrasted to better understand the two (partly) distinct components and their impact on CV health. [ABSTRACT FROM AUTHOR]

Background: Mountain activities characterized by strenuous exercise in a hypoxic setting place unique demands on the body. The mortality rate associated with mountain activities is high, with sudden cardiac death (SCD) representing the most frequent of all nontraumatic deaths. We evaluated the possible effect of acclimatization in reduction of SCD during high-altitude sojourns. Methods: This was a retrospective cohort study involving all deaths (N = 559) that occurred during mountain activities in Austria from 1985 through 1993. Baseline patient demographics, cardiovascular comorbidities, smoking history, family history of SCD, sleeping altitude, annual mountaineering frequency, and physical activity on the day of SCD were included in a questionnaire previously used in a pilot study. Results: Data from 301 of 599 individuals without prespecified exclusions were available for analysis (79% of eligible cohort). Sudden cardiac deaths happened mostly around noon (29%), and mean altitude at which SCDs occurred was 1,710 ± 501 m. When sleeping altitude was divided into quartiles (<700 m, 700-999 m, 1,000-1,299 m, and >1,299 m), the odds ratio for SCD on the first day at altitude when sleeping below 700 m was 5.7 (95% CI 2.8-11.6) as compared with sleeping above 1,299 m. Conclusion: For males >34 years, those with history of coronary artery disease and/or prior infarction, and those unaccustomed to physical activity at altitude, sleeping at moderate altitude before exercising at altitude may reduce the risk of SCD. [Copyright &y& Elsevier]

Background: Heart failure with preserved ejection fraction (HFpEF) is a disease of the elderly with cardiovascular stiffening and reduced exercise capacity. Exercise training appears to improve exercise capacity and cardiovascular function in heart failure with reduced ejection fraction. However, it is unclear whether exercise training could improve cardiovascular stiffness, exercise capacity, and ventricular-arterial coupling in HFpEF. Methods: Eleven HFpEF patients and 13 healthy controls underwent invasive measurements with right heart catheterization to define Starling and left ventricular (LV) pressure-volume curves; secondary functional outcomes included Doppler echocardiography, arterial stiffness, cardiopulmonary exercise testing with cardiac output measurement, and ventricular-arterial coupling assessed by the dynamic Starling mechanism. Seven of 11 HFpEF patients (74.9 ± 6 years; 3 men/4 women) completed 1 year of endurance training followed by repeat measurements. Pulmonary capillary wedge pressures and LV end-diastolic volumes were measured at baseline during decreased and increased cardiac filling. LV compliance was assessed by the slope of the pressure-volume curve. Beat-to-beat LV end-diastolic pressure (estimated from pulmonary arterial diastolic pressure) and stroke volume index were obtained, and spectral transfer function analysis was used to assess the dynamic Starling mechanism. Results: Before training, HFpEF patients had reduced exercise capacity, distensibility and dynamic Starling mechanism but similar LV compliance and end-diastolic volumes compared to controls albeit with elevated filling pressure and increased wall stress. One year of training had little effect on LV compliance and volumes, arterial stiffness, exercise capacity or ventricular-arterial coupling. Conclusion: Contrary to our hypothesis, 1 year of endurance training failed to impart favorable effects on cardiovascular stiffness or function in HFpEF. [Copyright &y& Elsevier]

Abstract: Syncope is a common but concerning event in athletic patients. As such, efforts must be made to distinguish presyncope from syncope with a critical distinction of syncope during exercise and postexercise syncope. Syncope most often occurs just after exercise and is usually benign; however, syncope during exercise may be a sign of pathologic structural or electrical cardiac issues. Solving this diagnostic puzzle mandates a detailed history and examination frequently augmented with diagnostic testing and imaging studies. Recommendations for treatment and potential restriction from activity also present challenging decisions to the health care provider. [Copyright &y& Elsevier]

