Cardiac rehabilitation (CR) is indicated in all patients after acute myocardial infarction (AMI) to improve prognosis and exercise capacity (EC). Previous studies reported that up to a third of patients did not improve their EC after CR (non-responders). Our aim was to assess the cardiac and peripheral mechanisms of EC improvement after CR using combined exercise echocardiography and cardiopulmonary exercise testing (CPET-SE). The responders included patients with an improved EC assessed as a rise in peak oxygen uptake (VO2) ≥1 mL/kg/min. Peripheral oxygen extraction was calculated as arteriovenous oxygen difference (A-VO2Diff). Out of 41 patients (67% male, mean age 57.5 ± 10 years) after AMI with left ventricular ejection fraction (LVEF) ≥40%, 73% improved their EC. In responders, peak VO2 improved by 27% from 17.9 ± 5.2 mL/kg/min to 22.7 ± 5.1 mL/kg/min, p < 0.001, while non-responders had a non-significant 5% decrease in peak VO2. In the responder group, the peak exercise heart rate, early diastolic myocardial velocity at peak exercise, LVEF at rest and at peak exercise, and A-VO2Diff at peak exercise increased, the minute ventilation to carbon dioxide production slope decreased, but the stroke volume and cardiac index were unchanged after CR. Non-responders had no changes in assessed parameters. EC improvement after CR of patients with preserved LVEF after AMI is associated with an increased heart rate response and better peripheral oxygen extraction during exercise.

of experts from the Working Group on Cardiac Rehabilitation and Exercise Physiology of the Polish Cardiac Society concerning the indications, performance technique, and interpretation of results for CPET in adult cardiology. Cardiopulmonary exercise testing CPET is an electrocardiographic exercise test expanded with exercise evaluation of ventilation and

Exercise intolerance after acute myocardial infarction (AMI) is a predictor of worse prognosis, but its causes are complex and poorly studied. This study assessed the determinants of exercise intolerance using combined stress echocardiography and cardiopulmonary exercise testing (CPET-SE) in patients treated for AMI. We prospectively enrolled patients with left ventricular ejection fraction (LV EF) ≥40% for more than 4 weeks after the first AMI. Stroke volume, heart rate, and arteriovenous oxygen difference (A-VO2Diff) were assessed during symptom-limited CPET-SE. Patients were divided into four groups according to the percentage of predicted oxygen uptake (VO2) (Group 1, <50%; Group 2, 50–74%; Group 3, 75–99%; and Group 4, ≥100%). Among 81 patients (70% male, mean age 58 ± 11 years, 47% ST-segment elevation AMI) mean peak VO2 was 19.5 ± 5.4 mL/kg/min. A better exercise capacity was related to a higher percent predicted heart rate (Group 2 vs. Group 4, p <0.01), higher peak A-VO2Diff (Group 1 vs. Group 3, p <0.01) but without differences in stroke volume. Peak VO2 and percent predicted VO2 had a significant positive correlation with percent predicted heart rate at peak exercise (r = 0.28, p = 0.01 and r = 0.46, p < 0.001) and peak A-VO2Diff (r = 0.68, p <0.001 and r = 0.36, p = 0.001) but not with peak stroke volume. Exercise capacity in patients treated for AMI with LV EF ≥40% is related to heart rate response during exercise and peak peripheral oxygen extraction. CPET-SE enables non-invasive assessment of the mechanisms of exercise intolerance.

Decreased exercise capacity (EC) is an established predictor of cardiac and all-cause mortality in patients with chronic heart failure (HF). No correlation has been found between EC and left ventricular (LV) ejection fraction. Moreover, data about the effect of right ventricular (RV) function on EC in HF with severe LV dysfunction are limited and contradictory. In this study, we aimed to investigate the relationship between EC and myocardial mechanics in patients with HF with reduced ejection fraction.Consecutive patients with symptomatic HF and LV ejection fraction ≤35% were prospectively assessed. All patients were evaluated with enhanced echocardiography. A symptom-limited treadmill cardiopulmonary exercise test (CPX) was performed within 24-hour interval. Patients were stratified into 4 groups according to their EC defined by Weber's classification. Prognosis of EC, expressed as oxygen uptake at peak exercise (peak VO2), was evaluated in multivariate linear regression analysis model.Sixty-seven patients with New York Heart Association classes II to III and a mean LV ejection fraction of 26 ± 7% were enrolled. A wide range of peak VO2 was observed in CPX with patient exercise performance distributed to all classes according to Weber's classification. Significant differences were found in RV systolic and diastolic functions between groups with different classes of EC: RV peak systolic myocardial velocity (S′) (P < .001), tricuspid annular plane systolic excursion (TAPSE) (P = .003), RV E’ (P = .003). In patients with functional decline, systolic pulmonary artery pressure (PASP) was higher (P = .029) and TAPSE/PASP ratio was lower (P = .006). No significant differences were found in LV diameter, systolic and diastolic function, and degree of mitral regurgitation. Thirty three patients with RV systolic dysfunction showed lower peak VO2 and oxygen uptake at anaerobic threshold (P = .008, P = .006, respectively), shorter exercise time (P = .003), and lower systolic blood pressure (P = .01) than in patients with normal RV systolic function. Logistic multivariate linear regression analysis with stepwise inclusion and exclusion revealed that gender, RV S′, and RV free wall strain were independent predictors of peak VO2.RV function, assessed as S′ and free wall strain, was independently related to EC, measured using CPX, in patients with HF and severe LV systolic dysfunction.

