title: Coronary-aortic interaction during ventricular isovolumic contraction.
abstract: In earlier work, we suggested that the start of the isovolumic contraction period could be detected in arterial pressure waveforms as the start of a temporary pre-systolic pressure perturbation (AIC(start), start of the Arterially detected Isovolumic Contraction), and proposed the retrograde coronary blood volume flow in combination with a backwards traveling pressure wave as its most likely origin. In this study, we tested this hypothesis by means of a coronary artery occlusion protocol. In six Yorkshire × Landrace swine, we simultaneously occluded the left anterior descending (LAD) and left circumflex (LCx) artery for 5 s followed by a 20-s reperfusion period and repeated this sequence at least two more times. A similar procedure was used to occlude only the right coronary artery (RCA) and finally all three main coronary arteries simultaneously. None of the occlusion protocols caused a decrease in the arterial pressure perturbation in the aorta during occlusion (P > 0.20) nor an increase during reactive hyperemia (P > 0.22), despite a higher deceleration of coronary blood volume flow (P = 0.03) or increased coronary conductance (P = 0.04) during hyperemia. These results show that the pre-systolic aortic pressure perturbation does not originate from the coronary arteries.
authors.affiliation: Experimental Cardiology, Thoraxcenter, Cardiovascular Research Institute COEUR, Erasmus MC, University Medical Center Rotterdam, Dr Molewaterplein 50, P.O. Box 2040, 3000 CA, Rotterdam, The Netherlands. m.vanhouwelingen@erasmusmc.nl
authors.forename: Marc J
authors.initials: MJ
authors.lastname: van Houwelingen
authors.forename: Daphne
authors.initials: D
authors.lastname: Merkus
authors.forename: Maaike
authors.initials: M
authors.lastname: Te Lintel Hekkert
authors.forename: Geert
authors.initials: G
authors.lastname: van Dijk
authors.forename: Arnold P G
authors.initials: AP
authors.lastname: Hoeks
authors.forename: Dirk J
authors.initials: DJ
authors.lastname: Duncker
mesh_terms: D000818:Animals; D001011:Aorta / Q000503:physiopathology*; D023921:Coronary Stenosis / Q000503:physiopathology*; D003331:Coronary Vessels / Q000503:physiopathology*; D004562:Electrocardiography; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006940:Hyperemia / Q000503:physiopathology; D009200:Myocardial Contraction / Q000502:physiology*; D034421:Sus scrofa