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Theleadless pacemaker (LLPM) therapy has been developed in recent years to overcome the transvenous lead and device pocket-related complications. The LLPMs now available are self-contained right ventricular pacemakers and are limited to single-chamber ventricular pacing modality. This literature review deals with the current status of LLPM technology and current areas of clinical applicability. The safety and efficacy outcomes published from randomized clinical trials and real world registries are analyzed and compared with historical conventional transvenous pacemaker data. Furthermore, new pacing modalities and future perspectives to broaden the clinical use and cover most of pacing indications are discussed. Due to the overall safe and effective profile in the short term and intermediate term, also in fragile patients, the LLPM use is constantly growing in daily clinical practice. Actually, it can be considered a landmark innovation, through which a new era of cardiac pacing has begun.

This is an analysis involving 134 heart failure patients with reduced ejection fraction versus 80 controls investigated during functional evaluation with gas exchange and hemodynamic, addressing the severe mitral regurgitation phenotype and testing the hypothesis that the backward cardiac output redistribution to the lung during exercise impairs delivery and overexpresses peripheral extraction. This information is new and has important implications in the management of heart failure.

AIMS In heart failure (HF), the haemodynamic response to exercise in relation to left atrial (LA) dynamics is unexplored. We sought to define whether abnormal LA dynamics during exercise may play a role in cardiac output (CO) limitation and tested its ability to predict outcome. METHODS AND RESULTS A total of 195 HF patients with reduced (n = 105), mid-range (n = 48), and preserved (n = 42) left ventricular ejection fraction (LVEF) and 46 non-cardiac dyspnoea (NCD) subjects underwent cardiopulmonary imaging with assessment of LA strain and strain rate (sra). HF patients, irrespective of LVEF, exhibited a significantly impaired LA strain and LA sra at rest, during exercise and recovery compared to NCD subjects with a blunted response in CO and right ventricular to pulmonary circulation coupling. LA strain and LA sra during exertion were significantly correlated with peak stroke volume index, peak CO and peak cardiac power output (R = 0.33, 0.48, 0.50 and R = 0.36, 0.51, 0.52 for LA strain and LA sra, respectively; all P 2, peak LVEF and peak heart rate, a higher LA strain (1% increase) during exercise was associated with a higher peak stroke volume index (mL/m2 ), CO (L/min) and cardiac power output (mmHg L/min) at multivariable analyses (β-coefficients ± standard error = 0.23 ± 0.07, 0.046 ± 0.014 and 0.012 ± 0.004, respectively; P

Introduction: The hemodynamic impact of left atrial (LA) intrinsic properties in heart failure (HF) in relation to heart rate (HR) response to exercise has not received attention. Hypothesis: We aimed at investigating the link between LA stiffness and function vs HR reserve (rest to peak exercise) in patients with HF. Methods: A total of 191 patients with HF: 157 β blockers user (LVEF 38 ± 12%, HR reserve 42 ± 18 beats/min) and 34 Non-β blockers user (LVEF 45 ± 19%, HR reserve 36 ± 19 beats/min) underwent cardiopulmonary exercise testing combined with exercise Echo with assessment of LA strain. LA stiffness (median 0.84, IQR 0.44 to 1.89) was assessed using mitral E/E’ /LA strain ratio at rest. Results: HR reserve was positively associated with LA-strain both at rest (20 ± 11%, R = 0.29) and during exercise (20 ± 11%, R = 0.19), LA-strain rate [absolute value] both at rest (1.7 ± 1.0 /s, R = 0.27) and during exercise (1.6 ± 1.2 /s, R = 0.26) and peak VO 2 (14 ± 4 mL/kg/min, R = 0.62), and negatively associated with LA volume index (44 ± 23 ml/m 2 , R = -0.29), log-transformed LA stiffness (R = -0.35), mitral regurgitation (from 0 to 4+) both at rest (R = -0.28:) and peak exercise (R = -0.25) and VE/VCO 2 slope (32 ± 8, R = -0.32)(figure) (P Conclusions: In HF patients, age and LA stiffness play a key role in HR response to exercise irrespective of β blockers prescription. These data may offer additional insights in the concepts of exercise limitation in HF.

