High intensity statin reduces atheroma volume in patients with acute STEMI
ESC 2014 - BarcelonaNews - Sep. 9, 2014
Presented at the ESC Congress 2014 by: Lorenz RABER (Bern, CH)
Effect of high-intensity statin therapy on atherosclerosis in patients with ST-elevation myocardial infarction: Results of the prospective, longitudinal intravascular ultrasound follow-up study
BackgroundStatins can importantly reduce the number of CV events, and IVUS studies have shown that high-intensity statin treatment can lead to atheroma regression in patients with stable coronary artery disease. In previous IVUS regression studies no patients with acute STEMI were included, despite their high risk of recurrent events and the high frequency of vulnerable plaques; often not only in the culprit vessel. The phenotype of the plaque has consequences for the occurrence of future events. It is therefore useful to study changes in the composition of the plaque in response to high-intensity statin treatment.
The IBIS 4 study tested the hypothesis that regression of coronary atherosclerosis can be achieved in proximal segments of non-infarct-related arteries with the highest dose rosuvastatin (40 mg daily), in 13 months in STEMI patients. It was also tested whether a reduction of radiofrequency (RF)-defined necrotic core and ‘thin cap fibroatheromas’ (TCFA) could be induced. To this extent, 103 acute STEMI patients from the COMFORTABLE AMI study, in whom the infarct-related vessel was treated, got rosuvastatin 20 mg during 2 weeks, followed by 13 months of rosuvastatin 40 mg.
- After 13 months, IVUS showed a reduction of atheroma volume of 0.9% (95%CI: -1.56 to -0.25, P=0.007) (of 43.95+9.66% to 43.02+9.82%).
- No significant change in percentage necrotic core was detected with RF after 13 months (21.13+7.43% by baseline and 21.02+7.04% after 13 months, change: -0.05%, 95%CI: -1.05 to 0.96, P=0.93).
- After 13 months the proportions of plaques with necrotic core and different plaque phenotypes had nog changed.
ConclusionThis IBIS 4 study demonstrated that the proximal segments of non-infarct-related arteries of STEMI patients have a high atherosclerotic plaque load, with the majority of the lesions being TCFA. Treatment with high intensity statins during 13 months was also in patients with acute STEMI associated with significantly less atherosclerosis (atheroma volume). This treatment did not change the proportion of plaque phenotypes.
In the discussion during the press conference was noted that there might be other means to characterise the phenotype of plaques, and that other methods may have detected phenotypic changes, because the atheroma volume did diminish. It is possible that more advanced techniques are required to see changes.
An advantage of this treatment is that atherosclerosis did not increase, thus rosuvastatin seems to halt the atherogenic process.
- Our reports are based on information made available at the ESC congress -
These data were published in the Eur. Heart J.