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Background Both secondary tricuspid regurgitation (STR) and heart failure with preserved ejection fraction (HFpEF) are relevant public health problems in the elderly population, presenting with potential overlaps and sharing similar risk factors. However, the impact of severe STR on hemodynamics and cardiorespiratory adaptation to exercise in HFpEF remains to be clarified. Aim To explore the impact of STR on exercise hemodynamics and cardiorespiratory adaptation in HFpEF. Methods We analyzed invasive hemodynamics and gas-exchange data obtained at rest and during exercise from HFpEF patients with severe STR (HFpEF-STR), compared with 1:1 age-, sex-, and body mass index (BMI)- matched HFpEF patients with mild or no STR (HFpEF-controls). Results Twelve HFpEF with atrial-STR (mean age 72 years, 92% females, BMI 28 Kg/m 2 ) and 12 HFpEF-controls patients were analyzed. HFpEF-STR had higher ( p < 0.01) right atrial pressure than HFpEF-controls both at rest (10 ± 1 vs. 5 ± 1 mmHg) and during exercise (23 ± 2 vs. 14 ± 2 mmHg). Despite higher pulmonary artery wedge pressure (PAWP) at rest in HFpEF-STR than in HFpEF-controls (17 ± 2 vs. 11 ± 2, p = 0.04), PAWP at peak exercise was no more different (28 ± 2 vs. 29 ± 2). Left ventricular transmural pressure and cardiac output (CO) increased less in HFpEF-STR than in HFpEF-controls (interaction p -value < 0.05). This latter was due to lower stroke volume (SV) values both at rest (48 ± 9 vs. 77 ± 9 mL, p < 0.05) and at peak exercise (54 ± 10 vs. 93 ± 10 mL, p < 0.05). Despite these differences, the two groups of patients laid on the same oxygen consumption isophlets because of the increased peripheral oxygen extraction in HFpEF-STR ( p < 0.01). We found an inverse relationship between pulmonary vascular resistance and SV, both at rest and at peak exercise ( R 2 = 0.12 and 0.19, respectively). Conclusions Severe STR complicating HFpEF impairs SV and CO reserve, leading to pulmonary vascular de-recruitment and relati, SCOPUS: ar.j, info:eu-repo/semantics/published

Background: Although the assessment of left atrial (LA) mechanics has been reported to refine atrial fibrillation (AF) risk prediction, it doesn't completely predict AF recurrences. The potential added role of right atrial (RA) function in this setting is unknown. Accordingly, this study sought to evaluate the added value of RA longitudinal reservoir strain (RASr) for the prediction of AF recurrence after electrical cardioversion (ECV). Methods: We retrospectively studied 132 consecutive patients with persistent AF who underwent elective ECV. Complete two-dimensional and speckle-tracking echocardiography analyses of LA and RA size and function were obtained in all patients before ECV. The endpoint was AF recurrence. Results: During a 12-month follow-up of, 63 patients (48%) showed AF recurrence. Both LA and RASr were significantly lower in patients experiencing AF recurrence than in patients with persistent sinus rhythm (LASr 10±6 vs 13±7%, and RASr 14±10 vs 20±9 %, respectively, p<0.001 for both). RASr (AUC=0.77, 95%IC 0.69-0.84, p<0.0001) was more strongly associated with the recurrence of AF after ECV than LASr (AUC=0.69 (95%IC 0.60-0.77), p<0.0001]. Kaplan-Meier curves showed that patients with both LASr≤10% and RASr ≤15% had a significantly increased risk for AF recurrences (log-rank, p<0.001). However, at multivariable Cox regression, RASr [HR 3.26, 95%CI (1.73-6.13), p< 0.001] was the only parameter independently associated with the AF recurrence. RASr was more strongly associated with the occurrence of AF relapse after ECV than LASr, LA and RA volumes. Conclusions: RASr was independently and more strongly associated than LASr with AF recurrence after elective ECV. This study highlights the importance of assessing the functional remodeling of both RA and LA in patients with persistent AF.

