Bradyarrhythmias in Type 2 Myocardial Infarction: Cause or Consequence?

We read with interest the recent study by Puchongmart et al., who reported that bradycardia/atrioventricular (AV) conduction disorders occur in 6% of type 2 myocardial infarction (T2MI) hospitalizations and are associated with higher in-hospital mortality and cardiogenic shock [1]. However, the available data do not permit causal interpretation of this association. First, T2MI is defined by a supply–demand mismatch driven by an acute precipitant, and outcomes vary substantially by trigger and comorbidity burden [2, 3]. Accordingly, the co-occurrence of bradyarrhythmias with a higher comorbidity burden may be clinically meaningful as a severity marker, reflecting reduced compensatory reserve and vulnerability to hypoperfusion and metabolic derangement. The same processes that precipitate T2MI—shock and tissue hypoperfusion with metabolic acidosis, electrolyte disturbance, and acute kidney injury—are also well-recognized causes of bradyarrhythmias and AV block. Experimental evidence shows that acidosis can markedly slow AV nodal conduction and, under certain conditions, produce partial or even complete AV block, underscoring that even “complete” block may be reversible once the metabolic milieu is corrected [4]. BRASH syndrome provides a clinical framework for this bradycardia–renal dysfunction–hyperkalemia–shock vicious cycle [5]. Consistent with this framework, bradyarrhythmias in T2MI may be better interpreted as markers of advanced physiological decompensation than as mortality-mediating mechanisms. Second, key dataset limitations preclude interpretation of “transient” versus “permanent” conduction disease. Administrative coding cannot distinguish pre-existing conduction abnormalities from new-onset bradyarrhythmias during the index admission, nor can it establish temporality. The absence of granular severity and metabolic markers (hemoglobin, creatinine, potassium, lactate, and arterial pH) prevents adequate severity adjustment and trigger phenotyping. Although the authors state that causes of T2MI were compared, these precipitating triggers are not reported in the presented results, further limiting interpretation of whether bradyarrhythmias merely reflect the severity of the underlying trigger. Moreover, irreversibility is a clinical decision often reflected in pacing strategy: if high-grade AV block truly represented intrinsic, nonreversible conduction system disease, one would expect clear alignment with permanent pacemaker implantation—ideally reported by AV block degree and inclusive of post-discharge device placement. Without these details, contrasting lower-grade AV block as “transient” while implying complete AV block is “non-reversible” risks post hoc speculation rather than evidence-based interpretation. We encourage reporting permanent pacemaker implantation stratified by AV block degree and incorporating available severity proxies (e.g., AKI/dialysis, mechanical ventilation, and vasopressor use) to better distinguish reversible metabolic conduction disturbances from intrinsic conduction disease. Overall, in the absence of temporality, trigger phenotyping, and objective metabolic severity markers, bradyarrhythmias in T2MI should be interpreted primarily as indicators of advanced physiological decompensation. Clarifying whether these disturbances are reversible metabolic phenomena or intrinsic conduction disease will require prospective studies integrating temporal rhythm characterization with detailed metabolic/hemodynamic profiling and clinically actionable endpoints, including pacing decisions. The authors declare no conflicts of interest. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.