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Methamphetamine‐associated cardiomyopathy (MaCM) is an increasingly recognised serious complication from methamphetamine (MA) use. It is characterised as the development of otherwise unexplained heart failure in the context of MA use. MaCM predominantly affects a young and vulnerable population with high morbidity and mortality. It is the second leading cause of mortality in patients with MA use disorder (MUD). Our understanding of MaCM pathogenesis is based on observational cohorts and autopsy studies. Currently, the treatment of MaCM is predicated on abstinence. Medical therapies offer some benefit to a minority of patients; however, without abstinence, medical therapies are often ineffective. Abstinence is difficult for most patients to achieve; all clinicians require an understanding of MaCM and how to educate patients on the risks of ongoing use. Where available, referral to addiction medicine specialists to assist with treatment of MUD is recommended. This review aims to: (i) explain the proposed pathologic mechanisms of MaCM; (ii) summarise recent recommendations of the screening and treatment of MaCM; and (iii) highlight the role of addiction medicine in the management of patient with MaCM.

Introduction: Pacing-induced cardiomyopathy (PiCM) is a potential adverse sequela of right ventricular pacing. Definition varies between studies and the optimal management approach is uncertain. We aimed to characterize definition, incidence, risk factors and treatment strategies of PiCM. Methods: We performed a systematic review and meta-analysis of human studies that evaluated PiCM following pacemaker implantation identified through a literature search of PubMed and EMBASE up to March 2022. Included studies had fifty or more participants. We collected data regarding study definition of PiCM and calculated pooled prevalence across studies. Meta-analysis with random-effects modelling was used to assess association between risk factors and PiCM, reported as odds ratio (OR) with 95% confidence interval (CI). Results: Twenty-six studies (six prospective studies) with a total of 57993 patients (mean/median age 51-78 years, female 45%) were included in final analysis. Fifteen unique definitions of PiCM were reported; the most common definition was left ventricular ejection fraction (LVEF) <50% and LVEF decline ≥10% after pacemaker insertion. Pooled prevalence of PiCM was 12% (95%CI, 11-14%; Figure 1). On meta-analyses, risk factors included male sex (OR 1.23 95%CI 1.12-1.35), baseline LVEF (OR 0.95 per 1% increase, 95%CI 0.93-0.97), paced QRS complex duration (OR 1.02 per msec, 95%CI 1.01-1.03) and right ventricular pacing (RVP) burden (OR 1.02 per 1% increase, 95%CI 1.01-1.02). Treatment strategies identified included cardiac resynchronisation therapy (five studies) and his bundle pacing (three studies). Conclusions: Definition of PiCM varied significantly between studies. More than one in ten patients with a pacemaker with RV pacing developed PiCM. Risk factors included male sex, baseline LVEF, paced QRS duration and RVP. The optimal management strategy is not yet established. Further research is needed to define and treat this understated complication.

Case presentation: A 36-year-old male was admitted to a local hospital with respiratory failure secondary to COVID-19 pneumonia. Initial management included oxygen, dexamethasone and baricitinib. On day 14 of illness the patient developed severe chest pain associated with widespread dynamic ST segment elevation and an elevated high sensitivity troponin I (17516 ng/L). He was transferred to a tertiary center for cardiac evaluation. Cardiovascular risk factors included treated hypertension and obesity (BMI 34). Physical exam revealed a blood pressure of 145/95 mmHg, regular heart rate at 90 bpm and coarse crepitations in bilateral lower lungs with a 3L oxygen requirement. Differentials included myopericarditis however, clinical suspicion for an acute coronary syndrome remained high. Urgent coronary angiogram revealed a large filling defect (figure 1A) at the mid-vessel of the LAD at the 1st diagonal bifurcation, likely a thrombus. Dual antiplatelet therapy, heparin and tirofiban infusion were commenced. Furthermore, echocardiography performed the same day revealed a reduced LVEF secondary to LAD territory hypokinesis and an associated apical left ventricular thrombus measuring 2.2x1.3 cm (figure 1B). Once established on anticoagulation the patient experienced no further chest pain and was discharged home on warfarin.The left ventricular thrombus was monitored for resolution in the community with serial transthoracic echocardiograms. Discussion: Raised highly sensitive troponin in the vicinity of severe COVID-19 infection is common, however, when associated with chest pain and or dynamic ECG changes myocarditis must be considered. The cytokine storm triggered by a SARS-CoV-2 infection can be thrombogenic, resulting from increased platelet activation and decreased fibrinolysis. This process may further complicate the evaluation and acute coronary syndrome does need consideration, even in those patients at a younger age with minimal risk factors.