Altered coronary vasodilator reserve and metabolism in myocardium subtended by normal arteries in patients with coronary artery disease

Neal G. Uren, Paolo Marraccini, Roberto Gistri, Ranil de Silva, Paolo G. Camici

Research output: Contribution to journalArticle

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Abstract

Objectives. The aim of this study was to investigate coronary vasodilator reserve and metabolism in myocardium subtended by angiographically normal arteries remote from ischemia. Background. After infarction, structural and functional changes occur in remote myocardium often subtended by normal arteries. Whether changes occur in regions remote from ischemic but noninfarcted myocardium is unknown. Methods. Coronary vasodilator reserve was measured with positron emission tomography in 12 patients with single-vessel disease using intravenous dipyridamole (0.56 mg/kg for 4 min). In another 10 patients, simultaneous arterial/great cardiac vein catheterization was performed during atrial pacing to measure myocardial metabolism in regions subtended by diseased or normal arteries. Results. Basal myocardial blood flow in stenosis-related regions was comparable to that in remote regions but was lower after dipyridamole administration (1.73 ± 0.91 vs. 2.89 ± 0.93 ml/min per g, p <0.01), giving coronary vasodilator reserve values of 1.80 ± 0.82 and 2.73 ± 0.89 (p <0.01). In normal control subjects, basal myocardial blood flow was 0.92 ± 0.13 and 3.67 ±0.94 ml/min per g in the basal state and after dipyridamole (both p <0.05 vs. values in remote regions), and coronary vasodilator reserve was 4.07 ± 0.98 (p <0.01 vs. values in remote regions). During pacing there was net lactate release in diseased regions (-18 ± 27%, p <0.05 vs. values in remote regions and control subjects) and extraction in remote regions (38 ± 17%) and in normal control subjects (26 ± 11%). Glucose and alanine extraction were increased in diseased (8 ± 6% and 6 ± 6%) and remote regions (6 ± 3% and 4 ± 3%), compared with values in normal control subjects (2 ± 3% and -1 ± 3%, both p <0.05 vs. diseased and remote regions). Conclusions. Coronary vasodilator reserve is reduced and glucose and alanine metabolism is abnormal in regions subtended by normal arteries remote from ischemic but noninfarcted myocardium.

Original languageEnglish
Pages (from-to)650-658
Number of pages9
JournalJournal of the American College of Cardiology
Volume22
Issue number3
DOIs
Publication statusPublished - 1993

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Vasodilator Agents
Coronary Artery Disease
Myocardium
Arteries
Dipyridamole
Alanine
Glucose
Cardiac Catheterization
Positron-Emission Tomography
Infarction
Veins
Lactic Acid
Pathologic Constriction
Reference Values
Ischemia

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Altered coronary vasodilator reserve and metabolism in myocardium subtended by normal arteries in patients with coronary artery disease. / Uren, Neal G.; Marraccini, Paolo; Gistri, Roberto; de Silva, Ranil; Camici, Paolo G.

In: Journal of the American College of Cardiology, Vol. 22, No. 3, 1993, p. 650-658.

Research output: Contribution to journalArticle

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abstract = "Objectives. The aim of this study was to investigate coronary vasodilator reserve and metabolism in myocardium subtended by angiographically normal arteries remote from ischemia. Background. After infarction, structural and functional changes occur in remote myocardium often subtended by normal arteries. Whether changes occur in regions remote from ischemic but noninfarcted myocardium is unknown. Methods. Coronary vasodilator reserve was measured with positron emission tomography in 12 patients with single-vessel disease using intravenous dipyridamole (0.56 mg/kg for 4 min). In another 10 patients, simultaneous arterial/great cardiac vein catheterization was performed during atrial pacing to measure myocardial metabolism in regions subtended by diseased or normal arteries. Results. Basal myocardial blood flow in stenosis-related regions was comparable to that in remote regions but was lower after dipyridamole administration (1.73 ± 0.91 vs. 2.89 ± 0.93 ml/min per g, p <0.01), giving coronary vasodilator reserve values of 1.80 ± 0.82 and 2.73 ± 0.89 (p <0.01). In normal control subjects, basal myocardial blood flow was 0.92 ± 0.13 and 3.67 ±0.94 ml/min per g in the basal state and after dipyridamole (both p <0.05 vs. values in remote regions), and coronary vasodilator reserve was 4.07 ± 0.98 (p <0.01 vs. values in remote regions). During pacing there was net lactate release in diseased regions (-18 ± 27{\%}, p <0.05 vs. values in remote regions and control subjects) and extraction in remote regions (38 ± 17{\%}) and in normal control subjects (26 ± 11{\%}). Glucose and alanine extraction were increased in diseased (8 ± 6{\%} and 6 ± 6{\%}) and remote regions (6 ± 3{\%} and 4 ± 3{\%}), compared with values in normal control subjects (2 ± 3{\%} and -1 ± 3{\%}, both p <0.05 vs. diseased and remote regions). Conclusions. Coronary vasodilator reserve is reduced and glucose and alanine metabolism is abnormal in regions subtended by normal arteries remote from ischemic but noninfarcted myocardium.",
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T1 - Altered coronary vasodilator reserve and metabolism in myocardium subtended by normal arteries in patients with coronary artery disease

AU - Uren, Neal G.

