Dengue virus infection is a leading cause of arboviral disease worldwide, with severe cases characterized by plasma leakage and hypovolemic shock. Increasing evidence suggests that cardiovascular involvement is clinically significant, challenging the conventional paradigm of dengue-associated hemodynamic compromise. This review synthesizes mechanistic, clinical, and population-based evidence to propose a temporal, phase-dependent framework of dengue cardiovascular pathology. Cardiovascular involvement evolves across distinct phases, beginning with direct viral myocardial effects and endothelial glycocalyx disruption during the febrile phase, followed by immune-mediated injury, vascular leak, and myocardial dysfunction. While vascular permeability typically resolves within 48–72 hours of defervescence, myocardial dysfunction may persist for up to 2 weeks, creating a temporal dissociation with important clinical consequences. Hemodynamic studies demonstrate that dengue shock frequently reflects a mixed phenotype, with approximately equal contributions of hypovolemic and cardiogenic shock. This mismatch creates a narrow therapeutic window in which aggressive fluid resuscitation may exacerbate cardiac dysfunction and increase the risk of pulmonary edema. Dengue-associated shock is therefore better understood as a dynamic, phase-dependent syndrome characterized by shifting contributions of vascular and myocardial dysfunction. Recognition of this mixed shock paradigm is essential for phase-specific management and highlights the need for accessible tools to identify shock phenotypes in real time.
Egli et al. (2026) studied this question.