Σφακιανάκης Αλέξανδρος
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5 Άγιος Νικόλαος
Κρήτη 72100
00302841026182
00306932607174
alsfakia@gmail.com

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Δευτέρα 4 Σεπτεμβρίου 2017

Hemodynamic Response to Nitroprusside in Patients With Low-Gradient Severe Aortic Stenosis and Preserved Ejection Fraction

AbstractBackground

Low-gradient severe aortic stenosis (LGSAS) with preserved ejection fraction (EF) is incompletely understood. The influence of arterial afterload and diastolic dysfunction on the hemodynamic presentation of LGSAS remains unknown.

Objectives

The authors sought to determine the acute hemodynamic response to sodium nitroprusside in LGSAS with preserved EF.

Methods

Symptomatic patients with LGSAS and preserved EF underwent cardiac catheterization with comparison of hemodynamic measurements before and after nitroprusside.

Results

Forty-one subjects (25 with low flow [LF], stroke volume index [SVI] ≤35 ml/m2, 16 with normal flow [NF]) were included. At baseline, LF patients had lower total arterial compliance (0.36 ± 0.12 ml/m2/mm Hg vs. 0.48 ± 0.16 ml/m2/mm Hg; p = 0.01) and greater effective arterial elastance (2.77 ± 0.84 mm Hg · m2/ml vs. 1.89 ± 0.82 mm Hg · m2/ml; p = 0.002). In all patients, nitroprusside reduced elastance, left ventricular filling pressures, and pulmonary artery pressures and improved compliance (p < 0.05). Aortic valve area increased to ≥1.0 cm2 in 6 LF (24%) and 4 NF (25%) subjects. Change in SVI with nitroprusside varied inversely to baseline SVI and demonstrated improvement in LF only (3 ± 6 ml/m2; p = 0.02).

Conclusions

Nitroprusside reduces afterload and left ventricular filling pressures in patients with LGSAS and preserved EF, enabling reclassification to moderate stenosis in 25% of patients. An inverse relationship between baseline SVI and change in SVI with afterload reduction was observed, suggesting that heightened sensitivity to afterload is a significant contributor to LF-LGSAS pathophysiology. These data highlight the utility of afterload reduction in the diagnostic assessment of LGSAS.



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