Background: Severe acute respiratory syndrome (SARS) is characterized by an overaggressive immune response. Myocardial performance may be impaired in cytokine-mediated immune reactions.
Methods and results: Forty-six patients with established clinical diagnosis of SARS were studied prospectively. Transthoracic echocardiographic examinations were done at the acute stage of infection and 30 days later. Among them, 14 patients required mechanical ventilation. The clinical course, laboratory data, SARS-CoV antibody titers, and results of reverse transcriptase-polymerase chain reaction were studied. Significantly higher left ventricular index of myocardial performance (IMP) (0.42+/-0.13 versus 0.33+/-0.09, P<0.001), longer isovolumic relaxation time (102.9+/-15.7 versus 81.6+/-14.7 ms, P<0.001), lower flow propagation velocity (69.6+/-15.7 versus 83.8+/-19.7 cm/s, P=0.011), and Doppler-derived cardiac output (4.69+/-1.01 versus 5.49+/-1.04 L/min, P<0.001) were observed during acute infection when compared with those at 30 days. No significant valvular disease or pulmonary hypertension was found. At baseline, a lower mean left ventricular ejection fraction (LVEF) (65.3+/-12.8% versus 71.4+/-5.7%, P=0.03) and a higher mean IMP (0.51+/-0.11 versus 0.40+/-0.12, P=0.017) were found in patients who required mechanical ventilation. A decrease in LVEF correlated moderately with an elevated lactate dehydrogenase level (r=-0.605, P<0.001), whereas a higher IMP correlated weakly with an increase in creatine kinase level (r=0.38, P=0.016). Histological examination of the heart in the patient with the lowest EF (30.2%) revealed no interstitial lymphocytic infiltrate or myocyte necrosis.
Conclusions: Subclinical diastolic impairment without systolic involvement was observed in patients with SARS. This impairment may be reversible on clinical recovery.