Introduction: The relationship between TAPSE vs heart rate (HR) during physical exercise may well represent the force-frequency relationship of the right ventricular (RV) whose impact on exercise performance and hemodynamics may translate in interesting insight. Aims: to phenotype heart failure (HF) patients based on the response in TAPSE vs HR. Methods: A total of 164 patients with HF and 32 healthy subjects with normal RV to pulmonary circulation (Pc) coupling, left atrium (LA) size and reservoir function (LA volume index 2 and LA-strain >23%) underwent cardiopulmonary exercise testing combined with exercise Echo. TAPSE/HR slope was assessed using (peak TAPSE - rest TAPSE)/(peak HR - rest HR) ratio. According to the 95% confidence interval of TAPSE/HR slope (0.03 - 0.13, median 0.06) in healthy subjects, HF patients were divided into 2 groups: responders (TAPSE/HR ≥0.03, n=108) and non-responders ( Results: There was no significant difference in age (65±12 vs 68±13 years), sex (70 vs 63% male), peak VO 2 (14±4 vs 13±4 ml/kg/min), and VE/VCO 2 slope (32±8 vs 33±10) between responder and non-responder group. However, responders exhibited a higher LA-strain at rest (21±12 vs 17±10%) and exercise (21±12 vs 17±10%), and a lower LA volume index (43±21 vs 52±27 ml/m 2 ) and mitral E/e’ (18±10 vs 22±11) than non-responders, respectively (P Conclusions: The RV force-frequency relationship may be impaired in HF. Especially in non-responders the lack of adaptive RV performance combines with worse RV to Pc coupling and atrial dysfunction. These data may offer additional insights in the concepts of exercise limitation in HF.

Background The hemodynamic impact of left atrial (LA) dynamics in aortic stenosis (AS) in relation to cardiopulmonary response to exercise has never been studied. We aimed at investigating the link between LA function vs hemodynamics and prognosis in asymptomatic severe AS patients. Methods A total of 106 patients: 76 asymptomatic severe AS patients (aortic valve area (AVA) Results Normal-flow low-gradient AS (NFLG: PV 35ml/m2, LVEF ≥50%, N=23), High-gradient AS (HG: PV ≥4 m/s or MPG ≥40 mmHg, LVEF ≥50%, N=23), Paradoxical low-flow low-gradient AS (PLFLG: PV Conclusions In asymptomatic severe AS, the study of LA functional adaptation to exercise plays a key role in the hemodynamic unfavorable cascade signaling major adaptive differences in dynamics during physical challenge. Overall, LA dynamics provides prognostic information also in AS patients. Funding Acknowledgement Type of funding sources: None.

Objectives The aim of this study was to identify the pattern of exercise left atrial (LA) dynamics, its gas exchange correlates, and prognosis in mitral regurgitation (MR) of primary and secondary origin. Background The adaptive response and clinical significance of LA function during exercise in MR is undefined. Methods A total of 196 patients with MR (81 with primary MR, 115 with secondary MR) and 54 control subjects underwent exercise stress echocardiography and cardiopulmonary exercise testing with LA function assessment. Patients with MR were divided into 4 groups according to etiology and severity using a cutoff of 3+. Results LA dynamics was studied using speckle-tracking echocardiography. Compared with control subjects, patients with MR had a lower LA strain and strain rate at rest. Exercise LA strain and LA strain rate progressively worsened from primary MR 3+ (25.5; IQR: 23.4 to 29.0); and those with secondary MR Conclusions In MR of any origin, exercise LA reservoir and pump function are impaired. For similar MR extent, secondary MR exhibits worse atrial function, resulting in the lowest exercise performance, limited cardiac output increase, impaired right ventricular–to–pulmonary circulation coupling, and the highest event rate.

