In Table 1, the authors described the characteristics of patients with A(H1N1) and cardiac dysfunction. However, if we look carefully at the table, the following points merit attention. All the patients had some underlying comorbidity that directly or indirectly affects the cardiac function. The baseline ejection fraction of case 4 was 40%, which might decrease not only because of A(H1N1) infection per se but also because of associated bacterial pneumonia/sepsis (which was not clearly described in the article). Cases 5 and 6 were pregnant patients in their third trimester. There is a possibility that these two cases may represent peripartum cardiomyopathy (criteria for diagnosis: cardiac failure within last months of pregnancy or within 5 months postpartum, no determinable cause for failure, no previous heart diseases, left ventricular dysfunction with ejection fraction <45%) that improved with treatment.2 More importantly, the Pao2/Fio2 fraction in all except case 5 (Pao2/Fio2 >300) fulfilled the criteria for ARDS (Pao2/Fio2 ≤200).3 ARDS is a reasonably well-characterized cause of acute cor pulmonale. Whether A(H1N1) virus induces disproportionate pulmonary vascular disease is not known, although preliminary autopsy results may be compatible with this finding.4 The thin-walled right side of the heart is particularly susceptible to ischemia and failure in the face of acute increases in afterload. Right-sided heart dysfunction has direct effects on left ventricular diastolic and systolic function. Except in cases 3 and 5, the APACHE (Acute Physiology And Chronic Health Evaluation) II score in the other four cases varied from 20 to 28, indicating that these patients were severely ill.5 In severely ill patients, multiple factors contribute to myocardial dysfunction, including sepsis, pneumonia, ARDS, and associated other organ dysfunction (as described in case 1, the dose of oseltamivir was reduced because of associated severe renal impairment). The rapid downhill course of case 1 (being intubated within 24 h of hospitalization) and partial response to diuretics and inotropes suggests the above possibilities rather than reversible cardiac dysfunction alone.