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This Article Full Text Full Text (PDF) All Versions of this Article: 288/1/H416    most recent 00615.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Popovic, Z. B. Articles by Thomas, J. D. Search for Related Content PubMed PubMed Citation Articles by Popovic, Z. B. Articles by Thomas, J. D.

Effects of sodium nitroprusside in aortic stenosis associated with severe heart failure: pressure-volume loop analysis using a numerical model

Zoran B. Popovi,¹ Umesh N. Khot,² Gian M. Novaro,¹ Fernando Casas,¹ Neil L. Greenberg,¹ Mario J. Garcia,¹ Gary S. Francis,¹ and James D. Thomas¹

¹Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio; and ²Indiana Heart Physicians, Indianapolis, Indiana

Submitted 21 June 2004 ; accepted in final form 27 August 2004

In the recently published clinical study [Use of Nitroprusside in Left Ventricular Dysfunction and Obstructive Aortic Valve Disease (UNLOAD)], sodium nitroprusside (SNP) improved cardiac function in patients with severe aortic stenosis (AS) and left ventricular (LV) systolic dysfunction. We explored the possible mechanisms of these findings using a series of numerical simulations. A closed-loop lumped parameters model that consists of 24 differential equations relating pressure and flow throughout the circulation was used to analyze the effects of varying hemodynamic conditions in AS. Hemodynamic data from UNLOAD study subjects were used to construct the initial simulation. Systemic vascular resistance (SVR), heart rate, and aortic valve area were directly entered into the model while end-systolic and end-diastolic pressure-volume (P-V) relationships were adjusted using previously published data to match modeled and observed end-systolic and end-diastolic pressures and volumes. Initial simulation of SNP treatment by a reduction of SVR was not adequate. To obtain realistic model hemodynamics that reliably reproduce SNP treatment effects, we performed a series of simulations while simultaneously changing end-systolic elastance (E_es), end-systolic volume at zero pressure (V₀), and diastolic P-V shift. Our data indicate that either an E_es increase or V₀ decrease is necessary to obtain realistic model hemodynamics. In five patients, we corroborated our findings by using the model to duplicate individual P-V loops obtained before and during SNP treatment. In conclusion, using a numerical model, we identified ventricular function parameters that are responsible for improved hemodynamics during SNP infusion in AS with LV dysfunction.

ventricular mechanics; contractility; afterload

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