scholarly journals Impaired myocardial reserve underlies reduced exercise capacity and heart rate recovery in preterm-born young adults

2020 ◽  
Author(s):  
Odaro J Huckstep ◽  
Holger Burchert ◽  
Wilby Williamson ◽  
Fernando Telles ◽  
Cheryl M J Tan ◽  
...  
Keyword(s):  
Heart Rate ◽  
Young Adults ◽  
Exercise Capacity ◽  
Heart Rate Recovery ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Functional Reserve ◽  
Peak Vo2 ◽  
Preterm Born ◽  
Myocardial Functional Reserve

Abstract Aims We tested the hypothesis that the known reduction in myocardial functional reserve in preterm-born young adults is an independent predictor of exercise capacity (peak VO2) and heart rate recovery (HRR). Methods and results We recruited 101 normotensive young adults (n = 47 born preterm; 32.8 ± 3.2 weeks’ gestation and n = 54 term-born controls). Peak VO2 was determined by cardiopulmonary exercise testing (CPET), and lung function assessed using spirometry. Percentage predicted values were then calculated. HRR was defined as the decrease from peak HR to 1 min (HRR1) and 2 min of recovery (HRR2). Four-chamber echocardiography views were acquired at rest and exercise at 40% and 60% of CPET peak power. Change in left ventricular ejection fraction from rest to each work intensity was calculated (EFΔ40% and EFΔ60%) to estimate myocardial functional reserve. Peak VO2 and per cent of predicted peak VO2 were lower in preterm-born young adults compared with controls (33.6 ± 8.6 vs. 40.1 ± 9.0 mL/kg/min, P = 0.003 and 94% ± 20% vs. 108% ± 25%, P = 0.001). HRR1 was similar between groups. HRR2 decreased less in preterm-born young adults compared with controls (−36 ± 13 vs. −43 ± 11 b.p.m., P = 0.039). In young adults born preterm, but not in controls, EFΔ40% and EFΔ60% correlated with per cent of predicted peak VO2 (r2 = 0.430, P = 0.015 and r2 = 0.345, P = 0.021). Similarly, EFΔ60% correlated with HRR1 and HRR2 only in those born preterm (r2 = 0.611, P = 0.002 and r2 = 0.663, P = 0.001). Conclusions Impaired myocardial functional reserve underlies reductions in peak VO2 and HRR in young adults born moderately preterm. Peak VO2 and HRR may aid risk stratification and treatment monitoring in this population.

scholarly journals Right ventricular systolic dysfunction but not dilatation correlates with prognostically significant reductions in exercise capacity in repaired Tetralogy of Fallot

2019 ◽  
Vol 21 (8) ◽  
pp. 906-913 ◽  
Author(s):  
Imran Rashid ◽  
Adil Mahmood ◽  
Tevfik F Ismail ◽  
Shamus O’Meagher ◽  
Shelby Kutty ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Tetralogy Of Fallot ◽  
Exercise Capacity ◽  
Multivariable Analysis ◽  
Cardiopulmonary Exercise Testing ◽  
Pulmonary Regurgitation ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Peak Vo2 ◽  
Repaired Tetralogy Of Fallot

Abstract Aims The optimal timing for pulmonary valve replacement in asymptomatic patients with repaired Tetralogy of Fallot (rTOF) and pulmonary regurgitation remains uncertain but is often guided by increases in right ventricular (RV) end-diastolic volume. As cardiopulmonary exercise testing (CPET) performance is a strong prognostic indicator, we assessed which cardiovascular magnetic resonance (CMR) parameters correlate with reductions in exercise capacity to potentially improve identification of high-risk patients. Methods and results In all, 163 patients with rTOF (mean age 24.5 ± 10.2 years) who had previously undergone CMR and standardized CPET protocols were included. The indexed right and left ventricular end-diastolic volumes (RVEDVi, LVEDVi), right and left ventricular ejection fractions (RVEF, LVEF), indexed RV stroke volume (RVSVi), and pulmonary regurgitant fraction (PRF) were quantified by CMR and correlated with CPET-determined peak oxygen consumption (VO2) or peak work. On univariable analysis, there was no significant correlation between RVEDVi and PRF with peak VO2 or peak work (% Jones-predicted). In contrast, RVEF and RVSVi had significant correlations with both peak VO2 and peak work that remained significant on multivariable analysis. For a previously established prognostic peak VO2 threshold of <27 mL/kg/min, receiver-operating characteristic curve analysis demonstrated a Harrell’s c of 0.70 for RVEF (95% confidence interval 0.61–0.79) with a sensitivity of 88% for RVEF <40%. Conclusion In rTOF, CMR indices of RV systolic function are better predictors of CPET performance than RV size. An RVEF <40% may be useful to identify prognostically significant reductions in exercise capacity in patients with varying degrees of RV dilatation.

