Cardiomyopathy
Effect of Successful Alcohol Septal Ablation on Microvascular Function in Patients With Obstructive Hypertrophic Cardiomyopathy

https://doi.org/10.1016/j.amjcard.2007.12.032Get rights and content

We hypothesized that relief of obstruction in patients with hypertrophic cardiomyopathy (HC) by percutaneous transluminal septal myocardial ablation (PTSMA) improves microvascular dysfunction by relief of extravascular compression. Microvascular dysfunction in obstructive HC is related to extravascular compression by increased left ventricular (LV) mass and LV end-diastolic pressure. The study included 14 patients with obstructive HC (mean age 55 ± 12 years, 11 men) who underwent successful PTSMA and 14 healthy volunteers (mean age 31 ± 4 years, 11 men). LV hemodynamics (by Doppler echocardiography) and intramyocardial flow dynamics (by adenosine myocardial contrast echocardiography) were evaluated in healthy volunteers and before and 6 months after PTSMA in patients with HC. LV end-diastolic pressure was estimated from the ratio of transmitral early LV filling velocity to early diastolic mitral annular velocity. PTSMA reduced the invasively measured LV outflow tract gradient (119 ± 35 vs 17 ± 16 mm Hg, p <0.0001) and LV end-diastolic pressure (23 ± 3 vs 16 ± 2 mm Hg, p <0.001). Six months after PTSMA, myocardial flow reserve improved (2.73 ± 0.56 vs 3.21 ± 0.49, p <0.001), but did not normalize compared with healthy controls (vs 3.95 ± 0.77, p <0.001). Also, septal hyperemic endo-to-epi myocardial blood flow ratio improved (0.70 ± 0.11 vs 0.92 ± 0.07, p <0.001). Changes in LV end-diastolic pressure, LV mass index, and LV outflow tract peak systolic gradient correlated well with changes in hyperemic perfusion (all p <0.05). In conclusion, microvascular dysfunction improves after PTSMA due to relief of extravascular compression forces.

Section snippets

Methods

The study comprised 14 consecutive patients (mean age 55 ± 12 years, 11 men) with obstructive HC and normal epicardial coronary arteries who underwent successful PTSMA and 14 healthy volunteers (mean age 31 ± 4 years, 11 men) who served as a control group. All patients with HC were in New York Heart Association functional class III with or without angina pectoris and had a LV outflow tract peak systolic gradient ≥50 mm Hg at rest or provocation.

The study protocol consisted of clinical

Results

Baseline and 6 months post-PTSMA characteristics of the 14 patients with HC are summarized in Table 1. New York Heart Association functional class decreased from 3.0 ± 0.3 to 1.2 ± 0.4 (p <0.0001), and none of the patients had angina pectoris at 6-month follow-up after PTSMA. After-PTSMA medications such as β blockers and calcium antagonists were withheld in most patients.

Immediately after PTSMA, the invasive LV outflow tract peak systolic gradient decreased from 119 ± 35 to 17 ± 16 mm Hg (p

Discussion

The main finding of our study is that patients with obstructive HC and normal epicardial coronary arteries have impaired vasodilator reserve, in particular in the subendocardium, as evidenced by adenosine stress MCE. After successful PTSMA, a decrease in LV outflow tract peak systolic gradient, LV mass index, and LV end-diastolic pressure and an improvement in vasodilator reserve in noninfarcted myocardium, including the endo-to-epi ratio, were seen. The degree of reduction in LV outflow tract

References (30)

Cited by (0)

View full text