Abstract: The level of circulating erythropoietin (EPO) in response to a fixed level of hypoxia shows substantial inter-individual variability, the source of which is undetermined. Arterial PO2 at altitude is regulated in part by the hypoxic ventilatory response, which also shows a wide inter-individual variability. We asked if the ventilatory response to hypoxia is related to the magnitude of EPO release at moderate altitude. Twenty-six national class US distance runners (17 M, 9 F) participated in a test of isocapnic hypoxic ventilatory response (HVR) at sea level, 2–7 days prior to departure to altitude. EPO measures were obtained at sea level and after 20h at 2500m. HVR for all subjects was 0.21±0.16Lmin−1 %SaO2 −1 (range 0.01–0.61Lmin−1 %SaO2 −1), with no significant difference between men and women. EPO was significantly increased from pre-altitude (8.6±2.6ngml−1, range 4.0–14.6ngml−1) to acute altitude (16.6±4.4ngml−1, range 5.0–27.0ngml−1), an increase of 92.2±70.1%. There was no significant sex difference in the EPO increase. ΔEPO for all subjects was not correlated with HVR (r =−0.17). Similarly, a statistically or physiologically significant correlation was not present between ΔEPO and HVR within the group of men (r =−0.22) or women (r =−0.19). The variability in the acute EPO response to moderate altitude is not explained by differences in peripheral chemoresponsiveness in elite distance runners. These results suggest that factors acting downstream from the lung influence the magnitude of the acute EPO response to altitude. [ABSTRACT FROM AUTHOR]

The article presents an overview of exertional collapse in runners, which is defined as the inability to stand or walk unaided as a result of lightheadedness, faintness, dizziness, or syncope. A discussion of research which has been conducted on exertional collapse is presented. The epidemiology, pathophysiology and diagnosis of exertional collapse is discussed.

Abstract: Background: Whether the absence of coronary artery calcium, or conversely the presence of high volumes of coronary artery calcium, may alter assessment of coronary heart disease risk based on traditional risk factors is uncertain. We sought to identify a potential threshold of coronary artery calcium for clinical use and examine the predictive power of coronary artery calcium in individuals categorized using conventional coronary heart disease risk assessment. Methods: The study included 10,746 men and women (36.3%) with a mean age of 53.8±9.9 years who were either physician- or self-referred for electron beam tomography scanning to a preventive medical clinic. Coronary heart disease risk factors were elicited by use of a questionnaire. Results: During a mean follow-up of 3.5 years, 81 primary events (coronary heart disease death or nonfatal myocardial infarction) occurred. Among individuals with a coronary artery calcium score of zero, the primary event rate was very low (0.4 events per 1000 person-years of observation). When participants were stratified by self-reported coronary heart disease risk factors (0–2, or 3–4), a coronary artery calcium score ≥100 was associated with substantially increased risk of coronary heart disease events within each level of stratification. In a subgroup of participants with available clinical data, similar results were found when participants were categorized by Framingham risk scores. Conclusions: Coronary artery calcium score can identify individuals at increased risk for coronary heart disease events who otherwise would be considered low-risk based on clinical assessment. A coronary artery calcium score of zero is associated with very low risk for coronary heart disease in the short to intermediate term (≈3.5 years) regardless of the number of risk factors present. [Copyright &y& Elsevier]

Syncope is a common clinical condition occurring even in otherwise healthy people without underlying cardiovascular disease. Neurally mediated syncope is by far the most common cause of syncope in individuals without any structural heart disease. Based on traditional wisdom, loss of sympathetic tone with relaxation of vascular smooth muscle is the key mechanism underlying the pathophysiology of syncope, especially in patients without an acute decrease in heart rate. However, this concept has recently been challenged. Some microneurographic studies indicate that sympathetic withdrawal may not always be a prerequisite even for the development of classic "vasodepressor" forms of syncope. Conversely, a decrease in cardiac output appears to be a determinant factor for syncope in most circumstances. This article reviews the relative contribution of cardiac output versus sympathetic vasoconstriction in neurally mediated syncope in otherwise healthy individuals. It is suggested that a moderate to severe fall in cardiac output with or without vasodilatation may contribute to syncope. [ABSTRACT FROM AUTHOR]

