By Michael H. Crawford, MD, Editor
SYNOPSIS: An observational study of hospitalized patients with type 1 or 2 myocardial infarction (MI) or myocardial injury showed that mortality is higher in type 2 MI or myocardial injury patients compared to type 1 MI patients.
SOURCE: Chapman AR, Shah ASV, Lee KK, et al. Long-term outcomes in patients with type 2 myocardial infarction and myocardial injury. Circulation 2018;137:1236-1245.
The third universal definition of myocardial infarction (MI) established three categories of myocardial injury in patients with elevated troponin levels: type 1 MI due to plaque rupture with atherothrombosis; type 2 MI due to myocardial oxygen supply-demand imbalance in the absence of atherothrombosis; and myocardial injury without other clinical signs of myocardial ischemia besides an elevated troponin. Clinically, the distinction between the latter two often is difficult because of uncertainty about the existence of atherosclerosis, which would carry therapeutic implications.
Investigators from a tertiary cardiac center in Scotland studied patients with type 1 or 2 MI or myocardial injury to improve risk stratification in these patients. Patients with type 3, 4, or 5 MI were excluded. The final study population included 2,122 patients: 55% were classified as type 1, 20% type 2, and 25% myocardial injury. All-cause mortality at five years was higher in those with type 2 MI (63%) or myocardial injury (72%) vs. those with type 1 MI (37%). Most deaths in type 2 and injury patients were due to non-cardiac causes (hazard ratio [HR], 2.3; 95% confidence interval [CI], 1.92-2.81 vs. type 1 MI). However, major adverse cardiovascular event (MACE) rates were similar in types 1, 2, and injury (33% vs. 30% vs. 31%, respectively). Notably, the presence of coronary artery disease (CAD) in type 2 or injury patients was an independent predictor of MACE (HR, 1.7; 95% CI, 1.3-2.2). At discharge, patients with type 2 MI or injury and known CAD compared to type 1 MI were less likely to received aspirin (66% vs. 91%, respectively), a statin (69% vs. 86%), or an angiotensin-converting enzyme or receptor blocker (53% vs. 71%; P < 0.001 for all). The authors concluded that in patients with type 2 MI or myocardial injury, identifying underlying CAD may inform decisions about risk reduction in these patients, which could improve their long-term outcomes.
Clinically, type 2 MI or injury patients are hospitalized for non-cardiac reasons and develop an adverse event that occasions obtaining a troponin level. Rarely are these diagnoses made in outpatients or patients presenting to the ED. Thus, it is not surprising that these patients demonstrate a high mortality rate, largely due to their non-cardiac diseases. It is well-known that an elevated troponin level is a bad prognostic sign, regardless of what is wrong with the patient. What is important about this study is that the rate of MACE was similar in all three classes of troponin elevation at about one-third over five years and that the major independent predictor of future MACE in type 2 and injury patients is the presence of CAD.
How do we identify those with CAD, and what do we do about it? Sometimes, the answer is straightforward if, for example, the patient has a history of CAD, or exhibits evidence of previous MI on ECG or echocardiography. However, the answer often is not straightforward, especially in the myocardial injury group, where there are no symptoms or sign of ischemia. Chapman et al suggested an approach based on the likelihood of CAD. If the likelihood is high, the authors suggested treating with aspirin and statins, as most of these patients would carry a > 7.5% risk of MACE over 10 years and would be candidates for these therapies anyway. If the risk is moderate, Chapman et al recommended coronary angiography by CT or invasive means. The authors did not discuss the low-risk patient.
Many U.S. cardiologists would take a different approach based on our current guidelines. In high-likelihood, high-risk patients, an invasive angiogram would make sense if appropriate for the patient’s condition. The intermediate-risk patient would either undergo CT angiography or a stress test, depending on other clinical factors. The low-likelihood, low-risk patient would undergo a stress test. Of course, none of these tests would happen until the patient had recovered from whatever brought him or her to the hospital.
The strengths of this study were the five-year follow-up and the identification of the cause of death. There also were several weaknesses, including the fact that the distinction between type 2 MI and injury was made by two cardiologists reviewing the records of the primary admission based on their clinical judgment alone. The patients were selected using a certain troponin assay, which may not apply to others with higher or lower sensitivities. Very few patients underwent angiography; thus, the incidence of CAD may have been underestimated. Also, there were few follow-up details beyond the cause of death.
Despite these limitations, this is the strongest study of this issue published to date and reinforces the concept that underlying CAD is common in type 2 MI and myocardial injury patients. Reasonable attempts to discover it or treat it should be taken.