1. What data in particular will be shared?
   Response - All of the individual participant data collected during the trial, after de-identification.
   


2. What additional supporting information will be shared?
   Response - Clinical Study Report
   
   
3. Who will be able to view these files?
   Response - Researchers who provide a methodologically sound proposal.
   


4. For what types of analyses will this data be available?
   Response - To achieve aims in the approved proposal.
   


5. By what mechanism will data be made available?
   Response - Proposals should be directed to [masterthulasi05@gmail.com].
   


6. For how long will this data be available start date provided 27-09-2024 and end date provided 27-01-2030?
   Response - Beginning 3 months and ending 5 years following article publication.
   


7. Any URL or additional information regarding plan/policy for sharing IPD? 
   Additional Information - NIL

Acute Myocardial Infarction is overwhelmingly the most important form of IHD which  

continues to be the leading cause of death in the industrialized and developing countries like  

India, despite spectacular progress in their prevention, detection and treatment over the last  

three decades. AMI has rapidly emerged as the major contributor towards the increasing  

morbidity and mortality. 

1 

A large number of asymptomatic individuals are at serious risk of developing MI because of  

their genetic predisposition, smoking behavior and sedentary lifestyle. About one third of  

patients with evolving myocardial infarction die before they reach the hospital to receive any  

effective treatment. Thus, myocardial infarction remains an important health problem and  

merits continued attention from basic and clinical researchers, epidemiologists and practicing  

physicians.  

A growing body of evidence supports the concept that local and systemic inflammation play a  

role in the initiation and progression of atherosclerosis and its complications. Inherent to the  

inflammatory process is the occurrence of an acute phase response.2,3 This response is induced  

by pro-inflammatory cytokines (Interleukin 1 and 6) which are released from the inflamed  

tissue by inflammatory and / or parenchymal cells. These in turn stimulate the liver to  

synthesize a number of acute phase proteins. CRP is a hepatically derived classical acute  

phase reactant, the serum level of which has long been known to increase after myocardial  

infarction.  

CRP levels partially reflect the extent of myocardial necrosis and can be used to predict in  

hospital and long terms, outcome in patients with AMI. Elevated plasma CRP levels in  

patients with acute coronary syndromes on admission and its persistence after discharge may  

indicate a state of persistent inflammation with poor short term and long term prognosis.  

Recent studies have shown CRP to be a risk predictor for future myocardial infarction, stroke  

and coronary heart disease in apparently healthy persons.

Due to the irreversibility of most acute cardiac events there is always an interest in searching  

for simple tests to single out patients with bad prognosis, so that timely revascularization is  

planned or they are put on intensive conservative regimens.6 

This study is designed to evaluate the serum concentration of CRP in AMI and its association  

with subsequent consequences in hospital morbidity and mortality.