Aims: Exercise right heart catheterization (RHC) is considered the gold-standard test to diagnose heart failure with preserved ejection fraction (HFpEF). However, exercise RHC is an insufficiently standardized technique, and current haemodynamic thresholds to define HFpEF are not universally accepted. We sought to describe the exercise haemodynamics profile of HFpEF cohorts reported in literature, as compared with control subjects. Methods and results: We performed a systematic literature review until December 2020. Studies reporting pulmonary artery wedge pressure (PAWP) at rest and peak exercise were extracted. Summary estimates of all haemodynamic variables were evaluated, stratified according to body position (supine/upright exercise). The PAWP/cardiac output (CO) slope during exercise was extrapolated. Twenty-seven studies were identified, providing data for 2180 HFpEF patients and 682 controls. At peak exercise, patients with HFpEF achieved higher PAWP (30 [29–31] vs. 16 [15–17] mmHg, P < 0.001) and mean right atrial pressure (P < 0.001) than controls. These differences persisted after adjustment for age, sex, body mass index, and body position. However, peak PAWP values were highly heterogeneous among the cohorts (I2 = 93%), with a relative overlap with controls. PAWP/CO slope was steeper in HFpEF than in controls (3.75 [3.20–4.28] vs. 0.95 [0.30–1.59] mmHg/L/min, P value < 0.0001), even after adjustment for covariates (P = 0.007). Conclusions: Despite methodological heterogeneity, as well as heterogeneity of pooled haemodynamic estimates, the exercise haemodynamic profile of HFpEF patients is consistent across studies and characterized by a steep PAWP rise during exercise. More standardization of exercise haemodynamics may be advisable for a wider application in clinical practice.

AIMS: In functional tricuspid regurgitation (FTR) patients, tricuspid leaflet tethering and relatively low jet velocity could result in proximal flow geometry distortions that lead to underestimation of TR. Application of correction factors on two-dimensional (2D) proximal isovelocity surface area (PISA) equation may increase its reliability. This study sought to evaluate the impact of the corrected 2D PISA method in quantifying FTR severity. METHODS AND RESULTS: In 102 patients with FTR, we compared both conventional and corrected 2D PISA measurements of effective regurgitant orifice area [EROA vs. corrected (EROAc)] and regurgitant volume (RegVol vs. RegVolc) with those obtained by volumetric method (VM) using three-dimensional echocardiography (3DE), as reference. Both EROAc and RegVolc were larger than EROA (0.29 ± 0.26 vs. 0.22 ± 0.21 cm2; P < 0.001) and RegVol (24.5 ± 20 vs. 18.5 ± 14.25 mL; P < 0.001), respectively. Compared with VM, both EROAc and RegVolc resulted more accurate than EROA [bias = -0.04 cm2, limits of agreement (LOA) ± 0.02 cm2 vs. bias = -0.15 cm2, LOA ± 0.31 cm2] and RegVol (bias = -3.29 mL, LOA ± 2.19 mL vs. bias = -10.9 mL, LOA ± 13.5 mL). Using EROAc and RegVolc, 37% of patients were reclassified in higher grades of FTR severity. Corrected 2D PISA method led to a higher concordance of TR severity grade with the VM method (ĸ = 0.84 vs. ĸ = 0.33 for uncorrected PISA, P < 0.001). CONCLUSION: Compared with VM by 3DE, the conventional PISA underestimated FTR severity in about 50% of patients. Correction for TV leaflets tethering angle and lower velocity of FTR jet improved 2D PISA accuracy and reclassified more than one-third of the patients.

Aims: Exercise right heart catheterization (RHC) is considered the gold-standard test to diagnose heart failure with preserved ejection fraction (HFpEF). However, exercise RHC is an insufficiently standardized technique, and current haemodynamic thresholds to define HFpEF are not universally accepted. We sought to describe the exercise haemodynamics profile of HFpEF cohorts reported in literature, as compared with control subjects. Methods and results: We performed a systematic literature review until December 2020. Studies reporting pulmonary artery wedge pressure (PAWP) at rest and peak exercise were extracted. Summary estimates of all haemodynamic variables were evaluated, stratified according to body position (supine/upright exercise). The PAWP/cardiac output (CO) slope during exercise was extrapolated. Twenty-seven studies were identified, providing data for 2180 HFpEF patients and 682 controls. At peak exercise, patients with HFpEF achieved higher PAWP (30 [29–31] vs. 16 [15–17] mmHg, P < 0.001) and mean right atrial pressure (P < 0.001) than controls. These differences persisted after adjustment for age, sex, body mass index, and body position. However, peak PAWP values were highly heterogeneous among the cohorts (I2 = 93%), with a relative overlap with controls. PAWP/CO slope was steeper in HFpEF than in controls (3.75 [3.20–4.28] vs. 0.95 [0.30–1.59] mmHg/L/min, P value < 0.0001), even after adjustment for covariates (P = 0.007). Conclusions: Despite methodological heterogeneity, as well as heterogeneity of pooled haemodynamic estimates, the exercise haemodynamic profile of HFpEF patients is consistent across studies and characterized by a steep PAWP rise during exercise. More standardization of exercise haemodynamics may be advisable for a wider application in clinical practice., SCOPUS: ar.j, info:eu-repo/semantics/published

