Bottom line: Enoxaparin is safe and efficacious when used during PCI. Patients who receive enoxaparin during PCI have reduced risk for death, MI, complications of MI, and major bleeding when compared with patients who receive unfractionated heparin.
Citation: Silvain J, Beygui F, Barthelmy O, et al. Efficacy and safety of enoxaparin versus unfractionated heparin during percutaneous coronary intervention: systematic review and meta-analysis. BMJ. 2012;344:e553.
Serum Potassium Levels and Mortality in Acute Myocardial Infarction
Clinical question: What is the relationship between serum potassium levels and mortality in acute myocardial infarction (AMI) patients?
Background: Several smaller studies in the pre-beta-blocker and pre-reperfusion era recommended maintaining serum potassium levels between 4.0 mEq/L and 5.0 mEq/L in AMI patients. However, current studies examining the relationship between potassium levels and mortality in AMI patients are lacking.
Study design: Retrospective cohort study.
Setting: Multicenter study involving 67 hospitals in the U.S.
Synopsis: Using the Cerner Health Facts database, which included 38,689 patients with biomarker-confirmed AMI, this study showed there was a U-shaped relationship between mean post-admission serum potassium level and in-hospital mortality.
Compared with the reference group of 3.5 mEq/L to less than 4.0 mEq/L (mortality rate 4.8%; 95% CI, 4.4% to 5.2%), mortality was comparable for those with mean post-admission potassium of 4.0 mEq/L to less than 4.5 mEq/L (5.0%; 95% CI, 4.7% to 5.3%). Mortality was twice as great for potassium of 4.5 mEq/L to less than 5.0 mEq/L (10.0%; 95% CI, 9.1% to 10.9%), and even greater for higher potassium strata. Similarly, mortality rates were higher for potassium levels of less than 3.5 mEq/L. Rates of ventricular fibrillation or cardiac arrest were higher among patients with potassium levels of less than 3.0 mEq/L or more than 5.0 mEq/L.
Bottom line: For inpatients with AMI, serum potassium levels of 3.5 mEq/L to 4.5 mEq/L should be maintained for the best outcomes. Repletion of serum potassium to levels greater than 4.5 mEq/L is associated with increased mortality and should be avoided.
Citation: Goyal A, Spertus JA, Gosch K, et al. Serum potassium levels and mortality in acute myocardial infarction. JAMA. 2012;307:157-164.
Proton-Pump Inhibitors Better than H2-Blockers in ACS and STEMI
Clinical question: Are proton-pump inhibitors (PPIs) better than H2-blockers at preventing UGI bleeding in patients after acute coronary syndrome (ACS) or ST-elevation myocardial infarction (STEMI)?
Background: It is not definitively known if PPIs are the same or better than H2-blockers in preventing UGI bleeding in patients on high-risk medications (aspirin, clopidogrel, and anticoagulants) after ACS or STEMI.
Study design: Randomized double-blinded controlled trial.
Setting: Single hospital.
Synopsis: Patients with ACS or STEMI were treated with aspirin, clopidogrel, and enoxaparin or thrombolytics. They were then randomized to either esomeprazole 20 mg or famotidine 40 mg, both administered nightly. They were followed throughout their hospital stay and were then followed between four and 52 weeks after discharge (mean duration: 19 weeks for esomeprazole, 18 weeks for famotidine). The primary end point was time to a composite outcome, consisting of UGI bleeding, obstruction, or perforation. Overall, 313 patients were randomized (164 to esomeprazole and 149 to famotidine).
The treatment groups were equivalent in baseline characteristics, and compliance in both groups was excellent (>98%). The primary endpoint occurred in three patients in the esomeprazole group and in 12 patients in the famotidine group (hazard ratio 0.21; 95% CI, 0.06 to 0.75; P=0.008).
Bottom line: PPIs are superior to H2-blockers in reducing UGI bleeding in patients on high-risk medications (aspirin, clopidogrel, and enoxaparin or thrombolytics) after ACS and STEMI. This confirms the recommendations of the 2010 ACCF/ACG/AHA Expert Consensus that PPIs should be used in those on dual antiplatelet therapy on anticoagulants.