¹Junior Resident, ²Professor, Department of Medicine, Patna Medical College and Hospital, Bihar, INDIA.

Email: dranand21@gmail.com

DISCUSSION

This study reports that higher levels of hsCRP and Trop-I at admission in AMI patients predicts heart failure. Inflammatory markers are important indicators for discrimination of different clinical forms of AMI. 

The incidence of AMI patients was found to be highest in the age group of 51-60 yrs i.e 66.7%, We have found mean and SD value of age was 55.650±6.84. Age and sex distribution of AMI patients is mentioned in Table 2. We divided total patients in 5 age groups i.e. 20-30, 31-40, 41-50, 51-60 and 61-70. Majority of patients i.e. 66.6% patients belonged to 51-60 years in age group, among them 30(50%) were male and 10(16.7%) patient was female.

Study of Gurunani RH et al. conducted¹², 100 patients, 68 were male and 32 were female as shown in. The age range of this study was 30-100 years. We divided these 100 patients in 7 age groups of 10 years range. The data obtained for individual patients were arranged according to the age group of patient. In our study, proportion of patients with Chest paint (90%) was significantly higher among others clinical findings. We have found another clinical finding is Sweating, Shortness of breath, palpitation, vomiting and syncope i.e 70%, 63%,35%,28% and 15% respectively.  In our study, among the patients with AMI, past history of DM (80.0%), Past history of hypertension present was (66.7 %), F/H of Ischemic Heart Disease (50%), Chronic smoker were (55%) and Alcohol abuse were (36.7%) found respectively. Clinical assessment sciences institute in Canada carried out a study on 4403 patients in Ontario Canada. They all had heart attack records which showed that mean of their age (67.3 years) and 33.7% were women. Statistics showed that numbers of married men who have been taken to hospital after heart attack faster were more than single ones, but in contrast there has been no relationship between marital statuses of women with arrival speed to hospital after experiencing chest pain related to heart attack which indicates that women take care of their husbands better (Chow et al.., 2007)¹³; “Iranian Students’ News Agency - ISNA,” 1998-2013). 48.4% of participants were illiterate in the present study. Results of a study showed that the majority of patients 79.1% did not have any information about the initial symptoms of MI (Akbari et al.., 2009)¹⁴. Illiteracy lead to ignorance and uneducated people certainly have lower level of health behaviors and preventive behaviors. Providing information by mass media and correct planning by health centers is needed for secondary prevention. It is recommended to provide necessary information for public education and also training and counseling for older patients with higher risk of heart disease. We have found in ECG-equal number of ST segment elevation and Q wave myocardial infarction and Non ST segment elevation and Non Q wave myocardial infarction was found 58.3% and 47.1% in AMI patients respectively.  The ECG is an important initial diagnostic tool in the evaluation and management of patients presenting with chest pain. ECG findings form the basis on which acute coronary syndromes are classified into STEMI, NSTEMI, or unstable angina, a classification which provides information regarding the extent of myocardium at risk and guides initial therapy. ST-segment elevation is a sign of transmural ischemia and identifies patients who are likely to benefit from urgent revascularization. The relation between ST-segment elevation on the ECG and the occluded coronary artery has been established in multiple clinical studies in patients with ACS¹⁵. LAD coronary artery obstruction most often results in ST-segment elevation in the precordial leads V1-V4 (anterior, anteroseptal patterns)¹⁶. In rare instances, ST-segment elevation in leads V1-V4 signifies RCA occlusion with concomitant right ventricular infarction¹⁵. Isolated ST elevation in leads V4–V6, without ST elevation in leads V1–V3, is usually due to an occlusion of the LCX or distal diagonal branch rather than the main LAD artery^[15]. ST-segment elevation in leads II, III, and aVF is associated with infarction of the inferior wall^[15,16]. The culprit vessel in inferior MI may be either the RCA (in the majority of cases) or the LCX artery^[16]. Consistent with prior studies, we found that all of our patients with anterior STEMI had LAD obstructive CAD, while among patients with inferior STEMI almost 80% had an occluded RCA and all but 1 of the remainder had an occluded LCX artery. we have found the Mean and SD value of T. Cholesterol is 242.833±38.91, Triglyceride is 228.716±46.29, HDL is 25.633±±2.10, LDL is 171.456 ±37.33, VLDL is 45.743±9.25 and random blood glucose is 129.983±19.31 respectively . Gorecki et al.