P6323Exercise capacity as predictor for anaemia or iron deficiency in patients with chronic heart failure

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N Ebner ◽  
G Dinopoulos ◽  
R Evertz ◽  
T Garfias Macedo ◽  
B Godoy ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Iron Deficiency ◽  
Exercise Capacity ◽  
Left Ventricular ◽  
World Health ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Peak Vo2 ◽  
Minute Walk

Abstract Background Anaemia and iron deficiency (ID) are important factors for muscle function and exercise capacity in patients with chronic heart failure (HF). Their interaction in HF remains to be defined. Methods A total of 280 out-patients with stable chronic HF were enrolled with mean age of 67.0±10.7 years, 21%female, mean left ventricular ejection fraction (LVEF) was 38.9±13.4%, mean Body Mass Index (BMI) 29.3±5.5 kg/m2]. Anaemia was defined according to World Health Organization criteria [Haemoglobin (Hb) <13 g/dL in men and <12 g/dL in women]. ID was defined as ferritin <100 μg/L or ferritin <100 <300 μg/L than with transferrin saturation (TSAT) <20%. Exercise capacity was assessed by spiroergometry (peakVO2), 6 minute walk test (6MWT), short physical performance battery test (SPPB), hang grip strength (HGS) and leg force (LF). All patients were followed up for a mean of 8 month. Results A total of 89 (32%) chronic HF patients had anaemia and 142 (51%) had iron deficiency at baseline. Patients with anaemia showed significant lower exercise capacity compared to patients without anaemia (peak VO2: 15.3±4.6 vs. 18.5±4.8 kg/min p<0.0001, 6MWT: 365.2±135.5 vs. 461.6±127.4 m p<0.0001, SPPB: 9.4±2.3 vs. 11.0±1.6 total points p<0.0001, HGS: 32.5±10.0 vs. 38.8±12.4 kg p<0.0001, LF: 31.4±11.0 vs. 41.3±21.6 kg p<0.0001). The same we found in patients with ID compared to patients without ID (peak VO2: 16.3±5.1 vs. 18.6±4.5 kg/min p=0.001, 6MWT: 400.0±140.8 vs. 458.8±128.4 m p=0.0008, SPPB: 10.0±2.1 vs. 10.9±1.7 total points p=0.0003, HGS: 34.5±11.9 vs. 39.3±11.7 kg p=0.001, LF: 35.7±23.4 vs. 40.5±13.6 kg p=0.04). After a Follow up of mean 8 month 53 patients develop a new onset of either anaemia (n=24) or ID (n=29). Logistic regression analysis showed that gender, 6 minute walk distance, SPPB, HGS and presence of diabetes mellitus at baseline are significantly associated with the development of anaemia or ID (all p<0.05). The strongest predictor was lower SPPB (p=0.0008). Interestingly known determinates lower peak VO2, higher age, higher NYHA class, Creatinine, and hsCRP were not predictive in our cohort to develop anaemia or ID after 8 month (all p>0.05). Conclusion Both anaemia and ID are strongly associated with reduced exercise capacity in patients with HF. The effect of anaemia and iron deficiency together is stronger than that of anemia and ID alone. Reduced SPPB, 6MWT, and HGS are important risk factors for the development of anaemia or ID.

