Carlos Collet1, Jeroen Sonck2, Bert Vandeloo3, Takuya Mizukami4, Bram Roosens3, Stijn Lochy3, Jean-Francois Argacha3, Danny Schoors3, Iginio Colaiori5, Giuseppe Di Gioia5, Monika Kodeboina5, Hiroshi Suzuki6, Marcel Van 't Veer7, Jozef Bartunek5, Emanuele Barbato2, Bernard Cosyns3, Bernard De Bruyne8. 1. Cardiovascular Center Aalst, OLV Clinic, Aalst, Belgium. Electronic address: carloscollet@gmail.com. 2. Cardiovascular Center Aalst, OLV Clinic, Aalst, Belgium; Department of Advanced Biomedical Sciences, University of Naples, Federico II, Naples, Italy. 3. Centrum voor Hart- en Vaatziekten, Universitair Ziekenhuis Brussel, Brussels, Belgium. 4. Cardiovascular Center Aalst, OLV Clinic, Aalst, Belgium; Department of Cardiology, Showa University Fujigaoka Hospital, Kanagawa, Japan. 5. Cardiovascular Center Aalst, OLV Clinic, Aalst, Belgium. 6. Department of Cardiology, Showa University Fujigaoka Hospital, Kanagawa, Japan. 7. Department of Cardiology, Catharina Hospital, Eindhoven, the Netherlands. 8. Cardiovascular Center Aalst, OLV Clinic, Aalst, Belgium; Lausanne University Hospital, Lausanne, Switzerland.
Abstract
BACKGROUND: Diffuse atherosclerosis is commonly observed in angiographically normal segments in patients with stable coronary artery disease (CAD). The distribution of epicardial resistance along the vessel can be evaluated using coronary physiology. OBJECTIVES: The purpose of this study was to characterize the pathophysiological patterns of CAD using invasive pressure pullbacks during continuous hyperemia. METHODS: In this prospective, multicenter study of patients undergoing clinically-indicated coronary angiography due to stable angina, a pressure-wire pullback device was set at a speed of 1 mm/s. Based on coronary angiography and on the fractional flow reserve (FFR) pullback curve, the patterns of CAD were adjudicated as focal, diffuse, or a combination of both. The distribution of epicardial resistance was characterized using the hyperemic pullback pressure gradients (PPGs). The PPG index, a continuous metric based on the magnitude of pressure drop over 20 mm and on the extent of functional disease was computed to determine the pattern of CAD. Low PPG index indicates diffuse CAD. RESULTS: A total of 158 vessels (n = 117) were included. Overall, 984,813 FFR values were used to generate 100 FFR pullback curves. Using coronary physiology, 36% of the vessel disease patterns were reclassified compared to angiography. The median of maximal PPG over 20 mm was 0.083 (interquartile range: 0.063 to 0.118) FFR units, and the mean extent of functional disease was 39.3 ± 21.3 mm. The mean PPG index was 0.58 ± 0.18 and differentiated pathophysiological focal and diffuse disease (p < 0.001). CONCLUSIONS: Pathophysiological patterns of CAD can be characterized by motorized hyperemic PPGs. The evaluation of the FFR pullback curve reclassified one-third of the vessels' disease patterns compared with conventional angiography. The PPG index is a novel metric that quantifies the distribution of epicardial resistance and discriminates focal from diffuse CAD. (Physiological Patterns of Coronary Artery Disease; NCT03824600).
BACKGROUND: Diffuse atherosclerosis is commonly observed in angiographically normal segments in patients with stable coronary artery disease (CAD). The distribution of epicardial resistance along the vessel can be evaluated using coronary physiology. OBJECTIVES: The purpose of this study was to characterize the pathophysiological patterns of CAD using invasive pressure pullbacks during continuous hyperemia. METHODS: In this prospective, multicenter study of patients undergoing clinically-indicated coronary angiography due to stable angina, a pressure-wire pullback device was set at a speed of 1 mm/s. Based on coronary angiography and on the fractional flow reserve (FFR) pullback curve, the patterns of CAD were adjudicated as focal, diffuse, or a combination of both. The distribution of epicardial resistance was characterized using the hyperemic pullback pressure gradients (PPGs). The PPG index, a continuous metric based on the magnitude of pressure drop over 20 mm and on the extent of functional disease was computed to determine the pattern of CAD. Low PPG index indicates diffuse CAD. RESULTS: A total of 158 vessels (n = 117) were included. Overall, 984,813 FFR values were used to generate 100 FFR pullback curves. Using coronary physiology, 36% of the vessel disease patterns were reclassified compared to angiography. The median of maximal PPG over 20 mm was 0.083 (interquartile range: 0.063 to 0.118) FFR units, and the mean extent of functional disease was 39.3 ± 21.3 mm. The mean PPG index was 0.58 ± 0.18 and differentiated pathophysiological focal and diffuse disease (p < 0.001). CONCLUSIONS: Pathophysiological patterns of CAD can be characterized by motorized hyperemic PPGs. The evaluation of the FFR pullback curve reclassified one-third of the vessels' disease patterns compared with conventional angiography. The PPG index is a novel metric that quantifies the distribution of epicardial resistance and discriminates focal from diffuse CAD. (Physiological Patterns of Coronary Artery Disease; NCT03824600).
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