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Phosphodiesterases as targets for intermittent claudication.

Yongge Liu¹, Yasmin Shakur, Junichi Kambayashi

¹Otsuka Maryland Medicinal Laboratories, Rockville, MD, USA. yonggel@yahoo.com

Handbook of Experimental Pharmacology

|June 23, 2011

Summary

Intermittent claudication (IC) symptoms, caused by peripheral arterial disease (PAD), can be improved with cilostazol. This phosphodiesterase 3 (PDE3) inhibitor offers multifactorial benefits for patients with leg pain during exercise.

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Area of Science:

Vascular Medicine
Pharmacology
Biochemistry

Background:

Intermittent claudication (IC) is a common manifestation of lower extremity peripheral arterial disease (PAD), primarily caused by atherosclerosis.
IC symptoms include exercise-induced leg muscle pain and fatigue due to an oxygen supply-demand mismatch.
Current pharmacological options for IC are limited, with cilostazol and pentoxifylline being the only indicated drugs.

Purpose of the Study:

To review the pharmacological actions of cilostazol in treating intermittent claudication.
To discuss the rationale and challenges of targeting phosphodiesterases (PDEs) for IC treatment.
To explore strategies for developing novel and more effective therapies for IC.

Main Methods:

Literature review of studies on intermittent claudication, peripheral arterial disease, and phosphodiesterase inhibitors.
Analysis of cilostazol's mechanism of action and clinical efficacy.
Discussion of current therapeutic limitations and future research directions.

Main Results:

Cilostazol, a PDE3 inhibitor, significantly improves walking distance and quality of life in IC patients.
Cilostazol exerts multifactorial effects, including antiplatelet, endothelial, smooth muscle, and lipid-modulating actions.
Existing treatments for IC have limitations, highlighting the need for improved therapeutic strategies.

Conclusions:

Cilostazol represents a valuable therapeutic option for managing intermittent claudication symptoms.
Targeting PDEs offers potential for developing new treatments, but challenges remain.
Further research is needed to optimize PDE-targeted therapies for peripheral arterial disease.