Angadi, Siddhartha S.

Background Data regarding changes in markers of cardiovascular and all‐cause mortality, namely, VO 2peak and minute ventilation/carbon dioxide production (V E /VCO 2 ) slope following renal transplantation past 1‐year post‐transplant are lacking. We examined changes in VO 2peak and V E /VCO 2 before and after ~3‐years after renal transplantation. Methods Eighteen patients (age 56.2 ± 2.5 years; 82.9 ± 4.9 kg; 9 male) completed an exercise test to exhaustion using a ramp treadmill protocol. Subjects underwent pre‐transplant exercise testing (PreTx) following which they were placed on the transplant wait‐list. Average time on the waitlist was 15.6 ± 2 months. Following transplant, subjects underwent follow‐up maximal exercise testing using the same protocol (PostTx). Mean duration to post‐transplant exercise testing was 35 ± 2 months. Gas exchange data, heart rate and respiratory exchange ratios were recorded throughout exercise testing. All variables are reported as mean ± standard error. α was set at 0.05 and a paired t‐test carried out to examine changes in VO 2peak and maximal V E /VCO 2 slope before and after transplant. Results Significant reductions in relative VO 2peak were observed from PreTx = 15.2 ± 0.8 mL/kg/min to PostTX = 12.2 ± 0.4 mL/kg/min (p = 0.002 ). Also, significant increases in V e /VCO 2 were observed from PreTx = 30 ± 1.4 to PostTx = 43 ± 1.6 (p < .001). Conclusions Long term follow‐up (~3‐years) in this small cohort of patients following renal transplantation demonstrated significant reductions in VO 2peak (20%) and worsening of the V E /VCO 2 slope (30%) which are modifiable markers of mortality risk. This underscores the need for larger cohort studies to be undertaken in this population given that these markers are independently linked to cardiovascular and all‐cause mortality risk. These data may have implications for cardiovascular stratification and cardiovascular risk reduction in this population. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Abstract Introduction Insomnia is a novel and modifiable risk factor for incident cardiovascular disease (CVD). However, identification of early markers of subclinical CVD in diagnosed insomnia is understudied. Our aim for this ongoing study is to contrast markers of cardiovascular structure and function between people with insomnia and good-sleeping controls. Methods Persons with insomnia (met ICSD-III criteria) and good sleeping controls (&lt;8 Insomnia Severity Index, mean 8-night SOL and WASO&lt;31min) were recruited from the community. Twenty-two adults (21-39y; 55% women) with no history of CVD, diabetes, inflammatory conditions, significant hypertension, or current sleep-disordered breathing (WatchPat200, Itamar Medical) were enrolled and underwent fasting cardiovascular testing. Testing included: Central augmented aortic pressure (AP) and carotid-femoral pulse wave velocity (cfPWV) for vascular stiffness; brachial artery flow mediated dilation (FMD) to assess endothelial function; and 2D echocardiography to assess ejection fraction (EF%), left ventricular global longitudinal strain (LVGLS), left atrial volume index (LAVI), mitral valve E/e’ ratio (E/e’), and lateral e’. ANCOVA models, adjusting for age, comparing persons with insomnia (n=6) to good sleeping controls (n=16) on each cardiovascular measure were conducted. Results AP (range:-5,10mmHg), cfPWV (range: 4.8-7.6m/s), EF% (range:55.0-72.0%), LVGLS (range:-26,-19%) LAVI (range:14.1-26.7mL/m2), E/e’ (range:3.2-7.8), and lateral e’ (range:0.09-0.22cm/sec) were all within normal ranges according to age and sex normative standards. Mean FMD was 8.8% (SD=4.3, range:4.3-19.8%). Age adjusted ANCOVA models indicated that the insomnia group had significantly worse cardiovascular function than good sleeping controls on cfPWV (M=6.8±0.3 vs. M=5.7±0.2; p=0.004), EF% (M=60.0±1.7 vs. M=65.2±1.0; p=0.017), LVGLS (M=-21.6±0.6 vs. M=-24.3±0.4; p=0.001), and lateral e’ (M=0.12±0.01 vs. M=0.18±0.01; p=0.003). No group differences were found for AP, FMD, LAVI, and E/e’. Conclusion Among relatively healthy young adults, people with insomnia had greater arterial stiffness and worse left ventricular systolic and diastolic functioning. Support American Academy of Sleep Medicine Foundation Focused Projects Award for Junior Investigators 179-FP-18

ABSTRACT Purpose We assessed resting central/peripheral blood pressure (BP), postexercise BP, and hemodynamic responses (stroke volume, cardiac output, and systemic vascular resistance) after acute exercise and 2 wk of aerobic training in lean and centrally obese men matched for BP. Methods Eight lean (body mass index < 25 kg·m −2 , visceral fat = 279 ± 224 cm 3 ) and eight centrally obese (body mass index > 30 kg·m −2 , visceral fat = 1471 ± 374 cm 3 ) men performed six training sessions (3 d·wk −1 for 40 min at 65%–70% HR max ). Resting BP and hemodynamic measurements were obtained at baseline, after exercise for 60 min, and at 24 h and 48 h after the last training session. Results Postexercise brachial and central systolic BP (SBP) and mean arterial BP decreased 3–4 mm Hg below resting in lean ( P < 0.001) and increased by 3 mm Hg in obese ( P < 0.02). Posttraining resting brachial/central SBP were reduced by 3–4 mm Hg only in lean men ( P < 0.05). Pretraining postexercise hypotension was significantly correlated with the training-induced change in resting brachial SBP at 48 h ( r = 0.58, P = 0.02), but not at 24 h ( r = 0.38, P = 0.15). Similar correlations were observed between acute reductions in central SBP and central SBP at 24 h ( r = 0.43, P = 0.09) and 48 h ( r = 0.54, P = 0.03) posttraining. Conclusions In contrast to the consistent results for lean men, postexercise hypotension was not observed in centrally obese men, and resting SBP was not reduced after a short aerobic training program. Considerable individual variation in postexercise BP response among obese men may have implications for design of exercise interventions to lower BP in these individuals.

