Incidence, Trends, and Outcomes of Type 2 Myocardial Infarction in a Community Cohort

Abstract

Background: Type 2 myocardial infarction (T2MI) occurs because of an acute imbalance in myocardial oxygen supply and demand in the absence of atherothrombosis. Despite being frequently encountered in clinical practice, the population-based incidence and trends remain unknown, and the long-term outcomes are incompletely characterized.

Methods: We prospectively recruited residents of Olmsted County, Minnesota, who experienced an event associated with a cardiac troponin T >99th percentile of a normal reference population (≥0.01 ng/mL) between January 1, 2003, and December 31, 2012. Events were retrospectively classified into type 1 myocardial infarction (T1MI, atherothombotic event), T2MI, or myocardial injury (troponin rise not meeting criteria for myocardial infarction [MI]) using the universal definition. Outcomes were long-term all-cause and cardiovascular mortality and recurrent MI. T2MI was further subclassified by the inciting event for supply/demand mismatch.

Results: A total of 5460 patients had at least one cardiac troponin T ≥0.01 ng/mL; 1365 of these patients were classified as index T1MI (age, 68.5±14.8 years; 63% male) and 1054 were classified as T2MI (age, 73.7±15.8 years; 46% male). The annual incidence of T1MI decreased markedly from 202 to 84 per 100 000 persons between 2003 and 2012 (P<0.001), whereas the incidence of T2MI declined from 130 to 78 per 100 000 persons (P=0.02). In comparison with patients with T1MI, patients with T2MI had higher long-term all-cause mortality after adjustment for age and sex, driven by early and noncardiovascular death. Rates of cardiovascular death were similar after either type of MI (hazard ratio, 0.8 [95% CI, 0.7-1.0], P=0.11). Subclassification of T2MI by cause demonstrated a more favorable prognosis when the principal provoking mechanism was arrhythmia, in comparison with postoperative status, hypotension, anemia, and hypoxia. After index T2MI, the most common MI during follow-up was a recurrent T2MI, whereas the occurrence of a new T1MI was relatively rare (estimated rates at 5 years, 9.7% and 1.7%).

Conclusions: There has been an evolution in the type of MI occurring in the community over a decade, with the incidence of T2MI now being similar to T1MI. Mortality after T2MI is higher and driven by early and noncardiovascular death. The provoking mechanism of supply/demand mismatch affects long-term survival. These findings underscore the healthcare burden of T2MI and provide benchmarks for clinical trial design.

Keywords: biological oxygen demand analysis; epidemiology; incidence; mortality; myocardial infarction; myocardial infarction, classification; myocardial ischemia; prognosis; trends.

Figure 1.

Study outline and event classification. URL – upper reference limit. UDMI – Universal Definition of MI.

Figure 2.. Temporal trends in T1MI and T2MI.

The annual incidence of T1MI decreased markedly between 2003 and 2012, with a more modest decline in T2MI such that the incidence of T2MI is similar to that of T1MI in contemporary years.

Figure 3.. A and B. Mortality after T2MI and T1MI.

Adjusted rates of long-term all-cause adjusted mortality were markedly higher following T2MI compared to T1MI whereas rates of cardiovascular mortality were similar after either MI type. Mortality risk was highest early after the index event. C and D. Recurrent MI after T2MI and T1MI. Following index T2MI, the most common recurrent MI was another T2MI event, with notably low rates of T1MI occurring during long-term follow-up. The reverse pattern was seen following index T1MI

Figure 4.. Troponin and mortality risk.

Peak cTNT was a strong predictor of one year all-cause (A), cardiovascular (B) and non cardiovascular (C) death in the T2MI population. CI – confidence interval

Figure 5:. A: Subclassification of T2MI and all-cause mortality.

Risk of long-term mortality was associated with the principal inciting cause of T2MI. Arrhythmic and post-operative precipitants conferred more favorable prognoses than anemia, hypotension and hypoxic insults. Rarer inciting causes of T2MI (n=49) were not included in panel A due to low number of patients in each category: structural heart disease (14), malignant hypertension (4), coronary embolism (8), spontaneous coronary artery dissection (19), coronary vasospasm (4).B: Patients with a single inciting cause of T2MI had a more favorable prognosis than those with multiple causes