- Myocardial Injury after Noncardiac Surgery (MINS)
It is defined as myocardial injury owing to ischemia occurring within 30 days after noncardiac surgery.
MINS includes postoperative MI in addition to postoperative elevation in cardiac biomarkers in patients with cardiovascular symptoms or evidence of ischemia on ECG.
MINS likely involves both supply–demand mismatch from CAD and ischemia secondary to obstructive CAD.
Other causes of myocardial ischemia after surgery such as sepsis, pulmonary embolism, or cardioversion are not included in the definition of MINS.
Thirty-day morality increases with increasing values of postoperative high-sensitivity cardiac troponin T (hs-cTnT), from 0.5% for hs-cTnT<20 ng/L to almost 30% for hs-cTnT≥1000 ng/L.
This increase in mortality is not limited to 30 days with postoperative elevation of cardiac biomarkers signifying increased mortality after 30 days as well.
Approximately 8% of patients experience MINS after noncardiac surgery, affecting 8 million adults annually.
A large proportion of MINS patients are asymptomatic, making diagnosis challenging.
Guidelines recommend measuring a BNP or NT-proBNP in patients who have a baseline risk greater than 5%, defined as patients age 65 years and older, or who are 45 to 64 years old with a history of cardiovascular disease, or who have a RCRI score greater than
Management of MINS is evolving. For patients who develop an MI postoperatively, management is similar to patients who develop MI in the non-perioperative period.
For patients who have evidence of myocardial injury without MI, management guidelines are less clear.
Evidence supports improved outcomes at 12 months in patients who received medical management.
Recommendations for chronic stable angina include β-blockers, ACE inhibitors, antiplatelet agents, and statins.
In addition, patients who experience MINS had a reduction in 30-day mortality if they received statin and aspirin.
Guidelines recommend at least initiating statin and aspirin in patients who experience MINS with appropriate follow-up care in the outpatient setting.
Recent evidence might support the initiation of anticoagulation in the setting of MINS: dabigatran, when continued for 2 years, reduced the composite outcome of vascular mortality, all-cause mortality, MI, cardiac revascularization, nonhemorrhagic stroke, peripheral arterial thrombosis, amputation, symptomatic venous thromboembolism, and readmission to hospital for vascular reasons.
Although anticoagulation might eventually play a role in the management of MINS, the current evidence is insufficient to warrant therapeutic anticoagulation for treatment of myocardial injury, particularly in the absence of an MI.