Routine exercise leads to cardiovascular adaptations that differ based on sex. Use of cardiac testing to screen athletes has driven research to define how these sex-based adaptations manifest on the electrocardiogram and cardiac imaging. Importantly, sex-based differences in cardiovascular structure and outcomes in athletes often parallel findings in the general population, underscoring the importance of understanding their mechanisms. Substantial gaps exist in the understanding of why cardiovascular adaptations and outcomes related to exercise differ by sex because of underrepresentation of female participants in research. As female sports participation rates have increased dramatically over several decades, it also remains unknown if differences observed in older athletes reflect biological mechanisms vs less lifetime access to sports in females. In this review, we will assess the effect of sex on cardiovascular adaptations and outcomes related to exercise, identify the impact of sex hormones on exercise performance, and highlight key areas for future research. [Display omitted] • Exercise performance, cardiac adaptation, and outcomes of exercise differ based on sex. • Female sex appears protective against exercise-associated coronary artery calcification, myocardial fibrosis, atrial fibrillation, and sudden cardiac death. • Greater representation of females in research will improve understanding of the causes of sex-based differences in the effect of exercise on the cardiovascular system. [ABSTRACT FROM AUTHOR]

Current guidelines recommend that patients with hypertrophic cardiomyopathy (HCM) not partake in high-intensity exercise due to the increased risk of sudden cardiac death. But individuals with genetic cardiomyopathies are not immune from cardiometabolic diseases, and inactivity is common in patients with HCM, likely due to fear of exercise-induced adverse events. The RESET-HCM trial (Study of Exercise Training in Hypertrophic Cardiomyopathy) illustrated that although moderate-intensity exercise may be safe in this population, the increase in cardiorespiratory fitness achieved with this training paradigm is modest. High-intensity exercise is an efficacious stimulus for increasing cardiorespiratory fitness in chronic disease populations. Such increases in fitness are associated with substantial reductions in cardiovascular mortality and may outweigh the theoretical risks associated with exercise in patients with HCM. The goal of this review is to examine the evidence supporting the safety and efficacy of different intensities of exercise training in HCM, and consider novel strategies to improve fitness. [ABSTRACT FROM AUTHOR]

Ventricular mass responds to changes in physical activity and loading, with cardiac hypertrophy after exercise training, and cardiac atrophy after sustained inactivity. Ventricular wall stress (ie, loading) decreases during microgravity. Cardiac atrophy does not plateau during 12 weeks of simulated microgravity but is mitigated by concurrent exercise training. The goal of this study was to determine whether the current exercise countermeasures on the International Space Station (ISS) offset cardiac atrophy during prolonged space flight. We measured left ventricular (LV) and right ventricular (RV) mass and volumes (via magnetic resonance imaging) in 13 astronauts (4 females; age 49 ± 4 years), between 75 and 60 days before and 3 days after 155 ± 31 days aboard the ISS. Furthermore, we assessed total cardiac work between 21 and 7 days before space flight and 15 days before the end of the mission. Data were compared via paired-samples t -tests. Total cardiac work was lower during space flight (P = 0.008); however, we observed no meaningful difference in LV mass postflight (pre: 115 ± 30 g vs post: 118 ± 29 g; P = 0.053), with marginally higher LV stroke volume (P = 0.074) and ejection fraction postflight (P = 0.075). RV mass (P = 0.999), RV ejection fraction (P = 0.147), and ventricular end-diastolic (P = 0.934) and end-systolic volumes (P = 0.145) were not different postflight. There were strong positive correlations between the relative change in LV mass with the relative changes in total cardiac output (r = 0.73; P = 0.015) and total cardiac work (r = 0.53; P = 0.112). The current exercise countermeasures used on the ISS appear effective in offsetting reductions in cardiac mass and volume, despite overall reductions in total cardiac work, during prolonged space flight. [Display omitted] [ABSTRACT FROM AUTHOR]

