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Microvascular dysfunction in collateral-dependent myocardium
G Sambuceti1, O Parodi, A Giorgetti
1CNR Institute of Clinical Physiology, Pisa, Italy.
Insights
Patients with coronary artery disease and collateral-dependent myocardium show reduced blood flow at rest and during stress. Despite this, collateral-dependent areas retain vasodilator reserve, suggesting a potential microvascular disorder.
Area of Science:
- Cardiovascular physiology
- Coronary artery disease research
- Myocardial blood flow dynamics
Background:
- Quantitative assessment of collateral circulation in humans is limited.
- Understanding myocardial blood flow regulation in coronary artery disease is clinically significant.
Purpose of the Study:
- To evaluate myocardial blood flow regulation in collateral-dependent areas of patients with coronary artery disease.
- To compare blood flow in collateral-dependent regions with remote and normal myocardium under various physiological conditions.
Main Methods:
- Positron emission tomography with nitrogen-13 ammonia was used for flow measurements.
- Flow was assessed at rest, during pacing-induced tachycardia, and after dipyridamole administration.
- Nineteen patients with isolated coronary artery occlusion were compared to 13 normal subjects.
Main Results:
- Collateral-dependent myocardium exhibited reduced resting and stress-induced blood flow compared to normal subjects.
- While remote myocardium responded to dipyridamole, collateral-dependent regions showed limited increase, indicating utilized vasodilator reserve.
- Poorer collateral development correlated with higher flow inhomogeneity and lower dipyridamole flow.
Conclusions:
- Collateral-dependent myocardium maintains vasodilator reserve, though it's nearly fully utilized during increased demand.
- Reduced blood flow adaptation suggests a potential global microvascular disorder in chronic coronary occlusion.
Objectives:
The aim of this study was to evaluate myocardial blood flow regulation in collateral-dependent myocardium of patients with coronary artery disease.
Background:
Despite great clinical relevance, perfusion correlates of collateral circulation in humans have rarely been estimated by quantitative methods at rest and during stress.
Methods:
Nineteen patients with angina and isolated occlusion of the left anterior descending (n = 14) or left circumflex (n = 5) coronary artery were evaluated. Using positron emission tomography and nitrogen-13 ammonia, we obtained flow measurements at baseline, during atrial pacing-induced tachycardia and after intravenous administration of dipyridamole (0.56 mg/kg body weight over 4 min). Flow values in collateral-dependent and remote areas were compared with values in 13 normal subjects.
Results:
Flow at rest was similar in collateralized and remote myocardium (0.61 +/- 0.11 vs. 0.63 +/- 0.17 ml/min per g, mean +/- 1 SD), and both values were lower than normal (1.00 +/- 0.20 ml/min per g, p < 0.01). During pacing, blood flow increased to 0.83 +/- 0.25 and 1.11 +/- 0.39 ml/min per g in collateral-dependent and remote areas, respectively (p < 0.05 vs. baseline); both values were lower than normal (1.86 +/- 0.61 ml/min per g, p < 0.01). Dipyridamole induced a further increase in perfusion in remote areas (1.36 +/- 0.57 ml/min per g, p < 0.01 vs. pacing) but not in collateral-dependent regions (0.93 +/- 0.37 ml/min per g, p = NS vs. pacing); again, both values were lower (p < 0.01) than normal (3.46 +/- 0.78 ml/min per g). Dipyridamole flow in collateral-dependent myocardium was slightly lower in patients with poorly developed than in those with well developed collateral channels (0.75 +/- 0.29 vs. 1.06 +/- 0.38 ml/min per g, respectively, p = 0.06); however, the former showed higher flow inhomogeneity (collateral/control flow ratio 0.58 +/- 0.10 vs. 0.81 +/- 0.22, respectively, p < 0.02). A linear direct correlation was observed between flow reserve of collateral-dependent and remote regions (r = 0.83, p < 0.01).
Conclusions:
Despite rest hypoperfusion, collateral-dependent myocardium maintains a vasodilator reserve that is almost fully utilized during increases in oxygen consumption. A global microvascular disorder might hamper adaptation to chronic coronary occlusion.