The loss of left atrial contractile function predicts a worse outcome in HFrEF patients.

Background: In chronic heart failure, high intracardiac pressures induce a progressive remodeling of small pulmonary arteries up to pulmonary hypertension. At the end of left atrial conduit function, pulmonary and left heart end-systolic pressures equalization might affect left atrial systole. In this single-center prospective study, we aimed to investigate whether peak atrial contraction strain (PACS), measured by speckle tracking echocardiography, was independently associated with prognosis in heart failure with reduced ejection fraction (HFrEF). Materials and methods: Outpatients with HFrEF and sinus rhythm referred to our echo-labs were enrolled. After clinical and echocardiographic evaluation, off-line speckle tracking echocardiography analysis was performed. Primary and secondary endpoint were cardiovascular death and heart failure hospitalization, respectively. Spline knotted survival model identified the optimal prognostic cut-off for PACS. Results: The 152 patients were stratified based on PACS <8% (n = 76) or PACS ≥8% (n = 76). Patients with PACS <8% had lower left ventricle and left atrial reservoir strain and higher New York Heart Association (NYHA) class and left atrial volume index (LAVI). Over a mean follow-up of 3.4 ± 2 years, 117 events (51 cardiovascular death, 66 heart failure hospitalizations) were collected. By univariate and multivariate Cox analysis, PACS emerged as a strong and independent predictor of cardiovascular death and heart failure hospitalization, after adjusting for age, sex, left ventricle strain, and E/e', LAVI (HR 0.6 per 5 unit-decrease in PACS). Kaplan-Meier curves showed a sustained divergence in event-free survival rates for the two groups. Conclusion: The reduction of PACS significantly and independently affects cardiovascular outcome in HFrEF. Therefore, its assessment, although limited to patients with sinus rhythm, could offer additive prognostic information for HFrEF patients.

Excess Mortality Associated with Progression Rate in Asymptomatic Aortic Valve Stenosis.

BACKGROUND: Aortic valve stenosis (AS) is a progressive condition characterized by gradual calcification of the aortic cusps. Progression rate evaluated using echocardiography has been associated with survival. However, data from routine practice covering the whole spectrum of AS severity and the rate of symptom onset are sparse. The aim of this study was to assess outcomes under medical management related to disease progression in asymptomatic patients with a wide range of AS severity. METHODS: Two hundred twenty-nine consecutive asymptomatic patients (mean age, 77 ± 10 years; 55% men) with AS, preserved left ventricular ejection fraction, and two or more echocardiographic examinations performed from 2004 to 2014 were retrospectively included. The median time between the two echocardiographic examinations was 24 months (interquartile range, 15-46 months). Patients were identified as rapid progressors if the annualized difference in peak aortic velocity between two echocardiographic examinations was ≥0.3 m/sec/y; others were labeled as slow progressors. The primary end point was mortality during medical follow-up (censoring on aortic valve interventions). The secondary end point was overall mortality. RESULTS: Rapid progressors accounted for 67 of the 229 patients (29%), and this feature was not associated with baseline characteristics. During a median of 5.8 years (interquartile range, 3.4-8.3 years) of follow-up from the first echocardiographic examination, 102 patients (45%) died, 86 (84%) during medical follow-up. Rapid progression rate predicted excess mortality (vs slow progression rate) after adjustment for age, sex, symptoms, baseline left ventricular ejection fraction, and baseline aortic valve area (hazard ratio, 2.50; 95% CI, 1.48-4.21; P = .0006) and after adjusting for peak aortic velocity and left ventricular ejection fraction obtained at the last echocardiographic examination (hazard ratio, 2.07; 95% CI, 1.25-3.46; P = .005). Among patients with baseline peak aortic velocity < 4 m/sec (nonsevere AS), rapid progression rate was associated with higher 5-year mortality compared with slow progression (57% vs 22% [P < .0001] under medical management and 44% vs 18% [P = .005] overall). Outcomes were comparable between nonsevere AS rapid progressors and baseline severe AS. Progression rate showed incremental prognostic value on receiver operating characteristic curve analysis versus AS severity. Of note, among slow progressors, 11 patients (5%) presented with high rates of symptom development and poor outcomes related to ventricular dysfunction or other advanced AS features. CONCLUSIONS: Progression rate is an individual, almost unpredictable feature among patients with AS. Rapid progression is an incremental marker of excess mortality in asymptomatic patients with AS, independent of clinical and hemodynamic characteristics. Rapid progression rate may identify patients with nonsevere AS at higher risk for events.