Abstract 2424: Improvement Of Cardiopulmonary Exercise Capacity In Patients With Chronic Post-infarction Heart Failure (CHF) After Intracoronary Infusion Of Bone Marrow-derived Progenitor Cells (BMC)

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Joerg Honold ◽  
Lenka Geiger ◽  
Ulrich Fischer-Rasokat ◽  
Birgit Assmus ◽  
Volker Schaechinger ◽  
...  
Keyword(s):  
Heart Failure ◽  
Oxygen Uptake ◽  
Exercise Capacity ◽  
Serum Levels ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Cardiopulmonary Exercise ◽  
Cardiopulmonary Exercise Capacity ◽  
Peak Vo2

Intracoronary (i.c.) infusion of BMC in patients (pts.) with CHF is associated with improvements in left ventricular ejection fraction (LVEF) and reduction of NT-proBNP serum-levels, especially in pts. with more severe heart failure. However, ist is unknown whether the modest improvements in cardiac function translate into an increase in cardiopulmonary exercise capacity. A total of 52 CHF-pts. performed cardiopulmonary exercise tests (CPET) according to a modified Bruce protocol before and 3 months after i.c. infusion of BMC into the infarct-related artery. Anaerobic threshold (AT) was determined by the v-slope method. Overall, pts. were 58±12 years old with a moderately impaired LVEF (mean 42±11%) and a median NYHA-class 2±0.75. NT-proBNP-serum levels were elevated (1007±154 pmol/ml). All pts. received chronic optimized medical therapy with betablockers, ACE-inhibitors and combined diuretics, which was kept constant during the study duration. Initial CPET revealed reduced peak oxygen uptake (peak VO2: 14.0 ml/min/kg), maximal oxygen Pulse (O2Pmax: 11.4 ml/beat) and oxygen uptake at AT (VO2AT: 10.9 ml/min/kg), whereas CO2-equivalents (EqCO2) were elevated (29.7). 3 months after therapy, repeated CPET showed an increase in peak VO2 (14.0±3.9 to 15.3±4.3 ml/min/kg, p=0.07), whereas VO2 AT (10.8±2.5 to 10.8±2.5 ml/min/kg, p= n.s.), O2Pmax (11.2 ± 3.1 to 12.0±3.3 ml/beat, p= n.s.) or EqCO2 (29.7±6.4 to 29.8±6.8, p= n.s.) remained unchanged. However, after dichotomizating the patient cohort according to the median of VO2max at baseline, pts. with lower initial VO2max showed a significant improvement in VO2max (12.8±1.5 to 13.5±2.7ml/min/kg, p= 0.03) and an improvement in VO2AT (9.1±1.8 to 9.5±2.2 ml/min/kg, p= ns), as well as a reduction of EqCO2 (34.7±7.1 to 33.8±8.0, p= ns). In contrast, pts. with initial VO2max > median did not show any significant improvements. These findings indicate that intracoronary BMC-therapy improves exercise capacity in CHF-patients with more advanced heart failure. Therefore, cardiopulmonary exercise testing might help to identify pts. more likely to derive functional benefit from intracoronary BMC administration.

scholarly journals Chronic vagus nerve stimulation is associated with multi-year improvement in intrinsic heart rate recovery and left ventricular ejection fraction in ANTHEM-HF

2021 ◽  
Author(s):  
Bruce D. Nearing ◽  
Imad Libbus ◽  
Gerrard M. Carlson ◽  
Badri Amurthur ◽  
Bruce H. KenKnight ◽  
...  
Keyword(s):  
Heart Rate ◽  
Left Ventricular Ejection Fraction ◽  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Heart Rate Recovery ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Intrinsic Heart Rate

