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Updated: Aug 1, 2026
In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
Myocardial perfusion in patients with total occlusion of a single coronary artery with and without collateral
Z X He1, J J Mahmarian, M S Verani
1Department of Nuclear Medicine, Fu Wai Hospital, Beijing, China.
Insights
Coronary collateral circulation does not prevent stress-induced ischemia in single-vessel coronary occlusion without prior heart attack. Collaterals may preserve heart muscle viability but do not resolve perfusion defects during stress.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Myocardial Perfusion Imaging
Background:
- Previous studies on coronary collateral circulation were limited by patient selection criteria.
- This study focuses on patients with total occlusion of a single coronary artery, excluding prior myocardial infarction or multivessel disease.
Purpose of the Study:
- To investigate the relationship between angiographic collateral circulation and myocardial perfusion.
- To determine if collateral circulation prevents stress-induced ischemia in a specific patient cohort.
Main Methods:
- Seventy-one patients with single-vessel total coronary occlusion underwent stress myocardial single-photon emission computed tomography (SPECT).
- Patients were assessed for the presence or absence of collateral circulation via angiography.
- Myocardial perfusion was evaluated using SPECT within 90 days of angiography.
Main Results:
- Abnormal myocardial perfusion was nearly universal (97%) in patients with single-vessel total coronary occlusion.
- Myocardial perfusion defects occurred with similar frequency and extent in patients with and without collateral circulation.
- Collateral circulation did not significantly alter the presence, size, or reversibility of perfusion defects during stress.
Conclusions:
- Stress-induced myocardial ischemia is highly prevalent in patients with single-vessel total coronary occlusion, regardless of collateral circulation.
- Angiographic collateral circulation appears insufficient to prevent stress-induced ischemia.
- Collateral circulation may play a role in preserving myocardial viability despite ischemia.
Background:
Previous studies that investigated the effects of coronary collateral circulation on myocardial perfusion were compromised by inclusion of patients with multivessel coronary artery disease, incomplete occlusion, prior myocardial infarction, or a combination of these. In this study we ascertained the relationship between angiographic collateral circulation and myocardial perfusion only in patients with total occlusion of a single coronary artery, in the absence of myocardial infarction or significant stenosis in the other coronary arteries.
Methods And Results:
Seventy-one consecutive patients underwent stress myocardial single photon emission computed tomography within 90 days of angiography. Collateral circulation was present in 49 patients and absent in 22 patients. All but 2 patients had abnormal perfusion by single photon emission computed tomography imaging, with a mean defect size of 19% +/- 12%, and most (83%) had reversible perfusion defects. Defect count activities improved from stress to rest (or redistribution) (45% +/- 13% to 59% +/- 14%, P <.001). Abnormal myocardial perfusion occurred with similar frequency in patients with collateral circulation and in those without it. Total defect size was 19% +/- 12% in patients with and 18% +/- 11% in those without collateral circulation (P = not significant). The extent of reversibility and defect count activity during stress and rest were similar in patients with collateral circulation and in those without it.
Conclusions:
In patients with a single-vessel total coronary occlusion and without myocardial infarction, stress-induced myocardial ischemia is almost always present, irrespective of presence or absence of angiographic collaterals. These data lend support to the premise that collateral circulation is rather insufficient to prevent stress-induced ischemia, although it can preserve myocardial viability.
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