title: Clinical evidence for myocardial derecruitment downstream from severe stenosis: pressure-flow control interaction.
abstract: 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 (133)Xe 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.
authors.affiliation: Consiglio Nazionale delle Ricerche Institute of Clinical Physiology, Pisa 56100, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Sambuceti
authors.forename: M
authors.initials: M
authors.lastname: Marzilli
authors.forename: A
authors.initials: A
authors.lastname: Mari
authors.forename: C
authors.initials: C
authors.lastname: Marini
authors.forename: P
authors.initials: P
authors.lastname: Marzullo
authors.forename: R
authors.initials: R
authors.lastname: Testa
authors.forename: I
authors.initials: I
authors.lastname: Raugei
authors.forename: M
authors.initials: M
authors.lastname: Papini
authors.forename: M
authors.initials: M
authors.lastname: Schluter
authors.forename: A
authors.initials: A
authors.lastname: L'Abbate
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D001011:Aorta / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D003251:Constriction, Pathologic / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000502:physiology*; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*; D015150:Echocardiography, Doppler; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D008833:Microcirculation / Q000502:physiology; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000502:physiology