Left atrial conduit flow rate at baseline and during exercise: an index of impaired relaxation in HFpEF patients.

AIMS: In healthy subjects, adrenergic stimulation augments left ventricular (LV) long-axis shortening and lengthening, and increases left atrial (LA) to LV intracavitary pressure gradients in early diastole. Lower increments are observed in patients with heart failure with preserved ejection fraction (HFpEF). We hypothesized that exercise in HFpEF would further impair passive LV filling in early-mid diastole, during conduit flow from pulmonary veins. METHODS AND RESULTS: Twenty HFpEF patients (67.8 ± 9.8 years; 11 women), diagnosed using 2007 ESC recommendations, underwent ramped semi-supine bicycle exercise to submaximal target heart rate (∼100 bpm) or symptoms. Seventeen asymptomatic subjects (64.3 ± 8.9 years; 7 women) were controls. Simultaneous LA and LV volumes were measured from pyramidal 3D-echocardiographic full-volume datasets acquired from an apical window at baseline and during stress, together with brachial arterial pressure. LA conduit flow was computed from the increase in LV volume from its minimum at end-systole to the last frame before atrial contraction (onset of the P wave), minus the reduction in LA volume during the same time interval; the difference was integrated and expressed as average flow rate, according to a published formula. The slope of single-beat preload recruitable stroke work (PRSW) quantified LV inotropic state. 3D LV torsion (rotation of the apex minus rotation of the base divided by LV length) was also measurable, both at rest and during stress, in 10 HFpEF patients and 4 controls. There were divergent responses in conduit flow rate, which increased by 40% during exercise in controls (+17.8 ± 37.3 mL/s) but decreased by 18% in patients with HFpEF (-9.6 ± 42.3 mL/s) (P = 0.046), along with congruent changes (+1.77 ± 1.13°/cm vs. -1.94 ± 2.73°/cm) in apical torsion (P = 0.032). Increments of conduit flow rate and apical torsion during stress correlated with changes in PRSW slope (P = 0.003 and P = 0.006, respectively). CONCLUSIONS: In HFpEF, conduit flow rate decreases when diastolic dysfunction develops during exercise, in parallel with changes in LV inotropic state and torsion, contributing to impaired stroke volume reserve. Conduit flow is measurable using 3D-echocardiographic full-volume atrio-ventricular datasets, and as a marker of LV relaxation can contribute to the diagnosis of HFpEF.

Left atrial conduit function modulates right ventricular afterload, exercise capacity and survival in heart failure patients.

AIMS: To assess if left atrial phasic function characteristics modulate functional capacity/survival by impacting on the pulsatile component of right ventricular (RV) afterload, as represented by pulmonary arterial compliance (PAC). MATERIALS AND METHODS: Sixty heart failure patients (67 ±â€Š11 years, ejection fraction 39 ±â€Š11%, range 20--62%) underwent 6 min walk test (6MWT) and 3D transthoracic echocardiography. Left atrial conduit was computed off-line, gathering simultaneous real-time 3D multibeats (six cycles) left atrial and left ventricular (LV) volume curves, with conduit (time) = [LV (time) - LV minimum volume] - [left atrial maximum volume - left atrial (time)], expressed as % LV stroke volume. Atrial stiffness (Kla) was computed using noninvasively assessed wedge pressure divided by left atrial reservoir (maximum - minimum) volume. PAC was obtained as ratio between RV stroke volume, obtained as pulsed Doppler RV outflow tract envelope∗cross-sectional area, and pulmonary pulse pressure, obtained by transforming tricuspid regurgitant velocity in millimetres of mercury and considering diastolic pulmonary as a fixed fraction of systolic pressure. RESULTS: Conduit averaged 34 ±â€Š12%, PAC 3.1 ±â€Š1.1 ml/mmHg, 6MWT 404 ±â€Š154 m. Conduit was independent of LV volumes and ejection fraction, showing a direct dependence on noninvasive Kla (r = 0.56; P < 0.001). Dividing patients into tertiles according to 6MWT and to PAC, the largest conduit fraction was associated with the lowest functional capacity (P < 0.001) and most deranged PAC (P < 0.001), respectively, suggesting outmost RV haemodynamic burden. Tertiles of conduit predicted survival (P = 0.01). CONCLUSION: Conduit depends on noninvasively assessed Kla and appears to be increased in heart failure patients with lowest capacity and worst survival, likely as RV pulsatile afterload, as reflected by PAC, is highest in these individuals.

