Key result
Inodilators abolish the correlation between septal E/e' and PAOP in decompensated end-stage HFrEF.
Why the study?
Does the use of inodilator drugs affect the accuracy of the E/e' ratio as a surrogate for pulmonary artery occlusion pressure in patients with decompensated end-stage systolic heart failure?
Observational (n=39)
Does the use of inodilator drugs affect the accuracy of the E/e' ratio as a surrogate for pulmonary artery occlusion pressure in patients with decompensated end-stage systolic heart failure?
p-value: p=<0.001
Inodilator agents severely impair the correlation between the E/e' ratio and pulmonary artery occlusion pressure in patients with decompensated end-stage systolic heart failure, limiting its utility as a non-invasive surrogate in this setting.
Inodilators may invalidate E/e' as a PAOP surrogate in decompensated end-stage HF; this cohort finding leaves open the need for prospective validation.
OBJECTIVES: We investigated the impact of inodilators on the accuracy of E/e' ratio as a surrogate for pulmonary artery occlusion pressure in patients with decompensated end-stage systolic heart failure. SETTING: The ratio of early diastolic transmitral flow velocity to tissue Doppler mitral annular early diastolic velocity, E/e', and pulmonary artery occlusion pressure have been shown to be correlated. The validity of E/e' for predicting pulmonary artery occlusion pressure in patients with decompensated end-stage systolic heart failure was recently challenged, but the influence of inodilators was not taken into account, despite the reported influence of these drugs on left ventricular relaxation properties. PATIENTS AND INTERVENTION: Invasive hemodynamic monitoring and echocardiographic data were collected prospectively from 39 patients with decompensated end-stage systolic heart failure (92% male), aged 56 ± 13 years. These patients had dilated ventricles with a low cardiac index (1.9 ± 0.6 L/min/m) and high pulmonary artery occlusion pressure (22 ± 8 mm Hg), and 90% required inodilator support during hospitalization. MEASUREMENTS AND MAIN RESULTS: The correlation between septal E/e' and pulmonary artery occlusion pressure was good for examinations in the absence of inodilators (n = 21) (r = 0.7; p < 0.001), but no correlation was found when inodilators were used (n = 31). Lateral and mean E/e' were poorly correlated with pulmonary artery occlusion pressure, if at all, in both cases. CONCLUSIONS: By modifying ventricular relaxation properties and the influence of filling pressure on e', inodilator agents severely impair the correlation between E/e' and pulmonary artery occlusion pressure in patients with decompensated end-stage systolic heart failure.
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Salem et al. (2014) conducted an observational in Decompensated end-stage systolic heart failure (n=39). Inodilator drugs vs. Absence of inodilators was evaluated on Correlation between septal E/e' and pulmonary artery occlusion pressure (p=<0.001). Inodilator use in decompensated end-stage systolic heart failure abolished the correlation between septal E/e' and pulmonary artery occlusion pressure (r=0.7, P<0.001 without inodilators).
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