Impaired Heart Rate Recovery and Chronotropic Incompetence in Patients With Heart Failure With Preserved Ejection Fraction (original) (raw)
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Circulation: Heart …, 2010
Background-This study assessed the chronotropic response to exercise and heart rate (HR) recovery after exercise in a carefully phenotyped group of patients with heart failure with preserved left ventricular ejection fraction (HfpEF) and a control group of similar age and gender distribution. Methods and Results-We studied 41 patients with HfpEF, 41 healthy controls, and 16 hypertensive controls. None were taking HR-limiting medications. All study participants had clinical examination, 12-lead ECG, pulmonary function test, echocardiogram, and metabolic exercise test with HR monitoring throughout exercise. Chronotropic response was measured by the percentage of the HR reserve used during maximal exercise and the peak exercise HR as a percentage of predicted maximal HR. Patients with HfpEF were generally women (70%), overweight, aged 69Ϯ8 years. Controls were of similar gender (63%) and age (67Ϯ6 years). Patients with HfpEF had significantly reduced peak VO 2 compared with controls (20Ϯ4 mL ⅐ kg Ϫ1 ⅐ min Ϫ1 versus 31Ϯ6 mL ⅐ kg Ϫ1 ⅐ min Ϫ1 , PϽ0.001) and greater minute ventilationcarbon dioxide production relationship (VE/VCO 2 slope) (33Ϯ6 versus 29Ϯ4, PϽ0.001). Chronotropic incompetence was significantly more common in patients with HfpEF compared with matched healthy controls as measured by the percentage of the HR reserve used during maximal exercise (63% versus 2%, Ͻ0.001) and percentage of predicted maximal HR (34% versus 2%, Ͻ0.001). In addition, abnormal HR recovery 1-minute after exercise (defined as the reduction in the HR from peak exercise 1-minute after exercise) was also significantly more common in patients with HfpEF compared with controls (23% versus 2%, Pϭ0.01). Hypertensive controls showed similar chronotropic response to peak exercise and HR recovery after exercise as healthy controls.
International Heart Journal, 2006
An attenuated heart rate recovery (HRR) immediately after exercise has been shown to be predictive of mortality. It is not known whether HRR predicts mortality when measured in patients with heart failure. The present study was undertaken to evaluate the ability of HRR to predict mortality in patients with heart failure. We studied 84 NYHA class II or III chronic congestive heart failure patients who had a left ventricular ejection fraction ≤ 40%. All patients underwent symptom limited cardiopulmonary exercise testing. The value for the HRR was defined as the difference in heart rate between peak exercise and one-minute later; a value ≤ 18 beats per minute was considered abnormal. The patients were divided into 2 groups according to the value of HRR. Those with abnormal HRR were assigned to group I and those with normal HRR were assigned to group II. The 2 groups were compared with each other regarding baseline characteristics and exercise capacity assessed by peak VO 2. There were 26 patients (31%) in group I and 58 patients (69%) in group II. Group II patients had better performance on treadmill exercise testing than group I patients. They had greater exercise duration (7.5 ± 3.8 minutes versus 5 ± 3.5 minutes, P = 0.006), better heart-rate reserve (79 ± 25% versus 63 ± 27%, P = 0.01), and higher values of maximal heart-rate (141 ± 18 beats/min versus 132 ± 17 beats/min, P = 0.04). Group II patients also had higher peak VO 2 values (16.8 ± 4.4 mL/kg/min versus 14.4 ± 3.6 mL/ kg/min, P = 0.01). When we separated the groups according to beta-blocker usage, betablockers had no prominent effect on HRR. In the follow-up period (mean 14.1 ± 6.1 months), the presence of abnormal HRR and lower peak VO 2 (≤ 14 mL/kg/min) were the only significant predictors of mortality in our patient population (adjusted hazard ratio [HR] 5.2, 95% CI, 1.3 to 24, P = 0.03 and adjusted HR 13, 95% CI, 2.1 to 25.6, P = 0.005, respectively). It seems that the attenuated HRR value one minute after peak exercise appears to be a reliable index of the severity of exercise intolerance in heart failure patients and this study supports the value of HRR as a prognostic marker among heart failure patients referred for cardiopulmonary exercise testing for prediction of prognosis.
Heart Failure Reviews, 2018
Exercise intolerance is a typical manifestation of patients affected by heart failure with reduced ejection fraction (HFrEF); however, the relationship among functional capacity, mortality, and exercise-induced heart rate response during exercise remains unclear in either sinus rhythm or atrial fibrillation subjects. Heart rate increase during incremental load exercise has a typical pattern in normal subjects, whereas it is commonly compromised in HFrEF patients, mainly due to the imbalance of the autonomic nervous system. In the present review, we aim to describe the behavior of heart rate during exercise in normal subjects and in HFrEF patients in sinus rhythm and atrial fibrillation, understanding and explaining the mechanism leading to a different exercise performance and functional limitation. Moreover, the role of chronotropic incompetence and the need of standardizing the cutoff criteria are also discussed in order to clarify the clinical importance, the prognostic relevance, and the potential therapeutic implications of this condition. Looking into the relative contribution and interaction of heart rate response during exercise might represent an important issue to guide individualized therapeutic interventions and prognostic assessment in HFrEF patients.
