Myocardial contrast echocardiography can be used to quantify intramyocardial blood volume

New insights into structural mechanisms of coronary autoregulation

Clarence C. Wu, Marc D Feldman, James D. Mills, Christine A. Manaugh, David Fischer, M. Zubair Jafar, Flordeliza S. Villanueva

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

Background: Changes in intramyocardial blood volume (IBV) mediate autoregulatory adaptations to coronary stenosis. This study investigated whether (1) myocardial contrast echocardiography (MCE) can quantify changes in IBV during coronary stenosis and (2) the relation between coronary resistance- and MCE-derived IBV could yield insight into structural mechanisms of IBV change. Methods and Results: A circulating in vitro model with constant flow and varying volume was used to determine whether 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 transit time was linearly related to volume (r=.91). To determine whether changes in IBV could be quantified in vivo, the left anterior descending coronary artery in 12 dogs was instrumented with a flow probe, occluder, and intracoronary pressure catheter, and non-flow-limiting stenoses were created. IBV was derived by use of coronary resistance measurements applied to models that assumed autoregulation to occur via vasodilatation or microvascular recruitment. MCE- IBV was calculated from microbubble transit rates. At constant flow, MCE and resistance IBV increased with stenosis. Although MCE and resistance IBV were linearly related, MCE overestimated IBV derived from the vasodilatation model and underestimated IBV calculated from the recruitment model. Conclusions: MCE can quantify autoregulatory increases in IBV that maintain resting myocardial perfusion. These data suggest that both microvessel vasodilatation and recruitment are dual mechanisms of IBV change. MCE thus may be a clinically useful technique for the detection and quantification of coronary artery disease at rest.

Original languageEnglish (US)
Pages (from-to)1004-1011
Number of pages8
JournalCirculation
Volume96
Issue number3
StatePublished - Aug 5 1997
Externally publishedYes

Fingerprint

Blood Volume
Echocardiography
Homeostasis
Vasodilation
Microbubbles
Coronary Stenosis
Pathologic Constriction
Microvessels
Coronary Artery Disease
Albumins
Coronary Vessels
Catheters
Perfusion
Dogs

Keywords

  • Contrast media
  • Coronary disease
  • Echocardiography
  • Stenosis

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Myocardial contrast echocardiography can be used to quantify intramyocardial blood volume : New insights into structural mechanisms of coronary autoregulation. / Wu, Clarence C.; Feldman, Marc D; Mills, James D.; Manaugh, Christine A.; Fischer, David; Jafar, M. Zubair; Villanueva, Flordeliza S.

In: Circulation, Vol. 96, No. 3, 05.08.1997, p. 1004-1011.

Research output: Contribution to journalArticle

Wu, Clarence C. ; Feldman, Marc D ; Mills, James D. ; Manaugh, Christine A. ; Fischer, David ; Jafar, M. Zubair ; Villanueva, Flordeliza S. / Myocardial contrast echocardiography can be used to quantify intramyocardial blood volume : New insights into structural mechanisms of coronary autoregulation. In: Circulation. 1997 ; Vol. 96, No. 3. pp. 1004-1011.
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AU - Feldman, Marc D

AU - Mills, James D.

AU - Manaugh, Christine A.

AU - Fischer, David

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AU - Villanueva, Flordeliza S.

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N2 - Background: Changes in intramyocardial blood volume (IBV) mediate autoregulatory adaptations to coronary stenosis. This study investigated whether (1) myocardial contrast echocardiography (MCE) can quantify changes in IBV during coronary stenosis and (2) the relation between coronary resistance- and MCE-derived IBV could yield insight into structural mechanisms of IBV change. Methods and Results: A circulating in vitro model with constant flow and varying volume was used to determine whether 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 transit time was linearly related to volume (r=.91). To determine whether changes in IBV could be quantified in vivo, the left anterior descending coronary artery in 12 dogs was instrumented with a flow probe, occluder, and intracoronary pressure catheter, and non-flow-limiting stenoses were created. IBV was derived by use of coronary resistance measurements applied to models that assumed autoregulation to occur via vasodilatation or microvascular recruitment. MCE- IBV was calculated from microbubble transit rates. At constant flow, MCE and resistance IBV increased with stenosis. Although MCE and resistance IBV were linearly related, MCE overestimated IBV derived from the vasodilatation model and underestimated IBV calculated from the recruitment model. Conclusions: MCE can quantify autoregulatory increases in IBV that maintain resting myocardial perfusion. These data suggest that both microvessel vasodilatation and recruitment are dual mechanisms of IBV change. MCE thus may be a clinically useful technique for the detection and quantification of coronary artery disease at rest.

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