Survival gains in the management of acute myocardial infarction in recent decades don’t apply to one increasingly common category of MI.
Type 2 MI, triggered by a surge in myocardial oxygen demand or a drop in its supply, is on the rise and might be more prognostically serious than the “classic” atherothrombotic type 1 form, for which there have been such impressive strides in therapy.
Strategies for assessing and treating type 2 MI and another condition it can resemble clinically – nonischemic myocardial injury – have been less rigorously explored and are far less settled.
That could be partly because recent iterations of the consensus-based universal definition of MI define type 1 MI primarily by the atherothrombotic process, whereas “demand” type 2 MI is characterized as secondary to other disorders. The list of potential primary conditions, cardiac and noncardiac, is long.
As a result, patients with type 1 MI are clinically well defined, but those with type 2 MI have so far defied efforts to be clinically characterized in a consistent way. However, recent efforts might change that, given growing appreciation that all-cause and cardiovascular (CV) mortality outcomes are actually worse for patients with type 2 MI.
“That’s because we have lots of treatments for type 1 MI. Type 2 and myocardial injury? We don’t know how to treat them,” David E. Newby, MD, PhD, University of Edinburgh, said in an interview.
Dr. Newby pointed to a widely cited 2018 publication, of which he is a coauthor, documenting 5-year outcomes of 2,122 patients with type 1 MI, type 2 MI, or nonischemic myocardial injury per the newly minted fourth universal definition.
Risk-factor profiles for patients with the latter two conditions contrasted with those of patients with type 1 MI, he observed. They were “a lot older,” were less likely to be smokers, had more hypertension and previous stroke, and a less prominent CV family history.
“So they’re a different beast,” Dr. Newby said. And their prognosis tended to be worse: all-cause mortality was about 62% for patients with type 2 MI and 72% with nonischemic myocardial injury, but only 37% for patients with type 1 MI. The difference between the two types of infarction was driven by an excess of noncardiovascular death after type 2 MI.
Mortality in patients with type 2 MI is “quite high, but it may well be a marker of the fact that you’ve got other serious diseases on board that are associated with poorer outcome,” he said.
Risk varies
The degree of risk in type 2 MI seems to vary with the underlying condition, a recent cohort study suggests. In about 3,800 patients with cardiac troponin (cTn) elevations qualifying as MI – a younger group; most were in their 30s and 40s – mortality at 10 years was 12% for those with type 1 MI, but 34% for those with type 2 MI and 46% for the remainder with nonischemic myocardial injury.
Underlying precipitating conditions varied widely among the patients with type 2 MI or nonischemic myocardial injury, and there was broad variation in mortality by etiology among those with type 2 MI. Sepsis and anemia entailed some of the highest risk, and hypertension and arrhythmias some of the lowest.
A prospective, community-based study of 5,460 patients with type 1 MI or type 2 MI reached a similar conclusion, but with a twist. Five-year all-cause mortality contrasted significantly between types of MI at 31% and 52%, respectively, but CV mortality rates were similar in this study.
Mortality in type 2 MI again varied by the precipitating etiology, suggesting that patients can be risk stratified according to pathophysiological mechanism behind their demand infarction, the authors concluded, “underscoring that type 2 MI is not a single entity, rather a group of phenotypic clusters.”
The usually high comorbidity burden and CV risk in patients with type 2 MI, one of those authors said in an interview, suggest there are “opportunities to see whether we can reduce that risk.”
Formal recommendations consistently say that, in patients with type 2 MI, “your first and foremost target should be to treat the underlying trigger and cause,” said Yader Sandoval, MD, Mayo Clinic, Rochester, Minn. That means such opportunities for further CV risk reduction tend to be “underappreciated.”
Dr. James L. Januzzi
“In principle, treating the inciting cause of type 2 MI or the injury is important,” said James L. Januzzi, MD, Massachusetts General Hospital, Boston, in an interview, “but I feel quite strongly that there must be more that we can do for these folks.”
Dr. Januzzi is senior author on a recent analysis based on more than 200,000 admissions across the United States that saw a 43% lower risk for in-hospital death and 54% lower risk for 30-day MI readmission for patients with type 2 MI than those with type 1, adjusted for risk factors and comorbidities.
But, “it is important to emphasize that type 2 MI patients had a substantial risk for adverse outcome, nonetheless, and lack a clear management approach,” Dr. Januzzi and colleagues stated in their publication, as reported by this news organization.
“Due to the high rates of long-term cardiovascular events experienced by the frequently encountered type 2 MI patients,” they wrote, “identifying evidence-based therapies represents a major unmet need.”
That such patients tend to be sick with multiple comorbidities and have not yet been clinically well characterized, Dr. Januzzi said, “has stymied our ability to develop a treatment strategy.”