Coronary microcirculatory vasoconstriction is heterogeneously distributed in acutely ischemic myocardium.
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.
Sambuceti
Gianmario
G
Institute of Clinical Physiology, Italian National Research Council, Pisa, Italy. battesto@ifc.cnr.it
Marzilli
Mario
M
Mari
Andrea
A
Marini
Cecilia
C
Schluter
Mathis
M
Testa
Roberto
R
Papini
Michaela
M
Marraccini
Paolo
P
Ciriello
Giuseppe
G
Marzullo
Paolo
P
L'Abbate
Antonio
A
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
D014979:Xenon Isotopes