Refractory Hypertension is not Attributable to Intravascular Fluid Retention as Determined by Intracardiac Volumes

摘要

Refractory hypertension is an extreme phenotype of antihypertensive treatment failure defined as lack of blood pressure (BP) control with ≥5 medications, including a long-acting thiazide and a mineralocorticoid receptor antagonist. Refractory hypertension is a subgroup of resistant hypertension, which is defined as BP > 135/85mmHg with three or more antihypertensive medications, including a diuretic. Resistant hypertension is generally attributed to persistent intravascular fluid retention. It is unknown whether alternative mechanisms are operative in refractory hypertension. Our objective was to determine whether refractory hypertension is characterized by persistent fluid retention, indexed by greater intracardiac volumes determined by cardiac magnetic resonance when compared to controlled resistant hypertension patients. Consecutive patients evaluated in our institution with refractory hypertension and controlled-resistant hypertension were prospectively enrolled. Exclusion criteria included advanced chronic kidney disease and masked or white coat hypertension. All enrolled patients underwent biochemical testing and cardiac magnetic resonance. The refractory hypertension group (n=24) was younger (mean age 51.7±8.9 vs. 60.6±11.5yrs, p=0.003) and had a greater proportion of females (75.0% vs. 43%, p=0.02) compared with the controlled-resistant hypertension group (n=30). Refractory hypertension patients had a greater left ventricular mass index (88.3±35.0 vs. 54.6 ±12.5g/m2, p<0.001), posterior (10.1±3.1 vs. 7.7±1.5mm, p=0.001) and septal wall thickness (14.5±3.8 vs. 10.0±2.2mm, p<0.001). There was no difference in B-type natriuretic peptide levels and left atrial or ventricular volumes. Diastolic dysfunction was noted in refractory hypertension. Our findings demonstrate greater left ventricular hypertrophy without chamber enlargement in refractory hypertension, suggesting that antihypertensive treatment failure is not attributable to intravascular volume retention.