Coronaryheart disease (CHD) alone caused ?1 of every 6 deaths in the United States in2009. Each year, it is estimated that ?635,000 Americans have a new coronaryattack (defined as first hospital myocardial infarction (MI) hospitalization ordeath by disease coronary) and ?280000 have a recurrent attack. It is estimatedthat 150,000 additional silent myocardial infarctions occur each year. (Go, etal, 2013). The cholesterol reduction represented 42.7% of the reduction of themortality rate in asymptomatic individuals, and for 34% in those with CHD.
(Young, et al, 2010).High sensitivity C-reactive protein (hs-CRP) increases acutely after tissueinjury, including myocardial infarction. This increase in hs-CRP levels, in part,correlates with the size of the infarct (Suleiman, et al, 2006) and with anincreased risk of cardiac rupture.
(Mueller, et al, 2002). In short-termstudies of patients with acute coronary syndromes (ACS), it has been shown thathigh levels of CRP are predictive of death, but not of recurrent AMI. (Ridker,2003).Patients with CRP concentrations> 5 mg / L at the time of hospital admissionhad an increase of 50% to 330% in the risk of death from any cause. Thisincrease in risk was present in the short and long term follow-ups, andincreased in magnitude as CRP concentrations increased to> 10 mg / l.(Marsik, et al, 2008).Patients with myocardial infarction with ST segment elevation (STEMI) havesignificantly higher peak CRP levels compared to patients with myocardialinfarction with ST-segment elevation (NSTEMI).
(Habib, et al, 2011). Themaximum level of CRP was 67 (36-112) mg / L in the STEMI group, 29 (20-87) mg /L in the NSTEMI group and 18 (12-36) mg / L in the unstable angina group.(Sánchez, et al, 2006)Left ventricular remodeling (LVR) postinfarction leads to a progressiveincrease in left ventricular systolic and diastolic volumes, distortion of theventricular shape and mural hypertrophy, in the weeks and months after STEMI.(Pfeffer, et al, 1990). It has been identified as an important marker of poorprognosis, related to excessive cardiovascular mortality and the risk of heartfailure.
(Cohn, et al, 2000). The main determinants of LVR after STEMI includethe size of the infarction, the anterior location of the infarction and thelate or failed reperfusion therapy at both the epicardial and microvascularlevels, the transmurality of the infarction and the degree of stunning of themyocardium (Pfeffer, et al, 1990)A relation was found between the level of CRP in the hospital and LVR in thelong-term follow-up in 226 patients with a first anterior myocardialinfarction, however, the CRP concentration was not associated independentlywith the LVR. (Fertin, et al, 2010)Although lifestyle measures and some pharmacological agents reduce CRP levels,statins are used more frequently, and lower CRP levels are around 15-35%.(Nambi, et al, 2005). Rosuvastatin and atorvastatin in higher doses have themost important properties of reducing CRP. (Nambi, et al, 2005).Several studies have evaluated the ability of statins to reduce hs-CRP inindividuals with ACS.
In the study of reduction of myocardial ischemia withaggressive cholesterol reduction (MIRACL), atorvastatin (80 mg) significantlyreduced CRP by 83%, compared with 74% with placebo, at 16 weeks. (Kinlay, etal, 2003).