Valentine’s Edition: Talking Anticoagulation and Acetaminophen

Volume 12, Issue 3

St Valentine’s Day has just passed, and with the color red plastered everywhere and all things heart-related on our minds, it seemed most fitting to focus this week on matters of the literal heart.

First, we discuss how extended anticoagulation can help mend a broken heart, and then we turn our focus to some new data suggesting that one of our most perceived-to-be-safe painkillers may, in fact, betray our trusting hearts.

Point 1: Does Extending Anticoagulation After Percutaneous Coronary Intervention Improve Outcomes?

The gold standard treatment for patients experiencing a ST-elevation myocardial infarction (STEMI) is percutaneous coronary intervention (PCI). While all STEMI patients should receive anticoagulation (typically with unfractionated heparin) prior to PCI, therapy is usually terminated after successful PCI.

This week, researchers used a large registry of over 35,000 patients from China to evaluate outcomes for patients who continued anticoagulation after PCI vs those who did not. In the patients who received post-procedure anticoagulation—which most commonly consisted of low-molecular weight heparin therapy—authors noted a significantly reduced risk of in-hospital mortality (.9% vs 1.8%; HR: .62; 95% CI: .43-.89; P < .001). There was no significant difference detected in risk of in-hospital major bleeding (2.5% vs 2.2%; HR: 1.05; 95% CI: .83-1.32; P = .14).

These results are interesting; however, treatment assignment was not randomized, and hence the mortality benefit perceived in the anticoagulation group could be due to residual confounding by indication. Additional randomized clinical trials are needed to determine if post-procedure anticoagulation truly has a place in the setting of contemporary PCI.

Point 2: A Broken Heart From Acetaminophen?

Acetaminophen has enjoyed a sterling reputation for being one of the safest drugs available when consumed at the recommended doses. This is in stark contrast to nonsteroidal anti-inflammatory drugs, which can interact with many important heart medications and can independently increase blood pressure when consumed chronically.

This week, the PATH-BP study was published, which was a randomized, placebo-controlled crossover trial of 103 patients; the intervention was acetaminophen 1 g by mouth 4 times daily for 2 weeks. The results of the study indicated acetaminophen use was associated with a roughly 5 mmHg increase in systolic blood pressure vs placebo (95% CI, 2.9–6.6).

These findings are still preliminary due to small sample size, but given the potential health implications of this increase in blood pressure, larger studies are urgently needed to determine the true effect of acetaminophen on blood pressure.