Editor's Note: Newer generations of troponin assays have increased sensitivity, allowing detection of small amounts of myocardial damage. Not infrequently, this increased sensitivity has led to diagnostic confusion, as at times it can be difficult to determine if the troponin increase is related to acute coronary syndrome, or a variety of other processes that can lead to acute/chronic myocardial damage.
The Cardiac Biomarkers editors asked experts in the field to comment on a case scenario that is not an infrequent occurrence for what their opinion was for the most appropriate diagnosis.
Case Presentation
HPI: The patient is a 57-year-old male with a history of dyspnea on exertion that began two days prior to the admission. The episodes last 10-15 minutes and have been relieved with rest. On the day of admission, the patient complained of severe dyspnea at rest with associated diaphoresis and nausea. The symptoms began approximately two hours prior to the emergency department visit and are still present during the evaluation.
PMHx HTN treated with and ACEI, diuretic and amlodipine, for which he has been non-compliant for the past two weeks.
No prior coronary history or prior cardiac evaluation.
PE: BP 260/140 mm Hg. P 110 bpm.
Cardiac: tachycardic, + S4.
Lungs: rales ¼ up bilaterally.
No edema.
Electrocardiogram (ECG): Sinus tachycardia with left ventricular hypertrophy (LVH) and 2 mm ST depression in V5 and V6 consistent with repolarization abnormalities or ischemia; no old ECG available for comparison.
Repeat ECG the next day at a heart rate of 80 bpm shows 1mm ST (or could have no change still with 2 mm ST depression) depression in V5 and V6.
Coronary angiography is performed and shows non-obstructive coronary disease (mid LAD-50%, proximal Cx 60%, and RCA diffuse 30%).
Echocardiogram shows EF -70%, moderate left ventricular hypertrophy (LVH), and no focal wall motion abnormalities.
Is this an acute myocardial infarction (AMI) as defined by the universal definition of AMI 2012?
Show Answer
The correct answer is: Yes
Joseph S. Alpert, MD, FACC: This is definitely an MI according to the American College of Cardiology/American Heart Association/European Society of Cardiology/World Heart Federation global definition of MI with three reports since its inception in 2000. Subsequent revisions were published in 2007 and 2012. The patient had appropriate symptoms as well as ECG changes, although the ECG changes could have been the result of LVH with ST-T changes and troponin elevation, which was modest in magnitude. The question is: Which type of MI is this – type 1 or type 2? On presentation, it could have been a combination of type 1 (plaque rupture or erosion and thrombosis) and/or type 2 (marked increase in myocardial oxygen demand secondary to severe and uncontrolled HTN with no coronary thrombosis). The catheterization demonstrated only modest coronary artery disease (CAD), so, in the end, I would have signed this out as a type 2 MI. The treatment would be to restart the evidence-based medication the patient was on and try to get the patient to adhere to this medical program. A statin should be added to his medical program.
Fred S. Apple, PhD: The increase and decrease of cardiac troponin I (cTnI) over the 24-hour sampling period is most likely real and not based on analytical noise of the assay's imprecision. The rapid clearance suggests a small myocardial injury with a short release of cTnI from the myocardium. Combined with the patients' poor clinical history for acute coronary syndrome (ACS), I would have to conclude that the increased and rise and fall of cTnI values were non-ACS in origin, but cannot rule out a type 2, supply demand, MI.
Allan S. Jaffe, MD, FACC: Although the case itself leaves some degree of ambiguity, it was probably configured to introduce the concept of a type 2 MI. That is one in which abnormalities in supply-demand balance with or without CAD lead to myocardial injury as documented by a rising and/or falling pattern of cTnI values as described in the case report. The presumption I suspect the authors want you to make is that the hypertension is the trigger and if so, this would be a type 2 AMI. However, the hypertension could be the result of acute ischemia. Given the angiogram was done 24 hours after presentation, one cannot be totally sure that a thrombus or some other process might have been acutely present and the hypertension was secondary. If so, this might have been a spontaneous type 1 AMI. Finally, if there were suspicion that some other cause such as pulmonary embolism had set off this cascade of events, the cTnI elevations might have been due to that with or without a component from the severe hypertensive response. The rapid increases and reductions in cTnI are commonly seen in patients with pulmonary emboli. Best diagnosis given the data as given is type 2 AMI, but the case exemplifies the need to think through these situations carefully.
Bertil Lindahl, MD, PhD: This is an AMI, type 2 according to the third universal definition of MI. The patient shows acute symptoms and signs consistent with ischemia, although the patient does not have chest pain. The patient shows clear cTnI elevation with rise and fall. Also, the high blood pressure and signs of LVH and no clear-cut cul-prit lesion at the coronary angiogram point at an imbalance between myocardial oxygen sypply and/or demand, hence a type 2 AMI.
L. Kristin Newby, MD, FACC: Yes, this is an MI. The patient had symptoms characteristic of ischemia, including a two-day history of new exertional symptoms and prolonged symptoms at rest on the day of presentation. Although the ECG had confounding LVH by description, there was a characteristic rise and fall in cardiac troponin above the 99th percentile reference limit. Although there was no obstructive disease at cath and normal EF and no focal WMA, these findings in and of themselves do not rule out a plaque rupture (Type 1) event (which could have exacerbated underlying hypertension). However, one might also consider a type 2 MI given the hypertensive emergency at presentation in the setting of medication noncompliance. I would treat as an MI with initiation of aspirin plus P2Y12 for a year, resumption of ACEi, addition of beta-blocker, and referral to cardiac rehab. Counsel re: medication compliance and ensure no barriers.
References
Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol 2012;60:1581-98.
Sandoval Y, Smith SW, Apple FS. Supply/demand type 2 myocardial infarction: should we be paying more attention? J Am Coll Cardiol 2014: 63:2079-87.
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