A steeper SBP/VO2 slope during exercise was associated with an increased risk of all-cause death and heart failure-related hospitalizations (HR 1.25; 95% CI 1.07-1.46).
Cohort (n=970)
Yes
Does a hypertensive response to exercise indexed to oxygen consumption predict all-cause death and heart failure hospitalizations in patients with established arterial hypertension and preserved LVEF?
In patients with established arterial hypertension, a steeper SBP/VO2 slope during exercise identifies a high-risk phenotype and independently predicts all-cause death and heart failure hospitalizations.
Hazard Ratio: 1.25 (95% CI 1.07–1.46)
Objective: In patients with established arterial hypertension (AH) and preserved left ventricular ejection fraction, the clinical significance of a hypertensive response to exercise (HRE) remains debated. This study aimed to determine whether HRE, defined by the slope of systolic blood pressure (SBP) increase indexed to oxygen consumption (VO2) to account for metabolic demand, is associated with distinct pathophysiological abnormalities and an increased risk of adverse outcomes.Design and method: We conducted a prospective cohort study, enrolling consecutive patients with established AH and preserved left ventricular ejection fraction, with or without heart failure (HF) from three European centers. All participants underwent a clinical and laboratory workup, transthoracic echocardiography at rest, and a combiner cardiopulmonary exercise test-exercise stress echocardiography (CPET-ESE). Patients were divided according to tertiles of SBP/VO2 slope, and HRE was defined as the highest tertile. The patients were prospectively followed for the composite endpoint of all-cause death and HF-related hospitalizations. Results: The final population included n=970 patients, with 425 females. Median age was 71 (62-77) years, median BMI was 27.7 (24.7-30.4) kg/m2. 308 patients (32%) had established HFpEF. Patients with HRE demonstrated a higher prevalence of significant albuminuria (albumin-to-creatinine ratio >=30 mg/g). The ultrasound evaluation revealed greater left ventricular mass, impaired myocardial systolic function (reduced global longitudinal strain), left atrial dilation, increased lung ultrasound B-lines at rest and peak effort, reduced total arterial compliance and impaired right ventricular-pulmonary arterial coupling during exercise. CPET confirmed a significantly lower peak VO2 in the HRE group, attributable to impaired peripheral oxygen delivery (due to lower haemoglobin) and utilisation (i.e., lower arteriovenous oxygen difference). Over a median follow-up of 24 months, a steeper SBP/VO2 slope was associated with an increased risk of the primary endpoint (Hazard Ratio 1.25, 95% Confidence Interval 1.07–1.46), independent of absolute SBP at rest and peak exercise. Conclusions: In patients with established AH, a steeper SBP/VO2 slope identifies a high-risk phenotype characterized by diffuse vascular stiffening, renal microvascular damage, subclinical cardiac dysfunction, and reduced functional reserve. This metric could be implemented in selected cases to refine risk stratification and tailor therapeutic strategies.
Biase et al. (Fri,) conducted a cohort in Arterial hypertension with preserved left ventricular ejection fraction (n=970). Steeper SBP/VO2 slope (hypertensive response to exercise) vs. Lower SBP/VO2 slope tertiles was evaluated on Composite of all-cause death and HF-related hospitalizations (HR 1.25, 95% CI 1.07-1.46). A steeper SBP/VO2 slope during exercise was associated with an increased risk of all-cause death and heart failure-related hospitalizations (HR 1.25; 95% CI 1.07-1.46).