Abstract Purpose Disturbed autonomic function is implicated in high mortality rates in heart failure patients. High-intensity vagus nerve stimulation therapy was shown to improve intrinsic heart rate recovery and left ventricular ejection fraction over a period of 1 year. Whether these beneficial effects are sustained across multiple years and are related to improved baroreceptor response was unknown. Methods All patients (n = 21) enrolled in the ANTHEM-HF clinical trial (NCT01823887, registered 4/3/2013) with 24 h ambulatory electrocardiograms at all time points and 54 normal subjects (PhysioNet database) were included. Intrinsic heart rate recovery, based on ~ 2000 spontaneous daily activity-induced heart rate acceleration/deceleration events per patient, was analyzed at screening and after 12, 24, and 36 months of chronic vagus nerve stimulation therapy (10 or 5 Hz, 250 μs pulse width, 18% duty cycle, maximum tolerable current amplitude). Results In response to chronic high-intensity vagus nerve stimulation (≥ 2.0 mA), intrinsic heart rate recovery (all time points, p < 0.0001), heart rate turbulence slope, an indicator of baroreceptor reflex gain (all, p ≤ 0.02), and left ventricular ejection fraction (all, p ≤ 0.04) were improved over screening at 12, 24, and 36 months. Intrinsic heart rate recovery and heart rate turbulence slope were inversely correlated at both screening (r = 0.67, p < 0.002) and 36 months (r = 0.78, p < 0.005). Conclusion This non-randomized study provides evidence of an association between improvement in intrinsic heart rate recovery and left ventricular ejection fraction during high-intensity vagus nerve stimulation for a period of ≥ 3 years. Correlated favorable effects on heart rate turbulence slope implicate enhanced baroreceptor function in response to chronic, continuously cyclic vagus nerve stimulation as a physiologic mechanism.

scholarly journals Cardiorespiratory fitness and heart rate recovery predict sudden cardiac death independent of ejection fraction

Heart ◽  
2019 ◽  
Vol 106 (6) ◽  
pp. 434-440 ◽  
Author(s):  
Jussi A Hernesniemi ◽  
Kalle Sipilä ◽  
Antti Tikkakoski ◽  
Juho T Tynkkynen ◽  
Pashupati P Mishra ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sudden Cardiac Death ◽  
Ejection Fraction ◽  
Cardiorespiratory Fitness ◽  
Exercise Testing ◽  
Cardiac Death ◽  
Heart Rate Recovery ◽  
Left Ventricular ◽  
Left Ventricular Ejection

ObjectiveTo evaluate whether cardiorespiratory fitness (CRF) and heart rate recovery (HRR) associate with the risk of sudden cardiac death (SCD) independently of left ventricular ejection fraction (LVEF).MethodsThe Finnish Cardiovascular Study is a prospective clinical study of patients referred to clinical exercise testing in 2001–2008 and follow-up until December 2013. Patients without pacemakers undergoing first maximal or submaximal exercise testing with cycle ergometer were included (n=3776). CRF in metabolic equivalents (METs) was estimated by achieving maximal work level. HRR was defined as the reduction in heart rate 1 min after maximal exertion. Adjudication of SCD was based on death certificates. LVEF was measured for clinical indications in 71.4% of the patients (n=2697).ResultsPopulation mean age was 55.7 years (SD 13.1; 61% men). 98 SCDs were recorded during a median follow-up of 9.1 years (6.9–10.7). Mean CRF and HRR were 7.7 (SD 2.9) METs and 25 (SD 12) beats/min/min. Both CRF and HRR were associated with the risk of SCD in the entire study population (HRCRF0.47 (0.37–0.59), p<0.001 and HRHRR0.57 (0.48–0.67), p<0.001 with HR estimates corresponding to one SD increase in the exposure variables) and with CRF, HRR and LVEF in the same model (HRCRF0.60 (0.45–0.79), p<0.001, HRHRR0.65 (0.51–0.82), p<0.001) or adjusting additionally for all significant risk factors for SCD (LVEF, sex, creatinine level, history of myocardial infarction and atrial fibrillation, corrected QT interval) (HRCRF0.69 (0.52–0.93), p<0.01, HRHRR0.74 (0.58–0.95) p=0.02).ConclusionsCRF and HRR are significantly associated with the risk of SCD regardless of LVEF.

scholarly journals Respiratory-related heart rate variability in progressive experimental heart failure

2005 ◽  
Vol 289 (4) ◽  
pp. H1729-H1735 ◽  
Author(s):  
Sophie Motte ◽  
Myrielle Mathieu ◽  
Serge Brimioulle ◽  
Anne Pensis ◽  
Lynn Ray ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Spectral Analysis ◽  
Left Ventricular ◽  
Right Atrial ◽  
Left Ventricular Ejection ◽  
Total Power ◽  
Progressive Heart Failure ◽  
Atrial Natriuretic