Background Significant heterogeneity exists in practice patterns and algorithms used for cardiac screening before kidney transplant. Cardiorespiratory fitness, as measured by peak oxygen uptake (VO 2peak ), is an established validated predictor of future cardiovascular morbidity and mortality in both healthy and diseased populations. The literature supports its use among asymptomatic patients in abrogating the need for further cardiac testing. Methods and Results We outlined a pre–renal transplant screening algorithm to incorporate VO 2peak testing among a population of asymptomatic high‐risk patients (with diabetes mellitus and/or >50 years of age). Only those with VO 2peak <17 mL/kg per minute (equivalent to <5 metabolic equivalents) underwent further noninvasive cardiac screening tests. We conducted a retrospective study of the a priori dichotomization of the VO 2peak <17 versus ≥17 mL/kg per minute to determine negative and positive predictive value of future cardiac events and all‐cause mortality. We report a high (>90%) negative predictive value, indicating that VO 2peak ≥17 mL/kg per minute is effective to rule out future cardiac events and all‐cause mortality. However, lower VO 2peak had low positive predictive value and should not be used as a reliable metric to predict future cardiac events and/or mortality. In addition, a simple mathematical calculation documented a cost savings of ≈$272 600 in the cardiac screening among our study cohort of 637 patients undergoing evaluation for kidney and/or pancreas transplant. Conclusions We conclude that incorporating an objective measure of cardiorespiratory fitness with VO 2peak is safe and allows for a cost savings in the cardiovascular screening protocol among higher‐risk phenotype (with diabetes mellitus and >50 years of age) being evaluated for kidney transplant.

Abstract Aims High-intensity interval training (HIIT) improves peak oxygen uptake and left ventricular diastology in patients with heart failure with preserved ejection fraction (HFpEF). However, its effects on myocardial strain in HFpEF remain unknown. We explored the effects of HIIT and moderate-intensity aerobic continuous training (MI-ACT) on left and right ventricular strain parameters in patients with HFpEF. Furthermore, we explored their relationship with peak oxygen uptake (VO2peak). Methods and results Fifteen patients with HFpEF (age = 70 ± 8.3 years) were randomized to either: (i) HIIT (4 × 4 min, 85–90% peak heart rate, interspersed with 3 min of active recovery; n = 9) or (ii) MI-ACT (30 min at 70% peak heart rate; n = 6). Patients were trained 3 days/week for 4 weeks and underwent VO2peak testing and 2D echocardiography at baseline and after completion of the 12 sessions of supervised exercise training. Left ventricular (LV) and right ventricular (RV) average global peak systolic longitudinal strain (GLS) and peak systolic longitudinal strain rate (GSR) were quantified. Paired t-tests were used to examine within-group differences and unpaired t-tests used for between-group differences (α = 0.05). Right ventricular average global peak systolic longitudinal strain improved significantly in the HIIT group after training (pre = −18.4 ± 3.2%, post = −21.4 ± 1.7%; P = 0.02) while RV-GSR, LV-GLS, and LV-GSR did not (P &gt; 0.2). No significant improvements were observed following MI-ACT. No significant between-group differences were observed for any strain measure. ΔLV-GLS and ΔRV-GLS were modestly correlated with ΔVO2peak (r = −0.48 and r = −0.45; P = 0.1, respectively). Conclusions In patients with HFpEF, 4 weeks of HIIT significantly improved RV-GLS.

Heart failure with preserved ejection fraction (HFpEF) is a major cause of morbidity and mortality. Exercise training is an established adjuvant therapy in heart failure; however, the effects of high-intensity interval training (HIIT) in HFpEF are unknown. We compared the effects of HIIT vs. moderate-intensity aerobic continuous training (MI-ACT) on peak oxygen uptake (V̇o2peak), left ventricular diastolic dysfunction, and endothelial function in patients with HFpEF. Nineteen patients with HFpEF (age 70 ± 8.3 yr) were randomized to either HIIT (4 × 4 min at 85-90% peak heart rate, with 3 min active recovery) or MI-ACT (30 min at 70% peak heart rate). Fifteen patients completed exercise training (HIIT: n = 9; MI-ACT: n = 6). Patients trained 3 days/wk for 4 wk. Before and after training patients underwent a treadmill test for V̇o2peak determination, 2D-echocardiography for assessment of left ventricular diastolic dysfunction, and brachial artery flow-mediated dilation (FMD) for assessment of endothelial function. HIIT improved V̇o2peak (pre = 19.2 ± 5.2 ml·kg−1·min−1; post = 21.0 ± 5.2 ml·kg−1·min−1; P = 0.04) and left ventricular diastolic dysfunction grade (pre = 2.1 ± 0.3; post = 1.3 ± 0.7; P = 0.02), but FMD was unchanged (pre = 6.9 ± 3.7%; post = 7.0 ± 4.2%). No changes were observed following MI-ACT. A trend for reduced left atrial volume index was observed following HIIT compared with MI-ACT (−3.3 ± 6.6 vs. +5.8 ± 10.7 ml/m2; P = 0.06). In HFpEF patients 4 wk of HIIT significantly improved V̇o2peak and left ventricular diastolic dysfunction. HIIT may provide a more robust stimulus than MI-ACT for early exercise training adaptations in HFpEF.