Abstract 18443: Impact of Left Ventricular Hypertrophy on Impaired Coronary Microvascular Dysfunction Determined by Direct Single-Wire Pressure and Flow Velocity Measurement
Introduction: Coronary microvascular (MV) dysfunction can be sustained by several pathogenic mechanisms (e.g. functional, structural and extravascular alterations). On the other hand, structural abnormalities (an adverse remodeling of intramural coronary arterioles consisting of vessel wall thickening mainly due to hypertrophy of smooth muscle cells and increased collagen deposition in the tunica media) responsible for coronary MV dysfunction have been consistently documented in patients with hypertrophic cardiomyopathy (HCM) and in those with pathologic left ventricular hypertrophy (LVH). However, there has been no technique that enables direct measurement of coronary MV dysfunction in vivo.
Methods: According to transthoracic echocardiographic data, patients without coronary obstruction (>50% diameter) on angiography were divided into 2 groups; LVH (n=17) and non-LVH (n=24). LVH was defined either interventricular septal thickness (IVST) or posterior wall thickness (PWT) thicker >11mm. To evaluate directly coronary MV dysfunction, a velocity-based index of hyperemic MV resistance (hMR) was measured using a dual-sensor (Doppler velocity and pressure)-equipped guidewire, and the guidewire-derived hemodynamic parameters were compared.
Results: There were no differences in clinical demographics between the groups except for more common male gender and HCM in LVH group. Although fractional flow reserve was comparable between the 2 groups, coronary flow reserve was significantly impaired (1.96±0.79 vs. 2.55±0.89, p=0.04), and hMR was significantly elevated (2.09±0.79 vs. 1.60±0.50, p=0.04) in LVH group compared with non-LVH group. Older age, worse estimated glomerular filtration rate, and LVH were significantly associated with MV dysfunction (≥median value of hMR [1.7]) in univariate analysis, and left ventricular mass index tended to predict MV dysfunction in multivariate logistic regression analysis (OR, 1.03; 95% CI, 1.00-1.06; p=0.10).
Conclusions: Compared with non-LVH patients, MV function was impaired in patients with LVH. In vivo assessment of hMR was a promising index of MV dysfunction in patients without epicardial obstruction to elucidate the pathophysiologic mechanisms underlying coronary MV dysfunction.
Author Disclosures: K. Tsujita: None. K. Yamanaga: None. N. Komura: None. K. Sakamoto: None. T. Miyazaki: None. M. Ishii: None. N. Tabata: None. T. Akasaka: None. T. Akasaka: None. Y. Arima: None. T. Ono: None. S. Kojima: None. S. Tayama: None. K. Kaikita: None. S. Hokimoto: None. H. Yamabe: None. S. Nakamura: None. H. Ogawa: Other Research Support; Modest; AstraZeneca, Astellas, Boehringer lngelheim, Bristol-Myers Squibb, Daiichi Sankyo, Dainippon Sumitomo Pharma, Kowa, MSD, Novartis, Pfizer, Sanofi, Takeda. Other Research Support; Significant; Bayer, Chugai, Otsuka. Honoraria; Modest; AstraZeneca, Bayer, Pfizer, Sanofi, Takeda. Honoraria; Significant; Daiichi Sankyo, MSD.
- © 2014 by American Heart Association, Inc.