Functional mitral regurgitation (MR) is prognostic in heart failure (HF). MR favors an nonphysiological exercise central cardiac output (CO) redistribution which adds to oxygen (O

Objectives The hypothesis of this study was that left atrial (LA) dynamic impairment during exercise may trigger right ventricular (RV)-to–pulmonary circulation (PC) uncoupling and ventilation inefficiency. Background LA function plays a key role in the hemodynamics of heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). Extensive investigation of LA dynamics, however, has been performed exclusively at rest. Methods A total of 49 patients with HFrEF, 20 patients with HFpEF, and 32 healthy subjects with normal LA size and reservoir function (LA volume index 23%) were prospectively enrolled. They underwent cardiopulmonary exercise testing and contemporary echo-Doppler assessment of LA-strain and LA-strain rate and of RV-to-PC coupling (pulmonary arterial systolic pressure/tricuspid annular peak systolic excursion ratio), measured at rest, at 40% of predicted peak oxygen consumption, and during recovery. Results In control subjects, LA-strain increased during exercise and recovery. Patients with HFpEF exhibited some LA-strain increase during exercise and recovery, whereas no changes occurred in those with HFrEF. The baseline LA-strain rate was greater in control subjects; a significant enhancement during recovery was observed only in this group. In both the HFpEF and HFrEF cohorts, RV-to-PC uncoupling and LA-strain at rest, exercise, and recovery significantly correlated with pulmonary arterial systolic pressure/tricuspid annular peak systolic excursion, as well as ventilation versus carbon dioxide slope, in a continuous fashion across groups (r = −0.63 and r = −0.59, r = −0.65 and r = −0.50, and r = −0.70 and r = −0.53 for control subjects, HFpEF, and HFrEF, respectively; p Conclusions In heart failure, an impaired LA-strain response is a key hemodynamic trigger for RV-to-PC uncoupling and exercise ventilation inefficiency with some overlap between HFpEF and HFrEF phenotypes. Reversibility of LA dynamics seems to be an unmet target of specific therapeutic interventions.

Objectives Right ventricular (RV) exercise contractile reserve (RVECR), its phenotypes, and its functional correlates are among the unresolved issues with regard to the role of the right ventricle in heart failure (HF) syndrome, and understanding these issues constitutes the objective of this study. Background Although the role of the right ventricle in HF syndrome might be fundamental, the pathophysiology of the failing right ventricle has not been extensively investigated. Methods Ninety-seven patients with HF (mean age 64 years, 70% men, mean left ventricular ejection fraction 33 ± 10%) underwent maximal exercise stress echocardiographic and cardiopulmonary exercise testing. RVECR and RV–to–pulmonary circulation (PC) coupling were assessed using the length-force relationship (tricuspid annular plane systolic excursion [TAPSE] vs. pulmonary artery systolic pressure) and the slope of mean pulmonary artery pressure versus cardiac output. On the basis of TAPSE, patients were categorized into 3 groups: those with TAPSE at rest ≥16 mm (group A, n = 60) and those with TAPSE at rest Results Although they had similar left ventricular ejection fractions and rest RV impairment, compared with patients in group C, those in group B showed some degree of RVECR (upward shift of the length-force relationship), better RV-to-PC coupling (lower mean pulmonary artery pressure vs. cardiac output slope), and greater ventilatory efficiency (lower slope of minute ventilation to carbon dioxide output). Rest mitral regurgitation and net changes in pulmonary artery systolic pressure were the variables retained in the best regression model as correlates of RVECR. Conclusions In patients with HF, RVECR unmasks different phenotypes. Impaired RV function at rest might not invariably lead to unfavorable RVECR and exercise RV-to-PC coupling. Testing these variables appears useful even in more advanced stages of HF to define various clinical conditions and, most likely, to define different levels of risk.