Exercise hemodynamics can differentiate heart failure with preserved ejection fraction (HFpEF) from noncardiac dyspnea. However, respiratory pressure swings may impact hemodynamic measurements, potentially leading to misdiagnosis of HFpEF. Moreover, threshold values for abnormal hemodynamic response indicative of HFpEF are not universally accepted. Thus, we sought to evaluate the impact of respiratory pressure swings on hemodynamic data interpretation as well as the concordance among 3 proposed exercise hemodynamic criteria for HFpEF: (1) end-expiratory pulmonary artery wedge pressure (PAWPexp) ≥25 mm Hg; (2) PAWPexp/cardiac output slope >2 mm Hg/L per minute; and (3) respiratory-averaged (avg) mean pulmonary artery pressure >30 mm Hg, total pulmonary resistanceavg >3 WU, PAWPavg ≥20 mm Hg.

Survivors from COVID-19 pneumonia can present with persisting multisystem involvement (lung, pulmonary vessels, heart, muscle, red blood cells) that may negatively affect exercise capacity. We sought to determine the extent and the determinants of exercise limitation in patients with COVID-19 at the time of hospital discharge. Eighteen consecutive patients with COVID-19 and 1:1 age-, sex-, and body mass index-matched controls underwent: spirometry, echocardiography, cardiopulmonary exercise test and exercise echocardiography for the study of pulmonary circulation. Arterial blood was sampled at rest and during exercise in patients with COVID-19. Patients with COVID-19 lie roughly on the same oxygen consumption isophlets than controls both at rest and during submaximal exercise, thanks to supernormal cardiac output (P < 0.05). Oxygen consumption at peak exercise was reduced by 30% in COVID-19 (P < 0.001), due to a peripheral extraction limit. In addition, within COVID-19 patients, hemoglobin content was associated with peak oxygen consumption (R2 = 0.46, P = 0.002). Respiratory reserve was not exhausted (median [IRQ], 0.59 [0.15]) in spite of moderate reduction of forced vital capacity (79 ± 40%). Pulmonary artery pressure increase during exercise was not different between patients and controls. Ventilatory equivalents for carbon dioxide were higher in patients with COVID-19 than in controls (39.5 [8.5] vs. 29.5 [8.8], P < 0.001), and such an increase was mainly explained by increased chemosensitivity. When recovering from COVID-19, patients present with reduced exercise capacity and augmented exercise hyperventilation. Peripheral factors, including anemia and reduced oxygen extraction by peripheral muscles were the major determinants of deranged exercise physiology. Pulmonary vascular function seemed unaffected, despite restrictive lung changes.NEW & NOTEWORTHY At the time of hospital discharge, patients with COVID-19 present with reduced funct

SCOPUS: no.j, info:eu-repo/semantics/published

Background: Exercise hemodynamics can differentiate heart failure with preserved ejection fraction (HFpEF) from noncardiac dyspnea. However, respiratory pressure swings may impact hemodynamic measurements, potentially leading to misdiagnosis of HFpEF. Moreover, threshold values for abnormal hemodynamic response indicative of HFpEF are not universally accepted. Thus, we sought to evaluate the impact of respiratory pressure swings on hemodynamic data interpretation as well as the concordance among 3 proposed exercise hemodynamic criteria for HFpEF: (1) end-expiratory pulmonary artery wedge pressure (PAWPexp) ≥25 mm Hg; (2) PAWPexp/cardiac output slope >2 mm Hg/L per minute; and (3) respiratory-averaged (avg) mean pulmonary artery pressure >30 mm Hg, total pulmonary resistanceavg>3 WU, PAWPavg≥20 mm Hg. Methods: Fifty-seven patients with unexplained dyspnea (70% women, 70±9 years) underwent exercise cardiac catheterization. The difference between end-expiratory and averaged hemodynamic values, as well as the concordance among the 3 hemodynamic definitions of HFpEF, were assessed. Results: End-expiratory hemodynamics measurements were higher than values averaged across the respiratory cycle. During exercise, a larger proportion of patients exceeded the threshold of 25 mm Hg for PAWPexprather than for PAWPavg(70% versus 53%, P<0.01). The concordance of 3/3 HFpEF exercise hemodynamic criteria was recorded in 70% of patients. PAWPexp/cardiac output slope identified HFpEF more frequently than the other 2 criteria (81% versus 64% to 69%), incorporating over 97% of abnormal responses to the latter. Patients with 3/3 positive criteria had worse clinical, gas-exchange, and hemodynamic profiles. Conclusions: Respiratory pressure swings impact on the exercise hemodynamic definitions of HFpEF that provide discordant results in 30% of patients. Equivocal diagnoses of HFpEF might be limited by adopting the most sensitive and inclusive criterion alone (ie, PAWPexp/cardiac output slop, SCOPUS: ar.j, info:eu-repo/semantics/published