**1. Introduction**

As many medical providers can attest first-hand, the devastation due to the methamphetamine problem does not spare a single person. Methamphetamine abuse is on the rise and recognition of its devastating cardiovascular risks are more important than ever. Similarly, cocaine use does not have benign effects on the heart. In the United States, heart failure (HF) is accountable for more than 1 million hospitalizations and \$32 billion in costs annually [1, 2]. Long-term stimulant abuse is a known cause of cardiomyopathy. Beta-blockers have shown improvement of systolic heart failure but use regarding prevention of stimulant-induced-cardiomyopathy is not well investigated. One of the proposed mechanisms of myocardial injury is thought due to catecholamine excess causing increased workload on the heart, which may benefit from BBT. However, BBT has been controversial in this patient population due to reported cases of worsening vasoconstriction due to unopposed alpha-receptor stimulation; and it has been suggested to avoid them altogether in this population with heart failure [1–4].

If BBT can decrease the extent and progression of stimulant-induced cardiomyopathy then patients might have a greater chance of regaining cardiac function if they one day decide to quite stimulant abuse. Patients may also have improvement in cardiac function and symptoms leading to less heart failure-related hospital admissions; which in turn could decrease the current financial burden placed on healthcare.

There is a lack of quality studies investigating the use of long-term BBT in active cocaine users and almost no data investigating this same issue in regards to methamphetamine. Recent research has suggested that the phenomenon of excessive alphastimulation might not be related to beta-blocker use [1, 2, 4]. Therefore, in patients who actively engage in stimulant drug abuse, how does long-term BBT (both selective and non-selective) affect cardiovascular outcomes compared to no BBT regarding prevention of stimulant-induced-cardiomyopathy?