The aim of this study was to identify the pattern of exercise left atrial (LA) dynamics, its gas exchange correlates, and prognosis in mitral regurgitation (MR) of primary and secondary origin.The adaptive response and clinical significance of LA function during exercise in MR is undefined.A total of 196 patients with MR (81 with primary MR, 115 with secondary MR) and 54 control subjects underwent exercise stress echocardiography and cardiopulmonary exercise testing with LA function assessment. Patients with MR were divided into 4 groups according to etiology and severity using a cutoff of 3+.LA dynamics was studied using speckle-tracking echocardiography. Compared with control subjects, patients with MR had a lower LA strain and strain rate at rest. Exercise LA strain and LA strain rate progressively worsened from primary MR 3+ through secondary MR ≥3+. In primary MR, some reserve in exercise LA strain and LA strain rate was observed, but not in secondary MR. In secondary MR, LA strain at rest and during exercise (18.1 ± 5.7 sIn MR of any origin, exercise LA reservoir and pump function are impaired. For similar MR extent, secondary MR exhibits worse atrial function, resulting in the lowest exercise performance, limited cardiac output increase, impaired right ventricular-to-pulmonary circulation coupling, and the highest event rate.

There has been a greater appreciation of several variables obtained by cardiopulmonary exercise testing (CPX). Exercise oscillatory ventilation (EOV) is a CPX pattern that has gained recognition as an ominous marker of poor prognosis in cardiac patients. The purpose of the present study is to characterize whether such an abnormal ventilatory pattern may also be detected in apparently healthy subjects and determine its clinical significance.The study involved 510 subjects (mean age 60 ± 14 years; 49% male) with a broad cardiovascular (CV) risk factor profile who underwent CPX.The population was divided into two groups according to the presence (17%) or absence of EOV. Subjects with EOV were significantly older and a higher percentage was female. Risk factor profile and medication use was significantly different between subgroups, indicating subjects with EOV had a worse CV risk factor profile and were prescribed CV-focused preventive medications at a significantly higher frequency. Subjects with EOV had comparatively poorer CPX performance and gas exchange phenotype. Multivariate binary logistic regression analysis found being female was the strongest predictor of EOV (odds ratio: 2.77, 95% confidence interval (CI): 1.66-4.61, p 0.001). A diagnosis of diabetes (odds ratio: 2.40, 95% CI: 1.34-4.15.2, p 0.001) added significant value for predicting EOV and was retained in the regression. The likelihood for EOV for subjects who were female and diagnosed with diabetes was 3.71 (95% CI 1.88-7.30, p 0.001).This is the first study to examine EOV prevalence and characterization in apparently healthy persons with results supporting an in-depth definition of abnormal exercise phenotypes.

Background— Several cardiovascular diseases are characterized by an impaired O 2 kinetic during exercise. The lack of a linear increase of Δoxygen consumption (V O 2 )/ΔWork Rate (WR) relationship, as assessed by expired gas analysis, is considered an indicator of abnormal cardiovascular efficiency. We aimed at describing the frequency of ΔVO 2 /ΔWR flattening in a symptomatic population of cardiac patients, characterizing its functional profile, and testing the hypothesis that dynamic pulmonary hypertension and right ventricular contractile reserve play a major role as cardiac determinants. Methods and Results— We studied 136 patients, with different cardiovascular diseases, referred for exertional dyspnoea. Cardiopulmonary exercise test combined with simultaneous exercise echocardiography was performed using a symptom-limited protocol. ΔVO 2 /ΔWR flattening was observed in 36 patients (group A, 26.5% of population) and was associated with a globally worse functional profile (reduced peak V O 2 , anaerobic threshold, O 2 pulse, impaired VE/VCO 2 ). At univariate analysis, exercise ejection fraction, exercise mitral regurgitation, rest and exercise tricuspid annular plane systolic excursion, exercise systolic pulmonary artery pressure, and exercise cardiac output were all significantly ( P P =0.01) and exercise tricuspid annular plane systolic excursion (odds ratio, 0.88; confidence interval, 0.80–0.97; P =0.01) as main cardiac determinants of ΔVO 2 /ΔWR flattening; female sex was strongly associated (odds ratio, 6.10; confidence interval, 2.11–17.7; P Conclusions— In patients symptomatic for dyspnea, the occurrence of ΔVO 2 /ΔWR flattening reflects a significantly impaired functional phenotype whose main cardiac determinants are the excessive systolic pulmonary artery pressure increase and the reduced peak right ventricular longitudinal systolic function.

