title: Right ventricular energetics in patients with hypertrophic cardiomyopathy and the effect of alcohol septal ablation.
abstract: BACKGROUND
  Diastolic dysfunction in hypertrophic cardiomyopathy (HCM) is accompanied by augmented left ventricular (LV) end-diastolic pressure, above all in the presence of LV outflow tract (LVOT) obstruction. Increased back-pressure may augment right ventricular (RV) afterload and induce an oxidative metabolic imbalance between the 2 ventricles. The aim was to study right-to-left ventricular oxidative metabolism in HCM and the effects of alcohol septal ablation (ASA).
  
  
  RESULTS
  Twenty-one HCM patients were enrolled. Eleven healthy subjects served as a control group. Subjects underwent 2-dimensional echocardiography to assess LVOT gradient, left atrial size, and diastolic function. [(11)C]Acetate positron-emission tomography (PET) was performed to determine RVk(2) and LVk(2), as a noninvasive index of oxidative metabolism. Seven HCM patients with LVOT obstruction, scheduled to undergo ASA, were also studied 6 months after the procedure. RVk(2) was higher in HCM patients than i control subjects (0.081 ± 0.021 min(-1) vs. 0.061 ± 0.017 min(-1); P = .05), whereas LVk(2) was similar between groups. Consequently, RVk(2)/LVk(2) was increased in the patients (0.85 ± 0.19 vs 0.59 ± 0.13; P = .004). In patients with obstructive HCM, ASA reduced RVk(2) (0.085 ± 0.021 min(-1) to 0.072 ± 0.022 min(-1); P = .001). Inasmuch as LVk(2) remained unaffected by the procedure, RVk(2)/LVk(2) was decreased after ASA (0.66 ± 0.18; P = .03). The absolute change in LVOT gradient was related to the absolute change in RVk(2) (r = 0.77; P = .044).
  
  
  CONCLUSIONS
  In HCM patients, RV oxygen consumption is increased in relation to the LV. ASA reduces RV oxygen consumption in HCM patients with LVOT obstruction, suggesting that increased LV loading conditions and diastolic dysfunction play a predominant role in augmenting RV workload in these patients.
authors.affiliation: Department of Cardiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands. s.timmer@vumc.nl
authors.forename: S A J
authors.initials: SA
authors.lastname: Timmer
authors.forename: P
authors.initials: P
authors.lastname: Knaapen
authors.forename: Tjeerd
authors.initials: T
authors.lastname: Germans
authors.forename: Mark
authors.initials: M
authors.lastname: Lubberink
authors.forename: Pieter A
authors.initials: PA
authors.lastname: Dijkmans
authors.forename: Anton
authors.initials: A
authors.lastname: Vonk-Noordegraaf
authors.forename: Jurrien M
authors.initials: JM
authors.lastname: Ten Berg
authors.forename: Folkert J
authors.initials: FJ
authors.lastname: Ten Cate
authors.forename: Adriaan A
authors.initials: AA
authors.lastname: Lammertsma
authors.forename: Albert C
authors.initials: AC
authors.lastname: van Rossum
mesh_terms: D055011:Ablation Techniques; D002312:Cardiomyopathy, Hypertrophic / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016022:Case-Control Studies; D003971:Diastole; D004452:Echocardiography; D000431:Ethanol; D005260:Female; D006346:Heart Septum / Q000601:surgery*; D006439:Hemodynamics; D006801:Humans; D008875:Middle Aged; D049268:Positron-Emission Tomography; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000503:physiopathology*
chemical_list: D000431:Ethanol