Ankle–Brachial Index and Ventricular–Arterial Coupling for the Assessment of Acute Left Ventricular Systolic Dysfunction

Background: The ankle–brachial index (ABI) has been extensively applied for the diagnosis and risk stratification of vascular disease. However, it can also provide information about the interaction between ventricular function and peripheral vascular compliance, defined as ventricular–arterial coupling (VAC), which has been extensively shown to predict the outcome of patients with heart failure (HF). So far, no study has addressed the use of ABI for the assessment and prognostic stratification of patients with acute decompensated left ventricular systolic dysfunction, which was the aim of our study. Methods: Patients hospitalized with acute HF and reduced left ventricular ejection fraction (EF < 50%) were prospectively included. Echocardiogram and ABI were performed after the resolution of the acute phase, before discharge, and on optimized medical therapy. Abnormal ABI was defined as values ≤0.90 or >1.4. Arterial and ventricular elastance and Ees/Ea (iVAC) were estimated from echocardiographic parameters. The normal range for iVAC was considered [0.5–1.0]. Results: We included 80 patients, of whom 81.3% were males, with a mean age of 67.98 ± 11.3 years. Among them, 57.5% were hypertensive, 32.5% were active smokers, 41.3% were hypercholesterolemic, 20% were diabetic and 11.3% had previous myocardial infarction. The mean ejection fraction was 36.8 ± 9.22%, stroke volume was 46.3 ± 14.3 mL, arterial elastance was (Ea) 2.48 ± 0.87 mmHg/mL and VA coupling was 0.64 ± 0.25. HF etiology was ischemic in 58 (72.5%) of the patients, of whom 31 displayed multivessel disease. Impaired ABI values were observed in 21 (26.3%) of the patients (≤0.90 in 11 patients and >1.4 in 10 patients). A significant non-linear (logistic) relationship was observed between ABI values and VA coupling (β = 1.07, p = 0.007), which became linear for iVAC ≥ 0.5 (β = 0.92, p < 0.001). A similar trend was observed in patients with ischemic (β = 1.06, p < 0.001) and non-ischemic etiology (β = 1.02, p = 0.12). Echocardiographic follow-up was available in 63 patients, as three died before re-assessment. At a median follow-up of 281.5 days, EF recovery was observed in 44 patients, and EF improvement in 76.2%. VA coupling was the only independent predictor of EF recovery (OR [95%CI] = 0.15 [0.03–0.69], p = 0.015 for iVAC < 0.5). Conclusions: Ventricular–arterial coupling can represent a useful tool for the prognostic stratification of patients hospitalized for acute decompensated left ventricular systolic dysfunction, with lower values being associated with worse outcomes. The ankle–brachial index is a widely available parameter displaying a good association with VAC; therefore, it could offer a faster bedside estimation of ventricular–arterial interaction. Future larger-scale studies are certainly needed to confirm our results and implement the use of the ABI in acute HF.