The hypothesis of this study was that left atrial (LA) dynamic impairment during exercise may trigger right ventricular (RV)-to-pulmonary circulation (PC) uncoupling and ventilation inefficiency.LA function plays a key role in the hemodynamics of heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). Extensive investigation of LA dynamics, however, has been performed exclusively at rest.A total of 49 patients with HFrEF, 20 patients with HFpEF, and 32 healthy subjects with normal LA size and reservoir function (LA volume index 34 ml/mIn control subjects, LA-strain increased during exercise and recovery. Patients with HFpEF exhibited some LA-strain increase during exercise and recovery, whereas no changes occurred in those with HFrEF. The baseline LA-strain rate was greater in control subjects; a significant enhancement during recovery was observed only in this group. In both the HFpEF and HFrEF cohorts, RV-to-PC uncoupling and LA-strain at rest, exercise, and recovery significantly correlated with pulmonary arterial systolic pressure/tricuspid annular peak systolic excursion, as well as ventilation versus carbon dioxide slope, in a continuous fashion across groups (r = -0.63 and r = -0.59, r = -0.65 and r = -0.50, and r = -0.70 and r = -0.53 for control subjects, HFpEF, and HFrEF, respectively; p 0.05).In heart failure, an impaired LA-strain response is a key hemodynamic trigger for RV-to-PC uncoupling and exercise ventilation inefficiency with some overlap between HFpEF and HFrEF phenotypes. Reversibility of LA dynamics seems to be an unmet target of specific therapeutic interventions.

The role that an increased stiffness of left atrial (LA) during exercise may play in mediating right ventricular (RV) -to-pulmonary circulation (PC) coupling during exercise in patients with left heart disease (LHD) is largely unexplored. 32 Controls and 179 patients with LHD [95 patients without

Right ventricular (RV) exercise contractile reserve (RVECR), its phenotypes, and its functional correlates are among the unresolved issues with regard to the role of the right ventricle in heart failure (HF) syndrome, and understanding these issues constitutes the objective of this study.Although the role of the right ventricle in HF syndrome might be fundamental, the pathophysiology of the failing right ventricle has not been extensively investigated.Ninety-seven patients with HF (mean age 64 years, 70% men, mean left ventricular ejection fraction 33 ± 10%) underwent maximal exercise stress echocardiographic and cardiopulmonary exercise testing. RVECR and RV-to-pulmonary circulation (PC) coupling were assessed using the length-force relationship (tricuspid annular plane systolic excursion [TAPSE] vs. pulmonary artery systolic pressure) and the slope of mean pulmonary artery pressure versus cardiac output. On the basis of TAPSE, patients were categorized into 3 groups: those with TAPSE at rest ≥16 mm (group A, n = 60) and those with TAPSE at rest 16 mm, who were divided according to median TAPSE at peak exercise (15.5 mm) into 2 subgroups (group B, ≥15.5 mm, n = 19; group C, 15.5 mm, n = 18).Although they had similar left ventricular ejection fractions and rest RV impairment, compared with patients in group C, those in group B showed some degree of RVECR (upward shift of the length-force relationship), better RV-to-PC coupling (lower mean pulmonary artery pressure vs. cardiac output slope), and greater ventilatory efficiency (lower slope of minute ventilation to carbon dioxide output). Rest mitral regurgitation and net changes in pulmonary artery systolic pressure were the variables retained in the best regression model as correlates of RVECR.In patients with HF, RVECR unmasks different phenotypes. Impaired RV function at rest might not invariably lead to unfavorable RVECR and exercise RV-to-PC coupling. Testing these variables appears useful even in more advanced stages of HF to define various clinical conditions and, most likely, to define different levels of risk.

