The findings were drawn from 6,253 unselected patients who presented to emergency departments in five European countries with chest discomfort. Type 1 myocardial infarction (T1MI) was diagnosed in 16.4% of the patients, with T2MI diagnosed in 4%.
Compared to the T1MI group, the T2MI had a lower proportion of current smokers (20% vs 26%) and a lower rate of hypercholesterolemia (53% vs 61%) but a higher proportion of females (36% vs 26%), researchers reported in JAMA Cardiology.
There was no significant difference between T2MI and T1MI patients, respectively, in rates of underlying coronary artery disease (41% vs 40%), previous MI (27% vs 30%) or previous revascularization (31% vs 32%).
High-sensitivity cardiac troponin (hs-cTn) levels showed clear differences, however. The baseline median hs-cTn was 30 ng/L in patients with T2MI and 63 ng/L in patients with T1MI. Median absolute change within 1 hour was 5 ng/L with T2MI and 11 ng/L with T1MI; median 6-hour peaks were 40 ng/L and 113 ng/L, respectively.
Whereas in T1MI the predominant pathophysiological mechanism was a primary atherothrombotic occlusion, in T2MI the predominant mechanisms underlying myocardial demand-supply mismatch were tachyarrhythmia (53.8%) and hypertension (18.7%). Coronary vasospasm was responsible for 5.6% of T2MI cases, anemia for 4.4%, hypoxemia for 3.9%, and coronary dissection for 1.2%.
All-cause mortality rates at two years were comparable:13.9% in T2MI and 11.7% in T1MI. Cardiovascular mortality at two years was 7.6% in T2MI and 9.3% in T1MI, with a hazard ratio (HR) of 0.80 for competing risks. The trend in increased all-cause mortality with T2MI was offset by increased CV mortality with T1MI. Mortality rates appeared to be greatly increased in T2MI patients with hypotension, hypoxia, anemia or multiple triggers, with a much lower risk for patients presenting with hypertension or tachyarrhythmia.
"We did not characterize tachyarrhythmia for this analysis. To qualify for T2MI, the documentation of a clear tachyarrhythmia was essential for the diagnosis. A heart rate of e.g. 110/min alone was not sufficient to make the diagnosis of T2MI, " coauthor Dr. Thomas Nestelberger from the University of Basel, Switzerland commented to Reuters Health in an email.
Only 1.6% of T2MI patients in this cohort had hypotension. However, the study excluded patients with sepsis, acute heart failure, myocarditis or Takotsubo's cardiomyopathy, as well as perioperative patients and critically ill patients in the intensive care unit.
Based on previous studies, the authors noted, "It is important to highlight that preexisting coronary artery disease (CAD) is a major confounder of mortality among patients with T2MI. In the absence of CAD, patients with T2MI have a very low risk of death."
Future T2MI was more likely to occur in patients who presented with T2MI compared to those initially diagnosed as T1MI (HR 3.2), whereas future T1MI was significantly more likely to occur in patients with T1MI at presentation (HR 2.91).
The diversity of T2MI phenotypic clusters, with supply-demand mismatch as the underlying mechanism, "also highlights that the immediate therapeutic approaches to T2MI must be highly individualized and focused on rapid reversal of the trigger," the authors conclude. However, "given the high risk of T2MI recurrence, these therapeutic measures should include optimal blood pressure and lipid control."
Treatment was left to the discretion of the attending consultant. At discharge, only 49% of patients with T2MI were receiving aspirin and 14% were receiving dual antiplatelet therapy (DAPT), whereas aspirin was prescribed to 91% and DAPT to 76% of patients discharged after T1MI. B-blockers were prescribed in 68% and 79% of T2MI and T1MI patients, respectively, and statins in 54% and 90%, respectively, suggesting a more aggressive approach for T1MI patients.
Although there was no breakdown of type of tachyarrhythmia, 31% of T2MI patients were discharged on anti-coagulation versus 14% of Type 1MI patients, which suggests that atrial fibrillation or atrial flutter may have been increased in T2MI.
Interventions varied by type of MI. Among T1MI patients, angiography was performed in 86%,percutaneous coronary intervention (PCI) in 67%, and coronary artery bypass grafting (CABG) in 8.6%. Among patients with T2MI, 27.5% underwent angiography, 3.2% had PCI, and 0.4% underwent CABG (all with P value <.001).
Dr. Nestelberger told Reuters Health that 17% of patients with T2MI underwent stress testing during the index hospitalization.
"Further work up for CAD in T2MI patients should be based on risk assessment," he said. "Patients with a low to moderate likelihood for CAD should undergo non-invasive stress testing or (computed tomography angiography), patients with a high likelihood for CAD should undergo invasive testing."
His team acknowledged that their study involved emergency department patients presenting with chest discomfort. In their population, the incidence of T1MI was four times as high as that of T2MI, but in earlier reports "restricting the assessment to the perioperative period and using hs-cTnt, T2MI was the clearly dominant MI etiology," the authors said.
Regarding patients with supply mismatch with acute heart failure with hypertension or with sepsis, hypotension and tachycardia but without chest discomfort, Dr. Nestelberger said, "Patients with evidence of myocardial injury (troponin elevation) but no clinical evidence of myocardial ischemia should be labelled as acute myocardial injury e.g. in the setting of acute heart failure. Those patients should not be labelled as T2MI."
SOURCE: https://bit.ly/3KwdNcm JAMA Cardiology, online March 9, 2022.
By Austin Kutscher MD FACC
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