HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Sambuceti, G. Articles by L'Abbate, A. Search for Related Content PubMed PubMed Citation Articles by Sambuceti, G. Articles by L'Abbate, A.

Coronary microcirculatory vasoconstriction is heterogeneously distributed in acutely ischemic myocardium

¹Institute of Clinical Physiology, Italian National Research Council, Pisa; ²Institute of Systems Science and Biomedical Engineering, Padova; ³Ospedale Santa Maria Nuova, Firenze; and ⁴Scuola Superiore di Studi Universitari Sant'Anna, Pisa, Italy

Submitted 24 August 2004 ; accepted in final form 18 November 2004

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.

coronary artery disease; myocardial ischemia; vascular recruitment; adenosine; blood flow

This article has been cited by other articles:

				A. L'Abbate, D. Neglia, C. Vecoli, M. Novelli, V. Ottaviano, S. Baldi, R. Barsacchi, A. Paolicchi, P. Masiello, G. S. Drummond, et al. Beneficial effect of heme oxygenase-1 expression on myocardial ischemia-reperfusion involves an increase in adiponectin in mildly diabetic rats Am J Physiol Heart Circ Physiol, December 1, 2007; 293(6): H3532 - H3541. [Abstract] [Full Text] [PDF]

				K. M. Marques, P. Knaapen, R. Boellaard, N. Westerhof, A. A. Lammertsma, C. A. Visser, and F. C. Visser Hyperaemic microvascular resistance is not increased in viable myocardium after chronic myocardial infarction Eur. Heart J., October 1, 2007; 28(19): 2320 - 2325. [Abstract] [Full Text] [PDF]

				N. H. J. Pijls Fractional flow reserve after previous myocardial infarction Eur. Heart J., October 1, 2007; 28(19): 2301 - 2302. [Full Text] [PDF]

				A. Abbate, G. G.L. Biondi-Zoccai, P. Agostoni, M. J. Lipinski, and G. W. Vetrovec Recurrent angina after coronary revascularization: a clinical challenge Eur. Heart J., May 1, 2007; 28(9): 1057 - 1065. [Abstract] [Full Text] [PDF]

				P. G. Camici and F. Crea Coronary Microvascular Dysfunction N. Engl. J. Med., February 22, 2007; 356(8): 830 - 840. [Full Text] [PDF]

				N. Westerhof, C. Boer, R. R. Lamberts, and P. Sipkema Cross-talk between cardiac muscle and coronary vasculature. Physiol Rev, October 1, 2006; 86(4): 1263 - 1308. [Abstract] [Full Text] [PDF]

				C. Kusmic, G. Lazzerini, F. Coceani, R. Barsacchi, A. L'Abbate, and G. Sambuceti Paradoxical coronary microcirculatory constriction during ischemia: a synergic function for nitric oxide and endothelin Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1814 - H1821. [Abstract] [Full Text] [PDF]