Heart failure is associated with autonomic imbalance, and this can be evaluated by a spectral analysis of heart rate variability. However, the time course of low-frequency (LF) and high-frequency (HF) heart rate variability changes, and their functional correlates during progression of the disease are not exactly known. Progressive heart failure was induced in 16 beagle dogs over a 7-wk period by rapid ventricular pacing. Spectral analysis of heart rate variability and respiration, echocardiography, hemodynamic measurements, plasma atrial natriuretic factor, and norepinephrine was obtained at baseline and every week, 30 min after pacing interruption. Progressive heart failure increased heart rate (from 91 ± 4 to 136 ± 5 beats/min; P < 0.001) and decreased absolute and normalized (percentage of total power) HF variability from week 1 and 2, respectively ( P < 0.01). Absolute LF variability did not change during the study until it disappeared in two dogs at week 7 ( P < 0.05). Normalized LF variability increased in moderate heart failure ( P < 0.01), leading to an increased LF-to-HF ratio ( P < 0.05), but decreased in severe heart failure ( P < 0.044; week 7 vs. week 5). Stepwise regression analysis revealed that among heart rate variables, absolute HF variability was closely associated with wedge pressure, right atrial and pulmonary arterial pressure, left ventricular ejection fraction and volume, ratio of maximal velocity of early (E) and atrial (A) mitral flow waves, left atrial diameter, plasma norepinephrine, and atrial natriuretic peptide (0.45 < r < 0.65, all P < 0.001). In tachycardia-induced heart failure, absolute HF heart rate variability is a more reliable indicator of cardiac dysfunction and neurohumoral activation than LF heart rate variability.

First clinical trial with etomoxir in patients with chronic congestive heart failure

2000 ◽  
Vol 99 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Stephan SCHMIDT-SCHWEDA ◽  
Christian HOLUBARSCH
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Sarcoplasmic Reticulum ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

In the failing human myocardium, both impaired calcium homoeostasis and alterations in the levels of contractile proteins have been observed, which may be responsible for reduced contractility as well as diastolic dysfunction. In addition, levels of a key protein in calcium cycling, i.e. the sarcoplasmic reticulum Ca2+-ATPase, and of the α-myosin heavy chain have been shown to be enhanced by treatment with etomoxir, a carnitine palmitoyltransferase inhibitor, in normal and pressure-overloaded rat myocardium. We therefore studied, for the first time, the influence of long-term oral application of etomoxir on cardiac function in patients with chronic heart failure. A dose of 80 mg of etomoxir was given once daily to 10 patients suffering from heart failure (NYHA functional class II–III; mean age 55±4 years; one patient with ischaemic heart disease and nine patients with dilated idiopathic cardiomyopathy; all male), in addition to standard therapy. The left ventricular ejection fraction was measured echocardiographically before and after a 3-month period of treatment. Central haemodynamics at rest and exercise (supine position bicycle) were defined by means of a pulmonary artery catheter and thermodilution. All 10 patients improved clinically; no patient had to stop taking the study medication because of side effects; and no patient died during the 3-month period. Maximum cardiac output during exercise increased from 9.72±1.25 l/min before to 13.44±1.50 l/min after treatment (P < 0.01); this increase was mainly due to an increased stroke volume [84±7 ml before and 109±9 ml after treatment (P < 0.01)]. Resting heart rate was slightly reduced (not statistically significant). During exercise, for any given heart rate, stroke volume was significantly enhanced (P < 0.05). The left ventricular ejection fraction increased significantly from 21.5±2.6% to 27.0±2.3% (P < 0.01). In acute studies, etomoxir showed neither a positive inotropic effect nor vasodilatory properties. Thus, although the results of this small pilot study are not placebo-controlled, all patients seem to have benefitted from etomoxir treatment. Etomoxir, which has no acute inotropic or vasodilatory properties and is thought to increase gene expression of the sarcoplasmic reticulum Ca2+-ATPase and the α-myosin heavy chain, improved clinical status, central haemodynamics at rest and during exercise, and left ventricular ejection fraction.

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