2 years ago at age 47 (female,with no family hx, nl lipid panel, no medical problems, non smoker, nl weight) I had an MI. I went to the ER with severe chest pain/pressure/SOB. My EKG was equivocal and my initial Troponin I level was equivocal at 0.24. I was admitted and 10 hours later my Troponin I level was 4.45. I had a cath the next day and had clear vessels (no obstruction). I was discharged home 3 days later on asa, plavix, beta blocker, ace ihibitor, statin. After 2 years I continue to have chest pain associated somethimes with EKG changes (flipped t waves was the last change assoc with pain). My pain is attributed to vasospastic angina and I am on a calcium channel blocker and recently Renexa was added which has helped. My questions: How significant was my MI with that troponin level? Was there a risk of mortality with that level of troponin? Sometimes I become complacent about taking my meds because I had clear vessels. Am I lulled into a false since of securtiy because I had clear vessels and no other risk factors? I take NTG spray with chest pain and it is relieved by the NTG but sometimes I have pain and don't take the spay and will just wait for the pain to go away if it is not too severe. Is it ok to not take NTG if the pain isn't severe?
The preferred cardiac markers are troponin I or T because of their specificity
CK-MB has lower specificity than troponins T and I, but may be used
Myoglobin or CK-MB isoforms should be considered for rapid diagnosis
Total CK, aspartate transaminase (serum glutamate oxaloacetate transaminase) and LDH have low specificity and are less satisfactory
Elevation of troponin or CK-MB is defined as a value exceeding the 99th centile of a reference control group
Sampling of troponins or CK-MB should be done at presentation, at 6–9 hours, and at 12–24 hours.
Electrocardiographic criteria are not specific enough to identify non-ST elevation MI
ST elevation MI is indicated by new ST elevation in at least two contiguous leads, measuring 0.1 mV in all other leads
Established MI (in the absence of confounders) is indicated by any Q wave in leads V1–V3 or by Q waves of 30 ms in two other contiguous leads
Presumed new left bundle branch block may not be accompanied by ST segment deviation; the characteristic changes indicative of acute MI in patients with prior left bundle branch block require further definition
It takes 6 hours for myocyte necrosis to become evident on histopathology
The pathological identification of MI depends in part on the staging of the inflammatory cell infiltrate: acute neutrophils; healing mononuclear cells; healed collagen without cellular infiltration
Infarcts are classified by size: microscopic (focal necrosis); small (30% of the left ventricle)
Manifestations of MI include regional wall motion abnormalities on echocardiography, contrast angiography, radionuclide scanning or magnetic resonance imaging
These abnormalities may include evidence of “infarct zone” wall thinning, changes in tissue texture, and/or abnormalities in wall motion
ACC, American College of Cardiology; CK, creatine kinase; ESC, European Society of Cardiology; MI, myocardial infarction
Heart. 2004 January; 90(1): 99–106.
Below is a must read for anyone interested in MI diagnoses, and the difference in male/female and African American/Caucausion male normal heart enzyme levels. Men have more muscle mass than women and African American males have, on average, 21% more muscle mass than Caucasion males.
Thus if the baseline, or differences in normal heart enzymes are not considered, false positives and negatives can occur.
An additional comment- I'm 43 woman with similar profile to above poster, I had a scad and received two stents, two days later in hospital had prolonged spasm leading to MI that could only be stopped by putting stents in the artery. My cardiologist thought the beta blocker I was on could have made the spasm worse than otherwise. So I am on calcium channel blocker (norvasc) . Can beta blockers make spasms worse? I read that beta blockers reduce recurrence of MI, but calcium channel blockers do not. Both MI's caused minimal heart damage ( was treated quickly) and I still have good EF. Also can a spasm lead to a dissection? Which is my primary condition? 8 yrs ago I had these symptoms (attributed to costochondritis in ER ) which are now supposed in hindsight to have healed on their own. I wonder what causes the spams or dissections and if any other diagnostic procedures to do.I want to return to normal exercise (walk/jog/run) I am on plavix, norvasc, coumadin and aspirin.
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