Across differing spectrums of cardiac function and cardiac pathologies, there are strong associations between measures of cardiorespiratory fitness and burden of symptoms, quality of life, and prognosis. In this part 2 of a 4-part series, we contend that there is a strong association among physical activity, cardiorespiratory fitness, and cardiac function. We argue that a chronic lack of exercise is a major risk factor for heart failure with preserved ejection fraction in some patients. In support of this hypothesis, increasing physical activity is associated with greater cardiac mass, greater stroke volumes, greater cardiac output and peak oxygen consumption, and fewer clinical events. Conversely, physical inactivity results in cardiac atrophy, reduced output, reduced chamber size, and decreased ability to augment cardiac performance with exercise. Moreover, physical inactivity is a strong predictor of heart failure risk and death. In sum, exercise deficiency should be considered part of the broad heart failure with preserved ejection fraction phenotype. [ABSTRACT FROM AUTHOR]

Abstract: Coronary artery calcium (CAC) scores ≥100 are predictive of CHD events in asymptomatic men. Exercise tolerance of ≥10METs predicts lower event rates in CHD patients; however, its relationship with events in individuals with subclinical atherosclerosis is less known. Participants were 710 asymptomatic men from the Aerobics Center Longitudinal Study whose exercise tolerance (ET) was quantified (<10 or ≥10METs) and whose CAC score was ≥100 as measured by electron beam tomography. During 3.5 years of follow-up 59 CHD events occurred. The age-adjusted hazard ratio (HR) of CHD events was 0.26 (95% CI=0.15–0.45) in men whose ET was ≥10METs compared with men whose ET was <10METs. Adjustment for CHD risk factors and abnormal exercise ECG did not change the association between ET and CHD. The extent of underlying atherosclerosis did not influence the association between ET and CHD; for example, the HR for CHD events in the ≥10MET group among men with CAC scores <400 and ≥400 was 0.16 (95% CI=0.05–0.56) and 0.23 (95% CI=0.11–0.46), respectively. In asymptomatic men with subclinical coronary atherosclerosis, an ET of ≥10METs identifies patients at lower risk for manifest CHD. [Copyright &y& Elsevier]

The role of the sports cardiologist has evolved into an essential component of the medical care of athletes. In addition to the improvement in health outcomes caused by reductions in cardiovascular risk, exercise results in adaptations in cardiovascular structure and function, termed exercise-induced cardiac remodeling. As diagnostic modalities have evolved over the last century, we have learned much about the healthy athletic adaptation that occurs with exercise. Sports cardiologists care for those with known or previously unknown cardiovascular conditions, distinguish findings on testing as physiological adaptation or pathological changes, and provide evidence-based and "best judgment" assessment of the risks of sports participation. We review the effects of exercise on the heart, the approach to common clinical scenarios in sports cardiology, and the importance of a patient/athlete-centered, shared decision-making approach in the care provided to athletes. [ABSTRACT FROM AUTHOR]

