Potent statin therapy affects disease progression in higher-risk patients
Factors underlying regression of coronary atheroma with potent statin therapy.Puri R, Nissen SE, Ballantyne CM, et al.
Eur Heart J. 2013 May 3. [Epub]
BackgroundHigh-dose statin regimens improve clinical outcomes in patients at high risk for future cardiovascular events [1 – 4]. Intensive statin therapy can halt the progression of atherosclerosis  and even induce disease regression  for reasons that are not yet fully understood.
Beyond their ability to lower levels of atherogenic lipoproteins, statins may also exert a direct effect upon the arterial wall . Arterial wall remodeling plays a pivotal role in the clinical expression of atherosclerotic disease.
It is of interest to understand whether factors that influence different measures of progression or regression of coronary atherosclerosis are similar. In the Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin (SATURN) the highest dose of rosuvastatin produced greater regression of total atheroma volume (TAV), but not of per cent atheroma volume (PAV), when compared with high-dose atorvastatin . Serial intravascular ultrasound (IVUS) was used to monitor these changes. The current analysis tried to characterize factors associated with regression of different measures of coronary atherosclerosis in 1039 patients included in SATURN, who were treated with atorvastatin (80 mg) or rosuvastatin (40 mg) daily for 24 months.
- Reductions in LDL-C were 40.1% and 47.2% for atorvastatin-treated patients and rosuvastatin-treated patients, respectively (P<0.001).
- HDL-C was increased with 10.0 vs 12.7%, respectively (P=0.02).
- The atorvastatin-treated group experienced greater per cent reductions in triglyceride levels (13.2% vs. 26.2%, P = 0.007).
- C-reactive protein decreased by 25.0% with atorvastatin and 23.7% with rosuvastatin (P= 0.34).
- TAV regression was 24.4 vs. 26.4 mm3 for atorvastatin-treated patients and rosuvastatin-treated patients, respectively; P = 0.01; PAV regression was20.99 vs. 21.22 %, respectively; P = 0.17.
- Both higher baseline TAV and PAV independently associated with TAV and PAV regression, respectively, in a multivariable analysis assessing change in TAV and PAV (standardized estimates: TAV -0.25, P < 0.001; PAV -0.23, P < 0.001)
ConclusionHigher-risk patients, particularly those with greater baseline coronary atheroma volume, are more likely to experience disease regression with potent statin therapy. These findings describe the variable clinical and biochemical characteristics affecting the natural course of coronary atherosclerosis, the arterial wall response, and highlight the need for additional therapeutic targets to tackle the residual burden of disease.
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