Atrial conduit function quantitation precardioversion predicts early arrhythmia recurrence in persistent atrial fibrillation patients.

AIMS: Atrial fibrillation incidence is increasing due to ageing population and electrical cardioversion (ECV) is overused because of atrial fibrillation recurrences. Study's aim was to evaluate value of novel three-dimensional echocardiographic-derived left atrial conduit (LAC) function quantification in predicting early atrial fibrillation recurrence after ECV. METHODS: We included 106 patients [74 (64-78) years] who underwent ECV for persistent nonvalvular atrial fibrillation. For all clinical data and simultaneous left atrial and left ventricular (LV) three-dimensional full-volume data sets were available before ECV. We computed LAC as: [(LV maximum - LV minimum) - (left atrial maximum - left atrial minimum) volume], expressed as % LV stroke volume. Atrial fibrillation recurrence was checked with Holter monitoring. RESULTS: One month after ECV 66 patients were in sinus rhythm and 40 experienced atrial fibrillation recurrence. Pre-ECV patients with atrial fibrillation recurrence showed higher LAC contribution to LV filling (P < 0.0001) and noninvasively estimated left atrial stiffness (P < 0.0001) compared with sinus rhythm patients. There were no other differences, neither in clinical characteristics nor in LV properties. At multivariate LAC (P < 0.001), left atrial stiffness (P = 0.002) and volume (P = 0.043) predicted early atrial fibrillation relapse, even when compared with other confounding factors. Receiver-operating characteristics area (ROC) analysis confirmed LAC as best atrial fibrillation recurrence predictor (0.84, P < 0.0001), cut-off value more than 54% exhibiting reasonable sensibility-specificity (76-75%). CONCLUSION: Atrial fibrillation makes LV filling dependent on reciprocation between left atrial reservoir/conduit phases. Our data suggest that LAC larger contribution to filling in persistent atrial fibrillation patients reflects left atrial and LV diastolic dysfunction, which skews atrio-ventricular interaction that leads to atrial fibrillation perpetuation, making LAC a powerful atrial fibrillation recurrence predictor after ECV.

Incremental value of right atrial strain for early diagnosis of hemodynamic deterioration in pulmonary hypertension: a new noninvasive tool for a more comprehensive diagnostic paradigma.

AIMS: Increased right atrial size is related to adverse prognosis in pulmonary hypertension. The potential incremental value of right atrial function assessment is still unclear. We tested the relationship between right atrial two-dimensional speckle-tracking echocardiography impairment and hemodynamic, functional and clinical deterioration in patients with pulmonary hypertension. METHODS: We prospectively evaluated 36 patients (27 female, 9 male; mean age 68 ±â€Š13 years) with suspected pulmonary hypertension undergoing right heart catheterization and 16 matched controls. All patients underwent baseline evaluation by New York Heart Association functional class, 6-min walking test, brain natriuretic peptide (BNP), and standard two-dimensional echocardiography in less than 48 h of right heart catheterization. Right atrial two-dimensional speckle-tracking echocardiography was assessed by averaging all segments in standard four-chamber apical view. RESULTS: Right atrial global integral strain was significantly lower in patients compared with controls (11.40 ±â€Š5.22% vs. 25.72 ±â€Š5.95 P < 0.001). Moreover, right atrial global strain, but not right atrial area or volume, was correlated with invasively measured cardiac index (CI) (r = 0.72; P < 0.0001) and pulmonary vascular resistances in all patients, even though stronger in subjects with precapillary pulmonary hypertension (r = -0.42, P = 0.018; r = -0.54, P = 0.007 respectively; P = 0.007). It was also correlated with New York Heart Association (P = 0.027), BNP (P = 0.002), and 6-min walking test (P = 0.006). After multivariate analysis including right atrial volume, tricuspid annular plane systolic excursion, left atrial strain, and BNP, right atrial global strain showed the strongest correlation with CI. Area under the curve optimal cutoff for predicting CI at least 2.4 l/min/m was 17% (area under the curve: 0.83, sensitivity: 90%, specificity: 54%). CONCLUSION: Right atrial global strain can identify right atrial functional impairment before structural changes and may be implemented in a comprehensive, noninvasive right heart assessment for diagnosis and follow-up of pulmonary hypertension patients.