The age-associated increase in cardiac and central arterial stiffness is attenuated with lifelong (>25 years) endurance exercise in a dose-dependent manner. Remodelling of the extracellular matrix of cardiovascular structures may underpin these lifelong exercise adaptations in structural stiffness. The primary aim was to examine whether matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) levels are associated with aging and lifelong exercise-related changes in cardiac and central arterial stiffness. Plasma MMPs and TIMPs, left ventricular (LV) (LV stiffness constant) and central arterial stiffness (pulse wave velocity) were examined in healthy adults stratified into five groups based on age and lifelong weekly exercise frequency: (1) young sedentary adults (28–50 years), and older adults (>60 years) who had performed either: (a) sedentary (0–1 sessions/week), (b) casual (2–3 sessions/week), (c) committed (4–5 sessions/week) or (d) athletic (≥6 sessions/week) frequency of exercise. MMP-1 was significantly lower in young compared to older sedentary (p = 0.049). Except for TIMP-2 (p = 0.018 versus committed) and the ratio of MMP-2/TIMP-4 (p = 0.047 versus committed), MMP and TIMP expression was not significantly different in lifelong exercise groups (≥casual) compared to the older sedentary group. MMP-1, -3 had a weak positive relationship with central PWV (r = 0.17–0.25, p ≤ 0.050) but there were no significant relationships between MMPs or TIMPs and LV stiffness constant (p ≥ 0.148). In conclusion, there was not a clear or consistent difference in plasma MMPs and TIMPs with lifelong exercise dose despite exhibiting lower cardiovascular stiffness at the highest exercise levels. • There was no clear or consistent effect of lifelong endurance exercise 'dose' on plasma MMPs and TIMPs levels. • Plasma MMPs and TIMPs were weakly associated with cardiac structure and central arterial stiffness. • Plasma levels of MMPs and TIMPs were not significantly associated with cardiac stiffness. • Alternative extracellular matrix pathways may explain the positive effect of lifelong exercise on cardiovascular stiffness. [ABSTRACT FROM AUTHOR]

Postural orthostatic tachycardia syndrome (POTS), the most common form of orthostatic intolerance in young people, affects approximately 500,000 people in the United States alone, typically young women at the peak of their education and the beginning of their working lives. This is a heterogeneous disorder, the pathophysiology and mechanisms of which are not well understood. There are multiple contributing factors and numerous potential mimics. This review details the most current views on the potential causes, comorbid conditions, proposed subtypes, differential diagnoses, evaluations, and treatment of POTS from cardiological and neurological perspectives. [ABSTRACT FROM AUTHOR]

The last few decades have seen substantial growth in the populations of competitive athletes and highly active people (CAHAP). Although vigorous physical exercise is an effective way to reduce the risk of cardiovascular (CV) disease, CAHAP remain susceptible to inherited and acquired CV disease, and may be most at risk for adverse CV outcomes during intense physical activity. Traditionally, multidisciplinary teams comprising athletic trainers, physical therapists, primary care sports medicine physicians, and orthopedic surgeons have provided clinical care for CAHAP. However, there is increasing recognition that a care team including qualified CV specialists optimizes care delivery for CAHAP. In recognition of the increasing demand for CV specialists competent in the care of CAHAP, the American College of Cardiology has recently established a Sports and Exercise Council. An important primary objective of this council is to define the essential skills necessary to practice effective sports cardiology. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD), is characterized by a progressive loss of renal function and increase in cardiovascular risk. In this review paper, we discuss the pathophysiology of increased sympathetic nerve activity in CKD patients and raise the possibility of endurance exercise being an effective countermeasure to address this problem. We specifically focus on the potential role of endurance training in altering renal sympathetic nerve activity as increased renal sympathetic nerve activity negatively impacts kidney function as well indirectly effects multiple other systems and organs. Recent technological advances in device based therapy have highlighted the detrimental effect of elevated renal sympathetic nerve activity in CKD patients, with kidney function and blood pressure being improved post renal artery nerve denervation in selected patients. These developments provide optimism for the development of alternative and/or complementary strategies to lower renal sympathetic nerve activity. However, appropriately designed studies are required to confirm preliminary observations, as the widespread use of the renal denervation approach to lower sympathetic activity presently has limited feasibility. Endurance training may be one alternative strategy to reduce renal sympathetic nerve activity. Here we review the role of endurance training as a potential alternative or adjunctive to current therapy in CKD patients. We also provide recommendations for future research to assist in establishing an evidence base for the use of endurance training to lower renal sympathetic activity in CKD patients. [ABSTRACT FROM AUTHOR]

We report the case of a 29-year-old man who developed acute congestive heart failure secondary to cardiac Chagas'' disease in the setting of Trypanosoma cruzi reactivation by acquired immune deficiency syndrome. [Copyright &y& Elsevier]

