Following ST Elevation Myocardial Infarction (STEMI) the myocardial ischemia causes an inflammatory response, which is a predictor of mortality and myocardial remodeling. Treatment with statins have been shown to be able to reduce the area at risk by reducing inflammation in hypercholesterolemic patients with unstable angina. It is unknown whether the anti-inflammatory effect can really reduce the size of myocardial necrosis in STEMI and if this is due to the anti-inflammatory effect of statins. What would be the best way to advance in the anti-inflammatory strategy for treating STEMI?
High dose statin are recommended treatment for both ST elevation as well as non ST myocardial infarction. Statins have anti-inflammatory effects and lower inflammatory markers such as CRP. In addition, several animal studies have shown that statin treatment during reperfusion reduces myocardial injury and reduces infarct size.
However, to the best of my knowledge no randomized study in patients with ST elevation myocardial infarction have showed significant effect.
Some prospective studies have investigated the effect of high dose statin in acute ST elevation myocardial infarction. The ROSEMARY study compared rousuvastatin 40 mg vs 10 mg in ST elevation MI and showed infarct size and clinical outcome. In a similar study REPERATOR pretreatment with atorvastatin 80 mg was compared with placebo and showed no difference in either infarct size or left ventricular function.
In contrast several but not all studies have shown positive effect on cardiovascular events and myocardial injury on elective patients with stable angina unstable angina pretreated with statin before PCI. Several attempts to reduce the anti-inflammatory strategy for treating STEMI. In experimental studies in animal models it works but despite several trials in human no trial have shown clear positive effects on outcome. The new very potent lipid lowering drugs such as the PCSK9 monoclonal antibodies might be effective strategy for treating STEMI but this must first be shown in future clinical trials.
OK Sven
Thank you for your comments. I think this is the way.
Paulo
regarding anti-inflammatory treatments in STEMI, you may find this review interesting
http://www.ncbi.nlm.nih.gov/pubmed/24530674
J Am Coll Cardiol. 2014 Apr 29;63(16):1593-603. doi: 10.1016/j.jacc.2014.01.014. Epub 2014 Feb 13.
Anti-inflammatory strategies for ventricular remodeling following ST-segment elevation acute myocardial infarction.
Seropian IM, Toldo S, Van Tassell BW, Abbate A.
Thanks for the input. Iam an investigator in kawasaki disease management.
This is the reason now now we prefer to add statin during acute illness due to its antiinfalmmatory action
It makes sense to start a statin if the patient is not already on one, in order to obtain stability, or hopefully remission, of arterial atherosclerotic lesions. I am not sure about whether the anti-inflammatory effect will reduce myocardial damage because trials of anti-inflammatory medication during myocardial infarction (e.g., steroids) have not been convincing enough to establish such treatment.
Most guideline agree on the use of statins in acute coronary syndrome. This is not only because they are able to act in secondary prevention, they are also plaque stabilizer and they reduce morbidity and mortality from many studies.
Paulo
CANTOS is a major multi-national randomized clinical trial that will test whether reducing inflammation in heart attack patients can reduce the risk of having another heart attack or stroke in the future. Thanks for your question.
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