heart disease (CHD) alone caused ?1 of every 6 deaths in the United States in
2009. Each year, it is estimated that ?635,000 Americans have a new coronary
attack (defined as first hospital myocardial infarction (MI) hospitalization or
death by disease coronary) and ?280000 have a recurrent attack. It is estimated
that 150,000 additional silent myocardial infarctions occur each year. (Go, et
al, 2013). The cholesterol reduction represented 42.7% of the reduction of the
mortality 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 tissue
injury, including myocardial infarction. This increase in hs-CRP levels, in part,
correlates with the size of the infarct (Suleiman, et al, 2006) and with an
increased risk of cardiac rupture. (Mueller, et al, 2002). In short-term
studies of patients with acute coronary syndromes (ACS), it has been shown that
high levels of CRP are predictive of death, but not of recurrent AMI. (Ridker,
Patients with CRP concentrations> 5 mg / L at the time of hospital admission
had an increase of 50% to 330% in the risk of death from any cause. This
increase in risk was present in the short and long term follow-ups, and
increased in magnitude as CRP concentrations increased to> 10 mg / l.
(Marsik, et al, 2008).
Patients with myocardial infarction with ST segment elevation (STEMI) have
significantly higher peak CRP levels compared to patients with myocardial
infarction with ST-segment elevation (NSTEMI). (Habib, et al, 2011). The
maximum 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 progressive
increase in left ventricular systolic and diastolic volumes, distortion of the
ventricular shape and mural hypertrophy, in the weeks and months after STEMI.
(Pfeffer, et al, 1990). It has been identified as an important marker of poor
prognosis, related to excessive cardiovascular mortality and the risk of heart
failure. (Cohn, et al, 2000). The main determinants of LVR after STEMI include
the size of the infarction, the anterior location of the infarction and the
late or failed reperfusion therapy at both the epicardial and microvascular
levels, the transmurality of the infarction and the degree of stunning of the
myocardium (Pfeffer, et al, 1990)
A relation was found between the level of CRP in the hospital and LVR in the
long-term follow-up in 226 patients with a first anterior myocardial
infarction, however, the CRP concentration was not associated independently
with 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 the
most important properties of reducing CRP. (Nambi, et al, 2005).
Several studies have evaluated the ability of statins to reduce hs-CRP in
individuals with ACS. In the study of reduction of myocardial ischemia with
aggressive cholesterol reduction (MIRACL), atorvastatin (80 mg) significantly
reduced CRP by 83%, compared with 74% with placebo, at 16 weeks. (Kinlay, et