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CLINICAL STUDY

Reduced procedural risk for coronary catheter interventions in carriers of the coagulation factor VII-Gln³⁵³ gene

Przemyslaw M. Mrozikiewicz, MD^*, Ingolf Cascorbi, MD, PhD^*, Sabine Ziemer, MD, Michael Laule, MD, Christian Meisel, MD^*, Verena Stangl, MD, Wolfgang Rutsch, MD, Klaus Wernecke, PhD, Gert Baumann, MD, Ivar Roots, MD^* and Karl Stangl, MD

^* Institute of Clinical Pharmacology, Charité University Medical Center, Humboldt University of Berlin, Berlin, Germany
Institute of Laboratory Medicine and Pathobiochemistry, Charité University Medical Center, Humboldt University of Berlin, Berlin, Germany
Department of Internal Medicine, Cardiology, Charité University Medical Center, Humboldt University of Berlin, Berlin, Germany
Institute of Biometry, Charité University Medical Center, Humboldt University of Berlin, Berlin, Germany

Manuscript received December 3, 1999; revised manuscript received April 28, 2000, accepted June 26, 2000.

Reprint requests and correspondence: Dr. Karl Stangl, Medizinische Klinik, Kardiologie, Angiologie, Pneumologie, Charité, Campus Mitte, Humboldt Universität zu Berlin, Schumannstrasse 20/21, D-10117 Berlin, Germany
karl.stangl{at}charite.de

OBJECTIVES

We have focused on the role of coagulation factor VII (FVII) Arg³⁵³Gln polymorphism as a risk predictor of complications following percutaneous transluminal coronary angioplasty (PTCA), directional coronary atherectomy (DCA), and stenting.

BACKGROUND

The FVII Arg³⁵³Gln mutation decreases FVII activity, and presence of the Gln³⁵³ allele could be protective against thrombus formation during catheter interventions.

METHODS

A total of 666 consecutive patients with coronary artery disease who had undergone PTCA (n = 280), DCA (n = 104), or stenting (n = 282) were followed up for a 30-day composite end point, which included need for target vessel revascularization, myocardial infarction, and death. The Arg³⁵³Gln polymorphism of FVII was determined by PCR/RFLP assay.

RESULTS

Carriers of the Gln³⁵³ allele had significantly lower levels of total FVII activity (FVIIc, –20.7%, p < 0.001) and of activated circulating FVII (FVIIa, –32.7%, p = 0.03) compared with Arg³⁵³/Arg³⁵³. The composite end point occurred in 43 patients: 4 were heterozygous Arg³⁵³/Gln³⁵³, and 39 were homozygous Arg³⁵³/Arg³⁵³. The incidence of the composite end point was 2.5% in carriers of the Gln³⁵³ allele and 7.7% in Arg³⁵³/Arg³⁵³ homozygotes (p = 0.013). This corresponds to a 72% risk reduction in carriers of the Gln³⁵³ allele (relative risk: 0.28; 95% confidence interval: 0.09–0.81; p = 0.02).

CONCLUSIONS

The Gln³⁵³ allele of FVII is associated with substantial risk reduction in adverse events that complicate coronary catheter interventions. With the perspective of active site-blocked activated FVII (FVIIai) as conjunctive medication, the results suggest that the FVII genotype should be taken into due consideration in assessment of FVIIai medication and of its dosage.

Abbreviations and Acronyms   CAD = coronary artery disease   DCA = directional coronary atherectomy   FVII = factor VII   FVIIa = activated FVII   FVIIai = active site-blocked activated FVII   FVIIc = total FVII activity   MI = myocardial infarction   nt = nucleotide   PTCA = percutaneous transluminal coronary angioplasty   TF = tissue factor   TIMI = thrombolysis in myocardial infarction   TVR = target-vessel revascularization

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