Yuhei Kobayashi1, Joo Myung Lee1, William F Fearon2, Jang Hoon Lee1, Takeshi Nishi1, Dong-Hyun Choi1, Frederik M Zimmermann1, Ji-Hyun Jung1, Hyun-Jung Lee1, Joon-Hyung Doh1, Chang-Wook Nam1, Eun-Seok Shin1, Bon-Kwon Koo1. 1. From the Division of Cardiovascular Medicine, Stanford University, CA (Y.K., W.F.F., T.N., D.-H.C.); Division of Cardiology, Department of Internal Medicine, Heart Vascular Stroke Institute, Samsung Medical Center, Seoul, Republic of Korea (J.M.L.); Department of Internal Medicine, Kyungpook National University Hospital, Daegu, Republic of Korea (J.H.L.); Department of Cardiology, Catharina Hospital Eindhoven, the Netherlands (F.M.Z.); Department of Medicine, Seoul National University Hospital, Republic of Korea (J.-H.J., H.-J.L., B.-K.K.); Department of Medicine, Inje University Ilsan Paik Hospital, Goyang, Republic of Korea (J.-H.D.); Department of Medicine, Keimyung University Dongsan Medical Center, Daegu, Republic of Korea (C.-W.N.); Department of Cardiology, Ulsan University Hospital, University of Ulsan College of Medicine, Republic of Korea (E.-S.S.); and Institute of Aging, Seoul National University, Republic of Korea (B.-K.K.). 2. From the Division of Cardiovascular Medicine, Stanford University, CA (Y.K., W.F.F., T.N., D.-H.C.); Division of Cardiology, Department of Internal Medicine, Heart Vascular Stroke Institute, Samsung Medical Center, Seoul, Republic of Korea (J.M.L.); Department of Internal Medicine, Kyungpook National University Hospital, Daegu, Republic of Korea (J.H.L.); Department of Cardiology, Catharina Hospital Eindhoven, the Netherlands (F.M.Z.); Department of Medicine, Seoul National University Hospital, Republic of Korea (J.-H.J., H.-J.L., B.-K.K.); Department of Medicine, Inje University Ilsan Paik Hospital, Goyang, Republic of Korea (J.-H.D.); Department of Medicine, Keimyung University Dongsan Medical Center, Daegu, Republic of Korea (C.-W.N.); Department of Cardiology, Ulsan University Hospital, University of Ulsan College of Medicine, Republic of Korea (E.-S.S.); and Institute of Aging, Seoul National University, Republic of Korea (B.-K.K.). wfearon@stanford.edu.
Abstract
BACKGROUND: Difficulty directly visualizing the coronary microvasculature as opposed to the epicardial coronary artery makes its assessment challenging. The goal of this study is to measure the index of microcirculatory resistance (IMR) in all 3 major coronary vessels to identify the clinical and angiographic predictors of an abnormal IMR. METHODS AND RESULTS: Ninety-three patients who underwent coronary physiological assessment in all 3 major coronary vessels were prospectively enrolled (59.8±9.4 years with 77.4% men). IMR was corrected using Yong's formula and coronary microvascular dysfunction (CMD) was defined using vessel-specific cutoffs. A global IMR was calculated as the sum of the IMR in all 3 major epicardial vessels. Angiographic epicardial disease severity was assessed with vessel-specific and overall SYNTAX score. Median IMR and fractional flow reserve was 17.2 (Q1-Q3: 13.3-22.9) and 0.92 (0.85-0.97). The majority of patients (59.1%) had no CMD, 23.7% had 1-vessel CMD, 14.0% had 2-vessel CMD, and 3.2% had 3-vessel CMD. CMD was observed at a similar rate in the territories supplied by all 3 major coronary vessels (left anterior descending coronary artery 28.0%, left circumflex artery 19.4%, and right coronary artery 23.7%; P=0.39). Fractional flow reserve had a weak, positive correlation with IMR (ρ=0.16; P<0.01). The SYNTAX score had no significant correlation with IMR, both at a patient level (ρ=-0.002; P=0.99) and a vessel-specific level (ρ=-0.06; P=0.36). By multivariable ordinal logistic regression analysis, no variable was left as an independent predictor of an abnormal IMR. CONCLUSIONS: Clinical factors and epicardial coronary disease severity are not predictors of the extent of CMD. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01621438.
BACKGROUND: Difficulty directly visualizing the coronary microvasculature as opposed to the epicardial coronary artery makes its assessment challenging. The goal of this study is to measure the index of microcirculatory resistance (IMR) in all 3 major coronary vessels to identify the clinical and angiographic predictors of an abnormal IMR. METHODS AND RESULTS: Ninety-three patients who underwent coronary physiological assessment in all 3 major coronary vessels were prospectively enrolled (59.8±9.4 years with 77.4% men). IMR was corrected using Yong's formula and coronary microvascular dysfunction (CMD) was defined using vessel-specific cutoffs. A global IMR was calculated as the sum of the IMR in all 3 major epicardial vessels. Angiographic epicardial disease severity was assessed with vessel-specific and overall SYNTAX score. Median IMR and fractional flow reserve was 17.2 (Q1-Q3: 13.3-22.9) and 0.92 (0.85-0.97). The majority of patients (59.1%) had no CMD, 23.7% had 1-vessel CMD, 14.0% had 2-vessel CMD, and 3.2% had 3-vessel CMD. CMD was observed at a similar rate in the territories supplied by all 3 major coronary vessels (left anterior descending coronary artery 28.0%, left circumflex artery 19.4%, and right coronary artery 23.7%; P=0.39). Fractional flow reserve had a weak, positive correlation with IMR (ρ=0.16; P<0.01). The SYNTAX score had no significant correlation with IMR, both at a patient level (ρ=-0.002; P=0.99) and a vessel-specific level (ρ=-0.06; P=0.36). By multivariable ordinal logistic regression analysis, no variable was left as an independent predictor of an abnormal IMR. CONCLUSIONS: Clinical factors and epicardial coronary disease severity are not predictors of the extent of CMD. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01621438.