Avatar of Larry Husten, PHD

Study Casts Doubt on Value of Genetic Testing for Familial Hypercholesterolemia (21 Feb 2013)

News

The recent introduction of two drugs specifically targeted to treat people with the rare but dangerous condition of homozygous familial hypercholesterolemia (FH) has caused increased interest in figuring out the best strategy to identify people with the disorder. Now a new study published online in the Lancet suggests that one of the main screening plans that relies on genetic…

This content is exclusive to CardioExchange. To continue reading, please log in or request an invitation.

Avatar of Larry Husten, PHD

Proof-of-Concept for Bedside Rapid Genotyping Test of CYP2C19 (28 Mar 2012)

News

A new point-of-care test can rapidly identify people with a common genetic variant associated with impaired clopidogrel function. The authors claim that this is the first study to demonstrate the feasibility of delivering a genetic test at bedside. In an article published online in the Lancet, Jason Roberts and colleagues report on a new point-of-care test that can…

This content is exclusive to CardioExchange. To continue reading, please log in or request an invitation.

Avatar of Richard A. Lange, MD, MBA

CYP2C19 Genotyping: Down For The Count? (30 Dec 2011)

Interventional Cardiology

Richard A. Lange, MD, MBA and L. David Hillis, MD

The controversy over the use of genetic testing to guide antiplatelet therapy reminds us of a WWF (Worldwide Wrestling Federation) tag team match.  What we agree upon (the match rules): Clopidogrel is a prodrug activated by several enzymes, including CYP2C19, and common genetic variations alter CYP2C19 activity. Here’s where the wrestling match begins: Are the CYP2C19 genetic…

This content is exclusive to CardioExchange. To continue reading, please log in or request an invitation.

Avatar of Larry Husten, PHD

ELEVATE-TIMI 56: One New Piece of the Clopidogrel Puzzle (16 Nov 2011)

News

Tripling the maintenance dose of clopidogrel in most but not all patients with a common genetic variation will lower platelet reactivity to levels achieved in patients without the variation.