Are coronary artery anomalies an accelerating factor for coronary atherosclerosis development?
Gianluca Rigatelli1, Marzio Gemelli, Alberto Zamboni
1Endocardiovascular Therapy Research, Legnago, Verona, Italy. jackyheart@hotmail.com
Insights
Benign congenital coronary anomalies (CAAs) do not appear to accelerate coronary artery disease (CAD) progression. Patients with CAAs and CAD had more cardiovascular events, but this was linked to existing risk factors, not the anomalies themselves.
Area of Science:
- Cardiology
- Vascular Biology
- Medical Imaging
Background:
- The role of benign congenital coronary anomalies (CAAs) in the development of coronary artery disease (CAD) remains unclear.
- Previous reports suggest a link between CAAs and CAD, but a comprehensive assessment is lacking.
- Understanding this relationship is crucial for accurate risk stratification and patient management.
Purpose of the Study:
- To investigate the influence of benign congenital coronary anomalies (CAAs) on the progression of coronary artery disease (CAD).
- To determine if CAAs act as an independent risk factor for accelerated atherosclerosis.
- To compare cardiovascular event rates and survival in patients with and without CAAs.
Main Methods:
- Retrospective review of 15,000 coronary angiographies to identify patients with CAAs.
- Patients with CAAs were divided into two groups: those with CAD (Group I) and those without CAD (Group II).
- Clinical data, cardiovascular events (myocardial infarction, angina, interventions, death), and follow-up angiography were analyzed.
Main Results:
- Group I (22 patients with CAAs and CAD) had a significantly higher incidence of cardiovascular events (50%) compared to Group II (17 patients with CAAs but no CAD, 12%).
- Higher prevalence of cardiovascular risk factors was observed in Group I.
- Mean actuarial survival (74.8% vs. 100%) and event-free survival (41.7% vs. 88.7%) were significantly lower in Group I compared to Group II.
Conclusions:
- Benign CAAs do not appear to be an independent accelerating factor for coronary atherosclerosis development.
- The increased cardiovascular events in patients with CAAs and CAD are likely attributable to the presence of classical risk factors.
- Further research is needed to fully elucidate the complex interplay between CAAs, atherosclerosis, and cardiovascular outcomes.
Abstract:
The relevance of benign congenital coronary anomalies (CAAs) in the atherosclerotic process is still confused despite the number of single reports of coronary artery disease in CAAs. The present study is aimed at assessing the role of CAAs on the progression of coronary artery disease (CAD). A review of the last 15,000 coronary angiographies was performed to select patients with CAAs, and they were divided into 2 groups on the basis of the presence (group I) or the absence (group II) of CAD. Clinical and instrumental records of the selected patients were reviewed and the numbers of cardiovascular events for each group (acute myocardial infarct, unstable angina, silent ischemia, bypass or percutaneous transluminal coronary angioplasty (PTCA) interventions, and cardiovascular death) were recorded from the date of diagnosis to July 2002. Group I (22 patients, mean age 64.1 +/- 9.1 years, F/M = 10/12) and group II (17 patients, mean age 66.5 +/- 10.6 years, F/M = 7/10) were similar for age and ejection fraction values. The presence of risk factors was statistically higher in group I. The number of patients with cardiovascular events was significantly higher in group I: 50% (11 patients) in group I vs 12% (2 patients) in group II, p<0.05). Repeated coronary angiography in 8/11 patients of group I and in the 2 patients of group II confirmed that the causes of the events were precedent atherosclerotic lesions in 7 patients and newly developed lesions in 3. At a mean follow-up of 60.4 +/- 12.3 months, mean actuarial survival was lower in group I than in group II (74.8% vs 100%, p=0.045), whereas mean event-free survival was 41.7% in group I and 88.7% in group II (p=0.02). Benign CAAs do not seem per se to be an accelerating factor for coronary atherosclerosis development in patients with no or few classical risk factors.
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