Synchronizing Cardiac Cycle Phase with Foot Strike to Optimize Cardiac Performance in Patients with Chronic Systolic Heart Failure and Cardiac Resynchronization Therapy (CRT)

Despite advances in medical and Cardiac Resynchronization Therapy (CRT), patients with chronic systolic heart failure (HF) have persistent symptoms including dyspnea on exertion and exercise intolerance. Novel strategies to improve exercise performance in these patients, such as optimizing cardio-locomotor coupling, could be particularly beneficial to improve functional capacity. For example, runners display a lower heart rate and higher oxygen pulse, suggestive of a higher stroke volume (SV), when foot strike occurs in diastole. Whether patients with HF undergoing CRT can similarly increase SV is unknown. PURPOSE: To compare the effects of diastolic versus systolic foot strike timing on exercise hemodynamics in patients with HF and CRT. METHODS: Ten patients (Age: 58 ± 17 years, 40% Female) with HF and previously implanted CRT pacemakers completed repeated 5-minute bouts of walking on a treadmill at a fixed but individualized speed (range: 1.5-3mph). Participants were randomized to walking to an auditory tone to synchronize their foot strike to either the systolic (ECG R-wave; 0 or 100%±15% or R-R interval) or diastolic phase (45±15% of the R-R interval) of their cardiac cycle. Participants were included if ≥50% of their steps were valid (i.e. in time). Patients wore a chest strap with an attached ECG sensor and accelerometer (CounterpaceR). Foot strike timing and associated valid step counts were assessed via CounterpaceR or post-hoc analysis of foot strike waveforms. Cardiopulmonary parameters were measured breath by breath via indirect calorimetry and cardiac output was measured via acetylene rebreathing, with SV calculated as the quotient of cardiac output and heart rate. RESULTS: There was no difference in oxygen uptake between conditions (1.02 ± 0.44 vs. 1.04 ± 0.44 L/min, P=0.298). When compared to systolic walking, stepping in diastole was associated with higher SV (Diastolic: 80 ± 28 vs. Systolic: 74 ± 26 ml, P=0.003) and cardiac output (8.3 ± 3.5 vs. 7.9 ± 3.4 L/min, P=0.004); heart rate (paced) was not different between conditions (101 ± 15 vs. 103 ± 14 bpm, P=0.300). Mean arterial pressure was significantly lower during diastolic walking (85 ± 12 vs. 98 ± 20 mmHg, P=0.007). CONCLUSION: In patients with HF and previous CRT, synchronizing foot strike with diastole during walking increased SV and cardiac output and reduced arterial pressure. Our findings indicate that in such paced hearts, diastolic stepping increases oxygen delivery and decreases afterload, which may facilitate increased exercise capacity. Therefore, if added to pacemakers, this cardio-locomotor coupling technology may maximize CRT efficiency and increase exercise participation and quality of life in patients with HF

Can We Calculate Mean Arterial Pressure in Humans?

Mean arterial pressure (MAP) is either measured with an oscillometric cuff and then systolic (SBP) and diastolic (DBP) blood pressures are estimated from an unknown algorithm; or SBP and DBP are measured via auscultation and MAP calculated using measures of systolic pressure (SBP), diastolic pressure (DBP), and a form-factor (FF; equation: [(SBP-DBP)*FF]+DBP). The typical FF used is 0.33 though others (0.4) have been proposed. Recent work indicates that estimation of aortic MAP via a FF leads to inaccurate values and should therefore be interpreted with caution, whether this is the case for local MAP is unknown. While the implications for hypertension (HTN) diagnosis are minimal, the calculation of local MAP is essential to the study of blood pressure regulation and exercise hemodynamics in patient populations (e.g. heart failure). PURPOSE: To compare the calculation of local MAP using catheter waveforms and a FF, against MAP derived from the pressure-time integral (PTI; i.e. average pressure across the cardiac cycle) measured via radial arterial catheterization. METHODS: We analyzed radial arterial catheter waveforms from 39 patients (Age: 71±7 years; BMI: 38.4±6.7; Female: 66%; HTN prevalence: 97%) with heart failure with preserved ejection fraction (HFpEF) at rest and during cycling exercise at 20 Watts. We compared the PTI (from the catheter waveform) with the calculation of MAP from the peak and nadir of the same waveforms (5-beat averages) using the 0.33 and 0.4 FF’s in the FF equation. RESULTS: Compared to the PTI (91±13 mmHg), resting MAP was not significantly different when calculated using the 0.33 FF (91±11 mmHg, P\u3e0.999) but was higher when using the 0.4 FF (96±12 mmHg, PCONCLUSION:While the 0.33 FF provides an accurate assessment of MAP on average during rest and exercise in the radial artery in patients with HFpEF, the limits of agreement are large reflecting a lack of precision in measurement at an individual level. Indirect calculations of MAP via a FF may lead to inaccurate conclusions regarding the mechanisms of blood pressure regulation both at rest and during exercise testing in this population

