Clinical Investigation
Right Ventricular Energetics in Patients With Hypertrophic Cardiomyopathy and the Effect of Alcohol Septal Ablation

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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).

Methods and 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. [11C]Acetate positron-emission tomography (PET) was performed to determine RVk2 and LVk2, 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. RVk2 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 LVk2 was similar between groups. Consequently, RVk2/LVk2 was increased in the patients (0.85 ± 0.19 vs 0.59 ± 0.13; P = .004). In patients with obstructive HCM, ASA reduced RVk2 (0.085 ± 0.021 min−1 to 0.072 ± 0.022 min−1; P = .001). Inasmuch as LVk2 remained unaffected by the procedure, RVk2/LVk2 was decreased after ASA (0.66 ± 0.18; P = .03). The absolute change in LVOT gradient was related to the absolute change in RVk2 (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.

Section snippets

Study Population

Twenty-one patients with HCM were enrolled in the study. HCM was diagnosed by the presence of a nondilated and hypertrophied LV, in the absence of any other systemic or cardiac causes of LV hypertrophy, on 2-dimensional (2D) echocardiography (maximal wall thickness >15 mm in adult patients). All patients exhibited an asymmetric pattern of septal hypertrophy. Eleven individuals with normal physical examination, electrocardiogram, and 2D echocardiography were enrolled to serve as a control group.

Results

Baseline characteristics, hemodynamics, and [11C]acetate clearance rates (k2) for all study groups are listed in Table 1. Heart rate and systolic blood pressure during the PET studies were similar between control subjects and HCM patients. RVk2 was higher in HCM patients, whereas LVk2 was not significantly different between the groups. As a result, RVk2/LVk2 was significantly higher in HCM patients (0.81 ± 0.21) compared with control subjects (0.59 ± 0.13; P = .004; Fig. 1).

In the HCM subset

Discussion

In the studied HCM population, RV oxidative metabolism was higher than in control subjects, despite the fact that heart rates were similar between the groups. In the subset of HCM patients with significant LVOT obstruction, ASA reduced RV oxygen consumption, indicating that the detrimental effects of outflow obstruction extend beyond the LV and, at least in part, augment RV workload. The linear relationship between the absolute change in LVOT gradient and the absolute change in RV oxidative

Limitations

The cohort of obstructive HCM patients was small, limiting the inferences that can be drawn from the present study. Nevertheless, the [11C]acetate PET data convincingly indicated augmented RV oxygen consumption in HCM and a significant reduction after ASA.

The presence of RV valvular disease, such as tricuspid regurgitation in HCM, could lead to increased demands on RV performance. Accordingly, RV oxidative metabolism less accurately reflects RV forward work, because part of the RV volume is

Disclosures

None.

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