In the Journals

AQUAMARINE: Statin therapy reduces high-intensity plaques in patients with CAD

Intensive statin therapy appears to decrease the plaque-to-myocardium signal-intensity ratio, or PMR, of high-intensity plaques detected by noncontrast T1-weighted MRI, according to findings from the AQUAMARINE pilot study.

This imaging technique has potential as a valuable means of quantitatively tracking changes in plaque composition, the researchers wrote.

The study included 48 patients with CAD who underwent prospective serial noncontrast T1-weighted MRI and CTA. These tests were performed at baseline and after 12 months of intensive pitavastatin (Livalo, Kowa Pharmaceuticals) therapy with an LDL target of less than 80 mg/dL. They used propensity score matching to identify a control group of 48 patients with CAD who were not treated with statins. The primary endpoint was change to the PMR of high-intensity plaque after 12 months, with secondary endpoints including change in CTA-measured indexes and levels of high-sensitivity C-reactive protein (hs-CRP).

The group receiving 12 months of statin therapy showed improvement to LDL (125 mg/dL to 70 mg/dL; P < .001), an 18.9% reduction in PMR (1.38 to 1.11; P < .001) and a significant reduction to hs-CRP (1.19 mg/L to 0.62 mg/L; P < .001), as well as improved low-attenuation plaque volume and a decrease in the proportion of total atheroma volume. The control group displayed a 19.2% increase in PMR, from 1.22 to 1.49 (P < .001).

Factors correlated with changes in PMR included: changes in LDL (r = 0.533; P < .001) hs-CRP (r = 0.347; P < .001) atheroma volume percentage (r = 0.477; P < .001) and low-attenuation plaque volume percentage (r = 0.416; P < .001).

Renu Virmani, MD

Renu Virmani

In a related editorial, Kazuyuki Yahagi, MD, Michael Joner, MD, and Cardiology Today Editorial Board member Renu Virmani, MD, of the CVPath Institute in Gaithersburg, Maryland, wrote that these findings were “tantalizing but not confirmatory.”

“There are recognized pitfalls involving small cohorts together with further limitations of [cardiac magnetic resonance], because coronary arteries are barely visualized by this low-resolution modality,” they wrote. “Nevertheless, PMR values may eventually prove to be a valuable surrogate for high-risk atherosclerotic plaques. Moreover, noninvasive [cardiac magnetic resonance] may be the future for risk stratification of CAD patients because the level of radiation exposure is reduced compared with CT.” – by Jennifer Byrne

Disclosures: One of the study researchers reports receiving research support from GE Healthcare and Philips Healthcare. Yahagi reports no relevant financial disclosures, but Joner and Virmani report numerous disclosures. Please see the editorial for a list of their relevant financial disclosures.

Intensive statin therapy appears to decrease the plaque-to-myocardium signal-intensity ratio, or PMR, of high-intensity plaques detected by noncontrast T1-weighted MRI, according to findings from the AQUAMARINE pilot study.

This imaging technique has potential as a valuable means of quantitatively tracking changes in plaque composition, the researchers wrote.

The study included 48 patients with CAD who underwent prospective serial noncontrast T1-weighted MRI and CTA. These tests were performed at baseline and after 12 months of intensive pitavastatin (Livalo, Kowa Pharmaceuticals) therapy with an LDL target of less than 80 mg/dL. They used propensity score matching to identify a control group of 48 patients with CAD who were not treated with statins. The primary endpoint was change to the PMR of high-intensity plaque after 12 months, with secondary endpoints including change in CTA-measured indexes and levels of high-sensitivity C-reactive protein (hs-CRP).

The group receiving 12 months of statin therapy showed improvement to LDL (125 mg/dL to 70 mg/dL; P < .001), an 18.9% reduction in PMR (1.38 to 1.11; P < .001) and a significant reduction to hs-CRP (1.19 mg/L to 0.62 mg/L; P < .001), as well as improved low-attenuation plaque volume and a decrease in the proportion of total atheroma volume. The control group displayed a 19.2% increase in PMR, from 1.22 to 1.49 (P < .001).

Factors correlated with changes in PMR included: changes in LDL (r = 0.533; P < .001) hs-CRP (r = 0.347; P < .001) atheroma volume percentage (r = 0.477; P < .001) and low-attenuation plaque volume percentage (r = 0.416; P < .001).

Renu Virmani, MD

Renu Virmani

In a related editorial, Kazuyuki Yahagi, MD, Michael Joner, MD, and Cardiology Today Editorial Board member Renu Virmani, MD, of the CVPath Institute in Gaithersburg, Maryland, wrote that these findings were “tantalizing but not confirmatory.”

“There are recognized pitfalls involving small cohorts together with further limitations of [cardiac magnetic resonance], because coronary arteries are barely visualized by this low-resolution modality,” they wrote. “Nevertheless, PMR values may eventually prove to be a valuable surrogate for high-risk atherosclerotic plaques. Moreover, noninvasive [cardiac magnetic resonance] may be the future for risk stratification of CAD patients because the level of radiation exposure is reduced compared with CT.” – by Jennifer Byrne

Disclosures: One of the study researchers reports receiving research support from GE Healthcare and Philips Healthcare. Yahagi reports no relevant financial disclosures, but Joner and Virmani report numerous disclosures. Please see the editorial for a list of their relevant financial disclosures.