Introduction after translation Coronary heartdisease (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 deathby disease coronary) and ?280000 have a recurrent attack.
It is estimated that150,000 additional silent myocardial infarctions occur each year. (Go, et al,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). In the trial Pravastatin or Atorvastatin Evaluation and InfectionTherapy-Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22),atorvastatin 80mg reduced the levels of hs-CRP and LDL-C 38% and 35% more,respectively, than pravatatin 40mg .
(Cannon, et al, 2004).The rationale for the use of statins in prevention: an intervention trialevaluating rosuvastatin (JUPITER), randomization to rosuvastatin 20 mg dailywas associated with a 54% reduction in myocardial infarction, a 48% reductionin accident cerebrovascular, a 46% reduction for bypass surgery or angioplasty,a 43% reduction in venous thromboembolism and a 20% reduction in mortality fromall causes. (Ridker, et al, 2008), (Ridker, et al, 2009), (Glynn, et al, 2009)Early treatment with statins during hospitalization improved in-hospitalsurvival as well as the clinical outcome at 12 months in patients withcardiogenic shock (CS) with acute MI undergoing revascularization therapy.(Sim, et al, 2013). Statin treatment was associated with a reduction inin-hospital mortality. (Sim, et al, 2013).
The National Registry of MyocardialInfarction (NRMI) 4 (Fonarow, et al, 2005) and the Global Registry of AcuteCoronary Events (G) It was found that the level of CRP measured 2 days afterreperfusion is a predictor of LVR at 3 months. (Mather, et al, 2013). Asignificant correlation was observed between the CRP plasma concentrationevaluated 2 days after the intervention and the LVR parameters at 2 monthsafter STEMI. (Ørn et al, 2009).
It is known that statins reduce the levels ofinflammatory biomarkers, such as CRP and the risk of CHD, and it has beensuggested that at least part of the cardioprotective effect of these drugscould be due to their pleiotropic and anti-inflammatory effects. In Pakistan,the association of STEMI, CRP and LVR levels has never been studied before.This study will provide the usefulness of hs-CRP for the evaluation of LVR andthe role of statin therapy in left ventricular remodeling after MI.This study has been designed to evaluate the relationship of the Hs-CRP levelswith the re-modeling of the left ventricle after MI and the beneficial effectsof standard therapy with high doses of statins in the reimplantation of theleft ventricle after MI in patients with first elevation of the ST MI segment.