¹⁷ observed higher levels of TC and LDL in patients with complicated versus those with uncomplicated clinical course of infarction, suggesting higher levels of these biomarkers during the first 24 hours of AMI have a strong negative prognostic value. Akosah et al.¹⁸ reported acceptable or optimal LDL levels in a series of 183 young adults experiencing AMI. High serum levels of HDL are associated with reduced risk for the development of atherosclerotic disease. HDL particles are believed to be antiatherogenic, secondary to their capacity to drive reverse cholesterol transport and antagonize pathways of inflammation, thrombosis, and oxidation. The majority of patients in both the primary and secondary prevention settings continue to experience significant residual risk for acute cardiovascular events, even when their LDL cholesterol is lowered aggressively via a combination of lifestyle modification and pharmacologic intervention.¹⁹ Al Aqeel et al.^[20] have observed that HDL appears to be the main lipid risk factor in patients presenting with AMI in Kuwaiti patients, suggesting that primary prevention strategies should focus on treatment modalities that increase HDL. Many conditions specific to the heart in diabetes affect global myocardial remodeling. Previous silent infarction may be present in as many as 40% of these patients at the time they present with their first clinically recognized MI. Cardiac autonomic neuropathy may be present in nearly 50% of the diabetic population with coronary artery disease²¹  Echocardiography is an accurate noninvasive test that enables detection of evidence of myocardial dysfunction caused by ischemia or necrosis ^[22]. Evaluation of wall motion while a patient is experiencing chest pain can be useful when the ECG is nondiagnostic^[129]. Evaluation of wall motion may also be useful if there is ECG or laboratory evidence of MI even in the absence of chest pain^[23]. Severe ischemia produces regional wall motion abnormalities (RWMAs) that can be visualized echocardiographically within seconds of coronary artery occlusion (12±5 and 19±8 seconds in two series of patients evaluated during transient coronary occlusions induced by angioplasty)²³. These changes occur prior to the onset of ECG changes or the development of symptoms²³. The RWMAs reflect a localized decrease in the amplitude and rate of myocardial excursion, as well as a blunted degree of myocardial thickening and local remodeling. Pearson correlation analysis of Trop-I with Echocardiographic parameters in all MI patients have found, positive correlation with hsCRP, LVIDd, LVIDs, LVPWD, and LA, Negative correlation with EF. And we have found significant correlation between LVIDs , EF and hsCRP. When correlation with hsCRP and Echocardiographic parameters , we have found positive correlation with, LVIDd, LVIDs, LVPWD, and LA, accept EF(Negative correlation). hsCRP have positive significant correlation with IVS and Trop-I. The study by Kavsak et al.²⁴ indicated that high CRP titers, independent of the subjects’ age, gender, and cTnI concentrations, predict long-term heart failure and mortality. Not only did CRP≥15 mg/L identify patients with heart failure at entry, it also predicted worsening of left ventricular function in patients presenting without clinical signs of heart failure at entry. Furthermore, in agreement with their results, CRP levels were a significant predictor of heart failure in our study in patients who did not have had any signs of heart failure at their first myocardial infarction. Although the exact role of CRP requires further exploration, our study focusing on hsCRP measurements within the first 3 days after AMI may prove useful for identification and prediction in patients who are at greater risk of heart failure and mortality. Scirica et al. have reported that both hsCRP and BNP measured 30 days after ACS are independently associated with the risk of heart failure and cardiovascular mortality, with the greatest risk occurring when both markers are simultaneously high.³⁰ CRP has been a marker of interest as a predictor of heart failure and pharmacological treatment benefits. ROC curve analysis to determine the cutoff points and Trop-I and hsCRP levels on admission with myocardial infarction for heart failure prediction. Compared with hsCRP measurement, troponin-I assays are substantially more sensitive in the detection of myocardial injury. The release kinetics of troponins T and I are similar; both are detectable in the serum within 4 to 12 h after the onset of myocardial necrosis and depending on the duration of ischemia and reperfusion status, peak values occur 12 to 48 h from symptom onset. Therefore, serial sampling, including a baseline sample and follow-up testing at 8 to 12 h after symptom onset, is recommended. allowing for diagnostic confirmation even when patients delay presentation after symptom onset. Because of their long serum half-lives, however, neither troponin I nor troponin T assays are ideal for detection of re-infarction after an index event.

