Key result
Intravenous flosequinan improved LV-pump function in dogs with acute heart failure, increasing cardiac output by 28% and decreasing characteristic aortic impedance by 11%.
Why the study?
Does intravenous flosequinan improve LV-pump function and reduce aortic impedance in a canine model of acute cardiac failure?
Does intravenous flosequinan improve LV-pump function and reduce aortic impedance in a canine model of acute cardiac failure?
In a canine model of acute heart failure, intravenous flosequinan exerted positive inotropic and lusitropic effects while significantly reducing both pulsatile and steady components of LV afterload.
Findings in canine acute HF should not change practice; leaves open human translation of flosequinan effects.
An arteriovenous vasodilator, flosequinan, has been shown to be effective for the treatment of acute heart failure. However, little is known as to its effect on aortic impedance, which is known to be a proper and precise expression of left ventricular (LV) afterload. To evaluate the acute cardiovascular effect of flosequinan in failing heart, we administered flosequinan intravenously to seven dogs with cardiac failure produced by an infusion of carbon powder (20-50 microm in diameter) into left main trunks of coronary artery. The LV-pump function was severely impaired after intracoronary injection of carbon powder, as evidenced by the findings that cardiac output, circumferential shortening velocity (mean Vcf), and peak +dP/dt of LV pressure were all decreased, associated with a significant increase in LV end-diastolic pressure. Flosequinan (0.9 mg/kg, i.v.) increased cardiac output by 28%, mean Vcf by 44%, and peak +dP/dt by 24%, whereas it decreased total systemic resistance by 32%, time constant of LV pressure decay by 22%, and LV end-diastolic pressure by 18%. Moreover, flosequinan substantially decreased the pulsatile components of LV afterload (i.e., characteristic impedance by 11% and arterial wave reflection coefficient by 45%). Thus flosequinan exerted not only positive inotropic but also positive lusitropic effects, in association with a significant reduction of both pulsatile and steady components of LV afterload, contributing to an improvement of LV-pump function in acute cardiac failure.
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Yano et al. (1998) studied Acute cardiac failure (n=7). Flosequinan was evaluated on Aortic impedance and LV-pump function. Intravenous flosequinan improved LV-pump function in dogs with acute heart failure, increasing cardiac output by 28% and decreasing characteristic aortic impedance by 11%.
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