Interpreting Elevated Troponins and Types of Myocardial Infarction

Elevations of cardiac biomarkers in the blood reflect injury leading to necrosis of myocardial cells but biomarkers do not indicate the underlying mechanism of this injury. Myocardial injury can be due to ischemic and non-ischemic causes. Therefore, small amounts of myocardial injury with necrosis may be detected, which are associated with CCF, renal failure, myocarditis, arrhythmias, pulmonary embolism and percutaneous or surgical coronary procedures. Troponin elevation in these contexts should not be called as Myocardial Infarction but Myocardial Injury.

Onset of myocardial ischaemia is the initial step resulting from an imbalance between oxygen supply and demand. This can be identified from history and ECG. Possible ischaemic symptoms include various combinations of chest, upper extremity, mandibular or epigastric discomfort or an ischaemic equivalent such as dyspnoea or fatigue (in women). Pain associated with vomiting, worse on exertion, sweating is definitely worrisome. The discomfort with acute MI usually lasts 20 min. In an ideal world, the sequence should be history, physical exam, ECG and troponins. Whenever symptoms recur, it is important to repeat the ECG. If you are ordering trop troponins, you must order serial ECGs as well. remember, ECG is more of a rule in test not a rule out test for ACS.

MI is classified into various types, based on pathological, clinical and prognostic differences, along with different treatment strategies 

References:

1. Roe MT, Harrington RA, Prosper DM, Pieper KS, Bhatt DL, Lincoff AM, Simoons ML, Akkerhuis M, Ohman EM, Kitt MM, Vahanian A, Ruzyllo W, Karsch K, Califf RM, Topol EJ. Clinical and therapeutic profile of patients pre- senting with acute coronary syndromes who do not have significant coronary artery disease. The Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial Investigators. Circulation. 2000;102:1101 – 1106.
2. Bugiardini R, Manfrini O, De Ferrari GM. Unanswered questions for manage- ment of acute coronary syndrome: risk stratification of patients with minimal disease or normal findings on coronary angiography. Arch Intern Med 2006; 166:1391 – 1395.
3. Reynolds HR, Srichai MB, Iqbal SN, Slater JN, Mancini GB, Feit F, Pena-Sing I, Axel L, Attubato MJ, Yatskar L, Kalhorn RT, Wood DA, Lobach IV, Hochman JS. Mechanisms of myocardial infarction in women without angiogra- phically obstructive coronary artery disease. Circulation 2011;124:1414 – 1425. 
4. Bertrand ME, LaBlanche JM, Tilmant PY, Thieuleux FA, Delforge MR, Carre AG, Asseman P, Berzin B, Libersa C, Laurent JM. Frequency of provoked coronary arterial spasm in 1089 consecutive patients undergoing coronary arteriography. Circulation 1982;65:1299 – 1306.
5. Suwaidi JA, Hamasaki S, Higano ST, Nishimura RA, Holmes DR Jr, Lerman A. Long-term follow-up of patients with mild coronary artery disease and endothe- lial dysfunction. Circulation 2000;101:948 – 954.
6. Bugiardini R, Manfrini O, Pizzi C, Fontana F, Morgagni G. Endothelial function predicts future development of coronary artery disease: a study on women with chest pain and normal angiograms. Circulation 2004;109:2518 – 2523. 
7. Kristian Thygesen, Joseph S. Alpert, Allan S. Jaffe, Maarten L. Simoons, Bernard R. Chaitman and Harvey D. White: the Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction 

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     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic