Abstract 2163: Extravascular Compressive Forces Limit Subendocardial Perfusion Reserve in Symptomatic Obstructive Hypertrophic Cardiomyopathy
Background. A blunted perfusion reserve is a hallmark of hypertrophic cardiomyopathy (HCM), which likely induces ischemia and serves as an important indepent marker for an unfavorable outcome. Although microvascular remodeling and decreased capillairy density are in part responsible this microvascular dysfunction, the contribution of potential reversible compressive extravascular forces is unknown.
Methods and Results. Eighteen patients with symptomatic HOCM (age 53±12 yrs, 13 men) and a normal coronary angiogram were studied with invasive pressure measure measurements, echocardiography to assess diastolic perfusion time, CMR to determine LV mass, and PET to quantify resting and hyperemic myocardial blood flow (MBF) in both the subendocardium and epicardium. Nt-pro-BNP was determined as a biochemical marker of wall stress. Resting (0.90±0.21 mL·min−1·mL−1) and stress MBF (2.26±0.97 mL·min−1·mL−1) were distributed homogeneously across the myocardium. The average subendocardial to epicardial ratio decreased from 1.20±0.11 at rest to 0.88±0.18 during hyperemia (p<0.01). Subendocardial hyperemic MBF inversely correlated with end-diastolic pressure (r=0.65, P<0.01) and nt-pro-BNP (r=0.78, p<0.01), but not with LV mass and diastolic perfusion time (p=NS).
Conclusions. Hyperemic perfusion impairment in HOCM is more pronounced at the subendocardial level and related to extravascular compressive forces such as end-diastolic pressure and wall stress rather than LV mass. Given these results, studies are warranted to elucidate the effects of wall stress lowering therapies on perfusion reserve.