Cardiac mechanisms for low aerobic power in anthracycline treated, older, long-term breast cancer survivors

Breast cancer survivors have reduced peak aerobic capacity (VO2peak) which may be related to latent or lingering chemotherapy induced cardiac damage. Nine, older (67 ± 3 years), long-term survivors (9.8 years) of anthracycline based chemotherapy and age- and sex-matched healthy controls were recruited and tested to determine whether: i) VO2peak remains reduced in long-term survivorship; and ii) reductions in VO2peak are due to cardiac dysfunction. VO2peak was significantly reduced in breast cancer survivors relative to healthy controls (15.9 ± 2.0 vs 19.9 ± 3.1 ml/kg/min, p = 0.006), however the heart rate and stroke volume responses to exercise were normal (heart rate reserve; 88 ± 9 vs 85 ± 10 bpm, p = 0.62: stroke volume reserve; 13 ± 6 vs 13 ± 9 ml,p = 0.94). These findings indicate low-normal ventricular size in long-term breast cancer survivors, but normal reserve function

Genetic and environmental determinants of diastolic heart function

Diastole is the sequence of physiological events that occur in the heart during ventricular filling and principally depends on myocardial relaxation and chamber stiffness. Abnormal diastolic function is related to many cardiovascular disease processes and is predictive of health outcomes, but its genetic architecture is largely unknown. Here, we use machine learning cardiac motion analysis to measure diastolic functional traits in 39,559 participants of the UK Biobank and perform a genome-wide association study. We identified 9 significant, independent loci near genes that are associated with maintaining sarcomeric function under biomechanical stress and genes implicated in the development of cardiomyopathy. Age, sex and diabetes were independent predictors of diastolic function and we found a causal relationship between genetically-determined ventricular stiffness and incident heart failure. Our results provide insights into the genetic and environmental factors influencing diastolic function that are relevant for identifying causal relationships and potential tractable targets

Genetic and environmental determinants of diastolic heart function

Diastole is the sequence of physiological events that occur in the heart during ventricular filling and principally depends on myocardial relaxation and chamber stiffness. Abnormal diastolic function is related to many cardiovascular disease processes and is predictive of health outcomes, but its genetic architecture is largely unknown. Here, we use machine learning cardiac motion analysis to measure diastolic functional traits in 39,559 participants of the UK Biobank and perform a genome-wide association study. We identified 9 significant, independent loci near genes that are associated with maintaining sarcomeric function under biomechanical stress and genes implicated in the development of cardiomyopathy. Age, sex and diabetes were independent predictors of diastolic function and we found a causal relationship between genetically-determined ventricular stiffness and incident heart failure. Our results provide insights into the genetic and environmental factors influencing diastolic function that are relevant for identifying causal relationships and potential tractable targets

Psychological resilience in sport performers: a review of stressors and protective factors

Psychological resilience is important in sport because athletes must utilize and optimize a range of mental qualities to withstand the pressures that they experience. In this paper, we discuss psychological resilience in sport performers via a review of the stressors athletes encounter and the protective factors that help them withstand these demands. It is hoped that synthesizing what is known in these areas will help researchers gain a deeper profundity of resilience in sport, and also provide a rigorous and robust foundation for the development of a sport-specific measure of resilience. With these points in mind, we divided the narrative into two main sections. In the first section, we review the different types of stressors encountered by sport performers under three main categories: competitive, organizational, and personal. Based on our recent research examining psychological resilience in Olympics champions (Fletcher & Sarkar, 2012), in the second section we discuss the five main families of psychological factors (viz. positive personality, motivation, confidence, focus, perceived social support) that protect the best athletes from the potential negative effect of stressors. It is anticipated that this review will help sport psychology researchers examine the interplay between stressors and protective factors which will, in turn, focus the analytical lens on the processes underlying psychological resilience in athletes