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Gene Therapy and Angiogenesis May be the Future of Treatment for Peripheral Vascular Disease

Gene Therapy and Angiogenesis May be the Future of Treatment for Peripheral Vascular Disease

Teaser: 

D'Arcy Little, MD, CCFP
Director of Medical Education,
York Community Services, Toronto, ON

Introduction and Epidemiology:
Peripheral vascular disease (PVD), a common and often disabling condition, usually results from the atherosclerotic occlusion of the arteries in the lower limbs.1 Symptomatic PVD is rare in men before the age of 50, but prevalence increases dramatically with age. The Edinburgh Artery Study states that the prevalence of symptomatic PVD increases from 2.2% in men aged 50 to 59, to 7.7% in men aged 70 to 74.2,3 Before the 7th decade, the prevalence in women is approximately half that seen in men, but this difference diminishes after that age.4

Definition and Diagnosis of Intermittent Claudication (IC)
Patients who suffer from intermittent claudication (IC) represent a subset of those patients with symptomatic lower extremity atherosclerotic disease. This review will focus on an approach to the investigation and management of this condition in the elderly population. Only 7-9% of patients with diagnosed lower extremity atherosclerosis suffer from intermittent claudication.5 In 1962, the Rose claudication questionnaire was developed as an epidemiologic instrument for the purposes of identifying patients with IC. It also serves as a good working definition of IC.

Gene Therapy May Play a Role in Reversing Heart Failure

Gene Therapy May Play a Role in Reversing Heart Failure

Teaser: 

heart locket imageGene Therapy May Play a Role in Reversing Heart Failure

In a potential breakthrough, a study has shown that failing heart muscle cells loaded with a gene called SERCA2a begin acting normal again.

Dr. Roger J. Hajjar and colleagues harvested muscle cells from 10 failed hearts removed from patients who had received heart transplants. The team injected these heart cells with a virus (vector) carrying the gene that makes SERCA2a, allowing the gene to become part of the cell's genetic code. Within 24 hours the gene induced overproduction of SERCA2a allowing the failed heart cells to begin beating and contracting at levels similar to those seen in normal hearts.

These results support the premise that gene-based therapies may offer a new modality for treating heart failure. However, further research should be conducted to see if improving the ability of cells to contract could lead to an improvement in symptoms and increased rates of survival for patients with heart failure.

Source: Journal of the American Heart Association 1999;2308-2311.