Related Experiment Videos
Coronary collateralization: determinants of adequate distal vessel filling after arterial occlusion
Jens G Kilian1, Anthony Keech, Mark R Adams
1Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia.
Insights
Factors influencing coronary collateral formation in coronary artery disease (CAD) were identified. Hyperlipidemia and calcium-channel blocker use promote rich collaterals, while diabetes, left anterior descending artery occlusion, and acute myocardial infarction are linked to poor collateralization.
Area of Science:
- Cardiology
- Vascular Biology
- Medical Research
Background:
- The protective role of collateral vessels in coronary artery disease (CAD) is recognized.
- Factors influencing the formation of these vital collateral vessels remain largely unknown.
Purpose of the Study:
- To investigate the patient characteristics and clinical factors associated with coronary collateral formation in patients with single-vessel coronary artery occlusion.
Main Methods:
- Coronary angiograms of 200 patients with single-vessel coronary artery occlusion were analyzed.
- Collateral circulation was graded as 'poor' or 'rich'.
- Patient data including demographics, medications, and cardiovascular risk factors were collected and analyzed.
Main Results:
- Rich collateralization was associated with hyperlipidemia and calcium-channel blocker (CCB) use.
- Poor collateralization was independently predicted by diabetes mellitus, left anterior descending (LAD) artery occlusion, and acute myocardial infarction (MI).
- Univariate analysis also identified age, statin use, nitrate use, stable angina presentation, and longer CAD duration as correlates of rich collaterals, while impaired left ventricular function correlated with poorer collaterals.
Conclusions:
- Diabetes mellitus, LAD occlusion, and acute MI are independently associated with poor coronary collateralization.
- Hyperlipidemia and CCB use are associated with rich collateralization.
- Understanding these factors may help predict outcomes following coronary artery occlusion.
Background:
The protective effect of collateral vessels in coronary artery disease (CAD) is well established. Little is known, however, about factors that influence collateral formation.
Methods:
We studied the coronary angiograms of 200 consecutive patients with single-vessel coronary artery occlusion. Patients were excluded if obstructive stenoses were present in other vessels or if prior revascularization had been undertaken. Collateral circulation to the occluded artery was graded as 'poor' (no or incomplete filling) or 'rich' (complete filling). Patient characteristics, including mode of presentation, medications and CAD risk factors, were assessed.
Results:
Positive univariate correlates of rich collaterals included increasing age [odds ratio (OR) 1.03, P = 0.016], 'statin' use (OR 2.50, P = 0.005), nitrate use (OR 1.96, P = 0.034), calcium-channel blocker (CCB) use (OR 4.07, P < 0.001), presentation with stable angina (OR 2.34, P = 0.006), longer time since diagnosis of CAD (OR 1.12, P = 0.002) and history of hyperlipidemia (OR 3.55, P < 0.001). Significantly poorer collateralization was observed in the setting of acute myocardial infarction (MI) (OR 0.23, P < 0.001), diabetes mellitus (OR 0.33, P = 0.003), impaired left ventricular function (OR 0.64, P = 0.015) and occlusion of the left anterior descending coronary artery (LAD) (OR 0.28, P < 0.001). On multivariate analysis, rich collateralization was associated with hyperlipidemia (P = 0.003) and CCB use (P = 0.028). Independent predictors of poor collaterals were presence of diabetes (P < 0.001), LAD occlusion (P = 0.001) and presentation with acute MI (P = 0.017).
Conclusion:
Diabetes mellitus, occlusion of the LAD and presentation with acute MI are independently associated with poor distal vessel collateralization, whereas hyperlipidemia and use of CCBs are associated with rich collateralization. Factors determining coronary collateral formation may in turn influence outcomes after coronary artery occlusion.