OBJECTIVE: To study left ventricular performance and hemodynamic abnormalities during different stages of dengue hemorrhagic fever (DHF). DESIGN AND SETTING: Observational study in a tertiary medical school hospital. PATIENTS: Twenty-four patients with serologically confirmed diagnosis of dengue virus infection and DHF according to the WHO criteria. METHODS: Echocardiography was performed during toxic, convalescent stages and at least 2 weeks after discharge (recovery). Left ventricular ejection fraction, rate-corrected velocity of circumferential fiber shortening adjusted for end-systolic meridional wall stress (VCFC/ESS) Z score, end-diastolic volume Z score, cardiac index, heart rate, mean arterial pressure, and total systemic vascular resistance (SVR) were compared between different stages of DHF. RESULTS: Ejection fraction and VCFC/ESS were significantly lower during the toxic stage than after recovery. End-diastolic volume was low during toxic stage and returned to normal during convalescence and recovery. Cardiac index was low during the toxic stage due to decreased preload (low end-diastolic volume) and depressed left ventricular ejection fraction. Cardiac index remained subnormal during convalescence due to sinus bradycardia. Wide variation in heart rate during toxic stage resulted in a small, nonsignificant increase compared to recovery. With treatment, heightened SVR resulted in relatively normal mean arterial pressure throughout the course of the illness. CONCLUSIONS: The mechanism of decreased cardiac output during toxic stage of DHF is complex. Decreased preload is accompanied by decreased left ventricular performance, and possibly a subnormal heart rate response in some patients.
OBJECTIVE: To study left ventricular performance and hemodynamic abnormalities during different stages of dengue hemorrhagic fever (DHF). DESIGN AND SETTING: Observational study in a tertiary medical school hospital. PATIENTS: Twenty-four patients with serologically confirmed diagnosis of dengue virus infection and DHF according to the WHO criteria. METHODS: Echocardiography was performed during toxic, convalescent stages and at least 2 weeks after discharge (recovery). Left ventricular ejection fraction, rate-corrected velocity of circumferential fiber shortening adjusted for end-systolic meridional wall stress (VCFC/ESS) Z score, end-diastolic volume Z score, cardiac index, heart rate, mean arterial pressure, and total systemic vascular resistance (SVR) were compared between different stages of DHF. RESULTS: Ejection fraction and VCFC/ESS were significantly lower during the toxic stage than after recovery. End-diastolic volume was low during toxic stage and returned to normal during convalescence and recovery. Cardiac index was low during the toxic stage due to decreased preload (low end-diastolic volume) and depressed left ventricular ejection fraction. Cardiac index remained subnormal during convalescence due to sinus bradycardia. Wide variation in heart rate during toxic stage resulted in a small, nonsignificant increase compared to recovery. With treatment, heightened SVR resulted in relatively normal mean arterial pressure throughout the course of the illness. CONCLUSIONS: The mechanism of decreased cardiac output during toxic stage of DHF is complex. Decreased preload is accompanied by decreased left ventricular performance, and possibly a subnormal heart rate response in some patients.
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