Preclinical systolic dysfunction relating to ankle-brachial index among high-risk PAD population with preserved left ventricular ejection fraction.

Peripheral artery disease (PAD) shares common clinical risk factors, for example, endothelial dysfunction, with preserved ejection fraction (LVEF) heart failure (HFpEF). Whether PAD is associated with preclinical systolic dysfunction and higher HF risk among individuals presenting preserved LVEF remains uncertain. We retrospectively included outpatients with at least one known or established cardiovascular (CV) risk factor with LVEF ≥ 50%. Patients were categorized into high risk and low risk of developing PAD (PAD vs Non-PAD) by ankle-brachial index (ABI) (≤ 0.90 or > 1.4) and further stratified based on their history of HFpEF (HFpEF vs. Non-HFpEF), resulting in the formation of four distinct strata. Preclinical systolic dysfunction was defined using dedicated speckle-tracking algorithm. A total of 2130 consecutive patients were enrolled in the study, with a median follow-up of 4.4 years. The analysis revealed a higher prevalence of high risk of developing PAD in patients with HFpEF compared to those without HFpEF (25.1% vs. 9.4%). Both high risk of developing PAD and HFpEF were independently associated with preclinical systolic dysfunction (global longitudinal strain, GLS ≥ - 18%) (odds ratio, OR: 1.38; 95% confidence interval, CI: 1.03-1.86). In comparison to patients at low risk of developing PAD without HFpEF (Non-PAD/Non-HFpEF group), those categorized as having a high risk of developing PAD with HFpEF (PAD/HFpEF group) exhibited the most impaired GLS and a heightened susceptibility to heart failure hospitalization (hazard ratio, HR: 6.51; 95% CI: 4.43-9.55), a twofold increased risk of all-cause mortality (HR: 2.01; 95% CI: 1.17-3.38), cardiovascular mortality (HR: 2.44; 95% CI: 1.08-5.51), and non-cardiovascular mortality (HR: 1.78; 95% CI: 0.82-3.84). A high risk of developing PAD was strongly linked to impaired preclinical systolic function and an increased likelihood for subsequent hospitalization for HF, all-cause mortality, CV mortality and non-CV mortality. There is a clear need for preventive strategies aimed at reducing hospitalizations for HF and mortality in this high-risk population.

Diagnostic accuracy of left atrial remodelling and natriuretic peptide levels for preclinical heart failure.

AIMS: Left atrial (LA) remodelling is an important predictor of cardiovascular events of heart failure (HF) and atrial fibrillation. Data regarding diagnostic value of LA remodelling on diastolic dysfunction (DD) and preclinical HF remain largely unexplored. METHODS AND RESULTS: We assessed LA dimension (LAD) in 8368 consecutive asymptomatic Asians (mean age: 49.7, 38.9% women) and related such measure to updated American Society of Echocardiography (ASE) DD criteria and newly revised N-terminal pro-brain natriuretic peptide (NT-proBNP) cut-off (≥125 pg/mL) and HF with preserved ejection fraction criteria incorporating NT-proBNP and echocardiography parameters by the European Society of Cardiology (ESC). LAD and indexed LAD (LADi) were both inversely correlated with myocardial relaxation e' and positively associated with indexed LA volume, left ventricular E/e', and tricuspid regurgitation velocity (all P < 0.001) and showed significantly graded increase across ASE-defined 'normal', 'inconclusive', and 'DD' categories (30.9, 34.4, and 36.5 mm; 16.7, 19.1, and 20.6 mm/m2 , for LAD/LADi, both P for trend: <0.001, respectively). Substantial differences of LAD/LADi (31.3 vs. 33.6 mm/16.7 vs. 19.2 mm/m2 , both P < 0.001) between ESC low and high HF probability using NT-proBNP cut-off were also observed. Multivariate linear and logistic models demonstrated that LAD set at 34 mm was independently associated with ASE-defined diastolic indices, DD existence, and elevated NT-proBNP (all P < 0.05). The use of LAD further yielded high diagnostic accuracy in DD (area under receiving operative characteristic curve: 0.77, 95% confidence interval [0.73, 0.80]; negative predictive value: 97.9%) and in ESC-recommended HF with preserved ejection fraction criteria (area under receiving operative characteristic curve: 0.70, 95% confidence interval [0.65, 0.75]; negative predictive value: 98.7%) with high predictive value in LA remodelling (>34 mL/m2 ; positive predictive value: 96%) and well-discriminated ESC-recommended NT-proBNP (≥125 pg/mL, LAD: 37 mm) for HF. CONCLUSIONS: Single utilization of atrial remodelling is highly useful for ruling out presence of DD and provides practical threshold for identifying preclinical HF based on most updated guidelines.

The relationship of renal function to segmental vascular stiffness, ankle-brachial index, and peripheral artery disease.