CONCLUSION

hsCRP levels on admission to hospital after first myocardial infarction are associated with an increased risk of heart failure. Our study shows that inflammatory processes plays an independent role in the development of heart failure after myocardial infarction. hsCRP and Trop I are a useful markers for predicting the time course of heart failure in patients with AMI. Thus, hsCRP measurements may assist in risk stratification after myocardial infarction. Measurement of hsCRP levels in patients earlier in AMI could help clinicians to discriminate those patients who are at increased risk of heart failure in the future. Measurement of cardiac troponins is rapidly assuming the position of gold standard for the biochemical diagnosis of myocardial necrosis. At the end of the study we can conclude that both biomarkers are very important diagnostic tool of acute in myocardial infarction detection, but we have found hsCRP is more sensitive then TROP-I and the specification is more in Trop-I compeared to hsCRP.

REFERENCES

• Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation. 2002;105:1135–43.
• Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 2005;352:1685–95.
• Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO, 3rd, Criqui M, et al.. Markers of inflammation and cardiovascular disease: Application to clinical and public health practice: A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation. 2003;107:499–511.
• Keller T, Zeller T, Peetz D, et al.. Sensitive troponin I assay in early diagnosis of acute myocardial infarction. N Engl J Med. 2009;361(9):868–877
• Omland T, de Lemos JA, Sabatine MS, et al.. A sensitive cardiac troponin T assay in stable coronary artery disease. N Engl J Med. 2009;361(26):2538–2547.
• Moran AE, Forouzanfar MH, Roth GA, Mensah GA, Ezzati M, Flaxman A, Murray CJ, Naghavi M (April 2014). "The global burden of ischemic heart disease in 1990 and 2010: the Global Burden of Disease 2010 study". Circulation. 129 (14): 1493– 501.
• Devlin RJ, Henry JA (2008). "Clinical review: Major consequences of illicit drug consumption". Critical Care. 12(1): 202.
• "How Is a Heart Attack Diagnosed?". www.nhlbi.nih.gov. December 17, 2013. A rchived from the original on 24 February 2015. Retrieved 24 February 2015.
• Casas JP, Shah T, Hingorani AD, Danesh J, Pepys MB (2008) C-reactive protein and coronary heart disease: a critical review. J Intern Med 264: 295-314.
• Ohman EM, Armstrong PW, Christenson RH, et al.. Cardiac troponin T levels for risk stratification in acute myocardial ischemia. GUSTO IIA Investigators. N Engl J Med. 1996;335(18):1333–1341.
• Morrow DA, Cannon CP, Jesse RL, et al.. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: clinical characteristics and utilization of biochemical markers in acute coronary syndromes. Clin Chem. 2007;53(4):552–574.
• Gurunani RH, Shrivastav A, Maru AM, Choksi TS, Agnihotri AS. Correlation of high sensitive C-reactive protein with cardiac markers in the diagnosis of acute coronary artery disease: A study of 100 cases. Med J DY Patil Univ 2015;8:614-8.
• Chow C, Pell A, Walker A, O'Dowd C, Dominiczak A, Pell J. Families of patients with premature coronary heart disease: an obvious but neglected target for primary prevention. BMJ. 2007;335(7618):481–485.
• Akbari M, Mohammadzadeh M, Rajabpoor M, AzimPoor A. Agents connection with awareness and act of patients that caused acute myocardial infarction encountering with clinical symptoms them to stay in urmia hospitals. Journal of Urmia Nursing And Midwifery Faculty. 2009;7(2):73–80. 
• Birnbaum Y, Drew BJ. The electrocardiogram in ST elevation acute myocardial infarction: correlation with coronary anatomy and prognosis. Postgrad Med J 2003;79:490-504. 10.1136/pmj.79.935.490.
• Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in acute myocardial infarction. N Engl J Med 2003;348:933-40. 10.1056/NEJMra022700.
• Gorecki A, Bednarz B, Jaxa-Chamiec T, et al.. Lipid profile during the first 24 hours after myocardial infarction has significant prognostic value. Kardiol Pol. 2004;60:229–36.
• Akosah KO, Cerniglia RM, Havlik P, Schaper A. Myocardial infarction in young adults with low-density lipoprotein cholesterol levels ≤ 100 mg/dL: clinical profile and 1-year outcomes. Chest. 2001;120:1953–8.
• Davidson MH, Toth PP. High-density lipoprotein metabolism: potential therapeutic targets. Am J Cardiol. 2007;100:n32–40. 
• Al Aqeel A, Mojiminiyi OA, Al Dashti R, Al Ozairi ES. Differences in physician compliance with guideline on lipid profile determination within 24 h after acute myocardial infarction. Med Princ Pract. 2005;14:41–5. 
• Toyry J, Niskanen L, Mantysaari M, Lansimies E, Uusitupa M. Occurrence, predictors, and clinical significance of autonomic neuropathy in NIDDM. Diabetes.1996; 45:308–315.
• 22 Cheitlin MD, Armstrong WF, Aurigemma GP, et al.. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation 2003; 108:1146.
• American College of Cardiology Foundation Appropriate Use Criteria Task Force, American Society of Echocardiography, American Heart Association, et al.. Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance Endorsed by the American College of Chest Physicians. J Am Coll Cardiol 2011; 57:1126.
• Kavsak PA, MacRae AR, Newman AM, et al.. Elevated C-reactive protein in acute coronary syndrome presentation is an independent predictor of long-term mortality and heart failure. Clin Biochem. 2007;40(5–6):326–329. doi:10.1016/j.clinbiochem.2006.10.025
• Liu D, Qi X, Li Q, et al.. Increased complements and high-sensitivity C-reactive protein predict heart failure in acutemyocardial infarction. Biomed Rep. 2016;5(6):761–765. doi:10.3892/br.2016.793.

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