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Related Experiment Video

Updated: Jun 21, 2026

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats

Published on: March 1, 2022

Treating heart failure with sildenafil.

¹Department of Internal Medicine, Baruch-Padeh Poria Medical Center, Lower Galilee, Israel. navablum@hotmail.com

Congestive Heart Failure (Greenwich, Conn.)

|July 25, 2009

Summary

This summary is machine-generated.

Sildenafil improves exercise capacity and quality of life in patients with heart failure and pulmonary hypertension. This phosphodiesterase type 5 inhibitor enhances endothelial function and ventilatory efficiency.

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Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

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Last Updated: Jun 21, 2026

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats

Published on: March 1, 2022

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

Published on: April 8, 2013

Area of Science:

Cardiology
Pulmonary Hypertension Research

Background:

Pulmonary hypertension is a complication of systolic heart failure.
Selective phosphodiesterase type 5 inhibitors are emerging treatments.

Purpose of the Study:

To evaluate sildenafil's efficacy in heart failure patients with secondary pulmonary hypertension.
To assess improvements in exercise capacity, quality of life, and physiological markers.

Main Methods:

Administered sildenafil to patients with systolic heart failure and pulmonary hypertension.
Monitored exercise capacity, oxygen consumption, ventilation, and endothelial function.
Assessed quality of life and breathlessness over 3 and 6 months.

Main Results:

Sildenafil improved peak oxygen consumption and reduced the minute ventilation/carbon dioxide output slope.
The drug acted as a selective pulmonary vasodilator at rest and during exercise.
Significant improvements in flow-mediated dilation, ergoreflex on ventilation, and breathlessness were observed.

Conclusions:

Sildenafil enhances endothelial activity and muscle perfusion in heart failure patients.
It improves signaling and ventilatory efficiencies, offering a potential new therapeutic strategy.
Sildenafil may represent a novel approach for managing heart failure with pulmonary hypertension.