Exercise Ventilatory Power (EVP; peak systolic blood pressure/exercise ventilation to CO2 production slope) is a new powerful prognostic marker that combines ventilator abnormalities with systemic hemodynamic during exercise. The phenotype and clinical relevance of patients with a worse EVP is broadly undefined and we aimed at this definition across a population of heart failure reduced ejection fraction (HFrEF) of different severity. Methods: 77 HFrEF patients (mean age 65±11; male 70%; ischemic etiology 59%; NYHA class I, II, III and IV 23%, 33%, 31% and 13%, respectively; mean LVEF 34±9 %) underwent cardiopulmonary exercise test (CPET) evaluation (ramp protocol on performed on a tilt-table cycleergometer) combined with simultaneous echocardiographic assessment. Results: Patients were divided in 2 EVP classes (cutoff 3) focusing on peak exercise echocardiographic variables. Conclusions: A low EVP translates in a very unfavorable phenotype characterized by a lower peak VO2 and CO response at peak exercise. Remarkable impairment in right heart function and pulmonary hemodynamics were also peculiar of a low EVP. All the LV-pulmonary circulation- RV apparatus is abnormally involved in the exercise response of the EVP HFrEF phenotype.

Background: in heart failure (HF) the mitral regurgitation (MR) is clinical and prognostic relevant. Cardiopulmonary exercise testing (CPET) allows evaluating functional capacity and provides indexes for HF risk stratification such as peak oxygen consumption (VO2). Since MR determines a severity-related backward flow to left atrium, it may result in an unfavorable central blood flow exercise redistribution that is physiological relevant to VO2 increase. Aim: To evaluate the cardiac output (CO) and VO2 exercise-response in HF reduced ejection fraction (HFrEF) patients according to MR severity to dissect what mechanism may be predominant in the VO2 increase. Methods: 104 HFrEF patients (mean age 64±11 y, male 72%, ischemic etiology 68%, mean LVEF 34±9%) underwent a maximal CPET (incremental ramp protocol) combined with exercise-echo. CO was non-invasive estimated by echo. Results: Population was divided into 2 groups according to the rest MR: group A (n=80) non-severe MR and B (N=24) severe MR. Despite the groups did not differ in rest CO (A vs B 3.8±1 vs 3.4±1.8 L/min, p=ns) and VO2 (0.27±0.06 vs 0.28±0.09 L/min, p=ns) group B showed higher peripheral extraction (C(a-v)O2 8±2 vs 9±4 mL/100 mL, p=0.036) already at rest (Figure). At peak exercise group B had an impaired increase both in CO (7,0±2,0 vs 5,2±3,3 L/min) and VO2 (1,0±0,3 vs 0,8±0,3 L/min, p=0.001) partially compensated by a greater C(a-v)O2 contribution (15±4 vs 18±5 for A vs B, p=0.047). Conclusions: Severe MR and consequent partial abnormal CO redistribution to the pulmonary circulation seems a relevant pathophysiological mechanisms that limits overall exercise performance in HFrEF. In this high risk subset of patients peripheral extraction compensates for the reduced CO and makes the basis for novel perspectives in these patients.

Background: Right ventricular (RV) dysfunction and pulmonary hypertension (PH) impact on clinical status and have a prognostic value in heart (HF) patients. There is interest in assessment the RV to pulmonary circulation (PC) uncoupling during exercise even though much needs to be defined on the functional phenotypes. Aim: to define how the degrees of RV-PC uncoupling may engender specific functional phenotypes. Methods: 94 HFrEF patients (mean age 66±11 y, male 70%, ischemic etiology 71%, mean LVEF 34±9%) underwent a maximal CPET (incremental ramp protocol) combined with exercise-echo. Results: Population was divided into 4 groups using the 4 quadrant approach (Figure) based on TAPSE vs systolic PAP (PASP) relationship as a length vs developed force of the RV during exercise (cutoff based on median values of 20 mm and 57 mmHg). At peak exercise patients with more favorable TAPSE vs PASP relationship (group A) showed the better functional CPET response (higher peak VO2; lower VE/VCO2 slope and prevalence of exercise oscillatory ventilation (EOV), p= 0.000, 0.005 and 0.000). Group B and C showed similar peak VO2 and the occurrence of dynamic PH (group C) was related to dynamic mitral regurgitation (MR) and high rate of EOV (B vs C p=0.001 and 0.000). Interestingly, for similar exercise tolerance and LV function parameters, group D patients had more severely impaired ventilatory efficiency associated with very high prevalence of rest severe (MR) and EOV (p=0.005, 0.002). Conclusions: This proposed non-invasive RV functional evaluation approach at peak exercise seems appealing for stageing HF syndrome severity based on the degree of the right heart dysfunction. It appears also useful to unmask different ventilatory phenotypes irrespective of a similar impairment in functional capacity and peak VO2.