BackgroundCryoballoon‐based pulmonary vein isolation (CB‐PVI) has been widely used for the treatment of atrial fibrillation. Although generally safe and effective, the procedure may be associated with pulmonary vein (PV) stenosis and bronchial or esophageal injury. The mechanisms leading to these complications have not been studied in detail. Our aim was to examine acute effects of cryoballoon on the pulmonary vessel and right heart pressures as well as PV wall morphology.Methods and ResultsIn 8 patients (5 men, mean age 55±14 years) undergoing CB‐PVI, pressure in each PV was measured by catheter located inside the PV directly before and after CB‐PVI. The right atrial, right ventricular, and pulmonary artery pressures as well as pulmonary arterial wedge capillary pressure in the pulmonary artery branch corresponding to target PV were also measured. Morphological changes in PVs were assessed using intravascular ultrasonography.There were no significant differences in PV pressures before and after ablation. The pulmonary arterial wedge capillary pressure significantly increased during cryoapplication (left superior: 20±10 versus 29±8.5 mm Hg, P=0.004; left inferior: 24±10 versus 32±6 mm Hg, P=0.012; right superior: 25±9 versus 35±10 mm Hg, P=0.002; right inferior: 24±10 versus 37±12 mm Hg, P=0.0036). The right atrial and pulmonary artery pressures increased significantly after CB‐PVI (9±6 versus 13±8 mm Hg, P=0.004, and 20±9 versus 24±10 mm Hg, P=0.048, respectively). Intravascular ultrasonography showed acute edema and dissection‐like changes causing relative lumen narrowing in 90% of PVs.Conclusions CB‐PVI causes significant rise in pulmonary artery and right atrial pressures as well as PV wall damage. The clinical significance of these findings warrants further investigations.

Background: Chronotropic incompetence in patients taking beta-blockers is associated with poor prognosis; however, its impact on exercise capacity (EC) remains unclear. Methods: We analyzed data from consecutive patients taking beta-blockers referred for cardiopulmonary exercise testing to assess EC. Chronotropic incompetence was defined as chronotropic index (CI) ≤ 62%. Results: Among 140 patients all taking beta-blockers (age 61 ± 9.7 years; 73% males), 64% with heart failure, chronotropic incompetence was present in 80.7%. EC assessed as peak oxygen uptake was lower in the group with chronotropic incompetence, 18.3 ± 5.7 vs. 24.0 ± 5.3 mL/kg/min, p < 0.001. EC correlated positively with CI (β = 0.14, p < 0.001) and male gender (β = 5.12, p < 0.001), and negatively with age (β = −0.17, p < 0.001) and presence of heart failure (β = −3.35, p < 0.001). Beta-blocker dose was not associated with EC. Partial correlation attributable to CI accounted for more than one-third of the variance in EC explained by the model (adjusted R2 = 59.8%). Conclusions: In patients taking beta-blockers, presence of chronotropic incompetence was associated with lower EC, regardless of the beta-blocker dose. CI accounted for more than one-third of EC variance explained by our model.

Galectin-3 is a biomarker of fibrosis, inflammation and oxidative stress, and its role in heart remodelling and exercise intolerance has not been conclusively proven in heart failure (HF) patients with reduced ejection fraction (rEF). We prospectively assessed 67 consecutive patients with symptomatic HF and left ventricular (LV) EF ≤ 35% during optimal medical therapy, with a mean serum galectin-3 concentration of 15.3 ± 6.4 and a median of 13.5 ng/mL. The group with galectin-3 concentrations greater than or equal to the median had significantly worse right ventricular (RV) systolic function parameters (s′, TAPSE), higher pulmonary artery systolic pressure, more advanced tricuspid regurgitation and lower RV-to-pulmonary circulation coupling index, while no significant differences were found in LV parameters. Moreover, this group achieved significantly lower parameters in cardiopulmonary exercise testing. Significant negative correlations were found between galectin-3 concentration and RV parameters and exercise capacity parameters and have persisted after adjustment for glomerular filtration rate, but not all of them have persisted after adjustment for NT-proBNP. Multivariate regression analysis revealed that TAPSE (β coefficient: − 0.605; p < 0.001) and heart rate at peak exercise (β coefficient: − 0.98; p = 0.009) were independently related to galectin-3 concentration. Elevated galectin-3 concentration in patients with HFrEF might indicate concomitant RV dysfunction and exercise intolerance.

No abstract