Coronary CT Angiography Can Track Regression of Noncalcified Plaques by Statin Therapy
July 25, 2016
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DURHAM, NC — Moderate and intensive statin treatment can retard or even bring about regression of noncalcified coronary plaque as shown by coronary CT angiography (CCTA), according to new research from China.
“Clinicians should know the potential usage of CT scans for high-risk patients, and if noncalcified plaques are found, strengthened statin therapy should be considered,” lead author Dr Bin Lu (Fuwai Hospital, Beijing) told heartwire from Medscape by email. “If clinicians know patients have positive coronary noncalcified plaques based on CT images, they should recommend to their patients to take statins regularly and follow up the disease after 1 or 2 years.”
Extensive clinical trial evidence points to serial coronary intravascular ultrasound (IVUS) as an imaging method to show that statin therapy can stop progression of coronary plaque or induce regression, but IVUS is invasive and unsuitable for nonischemic patients. However, CCTA has emerged as an imaging tool that can accurately and noninvasively measure luminal narrowing and characterize coronary plaques, according to the researchers.
They conducted a prospective multicenter observational study involving 206 consecutive patients with mild noncalcified plaque and undergoing CCTA.
The results were published online July 13, 2016 in the American Heart Journal.
The researchers divided patients into three groups: intensive statin therapy (n=55), moderate statin therapy (n=85), or no statin therapy (n=66). Patients in the intensive group took 20 to 40 mg/d atorvastatin or 10 to 20 mg/d rosuvastatin. Patients in the moderate group took 10 to 20 mg/d atorvastatin, 5 to 10 mg/d rosuvastatin, 20 to 40 mg/d fluvastatin, or 10 to 20 mg/d simvastatin.
The researchers performed serial scans after a median interval of 18 months to measure low-attenuation plaque (LAP) volume, total plaque volume, and percent plaque volume.
Patients in the intensive group experienced significantly improved lipid profiles during follow-up: total cholesterol, LDL-C, and triglycerides significantly decreased (P<0.001 all), while HDL-C increased nonsignificantly. Patients in the moderate-therapy group also experienced decreases in total cholesterol, LDL-C, and triglycerides (P<0.05), while HDL-C slightly increased.
Patients in the no-treatment group experienced no lipid-profile change.
On CCTA, the researchers observed significant regression of LAP volume, total plaque volume, and percent plaque volume in the intensive group compared with the no-treatment group (-7.1 vs. 0.9, -16.4 vs 12.3, -6.2 vs 3.5, respectively, P<0.001 all). They observed retarded progression of LAP, total plaque volume, and percent plaque volume in the moderate-treatment group.
Using a multivariable prediction model, the researchers found that total plaque volume, higher baseline LAP volume, and moderate and intensive therapy each predicted plaque regression (P<0.001, 0.004, and <0.001, respectively).
Based on their study results, they concluded, “This further confirms the feasibility of using serial CCTA to assess changes in plaque characteristics, allowing this method to potentially track atherosclerosis noninvasively.
“After this study, we are now full of confidence to treat our patients who have positive coronary plaques with statins. However, we need to do more about following up the patients for major adverse cardiac events after early detection and treatment of noncalcified coronary artery plaques,” Lu said.
The Capital Health Research and Development Special Fund supported this research. The researchers reported no relevant financial relationships.