Background: Speckle tracking analysis is an emerging technique that can be useful to assess abnormalities in cardiac contractility before traditional echo parameters. Purpose: To investigate whether right ventricular (RV) 2D speckle tracking analysis at peak exercise could stratify a heart failure reduced ejection fraction (HFrEF) population in different functional phenotypes, with particular emphasis on RV to pulmonary circulation relationship. Methods: 36 HFrEF patients (mean age 69±12; male 69%; NYHA I-II-III-IV 19-17-25-5 %) underwent a maximal cardiopulmonary exercise testing evaluation (bike, incremental ramp protocol) combined with Echo-Doppler and off-line speckle tracking analysis. Study population was divided in two groups according to median value of 2D right ventricle longitudinal strain at peak exercise (Group A RVLG at peak < -16, 17 patients vs Group B ≥ -16, 19 patients). In all patients we performed traditional echo and 2D longitudinal speckle tracking analysis at rest and peak exercise. Results: Despite similar left ventricle ejection fraction (Group A 36± 9% vs Group B 32±9%, p=ns) and global right ventricle longitudinal strain (RVLG) at rest (Group A -18.6±5.6% vs Group B -14.5±8.2%, p=ns), Group B patients showed a similar exercise performance (Peak VO 2 Group A 31.6±7.4 vs Group B 11.6±3.4 mlO 2 /Kg/min, p=ns) but more impaired ventilation (VE/VCO2 slope Group A 31.6±7.4 vs Group B 37.4±8.8, p Conclusions: In HFrEF RV speckle tracking analysis at peak exercise seems a useful technique for unmasking RV to PC uncoupling and the unfavorable gas exchange and ventilatory phenotypes.

Background: The ratio between the duration of right ventricular (RV) systole and diastole (S:D ratio) has been proposed as an index of RV performance in a pediatric population with pulmonary arterial hypertension in whom it may predict prognosis and functional capacity. In heart failure (HF) S:D may provide relevant insights in the exercise response. Aim: to analyze the correlation between rest and peak exercise S:D and functional and cardiac parameters in HFrEF. Methods: 94 HFrEF patients (mean age 66±11 y, male 70%, ischemic etiology 71%, mean LVEF 34±9%) underwent a symptom-limited cardiopulmonary exercise testing (incremental ramp protocol) combined with exercise-echo. RV S:D was assessed by echo at rest and peak exercise. Results: A good correlation was found between rest and peak S:D and CPET indexes of exercise capacity, such as peak oxygen consumption (VO2) (Sperman’s rho -0.40 and 0.38 respectively, p= 0.02 and 0.023) and maximal workload (Rho= -0.42 and -0.45, p=0.031 and 0.034). An higher S:D also correlated with more impaired ventilatory efficiency or higher VE/VCO2 slope (Rho 0.49 and 0.32, p=0.019 and 0.024). Looking at echo phenotype, interestingly S:D is associated with parameters of mitral regurgitation (MR) severity, such as effective regurgitant orifice (Rho rest 0.63, peak 0.35, p

