title: Coronary microcirculatory vasoconstriction is heterogeneously distributed in acutely ischemic myocardium.
abstract: The classical model of coronary physiology implies the presence of maximal microcirculatory vasodilation during myocardial ischemia. However, Doppler monitoring of coronary blood flow (CBF) documented severe microcirculatory vasoconstriction during pacing-induced ischemia in patients with coronary artery disease. This study investigates the mechanisms that underlie this paradoxical behavior in nine patients with stable angina and single-vessel coronary disease who were candidates for stenting. While transstenotic pressures were continuously monitored, input CBF (in ml/min) to the poststenotic myocardium was measured by Doppler catheter and angiographic cross-sectional area. Simultaneously, specific myocardial blood flow (MBF, in ml.min(-1).g(-1)) was measured by 133Xe washout. Perfused tissue mass was calculated as CBF/MBF. Measurements were obtained at baseline, during pacing-induced ischemia, and after stenting. CBF and distal coronary pressure values were also measured during pacing with intracoronary adenosine administration. During pacing, CBF decreased to 64 +/- 24% of baseline and increased to 265 +/- 100% of ischemic flow after adenosine administration. In contrast, pacing increased MBF to 184 +/- 66% of baseline, measured as a function of the increased rate-pressure product (r = 0.69; P < 0.05). Thus, during pacing, perfused myocardial mass drastically decreased from 30 +/- 23 to 12 +/- 11 g (P < 0.01). Distal coronary pressure remained stable during pacing but decreased after adenosine administration. Stenting increased perfused myocardial mass to 39 +/- 23 g (P < 0.05 vs. baseline) as a function of the increase in distal coronary pressure (r = 0.71; P < 0.02). In conclusion, the vasoconstrictor response to pacing-induced ischemia is heterogeneously distributed and excludes a tissue fraction from perfusion. Within perfused tissue, the metabolic demand still controls the vasomotor tone.
authors.affiliation: Institute of Clinical Physiology, Italian National Research Council, Pisa, Italy. battesto@ifc.cnr.it
authors.forename: Gianmario
authors.initials: G
authors.lastname: Sambuceti
authors.forename: Mario
authors.initials: M
authors.lastname: Marzilli
authors.forename: Andrea
authors.initials: A
authors.lastname: Mari
authors.forename: Cecilia
authors.initials: C
authors.lastname: Marini
authors.forename: Mathis
authors.initials: M
authors.lastname: Schluter
authors.forename: Roberto
authors.initials: R
authors.lastname: Testa
authors.forename: Michaela
authors.initials: M
authors.lastname: Papini
authors.forename: Paolo
authors.initials: P
authors.lastname: Marraccini
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Ciriello
authors.forename: Paolo
authors.initials: P
authors.lastname: Marzullo
authors.forename: Antonio
authors.initials: A
authors.lastname: L'Abbate
mesh_terms: D000208:Acute Disease; D000368:Aged; D000787:Angina Pectoris / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D003097:Collateral Circulation; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology*; D003326:Coronary Circulation; D004562:Electrocardiography; D004734:Energy Metabolism; D005260:Female; D006801:Humans; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology*; D010138:Pacemaker, Artificial; D011877:Radionuclide Imaging; D014655:Vascular Resistance; D014661:Vasoconstriction; D016277:Ventricular Function, Left; D014979:Xenon Isotopes
chemical_list: D014979:Xenon Isotopes