How to Increase the Rate of Optimal Medical Therapy following Acute Myocardial Infarction

To the Editor Haraguchi et al. showed that several baseline characteristics were associated with the failure of optimal medical therapy, including anti-platelets, angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers, beta-blockers, and statins, at the time of index discharge following acute myocardial infarction (1). Their findings may help improve the strategy for increasing the rate of delivering optimal medical therapy following acute myocardial infarction. I would like to highlight several points that I feel will improve the implications of their findings.

Since the optimal medical therapy defined in this study might not be essential for those with vasospastic angina (2), it may be best to exclude such cohorts from the analyses. Furthermore, the existence of asthma might not necessarily be a contraindication of beta-blocker therapy (3), so it might be better for the authors to revise the therapeutic strategy for those with asthma. Hemodialysis and an estimated glomerular filtration rate <30 mL/mg/1.73 m², both of which were included in the multivariate analysis, might have multicollinearity with each other, so their variance inflation factors should be calculated in advance. Finally, hypotension following myocardial infarction may also be an obstacle for the initiation of anti-heart failure medications that reduce systemic blood pressure. Ivabradine, an inhibitor of I_f channel in the sinoatrial node, might increase the systemic blood pressure by improving sinus tachycardia and thereby allow us to initiate these medications (4).

The author states that he has no Conflict of Interest (COI).