Early heart rate recovery after exercise predicts mortality in patients with chronic heart failure
International journal of …, 2006
Background: Patients with chronic heart failure (CHF) have multiple abnormalities of autonomic regulation that have been associated to their high mortality rate. Heart rate recovery immediately after exercise is an index of parasympathetic activity, but its prognostic role in CHF patients has not been determined yet. Methods: Ninety-two stable CHF patients (83M/9F, mean age: 51 T12 years) performed an incremental symptom-limited cardiopulmonary exercise testing. Measurements included peak O 2 uptake (VO 2 p), ventilatory response to exercise (V E /VCO 2 slope), the first-degree slope of VO 2 for the 1st minute of recovery (VO 2 /t-slope), heart rate recovery [(HRR 1 , bpm): HR difference from peak to 1 min after exercise] and chronotropic response to exercise [%chronotropic reserve (CR, %) = (peak HR À resting HR/220 À age À resting HR) Â 100]. Left ventricular ejection fraction (LVEF, %) was also measured by radionuclide ventriculography. Results: Fatal events occurred in 24 patients (26%) during 21 T 6 months of follow-up. HRR 1 was lower in non-survivors (11.4 T 6.4 vs. 20.4 T 8.1; p < 0.001). All cause-mortality rate was 65% in patients with HRR 1 12 bpm versus 11% in patients with HRR 1 > 12 bpm (logrank: 32.6; p < 0.001). By multivariate survival analysis, HRR 1 resulted as an independent predictor of mortality (v 2 = 19.2; odds ratio: 0.87; p < 0.001) after adjustment for LVEF, VO 2 p, V E /VCO 2 slope, CR and VO 2 /t-slope. In a subgroup of patients with intermediate exercise capacity (VO 2 p: 10 -18, ml/kg/min), HRR 1 was a strong predictor of mortality (v 2 : 14.3; odds ratio: 0.8; p < 0.001). Conclusions: Early heart rate recovery is an independent prognostic risk indicator in CHF patients and could be used in CHF risk stratification. D
ESC heart failure, 2018
The mechanisms of exercise intolerance in heart failure with preserved ejection fraction (HFpEF) are not yet elucidated. Chronotropic incompetence has emerged as a potential mechanism. We aimed to evaluate whether heart rate (HR) response to exercise is associated to functional capacity in patients with symptomatic HFpEF. We prospectively studied 74 HFpEF patients [35.1% New York Heart Association Class III, 53% female, age (mean ± standard deviation) 72.5 ± 9.1 years, and 59.5% atrial fibrillation]. Functional performance was assessed by peak oxygen consumption (peak VO). The mean (standard deviation) peak VOwas 10 ± 2.8 mL/min/kg. The following chronotropic parameters were calculated: Delta-HR (HR at peak exercise - HR at rest), chronotropic index (CI) = (HR at peak exercise - resting HR)/[(220 - age) - resting HR], and CI according to the equation developed by Keteyian et al. (CIK) (HR at peak exercise - HR at rest)/[119 + (HR at rest/2) - (age/2) - 5 - HR at rest]. In a bivariat...
PRILOZI, 2014
Objective: Exercise intolerance in patients with heart failure with preserved ejection fraction (HFpEF) is most often attributed to diastolic dysfunction (DD); however, chronotropic incompetence (CI) could also play an important role. We intended to examine whether there are predictive echocardiographic parameters of DD for impaired chronotropic response to exercise. Methods and Results: Patients (n = 143) with unexplained dyspnea and/or exercise intolerance who fulfilled clinical and echocardiographic criteria of HFpEF presence underwent a symptom-limited exercise test using a treadmill (ETT) according to the Bruce protocol. CI was defined as an achieved heart rate reserve (HRR) of ≤ 80%. Comparison of the groups with (n = 98) and without CI (n = 45) did not show any statistically significant difference regarding demographic and clinical character-ristics except for use of beta blockers (BB) that were more frequently present (p = 0.012) in patients with CI in comparison with those ...
Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction
European Journal of Heart Failure, 2011
Peak oxygen uptake (VO 2) is diminished in patients with heart failure with preserved ejection fraction (HFpEF) suggesting impaired cardiac reserve. To test this hypothesis, we assessed the haemodynamic response to exercise in HFpEF patients. Methods and results Eleven HFpEF patients (73 + 7 years, 7 females/4 males) and 13 healthy controls (70 + 4 years, 6 females/7 males) were studied during submaximal and maximal exercise. The cardiac output (Q c , acetylene rebreathing) response to exercise was determined from linear regression of Q c and VO 2 (Douglas bags) at rest, 30% and 60% of peak VO 2 , and maximal exercise. Peak VO 2 was lower in HFpEF patients than in controls (13.7 + 3.4 vs. 21.6 + 3.6 mL/kg/min; P , 0.001), while indices of cardiac reserve were not statistically different: peak cardiac power output [CPO ¼ Q c × mean arterial pressure (MAP); HFpEF 1790 + 509 vs. controls 2119 + 581 L/mmHg/min; P ¼ 0.20]; peak stroke work [SW ¼ stroke volume (SV) × MAP; HFpEF 13 429 + 2269 vs. controls 13 200 + 3610 mL/mmHg; P ¼ 0.80]. The DQ c /DVO 2 slope was abnormally elevated in HFpEF patients vs. controls (11.2 +3.6 vs. 8.3 + 1.5; P ¼ 0.015). Conclusion Contrary to our hypothesis, cardiac reserve is not significantly impaired in well-compensated outpatients with HFpEF. The abnormal haemodynamic response to exercise (decreased peak VO 2 , increased DQ c /DVO 2 slope) is similar to that observed in patients with mitochondrial myopathies, suggesting an element of impaired skeletal muscle oxidative metabolism. This impairment may limit functional capacity by two mechanisms: (i) premature skeletal muscle fatigue and (ii) metabolic signals to increase the cardiac output response to exercise which may be poorly tolerated by a left ventricle with impaired diastolic function.
Journal of Cardiopulmonary Rehabilitation and Prevention, 2020
H eart failure (HF) is a major health care problem associated with high morbidity and mortality. 1 Currently, >6 million Americans ≥20 y of age have HF, and its prevalence is expected to increase by 46% by 2030. 1,2 Nearly half of all HF patients have preserved left ventricular (LV) ejection fraction (heart failure with preserved ejection fraction [HF-pEF]) and this phenotype is more common in older individuals, women, and those with a history of hypertension, obesity, and anemia. 1,3 Decreased exercise tolerance is a hallmark feature in clinically stable HFpEF patients and is associated with reduced quality of life (QoL). 4,5 Given the relationship between cardiorespiratory fitness (CRF; ie, peak oxygen uptake, • Vo 2peak) and survival, 6,7 an important goal of therapy should be to improve CRF in HFpEF patients. 8-12 Currently, exercise training is the only proven effective intervention to improve • Vo 2peak , aerobic endurance, and QoL in HFpEF patients. 4,10 Several recent meta-analyses have reported that endurance exercise training, performed alone or combined with resistance training, improves • Vo 2peak and 6-min walk test distance by 2.2 mL/kg/min and 33 m, respectively. 4,13,14 Accordingly, understanding the mechanisms responsible for reduced • Vo 2peak and its improvement with exercise training is critical to optimally improve functional capacity and QoL in HFpEF patients. In this brief review, the pathophysiology of exercise intolerance and the role of exercise training to improve • Vo 2peak in clinically stable patients with HFpEF are discussed. Further discussion of the mechanisms responsible for the exercise training-mediated increase in • Vo 2peak is provided, along with evidence-based exercise prescription guidelines for clinically stable HFpEF patients participating in an exercise-based cardiac rehabilitation (CR) program. PATHOPHYSIOLOGY OF EXERCISE INTOLERANCE IN HFpEF Appreciating the Fick principle for • Vo 2 is fundamental to understanding the pathophysiology of exercise intolerance in patients with HFpEF. Specifically, the Fick principle dictates that • Vo 2 = cardiac output (Q) × arterial-venous O 2 content difference (a-vO 2 Diff), with Q and the a-vO 2 Diff each having their own modulating factors that ultimately drive the highest achievable • Vo 2 at peak exercise (Figure). ROLE OF CARDIAC FUNCTION ON EXERCISE LIMITATIONS IN HFpEF The reduction in • Vo 2peak observed in patients with HFpEF is due, in part, to a reduction in cardiac function during exercise. Several independent laboratories have demonstrated that peak Q is 30-40% lower in patients with HF-pEF compared with control subjects. 16-19 Evidence to date suggests that chronotropic incompetence rather than stroke volume (SV) is a fundamental concern for the blunted Q response to peak exercise in patients with HFpEF. 16-18,20-22 Indeed, significant relationships between Q (independent of major reductions in SV) 18 and heart rate (HR) 20 with • Vo 2peak have previously been reported, even when matched for important comorbidities, 21 supporting that underlying chronotropic incompetence is a major contributor to reduced Q and subsequent reductions in • Vo 2peak in HFpEF. Despite the major role that HR plays on the severely reduced peak exercise • Vo 2 in patients with HFpEF, several impairments in left ventricular function have also been reported (Figure). Normally, LV relaxation is augmented during exercise to compensate for the reduction in filling