TY - JOUR
T1 - Coronary microcirculatory vasoconstriction is heterogeneously distributed in acutely ischemic myocardium
AU - Sambuceti, Gianmario
AU - Marzilli, Mario
AU - Mari, Andrea
AU - Marini, Cecilia
AU - Schluter, Mathis
AU - Testa, Roberto
AU - Papini, Michaela
AU - Marraccini, Paolo
AU - Ciriello, Giuseppe
AU - Marzullo, Paolo
AU - L'Abbate, Antonio
PY - 2005/5
Y1 - 2005/5
N2 - 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.
AB - 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.
KW - Adenosine
KW - Blood flow
KW - Coronary artery disease
KW - Myocardial ischemia
KW - Vascular recruitment
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U2 - 10.1152/ajpheart.00870.2004
DO - 10.1152/ajpheart.00870.2004
M3 - Article
C2 - 15840905
AN - SCOPUS:18044385590
VL - 288
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 5 57-5
ER -