The hemodynamic impact of mitral regurgitation (MR), left atrial (LA) dynamics, and RV-to-PC coupling during exercise on cardiopulmonary function and clinical outcome has never been studied. 279 patients with exercise induced-dyspnea (120 HF, 56 aortic stenosis, 47 primary MR, 14 hypertrophic

The hemodynamic impact of left atrial (LA) dynamic response in heart failure (HF) on cardiopulmonary function and RV-to-PC coupling at exercise is a matter of recent interest. 120 patients with HF reduced (rEF, n=70), mid-range (mrEF, n=25) and preserved (pEF, n=25) ejection fraction underwent CPET

Exercise Ventilatory Power (EVP; peak systolic blood pressure/exercise ventilation to CO2 production slope) is a new powerful prognostic marker that combines ventilator abnormalities with systemic hemodynamic during exercise. The phenotype and clinical relevance of patients with a worse EVP is

Background: In heart failure (HF) patients the severity of mitral regurgitation (MR) at rest has a well established prognostic value and its increase during exercise further adds to an increased risk. Our goal was to define the relationship between the degree of exercise MR severity with cardiopulmonary and echocardiographic related phenotypes in a cohort of HF patients. Methods: 71 HF reduced ejection fraction patients (mean age 67±11; male 72%; ischemic etiology 61%; NYHA class I, II, III and IV 13%, 36%, 39% and 12%, mean ejection fraction 33±9%) underwent cardiopulmonary exercise test (CPET) on tiltable cycle-ergometer combined with echocardiography at rest and during exercise. The population was divided into two groups according to the degree of functional peak MR: no to mild/moderate MR (no MR, MR1+ and MR2+) vs moderate/severe MR (MR3+ and MR4+). Results: A good correlation (ρ coefficient= 0.49) was found between the degree of dynamic MR and PASP at peak exercise. Despite similar echocardiographic profile at rest patients with significant peak MR (MR≥3+) had worse exercise performance (lower peak VO2, O2 pulse and workload) and impaired ventilatory efficiency (higher VE/VCO2 slope). Conclusions: In HF patients the severity of exercise-induced MR is associated with the most unfavorable performance and pulmonary hemodynamic response. A combined approach with CPET and echocardiographic assessment can help to early unmask and target functional MR and its related unfavorable phenotypes.

Diabetes mellitus (DM) is a risk condition that may determine overall exercise limitation and reduced oxygen consumption (VO2). No study has addressed the cardiopulmonary exercise testing phenotype in diabetic subjects with normal left ventricular function. Their functional characterization by

Aortic stenosis (AS) is characterized by increased afterload and functional disability. Exercise intolerance may incur even without overt symptoms. Cardiopulmonary exercise testing (CPET) provides pathophysiological insights on mechanisms affecting exercise intolerance. Nonetheless, it has never

Aims In heart failure patients with reduced ejection fraction (HFrEF), exercise-induced functional mitral regurgitation (MR) may affect functional capacity and outcome. We sought to study functional and cardiac phenotypes of HFrEF patients according to the MR degree. Methods and results We performed rest and exercise echocardiography (Ex-Echo), simultaneously combined with cardiopulmonary exercise test (CPET), in 102 HFrEF patients, identifying 3 groups: non-severe (ERO

Group 2 pulmonary hypertension (PH) and exercise oscillatory ventilation (EOV) are prognostic signs in heart failure (HF). It is unknown what may characterize the exercise response of PH patients and EOV. Aim: To define the functional pattern in HF reduced ejection fraction (HFrEF) with PH according

The hemodynamic adaptation to exercise in heart failure preserved ejection fraction (HFpEF) has never been studied in terms of left atrial adaptations and right ventricular to pulmonary circulation (RV to PC) coupling. We aimed at investigating these responses. Ten HFpEF patients (LVEF >50%

We hypothesized that a failure of left atrial contribution to left ventricular filling would be involved in the right ventricular (RV) to pulmonary circulation (PC) uncoupling and exercise ventilation inefficiency. 44 patients with heart failure reduced ejection fraction (HFrEF) and 32 controls