Introduction elevation (STEMI) have significantly higher peak CRP levels

Introduction after translation

 

Coronary 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,
2003).
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
al, 2003). In the trial Pravastatin or Atorvastatin Evaluation and Infection
Therapy-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 trial
evaluating rosuvastatin (JUPITER), randomization to rosuvastatin 20 mg daily
was associated with a 54% reduction in myocardial infarction, a 48% reduction
in accident cerebrovascular, a 46% reduction for bypass surgery or angioplasty,
a 43% reduction in venous thromboembolism and a 20% reduction in mortality from
all causes. (Ridker, et al, 2008), (Ridker, et al, 2009), (Glynn, et al, 2009)
Early treatment with statins during hospitalization improved in-hospital
survival as well as the clinical outcome at 12 months in patients with
cardiogenic shock (CS) with acute MI undergoing revascularization therapy.
(Sim, et al, 2013). Statin treatment was associated with a reduction in
in-hospital mortality. (Sim, et al, 2013). The National Registry of Myocardial
Infarction (NRMI) 4 (Fonarow, et al, 2005) and the Global Registry of Acute
Coronary Events (G) It was found that the level of CRP measured 2 days after
reperfusion is a predictor of LVR at 3 months. (Mather, et al, 2013). A
significant correlation was observed between the CRP plasma concentration
evaluated 2 days after the intervention and the LVR parameters at 2 months
after STEMI. (Ørn et al, 2009). It is known that statins reduce the levels of
inflammatory biomarkers, such as CRP and the risk of CHD, and it has been
suggested that at least part of the cardioprotective effect of these drugs
could 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 and
the role of statin therapy in left ventricular remodeling after MI.
This study has been designed to evaluate the relationship of the Hs-CRP levels
with the re-modeling of the left ventricle after MI and the beneficial effects
of standard therapy with high doses of statins in the reimplantation of the
left ventricle after MI in patients with first elevation of the ST MI segment.

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