AU - Marraccini, Paolo

AU - Gistri, Roberto

AU - de Silva, Ranil

AU - Camici, Paolo G.

PY - 1993

Y1 - 1993

N2 - Objectives. The aim of this study was to investigate coronary vasodilator reserve and metabolism in myocardium subtended by angiographically normal arteries remote from ischemia. Background. After infarction, structural and functional changes occur in remote myocardium often subtended by normal arteries. Whether changes occur in regions remote from ischemic but noninfarcted myocardium is unknown. Methods. Coronary vasodilator reserve was measured with positron emission tomography in 12 patients with single-vessel disease using intravenous dipyridamole (0.56 mg/kg for 4 min). In another 10 patients, simultaneous arterial/great cardiac vein catheterization was performed during atrial pacing to measure myocardial metabolism in regions subtended by diseased or normal arteries. Results. Basal myocardial blood flow in stenosis-related regions was comparable to that in remote regions but was lower after dipyridamole administration (1.73 ± 0.91 vs. 2.89 ± 0.93 ml/min per g, p <0.01), giving coronary vasodilator reserve values of 1.80 ± 0.82 and 2.73 ± 0.89 (p <0.01). In normal control subjects, basal myocardial blood flow was 0.92 ± 0.13 and 3.67 ±0.94 ml/min per g in the basal state and after dipyridamole (both p <0.05 vs. values in remote regions), and coronary vasodilator reserve was 4.07 ± 0.98 (p <0.01 vs. values in remote regions). During pacing there was net lactate release in diseased regions (-18 ± 27%, p <0.05 vs. values in remote regions and control subjects) and extraction in remote regions (38 ± 17%) and in normal control subjects (26 ± 11%). Glucose and alanine extraction were increased in diseased (8 ± 6% and 6 ± 6%) and remote regions (6 ± 3% and 4 ± 3%), compared with values in normal control subjects (2 ± 3% and -1 ± 3%, both p <0.05 vs. diseased and remote regions). Conclusions. Coronary vasodilator reserve is reduced and glucose and alanine metabolism is abnormal in regions subtended by normal arteries remote from ischemic but noninfarcted myocardium.

AB - Objectives. The aim of this study was to investigate coronary vasodilator reserve and metabolism in myocardium subtended by angiographically normal arteries remote from ischemia. Background. After infarction, structural and functional changes occur in remote myocardium often subtended by normal arteries. Whether changes occur in regions remote from ischemic but noninfarcted myocardium is unknown. Methods. Coronary vasodilator reserve was measured with positron emission tomography in 12 patients with single-vessel disease using intravenous dipyridamole (0.56 mg/kg for 4 min). In another 10 patients, simultaneous arterial/great cardiac vein catheterization was performed during atrial pacing to measure myocardial metabolism in regions subtended by diseased or normal arteries. Results. Basal myocardial blood flow in stenosis-related regions was comparable to that in remote regions but was lower after dipyridamole administration (1.73 ± 0.91 vs. 2.89 ± 0.93 ml/min per g, p <0.01), giving coronary vasodilator reserve values of 1.80 ± 0.82 and 2.73 ± 0.89 (p <0.01). In normal control subjects, basal myocardial blood flow was 0.92 ± 0.13 and 3.67 ±0.94 ml/min per g in the basal state and after dipyridamole (both p <0.05 vs. values in remote regions), and coronary vasodilator reserve was 4.07 ± 0.98 (p <0.01 vs. values in remote regions). During pacing there was net lactate release in diseased regions (-18 ± 27%, p <0.05 vs. values in remote regions and control subjects) and extraction in remote regions (38 ± 17%) and in normal control subjects (26 ± 11%). Glucose and alanine extraction were increased in diseased (8 ± 6% and 6 ± 6%) and remote regions (6 ± 3% and 4 ± 3%), compared with values in normal control subjects (2 ± 3% and -1 ± 3%, both p <0.05 vs. diseased and remote regions). Conclusions. Coronary vasodilator reserve is reduced and glucose and alanine metabolism is abnormal in regions subtended by normal arteries remote from ischemic but noninfarcted myocardium.

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