Usefulness of the Right Parasternal Echocardiographic View to Improve the Hemodynamic Assessment After Valve Replacement for Aortic Stenosis.

Right-parasternal-view (RPV) often provides the best hemodynamic assessment of the aortic-valve-stenosis by echocardiography. However, no detailed study on patients with aortic prosthesis is available. Thus, RPV usefulness is left as an anecdotical notion in this context. We aimed to define feasibility and clinical-impact of RPV before and soon-after percutaneous implantation (TAVI) or surgical (SAVR) aortic-valve-replacement (AVR) for AS. Patients with severe-AS electively referred for AVR between September-2019 and February-2020 were prospectively evaluated. Echocardiographic examinations inclusive of apical and RPV to measure aortic-peak-velocity , gradients and area (AVA) were performed the day before AVR and at hospital discharge and compared by matched-pair-analysis. Forty-seven patients (mean age 79 ± 8 years, 63% female, ejection-fraction 61 ± 6%) referred for SAVR (24 [51%]) or TAVI (23 [49%]) were enrolled. RPV was feasible in 45 patients (96%) before-AVR but in only 32 after-AVR (68%), particularly after SAVR (50%) than TAVI (87% p = 0.005). RPV remained the best acoustic window after TAVI in 75% of cases. Hemodynamic assessment of TAVI, but not SAVR, invariably benefit from RPV versus apical evaluation (aortic-peak-velocity: 2.57 ± 0.39 vs 2.23 ± 0.47 m/sec, p = 0.002; mean gradient: 15 ± 5 vs 12 ± 5 mm Hg, p = 0.01). Five (11%) patients presented severe patient-prosthesis-mismatch, 4 of which were detectable only by RPV. This pilot-experience demonstrates that RPV feasibility is slightly reduced after AVR. RPV can improve the hemodynamic assessment of the prosthetic valve versus apical view, including the detection of patient-prosthesis-mismatch. Furthermore, when RPV is the best acoustic windows in patients with severe AS, it generally remains so after-TAVI.

Degree of left ventricular dilatation at end-diastole: Correlation and prognostic utility of quantitative volumes by 2D-echocardiography versus linear dimensions in patients with asymptomatic aortic regurgitation.

BACKGROUND: Guideline recommendations for aortic valve replacement (AVR) in asymptomatic patients with chronic aortic regurgitation (AR) have historically focused on linear dimensions without normalization for the body surface area (BSA). Values for grading the severity of end-diastolic volume dilatation by 2D echocardiography remain to be established. METHODS AND RESULTS: We retrospectively analyzed 543 consecutive asymptomatic patients with pure chronic moderate/severe AR (mean age 66 ± 17 years, 37.7% males). Applying the ASE/EACVI guidelines, BSA-indexed LV end-diastolic volume (LVEDVi) and indexed LV end-diastolic diameter (LVEDDi) were assessed. Then, we identified 192 patients with at least mild LV end-diastolic dilatation by volumetric or linear measurements. The outcome endpoint was the combination of cardiac death, hospitalization for acute heart failure or AVR during a median follow-up of 4.5 ± 3.6 years. Multivariable Cox regression analyses including age, LV ejection fraction (EF) and AR severity showed an independent prognostic value of the LVEDDi and LVEDVi (P < .001 and P < .01, respectively). Congruent severe LVEDDi and LVEDVi dilatation was associated with a higher event rate compared to discordant severe LV end-diastolic dilatation or nonsevere LV dilatation (P = .001) even after landmark analysis (P = .02). In patients with EF > 50%, only the LVEDVi showed and independent prognostic value (P < .001). CONCLUSIONS: In a cohort of asymptomatic patients with AR, the presence of severe LV volume and diameter dilatation on the basis of the cutoff values proposed by current recommendations and normalized for BSA may be instrumental in the identification of patients at increased risk of clinical progression regardless of EF.

