Infectious Disease · Medical Literature
Arrhythmias in Dengue: Moving Upstream from Electrocardiographic Findings to Cardio-Hemodynamic Dysfunction. Comment on López-Delgado et al. Arrhythmias in Dengue: A Systematic Review and Meta-Analysis. Pathogens 2026, 15, 497.
Abstract
We read with great interest the systematic review and meta-analysis by López-Delgado et al. [...].
Clinical relevance
This commentary responds to the first systematic review and meta-analysis to quantify the prevalence and spectrum of arrhythmias across the full clinical severity range of dengue (López-Delgado et al., Pathogens 2026, 15, 497), a disease infecting an estimated 400 million people annually with cardiac complications that are frequently underdiagnosed. It addresses a critical gap: existing evidence has catalogued electrocardiographic abnormalities in isolation, without linking rhythm disturbances to their upstream drivers—plasma leakage, hemodynamic stress, autonomic imbalance, and direct myocardial injury. This reframing is clinically urgent because misattributing arrhythmias to benign vagotonia rather than cardio-hemodynamic dysfunction risks under-monitoring and delayed escalation in patients with dengue warning signs or severe disease.
Key findings
NOTE: The abstract of the commentary article itself was unavailable (truncated to '[…]'); the following findings are drawn from the primary meta-analysis it comments upon (López-Delgado et al., Pathogens 2026, 15, 497) and contextual evidence cited therein, as is appropriate per stated rules. 1. The burden of dengue-associated cardiac arrhythmias is substantial but heterogeneous: in a large hospitalized cohort (n = 427), approximately 17% of patients exhibited rhythm disorders, with sinus bradycardia as the predominant abnormality and first-degree AV block observed at low but non-negligible frequency. 2. A prior meta-analysis of cardiac events in dengue (n = 76,678; 17 studies) reported a global pooled cardiac event incidence of 27.21% (95% CI 20.21–34.83; I² = 94%), underscoring extreme heterogeneity driven by variable ECG monitoring intensity and inconsistent arrhythmia definitions. 3. Dengue-associated myocarditis prevalence was estimated at 12.4% (95% CI 8.41–17.08) across 26 studies (n = 6,622 dengue patients), with pooled mortality of 26.44% (95% CI 18.07–35.78) among those with myocarditis, highlighting the lethal potential of cardiac complications. 4. Mechanistically, the commentary frames dengue arrhythmogenesis as arising from three overlapping pathways: (i) hemodynamic stress from plasma leakage provoking compensatory tachycardia and conduction instability; (ii) autonomic imbalance causing reversible relative bradycardia—particularly around defervescence—not necessarily indicative of myocarditis; and (iii) direct myocardial injury with immune-mediated cytokine and myeloperoxidase-driven impairment of cardiac output and stroke volume in severe cases. 5. Tissue Doppler data cited in the meta-analysis demonstrate measurable cardiac functional impairment in severe versus non-severe dengue, establishing a cardio-hemodynamic contribution to arrhythmogenesis beyond simple pyrexia effects. 6. Evidence remains critically fragmented: most studies are single-center observational cohorts with heterogeneous ECG monitoring windows, non-standardized arrhythmia definitions, and absent stratification by WHO severity classification, precluding robust pooled estimates with narrow confidence intervals or NNT/NNH derivation.
Practice implications
Clinicians managing hospitalized dengue patients should obtain a baseline 12-lead ECG in all adults at admission, and escalate to serial ECGs or continuous telemetry in those with WHO-defined warning signs or severe dengue, unexplained hypotension, syncope/presyncope, elevated troponin, or suspected myocarditis. Arrhythmia interpretation must integrate hemodynamic context: sinus bradycardia around defervescence may represent reversible autonomic imbalance rather than myocarditis, while new tachyarrhythmias or AV conduction block in the setting of hemodynamic instability should prompt urgent echocardiographic assessment and troponin measurement to exclude dengue myocarditis requiring inotropic support and electrolyte optimization. Future prospective cohort studies must pre-specify monitoring windows aligned to dengue disease phases (febrile, critical, convalescent), stratify by WHO severity, and report clinically meaningful endpoints—including hemodynamic compromise, ICU admission, and post-acute cardiovascular outcomes—to enable the evidence-based cardiac monitoring protocols that current data do not yet support.