Objective To assess the effect of cardiorespiratory fitness on the association between the initiation of statin therapy and incident diabetes. Patients and methods In a prospective observational study, we studied 6519 generally healthy men and 2334 women with two preventive health examinations from December 15, 1998 through December 18, 2013 which included measurement of fitness levels, statin therapy, risk factors for diabetes, and incident diabetes. Results 93 cases of incident diabetes occurred during an average follow-up of 3.0 years. After multivariable adjustment, an increased odds of incident diabetes with statin use was observed in those patients with impaired fasting glucose at baseline (odds ratio [OR]: 2.15, [95% CI:1.26 to 3.67]), but not among individuals with normal glucose levels (OR:1.85, [95% CI: 0.76 to 4.52]). Cardiorespiratory fitness attenuated but did not eliminate the increased risk of incident diabetes with statin use. Conclusion In a population of relatively healthy patients, statin use was not associated with incident diabetes in patients with normal fasting glucose at baseline. However, it was associated with incident diabetes in those patients with impaired fasting glucose at baseline, though this risk was substantially reduced by increasing fitness. In addition, increasing cardiorespiratory fitness was inversely associated with incident diabetes whether or not a patient was treated with a statin. [ABSTRACT FROM AUTHOR]

Background Insertion of a left ventricular assist device (LVAD) is an accepted therapy for advanced heart failure patients. However, the effects on end-organ perfusion, including cerebral autoregulation, are unclear in the presence of reduced pulsatility. Therefore, the objective of this study was to determine whether cerebral autoregulation is impaired in patients with continuous-flow (CF) LVADs. Methods Dynamic cerebral autoregulation was assessed in both time-domain (autoregulatory index) and frequency-domain (transfer function analysis) analyses in 9 CF-LVAD subjects, 5 pulsatile LVAD subjects and 10 healthy controls, by evaluating mean arterial pressure (MAP) and cerebral blood flow velocity (CBFV) during a sit–stand maneuver at 0.05 Hz (10-second sit, 10-second stand). The autoregulatory index was calculated as the percent change in mean CBFV per mm Hg change in MAP. Results The magnitude of oscillation in MAP and CBFV was greater in subjects with pulsatile LVADs than either CF-LVADs or healthy controls ( p = 0.065 for MAP, p = 0.004 for CBFV). The autoregulatory index and transfer function gain were similar among groups, indicating that dynamic cerebral autoregulation is preserved among patients with CF-LVADs. Conclusions Cerebral blood flow in patients with CF-LVADs is comparable to that of healthy controls across a range of blood pressures. Patients with pulsatile devices have greater oscillations in MAP and CBFV. However, dynamic cerebral autoregulation is preserved among subjects with either type of device. Thus, the reduction in pulsatility afforded by CF-LVADs does not impair normal autoregulatory processes. [ABSTRACT FROM AUTHOR]

Background: Sedentary aging has deleterious effects on the cardiovascular system, including decreased left ventricular compliance and distensibility (LVCD). Conversely, Masters level athletes, who train intensively throughout adulthood, retain youthful LVCD.Objectives: The purpose of this study was to test the hypothesis that preservation of LVCD may be possible with moderate lifelong exercise training.Methods: Healthy seniors (n = 102) were recruited from predefined populations, screened for lifelong patterns of exercise training, and stratified into 4 groups: "sedentary" (<2 sessions/week); "casual" (2 to 3 sessions/week); "committed" (4 to 5 sessions/week); and "competitive" Masters level athletes (6 to 7 sessions/week). Right heart catheterization and echocardiography were performed while preload was manipulated using lower body negative pressure and rapid saline infusion to define LV pressure-volume relationships and Frank-Starling curves.Results: Peak oxygen uptake and LV mass increased with escalating doses of lifelong exercise, with little change in systolic function. At baseline, LV distensibility was greater in committed (21%) and competitive (36%) exercisers than in sedentary subjects. Group LV stiffness constants (sedentary: 0.062 ± 0.039; casual: 0.079 ± 0.052; committed: 0.055 ± 0.033; and competitive: 0.035 ± 0.033) revealed: 1) increased stiffness in sedentary subjects compared to competitive athletes, whereas lifelong casual exercise had no effect; and 2) greater compliance in committed exercisers than in sedentary or casual exercisers.Conclusions: Low doses of casual, lifelong exercise do not prevent the decreased compliance and distensibility observed with healthy, sedentary aging. In contrast, 4 to 5 exercise sessions/week throughout adulthood prevent most of these age-related changes. As LV stiffening has been implicated in the pathophysiology of many cardiovascular conditions affecting the elderly, this "dose" of exercise training may have important implications for prevention of cardiovascular disease. [ABSTRACT FROM AUTHOR]

