MYOCARDIAL CONTRAST ECHOCARDIOGRAPHY CAN BE USED TO QUANTIFY INTRAMYOCARDIAL BLOOD-VOLUME - NEW INSIGHTS INTO STRUCTURAL MECHANISMS OF CORONARY AUTOREGULATION

Citation
Cc. Wu et al., MYOCARDIAL CONTRAST ECHOCARDIOGRAPHY CAN BE USED TO QUANTIFY INTRAMYOCARDIAL BLOOD-VOLUME - NEW INSIGHTS INTO STRUCTURAL MECHANISMS OF CORONARY AUTOREGULATION, Circulation, 96(3), 1997, pp. 1004-1011
Citations number
33
Categorie Soggetti
Peripheal Vascular Diseas",Hematology
Journal title
ISSN journal
00097322
Volume
96
Issue
3
Year of publication
1997
Pages
1004 - 1011
Database
ISI
SICI code
0009-7322(1997)96:3<1004:MCECBU>2.0.ZU;2-S
Abstract
Background Changes in intramyocardial blood volume (IBV) mediate autor egulatory adaptations to coronary stenosis. This study investigated wh ether (1) myocardial contrast echocardiography (MCE) can quantify chan ges in IBV during coronary stenosis and (2) the relation between coron ary resistance- and MCE-derived IBV could yield insight into structura l mechanisms of IBV change. Methods and Results A circulating in vitro model with constant flow and varying volume was used to determine whe ther indicator dilution theory could be applied to MCE. Contrast echo was performed with albumin microbubbles, and time-intensity data were fit to a gamma-variate function. With six different volumes, bubble tr ansit time was linearly related to volume (r=.91). To determine whethe r changes in IBV could be quantified in vivo, the left anterior descen ding coronary artery in 12 dogs was instrumented with a flow probe, oc cluder, and intracoronary pressure catheter, and non-flow-limiting ste noses were created. IBV was derived by use of coronary resistance meas urements applied to models that assumed autoregulation to occur via va sodilatation or microvascular recruitment. MCE-IBV was calculated from microbubble transit rates. At constant flow, MCE and resistance IBV i ncreased with stenosis. Although MCE and resistance IBV were linearly related, MCE overestimated IBV derived from the vasodilatation model a nd underestimated IBV calculated from the recruitment model. Conclusio ns MCE can quantify autoregulatory increases in IBV that maintain rest ing myocardial perfusion. These data suggest that both microvessel vas odilatation and recruitment are dual mechanisms of IBV change. MCE thu s may be a clinically useful technique for the detection and quantific ation of coronary artery disease at rest.