Mechanism of reversible 99mTc-sestamibi perfusion defects during pharmacologically induced vasodilatation

Kevin Wei, Dai-Trang (Elizabeth) Le, Jian Ping Bin, Matthew Coggins, Ananda R. Jayawera, Sanjiv Kaul

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Abstract

Reversible perfusion defects on 99mTc-sestamibi imaging during hyperemia are thought to occur due to myocardial blood flow (MBF) "mismatch" between regions with and without stenosis. We have recently shown that myocardial blood volume (MBV) distal to a stenosis decreases during hyperemia, resulting in a reversible perfusion defect on myocardial contrast echocardiography (MCE). In this study, we hypothesized that a reversible perfusion defect on 99mTc-sestamibi imaging during hyperemia results from the same mechanism. We tested our hypothesis under the following conditions: 1) increases in MBF in the absence of changes in MBV by using direct intracoronary infusion of adenosine (group I, n = 10 dogs); 2) decrease in MBV despite an increase in MBF by left main infusion of adenosine proximal to a noncritical coronary stenosis placed on either coronary artery (group II, n = 13 dogs); and 3) reduction in both resting MBF and MBV by placement of a severe stenosis (group III, n = 7 dogs). In group I dogs, no difference in MBV or 99mTc-sestamibi uptake was found between the two coronary beds despite an up to fourfold increase in MBF in one bed with adenosine. In group II dogs, MBV distal to the stenosis decreased during hyperemia despite a twofold increase in mean MBF. A good correlation was found between 99mTc-sestamibi uptake and MBV ratios from the stenosed versus normal bed (r = 0.91, P <0.001). In group III dogs, both MBF and MBV were decreased in the stenosed bed at rest with a good correlation noted between 99mTc-sestamibi uptake and MBV ratios from the stenosed versus normal bed (r = 0.92, P = 0.004). We conclude that reversible defects on 99mTc-sestamibi during vasodilator stress imaging are related to decreases in MBV distal to a stenosis and not to "flow mismatch" between beds. The decrease in MBV results in reduced 99mTc-sestamibi uptake during hyperemia.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume280
Issue number4 49-4
StatePublished - 2001
Externally publishedYes

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Technetium Tc 99m Sestamibi
Blood Volume
Vasodilation
Perfusion
Hyperemia
Dogs
Pathologic Constriction
Adenosine
Bed Rest
Coronary Stenosis
Vasodilator Agents
Echocardiography
Coronary Vessels

Keywords

  • Hyperemia
  • Myocardial blood flow
  • Myocardial blood volume

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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title = "Mechanism of reversible 99mTc-sestamibi perfusion defects during pharmacologically induced vasodilatation",
abstract = "Reversible perfusion defects on 99mTc-sestamibi imaging during hyperemia are thought to occur due to myocardial blood flow (MBF) {"}mismatch{"} between regions with and without stenosis. We have recently shown that myocardial blood volume (MBV) distal to a stenosis decreases during hyperemia, resulting in a reversible perfusion defect on myocardial contrast echocardiography (MCE). In this study, we hypothesized that a reversible perfusion defect on 99mTc-sestamibi imaging during hyperemia results from the same mechanism. We tested our hypothesis under the following conditions: 1) increases in MBF in the absence of changes in MBV by using direct intracoronary infusion of adenosine (group I, n = 10 dogs); 2) decrease in MBV despite an increase in MBF by left main infusion of adenosine proximal to a noncritical coronary stenosis placed on either coronary artery (group II, n = 13 dogs); and 3) reduction in both resting MBF and MBV by placement of a severe stenosis (group III, n = 7 dogs). In group I dogs, no difference in MBV or 99mTc-sestamibi uptake was found between the two coronary beds despite an up to fourfold increase in MBF in one bed with adenosine. In group II dogs, MBV distal to the stenosis decreased during hyperemia despite a twofold increase in mean MBF. A good correlation was found between 99mTc-sestamibi uptake and MBV ratios from the stenosed versus normal bed (r = 0.91, P <0.001). In group III dogs, both MBF and MBV were decreased in the stenosed bed at rest with a good correlation noted between 99mTc-sestamibi uptake and MBV ratios from the stenosed versus normal bed (r = 0.92, P = 0.004). We conclude that reversible defects on 99mTc-sestamibi during vasodilator stress imaging are related to decreases in MBV distal to a stenosis and not to {"}flow mismatch{"} between beds. The decrease in MBV results in reduced 99mTc-sestamibi uptake during hyperemia.",
keywords = "Hyperemia, Myocardial blood flow, Myocardial blood volume",
author = "Kevin Wei and Le, {Dai-Trang (Elizabeth)} and Bin, {Jian Ping} and Matthew Coggins and Jayawera, {Ananda R.} and Sanjiv Kaul",
year = "2001",
language = "English (US)",
volume = "280",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "4 49-4",