Abstract: Aging leads to accumulation of irreversible advanced glycation end-products (AGEs), contributing to vascular stiffening and endothelial dysfunction. When combined with the AGE-crosslink breaker Alagebrium, exercise training reverses cardiovascular aging in experimental animals. This study is the first to examine the effect of Alagebrium, with and without exercise training, on endothelial function, arterial stiffness and cardiovascular risk in older individuals. Forty-eight non-exercising individuals (mean age 70±4years) without manifest diseases or use of medication were allocated into 4 groups for a 1-year intervention: Exercise training & Alagebrium (200mg/day); exercise training & placebo; no exercise training & Alagebrium (200mg/day); and no exercise training & placebo. We performed a maximal exercise test (VO2max) and measured endothelial function using venous occlusion plethysmography and intra-arterial infusion of acetylcholine, sodium nitroprusside and NG-monomethyl-l-arginine. Arterial stiffness was measured using pulse wave velocity. Cardiovascular risk was calculated using the Lifetime Risk Score (LRS). In the exercise training groups, LRS and VO2max improved significantly (23.9±4.5 to 27.2±4.6mLO2/min/kg, p <0.001). Endothelial response to the vasoactive substances did not change, nor did arterial stiffness in any of the four groups. In conclusion, one year of exercise training significantly improved physical fitness and lifetime risk for cardiovascular disease without affecting endothelial function or arterial stiffness. The use of the AGE-crosslink breaker Alagebrium had no independent effect on vascular function, nor did it potentiate the effect of exercise training. Despite the clinical benefits of exercise training for older individuals, neither exercise training nor Alagebrium (alone or in combination) was able to reverse the vascular effects of decades of sedentary aging. [Copyright &y& Elsevier]

Objectives: The aim of this study was to determine the relative contribution of the muscle and ventilatory pumps to stroke volume in patients without a subpulmonic ventricle. Background: In patients with Fontan circulation, it is unclear how venous return is augmented to increase stroke volume and cardiac output during exercise. Methods: Cardiac output (acetylene rebreathing), heart rate (electrocardiography), oxygen uptake (Douglas bag technique), and ventilation were measured in 9 patients age 15.8 ± 6 years at 6.1 ± 1.8 years after Fontan operation and 8 matched controls. Data were obtained at rest, after 3 min of steady-state exercise (Ex) on a cycle ergometer at 50% of individual working capacity, during unloaded cycling at 0 W (muscle pump alone), during unloaded cycling with isocapnic hyperpnea (muscle and ventilatory pump), during Ex plus an inspiratory load of 12.8 ± 1.5 cm water, and during Ex plus an expiratory load of 12.8 ± 1.6 cm water. Results: In Fontan patients, the largest increases in stroke volume and stroke volume index were during zero-resistance cycling. An additional increase with submaximal exercise occurred in controls only. During Ex plus expiratory load, stroke volume indexes were reduced to baseline, non-exercise levels in Fontan patients, without significant changes in controls. Conclusions: With Fontan circulation increases in cardiac output and stroke volume during Ex were due to the muscle pump, with a small additional contribution by the ventilatory pump. An increase in intrathoracic pressure played a deleterious role in Fontan circulation by decreasing systemic venous return and stroke volume. [Copyright &y& Elsevier]