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Background: Type 2 myocardial infarction (MI) is an imbalance between myocardial oxygen demand and supply, leading to myocardial ischemia. It is not due to plaque rupture, and is usually caused by a condition other than coronary artery disease (CAD). However, limited data are available comparing the prevalence of traditional coronary risk factors and mortality between type 1 and type 2 MI. We hypothesize that type 2 MI carries a higher mortality than type 1. Methods:We searched the databases of PubMed, EMBASE, CENTRAL, and MEDLINE for studies comparing type 1 MI with type 2 MI. The baseline variables were compared in each cohort. Summary risk ratios and 95% confidence intervals were calculated using the random effects model to compare mortality between the two groups. Results:The included studies yielded 25,872 patients of whom 2,683 (10%) had type 2 MI. Compared to the type 1 cohort, the type 2 cohort had significantly higher inpatient (15% vs. 4.7%, P<0.00001), 30-day (17.6% vs. 5.3%, P<0.00001) and 1-yr mortality (27% vs. 13%, P<0.00001), as well as higher 30-day major adverse cardiovascular events (20% vs. 9%, P<0.0001). Operative stress (20%) was the most common trigger of type 2 MI, followed by sepsis (19%), arrhythmia (18.63%), heart failure (15%), and anemia (12%).Conclusions: Type 2 MI is a common entity and is more common in females, older age groups, and in patients with multiple comorbidities: it also tends to result in higher mortality.

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The present meta-analysis suggests that patients with high-risk AMI without cardiogenic shock do not seem to benefit from the use of IABP as measured by in-hospital mortality, rate of reinfarction, and recurrent angina. However, in patients with AMI with cardiogenic shock (systolic blood pressure [SBP] < 90), there was significant reduction in mortality using IABP. The use of IABP is associated with increase in the rate of both moderate and severe bleeding.

Statins therapy slows down the progression of carotid atherosclerosis as measured by CIMT, indicating benefits at subclinical stage of the disease process.