TY - JOUR
T1 - Clinical evidence for myocardial derecruitment downstream from severe stenosis
T2 - Pressure-flow control interaction
AU - Sambuceti, Gianmario
AU - Marzilli, Mario
AU - Mari, Andrea
AU - Marini, Cecilia
AU - Marzullo, Paolo
AU - Testa, Roberto
AU - Raugei, Isabella
AU - Papini, Micaela
AU - Schluter, Mathis
AU - L'Abbate, Antonio
PY - 2000
Y1 - 2000
N2 - To verify the interaction between coronary pressure (CP) and blood flow (CBF) control, we studied nine candidates for angioplasty of an isolated lesion of the left anterior descending coronary artery [i.e., percutaneous transluminal coronary angioplasty (PTCA)]. CBF (i.e., flow velocity x coronary cross-sectional area at the Doppler tip) and CP were monitored during washout of 2-5 mCi of 133Xe after bolus injection into the left main artery before and after PTCA. Xe mean transit time (MTT) was calculated as the area under the time-activity curve, acquired by a gamma camera, divided by the dose obtained from a model fit of the Xe curve in the anterior wall. CBF response to intracoronary adenosine (2 mg) was also assessed. PTCA increased baseline CBF (from 14.5 ± 9.4 to 20 ± 8 ml/min, P <0.01), coronary flow reserve (from 1.52 ± 0.24 to 2.33 ± 0.8, P <0.01), and CP (from 64 ± 9 to 100 ± 10 mmHg, P <0.05). MTT decreased from 89 ± 32 to 70 ± 19 s (P <0.05) after PTCA; however, MTT and CBF changes were not correlated (r = -0.09, not significant). Inasmuch as MTT is the ratio of distribution volume to CBF, MTT x CBF was used as an index of perfused myocardial volume. Volume increased after PTCA from 23 ± 18 to 56 ± 30 ml. A direct correlation was observed between the percent increase in distal CP and percent increase in perfused volume (r = 0.91, P <0.01). Thus low CP was not associated with exhaustion of flow reserve but, rather, with reduction of perfused myocardial volume. These data suggest that, in the presence of a severe coronary stenosis, derecruitment of vascular units occurs that is proportional to the decrease in driving pressure. Residual perfused units maintain a vasomotor tone, thus explaining the paradoxical persistence of coronary reserve.
AB - To verify the interaction between coronary pressure (CP) and blood flow (CBF) control, we studied nine candidates for angioplasty of an isolated lesion of the left anterior descending coronary artery [i.e., percutaneous transluminal coronary angioplasty (PTCA)]. CBF (i.e., flow velocity x coronary cross-sectional area at the Doppler tip) and CP were monitored during washout of 2-5 mCi of 133Xe after bolus injection into the left main artery before and after PTCA. Xe mean transit time (MTT) was calculated as the area under the time-activity curve, acquired by a gamma camera, divided by the dose obtained from a model fit of the Xe curve in the anterior wall. CBF response to intracoronary adenosine (2 mg) was also assessed. PTCA increased baseline CBF (from 14.5 ± 9.4 to 20 ± 8 ml/min, P <0.01), coronary flow reserve (from 1.52 ± 0.24 to 2.33 ± 0.8, P <0.01), and CP (from 64 ± 9 to 100 ± 10 mmHg, P <0.05). MTT decreased from 89 ± 32 to 70 ± 19 s (P <0.05) after PTCA; however, MTT and CBF changes were not correlated (r = -0.09, not significant). Inasmuch as MTT is the ratio of distribution volume to CBF, MTT x CBF was used as an index of perfused myocardial volume. Volume increased after PTCA from 23 ± 18 to 56 ± 30 ml. A direct correlation was observed between the percent increase in distal CP and percent increase in perfused volume (r = 0.91, P <0.01). Thus low CP was not associated with exhaustion of flow reserve but, rather, with reduction of perfused myocardial volume. These data suggest that, in the presence of a severe coronary stenosis, derecruitment of vascular units occurs that is proportional to the decrease in driving pressure. Residual perfused units maintain a vasomotor tone, thus explaining the paradoxical persistence of coronary reserve.
KW - Autoregulation
KW - Coronary angioplasty
KW - Coronary artery disease
KW - Coronary circulation
KW - Microcirculation
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M3 - Article
C2 - 11087216
AN - SCOPUS:0034537222
SN - 0363-6119
VL - 279
JO - American Journal of Physiology
JF - American Journal of Physiology
IS - 6 48-6
ER -