RESUMEN
BACKGROUND: Hypertensive heart disease (HHD) is a leading contributor to heart failure with preserved ejection fraction (HFpEF). However, the mechanisms behind the transition to the symptomatic phase remain unclear. OBJECTIVES: We sought to find the association of the exercise response of left atrial (LA) mechanical function with functional capacity, symptoms, and outcome across the heart failure (HF) spectrum in hypertension. METHODS: Echocardiography (including LA reservoir peak atrial longitudinal strain [PALS] and peak atrial contractile strain [PACS] and LA stiffness index) was performed at rest and immediately postexercise in 139 patients with HHD-35 with stage A, 48 with stage B, and 56 with stage C HFpEF. Patients were followed for HF and atrial fibrillation. RESULTS: Exercise capacity was progressively worse from stage A through stage B to stage C and was accompanied by a gradual impairment of changes in PALS and PACS from rest to exercise, whereas LA stiffness reserve remained unchanged until stage C. Peak atrial longitudinal strain and PACS reserves were independently associated with exercise capacity (P = .017 and .008, respectively). Left atrial stiffness reserve and E/e' were the strongest associations of symptomatic HF. Over a median of 25 months, 35 patients developed HF and/or atrial fibrillation. Peak atrial longitudinal strain and PACS reserves were associated with the study end points after adjusting for age, diabetes, N-terminal pro-B type natriuretic peptide, LA volume index, resting E/e', and resting PALS/PACS. CONCLUSIONS: Impaired exercise reserve of LA strain and stiffness are associated with reduced functional capacity in hypertension, and LA strain reserve is independently associated with outcome. These parameters appear to be determinants of progression to overt HF in HHD; however, their contribution may differ depending on HF stage.
RESUMEN
BACKGROUND: Skeletal muscle (SM)-associated mechanisms of exercise intolerance in HFpEF are insufficiently defined, and inadequate augmentation of SM blood flow during physical effort may be one of the contributors. Therefore, we sought to investigate the association of SM perfusion response to exertion with exercise capacity in this clinical condition. METHODS: Echocardiography and SM microvascular perfusion by contrast-enhanced ultrasound were performed at rest and immediately post-exercise test in 77 HFpEF patients in NYHA class II and III, and in 25 subjects with normal exercise tolerance (stage B). Exercise reserve of cardiac function and SM perfusion was calculated by subtracting resting value from exercise value. RESULTS: In addition to decreased cardiac functional reserve, HFpEF patients demonstrated significantly reduced SM perfusion reserve as compared to HF stage B, with the degree of impairment being greater in the subgroup with more profound left ventricular (LV) diastolic abnormalities (E/e' > 15 and TRV > 2.8 m/s). SM perfusion reserve was significantly associated with exercise capacity (beta = 0.33; SE 0.11; p = 0.003), cardiac output reserve (beta = 0.24; SE 0.12; p = 0.039), resting E/e' (beta = -0.33; SE 0.11; p = 0.006), and patient frailty expressed by the PRISMA 7 score (beta = -0.30; SE 0.11; p = 0.008). In multivariable analysis including clinical, demographic and cardiac functional variables, SM perfusion reserve was in addition to patient frailty, sex and LV longitudinal strain reserve among the independent correlates of exercise capacity. CONCLUSIONS: SM perfusion reserve is impaired in HFpEF, and is associated with reduced exercise capacity independent of clinical, demographic and "central" cardiac factors. This supports the need to consider the SM domain in patient management strategies in HFpEF.