Marlene Busko

July 21, 2015

LAS VEGAS, NV — In low- to intermediate-risk patients who presented to the emergency department with possible acute coronary syndrome (ACS) and had a coronary CT angiography (CCTA) scan to detect stenosis, those on statin therapy were less likely to have a high-risk plaque and more likely to have coronary artery calcification, according to a new analysis of the Multicenter Study to Rule Out Myocardial Infarction by Cardiac Computed Tomography (ROMICAT-II)[1].

The results, presented here at the Society of Cardiovascular Computed Tomography (SCCT) 2015 Annual Scientific Meeting, suggest that "statins may cause an increase in calcification in the coronary arteries . . . and that may not be a bad thing," according to lead investigator Dr Sumbal Janjua (Massachusetts General Hospital, Boston). "It may show that the statins are working."

Dr Todd Villines (Walter Reed Army Medical Center, Washington, DC), session cochair, said the effect of statins on plaque "has not been well assessed using coronary CT in less risky patients who are not having invasive studies." Despite inherent limitations, the current study is a hypothesis-generating "snapshot" that is "certainly consistent with other observations that statins may modulate plaque biology by decreasing lipid content, making [the plaques] less risky, and increasing the calcium content," he told heartwire from Medscape.

Do Statins Change Plaque Features?

Data from several intravascular ultrasound studies suggest that statins have a small stabilizing effect on atherosclerotic plaques, Janjua noted, referring to an earlier study by Dr Rishi Puri (Cleveland Clinic, OH) reported by heartwire . In addition, previous CCTA studies suggest that statins may reduce total and noncalcified plaque volume and high-risk plaque features.

In the present study, researchers investigated the relationship between statin use and plaque features in low- to intermediate-risk patients with chest pain and suspected ACS in ROMICAT-II. They analyzed data from 222 patients who presented to the emergency department with acute chest pain, had negative troponin and ECG results, and had coronary stenosis detected by CCTA. Of these patients, 147 were taking statins and 75 were not taking statins when they presented. About a third of patients were women and a quarter had a family history of CAD.

Compared with patients not on statin therapy, those receiving statins were older, more likely to have hypertension and type 2 diabetes, and less likely to be a current smoker. Patients on statin therapy also had a significantly lower mean LDL cholesterol (93.1 vs 119.3 mg/dL, P<0.001) and total cholesterol (172.9 vs 196.7 mg/dL, P<0.001). This suggests that the classification of statin therapy, based on self-report, was accurate, Janjua noted.

Three experts analyzed the CCTA images to identify calcified and noncalcified plaque, CAD severity, and high-risk plaque (defined as positive remodeling, <30 Hounsfield units, or a napkin-ring sign). Patients had two to four coronary artery segments with plaque.

In the overall cohort, those receiving statins were significantly more likely to have calcified plaque (93.3% vs 76.2%, P<0.001) and significantly less likely to have noncalcified plaque (64.0% vs 83.0%, P=0.002) or high-risk plaque (13.3% vs 31.1%, P=0.003) compared with patients not on statins.

In the subset of 186 patients with nonobstructive CAD, defined as a stenosis between 1% to 49%, patients receiving statins were also more likely to have calcified plaque and less likely to have noncalcified plaque or high-risk plaque.

In the overall cohort, patients who were older, male, or had more traditional cardiovascular risk factors, more coronary artery segments with plaque, or a coronary stenosis 50% or higher were more likely to have high-risk plaque.

Patients on statins were less likely to have high-risk plaque, and this association persisted after adjusting for age, gender, number of traditional cardiovascular risk factors, and CAD extent and severity (OR 0.30; 95% CI 0.12–0.73, P=0.008).

This was a retrospective, cross-sectional analysis that lacked information about the duration and dose of statin therapy (which would have been useful to determine plaque changes over time), and patients had a low number of high-risk plaques, Janjua acknowledged.

Nevertheless, "these observations generate the hypothesis that statin therapy may lead to the conversion of noncalcified, high-risk plaque to coronary artery calcium, and thus [coronary artery calcium] may represent a benign finding in patients on statin therapy," she concluded.

Janjua had no relevant financial relationships.


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