Femoral venous oxygen saturation may still be a valuable tool.

We thank Dr Das for his interest in our case series published in CHEST (May 2010). 1 In his letter, Dr Das emphasizes some of the key clinical data presented in Table 1 of our report on six patients with both pandemic 2009 infl uenza A(H1N1) (A[H1N1 ]) and cardiac dysfunction. We agree that other conditions, including but not limited to sepsis, multiple organ dysfunction syndrome, and peripartum cardiomyopathy, may have contributed to the cardiac dysfunction observed in our case series. Limited by the nature of a small case series, we were careful not to assign a causal relationship to the observed association between A(H1N1) and cardiac dysfunction. Regarding Dr Das’s proposal of right-sided heart dysfunction contributing to left-sided heart dysfunction, transthoracic echocardiographic assessment of right-sided heart function was normal in all of our cases except the patient in case 6, who had moderate right ventricular dysfunction. We agree that in hospitalized patients it is diffi cult to distinguish whether cardiac dysfunction is attributable to direct virally mediated myocarditis, systemic infl ammatory response, or other comorbidities. However, we believe it prudent for clinicians to be aware of a high prevalence of cardiomyopathy associated with A(H1N1) in hospitalized patients. Subsequent to submission of our case series, several reports have emerged suggesting a direct effect of A(H1N1) on the myocardium. For example, Puzelli et al 2 described an 11-year-old child with A(H1N1) in Italy who died of myopericarditis and had A(H1N1) isolated from both myocardial tissue and pericardial fl uid, providing direct evidence for A(H1N1) effects on myocardial cells. Histologic confi rmation of myocardial infi ltration with A(H1N1) was obtained in a 5-year-old girl whose death was documented in a series of four cases from a single hospital in California over just a 30-day time period. 3 Haessler et al 4 reported a case of a previously healthy 24-year-old woman with A(H1N1) and left ventricular dysfunction that improved on serial echocardiograms, consistent with our observations. Beyond traditional echocardiographic assessment, tissue Doppler measurements enabled detection of subclinical cardiac dysfunction in patients from Turkey hospitalized with A(H1N1). 5 Furthermore, a report from Japan identifi ed that myocarditis associated with A(H1N1) seemed more common than observed with prior seasonal infl uenza outbreaks. 6 We agree that it is diffi cult to causally relate cardiac dysfunction to a specifi c etiology in critically ill patients within a small case series. However, it is our belief that physicians managing patients with A(H1N1) should be aware that transient cardiac dysfunction can occur and may be related to viral myocarditis.