A recent study of autopsy data in Finland suggests nearly half of individuals who experience sudden cardiac death (SCD) without a prior diagnosis of coronary artery disease (CAD) actually had a history of silent MI (SMI)—but that history wasn’t detected until after their deaths.
Acute MI is highly treatable in today’s medical landscape, first author Juha H. Vahatalo, BM, and colleagues at the University of Oulu and Oulu University Hospital in Finland wrote in JAMA Cardiology July 10. But PCIs and antithrombotic therapies are useless against the approximate one-half of MIs that are estimated to be clinically unrecognized.
Outcomes are worse for patients with SMI, reflecting an increased risk of SCD and heart failure that’s much steeper than their counterparts with clinically recognized events, the authors said. In their study, Vahatalo et al. defined SMI as a scar detected by macroscopic and microscopic evaluation of the myocardium without previously diagnosed CAD.
The researchers’ case-control study compared autopsy findings, clinical characteristics and ECG markers associated with SMI in a consecutive cohort of patients enrolled in the Finnish Genetic Study of Arrhythmic Events (Fingesture) registry. All individuals had autopsy-verified SCD in Northern Finland between 1998 and 2017, and Vahatalo’s team obtained clinical history from their medical records, previously recorded ECGs and a standardized questionnaire provided to their next of kin.
A total of 5,869 patients were included in the analysis, the majority of them male and in their mid-sixties. The authors considered individuals with SCD, CAD and SMI as having had cases; those with SCD, CAD and no evidence of SMI were control participants.
The cause of SCD was CAD in 74.8% of cases, Vahatalo and colleagues reported, and more than 70% of that subgroup had no record of previously diagnosed CAD. SMI was noted in 1,322 individuals (42.4%) who experienced SCD without a clinical history of CAD, and those patients were on average older and more often men than control subjects. Heart weight was also higher in participants with SMI—483 grams compared to 438 grams in control patients.
In patients with SMI, SCD occurred during physical activity 18.2% of the time, while control patients met the same fate just 12.4% of the time. The prevalence of SMI among people with diabetes also seemed to be higher compared to nondiabetics.
Vahatalo and co-authors examined 438 patient ECGs recorded prior to SCD, further finding that a prior ECG was abnormal in 66.8% of patients who had SCD after SMI compared with 55.4% of those who had SCD without SMI. That means some individuals’ CAD diagnoses might have been identifiable via ECG before they died.
“In the future, other, more efficient methods might be useful for diagnosing SMI in addition to standard ECGs,” the authors wrote in JAMA. “These include the likelihood that greater sensitivity can be achieved by imaging techniques, such as cardiac MRI, but the cost-effectiveness for CMRI is likely to be unreasonable. Therefore, screening high-risk populations with ECG to identify individuals for further examinations would probably be reasonable.”
After those screenings, they said, physicians could identify the best candidates for further CMRI screening and echocardiographic strain analysis, possibly lowering costs while catching more cases of CAD.
In a corresponding commentary, William C. Roberts, MD, of Baylor University Medical Center, lauded Vahatalo and his team for their efforts, in particular their “huge” patient base. In Finland, Roberts explained, autopsies are mandatory for all unexpected deaths, giving scientists access to a wide range of data.
Still, he said, large numbers don’t necessarily connote “perfect data.” Vahatalo and co-authors’ research was completed over two decades, during which many different pathologists worked on the study and might have skewed the results with inconsistent practices.