The authors consecutively assessed various arterial pulse-wave velocity (PWV) indices and ankle-brachial index (ABI) by an automatic device (VP2000, OMRON Health Care Co. Ltd., Kyota, Japan) in outpatients with ≥ 1 cardiovascular risk. PAD was defined as ABI ≤ 0.9. Among 2309 outpatients (mean age 62.4 years), worse renal function was associated with higher brachial-ankle PWV, heart-carotid PWV, heart-femoral PWV (hf-PWV), and lower ABI (all P < .001). Multivariate regression models showed independent associations between lower eGFR, lower ABI (Coef: 0.42 & 0.41 for right and left), higher hf-PWV (Coef: -11.4 [95% CI: -15.4, -7.3]) and greater PAD risk (adjusted OR: 0.83 [95% CI: 0.76, 0.91], all P < .05). eGFR set at 77 mL/min/1.73m2 was observed to be useful clinical cutoff (c-statistics: 0.67) for identifying PAD (P for ΔAUROC: .009; likelihood X2 : 93.82 to 137.43, P < .001) when superimposed on clinical risks. This study suggested early renal insufficiency is tightly linked to region-specific vascular stiffness and PAD.

Relation of carotid artery diameter with cardiac geometry and mechanics in heart failure with preserved ejection fraction.

BACKGROUND: Central artery dilation and remodeling are associated with higher heart failure and cardiovascular risks. However, data regarding carotid artery diameter from hypertension to heart failure have remained elusive. We sought to investigate this issue by examining the association between carotid artery diameter and surrogates of ventricular dysfunction. METHODS AND RESULTS: Two hundred thirteen consecutive patients including 49 with heart failure and preserved ejection fraction (HFpEF), 116 with hypertension, and an additional 48 healthy participants underwent comprehensive echocardiography and tissue Doppler imaging. Ultrasonography of the common carotid arteries was performed for measurement of intima-media thickness and diameter (CCAD). Cardiac mechanics, including LV twist, were assessed by novel speckle-tracking software. A substantial graded enlargement of CCAD was observed across all 3 groups (6.8 ± 0.6, 7.7 ± 0.73, and 8.7 ± 0.95 mm for normal, hypertension, and HFpEF groups, respectively; ANOVA P<0.001) and correlated with serum brain natriuretic peptide level (R(2)=0.31, P<0.001). Multivariable models showed that CCAD was associated with increased LV mass, LV mass-to-volume ratio (ß-coefficient=10.9 and 0.11, both P<0.001), reduced LV longitudinal and radial strain (ß-coeffficient=0.81 and -3.1, both P<0.05), and twist (ß-coefficient=-0.84, P<0.05). CCAD set at 8.07 mm as a cut-off had a 77.6% sensitivity, 82.3% specificity, and area under the receiver operating characteristic curves (AUROC) of 0.86 (95% CI 0.80 to 0.92) in discriminating HFpEF. In addition, CCAD superimposed on myocardial deformation significantly expanded AUROC (for longitudinal strain, from 0.84 to 0.90, P of ΔAUROC=0.02) in heart failure discrimination models. CONCLUSIONS: Increased carotid artery diameter is associated with worse LV geometry, higher brain natriuretic peptide level, and reduced contractile mechanics in individuals with HFpEF.

Prevalence of symptomatic large pleural effusions first diagnosed more than 30 days after coronary artery bypass graft surgery.

BACKGROUND AND OBJECTIVE: Symptomatic large pleural effusions (>25% of hemithorax) are sometimes diagnosed after coronary artery bypass graft surgery (CABG). Their incidence and outcome have not been fully described. This study aims to discuss the prevalence and the clinical course in patients diagnosed with symptomatic newly developed large pleural effusions at least 30 days after CABG. METHODS: A retrospective study of 410 patients who underwent CABG over a three and a half year period was undertaken. The type of surgery, timing of occurrence of effusion after CABG, amount and characteristics of the pleural effusion, left ventricular dimension and ejection fraction were obtained from medical records and cardiac surgery databases. RESULTS: The records of 356 patients 1 month post CABG were available for evaluation. The initial diagnosis of a newly developed symptomatic large pleural effusions was made in 11 patients (3.1%) at least 30 days after CABG. Eight had a pleural effusion predominantly on the left side and three on the right. Patients were further divided into two groups: those who had effusions diagnosed between 30 and 90 days post CABG (group 1) and those diagnosed more than 90 days post-CABG (group 2). The pleural fluid LDH levels were higher in patients in group 1 (1262.0 +/- 921.3 U/L vs. 117.5 +/- 35.1 U/L, P = 0.02). Patients in group 2 had evidence of cardiac impairment compared with those in group 1, as evidenced by a lower ejection fraction (68.8 +/- 6.0% vs. 52.0 +/- 10.6% in groups 1 and 2, respectively, P = 0.01) and higher left ventricular end-diastolic dimension (45.2 +/- 6.0 mm vs. 55.3 +/- 8.4 mm in groups 1 and 2, respectively, P = 0.05). CONCLUSIONS: The incidence of symptomatic newly developed large pleural effusions first diagnosed at more than 30 days post CABG was 3.1%. Those who were diagnosed between 30 and 90 days post CABG tended to have exudative effusions, whereas those diagnosed more than 90 days post CABG often had left ventricular impairment and transudative effusions. Most of these effusions settled with conservative management and did not recur.