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TY - JOUR

T1 - Mechanism of reversible 99mTc-sestamibi perfusion defects during pharmacologically induced vasodilatation

AU - Wei, Kevin

AU - Le, Dai-Trang (Elizabeth)

AU - Bin, Jian Ping

AU - Coggins, Matthew

AU - Jayawera, Ananda R.

AU - Kaul, Sanjiv

PY - 2001

Y1 - 2001

N2 - Reversible perfusion defects on 99mTc-sestamibi imaging during hyperemia are thought to occur due to myocardial blood flow (MBF) "mismatch" between regions with and without stenosis. We have recently shown that myocardial blood volume (MBV) distal to a stenosis decreases during hyperemia, resulting in a reversible perfusion defect on myocardial contrast echocardiography (MCE). In this study, we hypothesized that a reversible perfusion defect on 99mTc-sestamibi imaging during hyperemia results from the same mechanism. We tested our hypothesis under the following conditions: 1) increases in MBF in the absence of changes in MBV by using direct intracoronary infusion of adenosine (group I, n = 10 dogs); 2) decrease in MBV despite an increase in MBF by left main infusion of adenosine proximal to a noncritical coronary stenosis placed on either coronary artery (group II, n = 13 dogs); and 3) reduction in both resting MBF and MBV by placement of a severe stenosis (group III, n = 7 dogs). In group I dogs, no difference in MBV or 99mTc-sestamibi uptake was found between the two coronary beds despite an up to fourfold increase in MBF in one bed with adenosine. In group II dogs, MBV distal to the stenosis decreased during hyperemia despite a twofold increase in mean MBF. A good correlation was found between 99mTc-sestamibi uptake and MBV ratios from the stenosed versus normal bed (r = 0.91, P <0.001). In group III dogs, both MBF and MBV were decreased in the stenosed bed at rest with a good correlation noted between 99mTc-sestamibi uptake and MBV ratios from the stenosed versus normal bed (r = 0.92, P = 0.004). We conclude that reversible defects on 99mTc-sestamibi during vasodilator stress imaging are related to decreases in MBV distal to a stenosis and not to "flow mismatch" between beds. The decrease in MBV results in reduced 99mTc-sestamibi uptake during hyperemia.

AB - Reversible perfusion defects on 99mTc-sestamibi imaging during hyperemia are thought to occur due to myocardial blood flow (MBF) "mismatch" between regions with and without stenosis. We have recently shown that myocardial blood volume (MBV) distal to a stenosis decreases during hyperemia, resulting in a reversible perfusion defect on myocardial contrast echocardiography (MCE). In this study, we hypothesized that a reversible perfusion defect on 99mTc-sestamibi imaging during hyperemia results from the same mechanism. We tested our hypothesis under the following conditions: 1) increases in MBF in the absence of changes in MBV by using direct intracoronary infusion of adenosine (group I, n = 10 dogs); 2) decrease in MBV despite an increase in MBF by left main infusion of adenosine proximal to a noncritical coronary stenosis placed on either coronary artery (group II, n = 13 dogs); and 3) reduction in both resting MBF and MBV by placement of a severe stenosis (group III, n = 7 dogs). In group I dogs, no difference in MBV or 99mTc-sestamibi uptake was found between the two coronary beds despite an up to fourfold increase in MBF in one bed with adenosine. In group II dogs, MBV distal to the stenosis decreased during hyperemia despite a twofold increase in mean MBF. A good correlation was found between 99mTc-sestamibi uptake and MBV ratios from the stenosed versus normal bed (r = 0.91, P <0.001). In group III dogs, both MBF and MBV were decreased in the stenosed bed at rest with a good correlation noted between 99mTc-sestamibi uptake and MBV ratios from the stenosed versus normal bed (r = 0.92, P = 0.004). We conclude that reversible defects on 99mTc-sestamibi during vasodilator stress imaging are related to decreases in MBV distal to a stenosis and not to "flow mismatch" between beds. The decrease in MBV results in reduced 99mTc-sestamibi uptake during hyperemia.

KW - Hyperemia

KW - Myocardial blood flow

KW - Myocardial blood volume

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