New-onset extreme right axis deviation in acute myocardial infarction: clinical characteristics and outcomes.

BACKGROUND: QRS axis deviation can occur during myocardial infarction (MI); to date, little is known about the significance of extreme right axis deviation (ERAD) in the frontal plane, i.e. a shift in QRS axis between +180° and +270°, during MI. We sought to investigate the clinical characteristics and outcomes of patients with new-onset ERAD in the absence of complete bundle branch blocks (BBB) in the setting of acute coronary syndromes (ACS). METHODS: A single-center retrospective observational study was conducted, including patients with new-onset ERAD in the absence of complete BBB admitted for ACS to our Cardiac Intensive Care Unit. Clinical, electrocardiographic, echocardiographic, angiographic features at baseline and cardiovascular events during hospitalization and at mid-term follow-up were collected. RESULTS: The study population consisted of 30 consecutive patients (23 men) from January 2014 to September 2018. The most frequent clinical presentation was ST-segment elevation MI (n = 22, 73.4%) and the most frequent electrocardiographic MI location was anterolateral (n = 11, 36.7%). Left anterior descending (LAD) was the most frequent infarct-related artery (n = 21, 70%); 15 patients (50%) had multivessel coronary artery disease. Cardiac arrest due to ventricular fibrillation (VF) at presentation (n = 5, 16.6%), cardiogenic shock during the hospital stay (n = 10, 33.3%), cardiac arrest due to VF after revascularization (n = 6, 20%) and cardiac death (n = 7, 23.3%) were common. CONCLUSION: New-onset ERAD during MI may be related to extensive myocardial ischemia and/or necrosis causing an "electrical escaping" with an extreme dislocation of the QRS axis. In our limited series we found several acute arrhythmic and hemodynamic complications and high mortality.

New insights to the potential mechanisms driving coronary flow reserve impairment in Cushing's syndrome: A pilot noninvasive study by transthoracic Doppler echocardiography.

BACKGROUND: The contribution of functional and/or structural remodeling to reduced coronary flow velocity reserve (CFVR), reflecting impaired coronary microcirculation in Cushing's syndrome (CS), has not been clearly elucidated. We aimed to identify the potential mechanisms of coronary microvascular impairment in CS. METHODS: We studied 15 CS patients (11 female, age 50 ±â€¯9 years) without clinical evidence of cardiovascular disease. Coronary flow velocity in the left anterior descending coronary artery was measured by transthoracic Doppler echocardiography, at rest, and during adenosine infusion. Average peak flow velocities, CFVR, and microvascular resistance in baseline (BMR) and hyperemic conditions (HMR) were assessed. CFVR ≤2.5 was considered a marker of microvascular disease (CMD). Diastolic function (E/e'), global longitudinal strain (GLS) and fractional pulse pressure (fPP), an index of arterial stiffness, were also assessed. RESULTS: CMD was present in 5 patients (33.3%). CMD was primarily driven by increased baseline peak flow velocity (29 ±â€¯12 versus 19.6 ±â€¯4.2 cm/s, p = .03) in the presence of decreased BMR (3.62 ±â€¯0.6 versus 5.46 ±â€¯1.4 mm Hg·s/cm, p = .03). Moreover, urinary cortisol and E/e' were higher (p = .001 and p = .001, respectively) and GLS was lower (p = .009) in patients with CMD. fPP was higher in patients with CMD (p = .01). Urinary cortisol correlated to CFVR (p = .008), E/e' (p < .0001) and GLS (p < .0001). fPP directly correlated to average peak flow velocities at rest (p = .01) and inversely to BMR (p = .03). CONCLUSIONS: Functional microvascular regulatory impairment seems to be the potential mechanism of CMD in CS. CMD seems to be related to decreased myocardial contractility and diastolic dysfunction associated with cortisol excess.