VTE increases risk for heart attack, stroke
November 23, 2007
MedWire News: Patients with venous thromboembolism (VTE) have a substantially increased risk for arterial cardiovascular events such as myocardial infarction and stroke, a Danish population-based study reveals.
The excess risk was most pronounced in the first year after VTE but persisted for up to 20 years, and was seen not only in patients with unprovoked VTE but also those with VTE secondary to pregnancy, surgery, or other predisposing conditions.
Henrik Toft Sørensen (Aarhus University Hospital, Denmark) and team explain that VTE events have generally been considered as distinct from thrombotic atherosclerotic diseases. However, recent studies suggested that both conditions involve activation of blood coagulation and platelets, they note.
To investigate further, the researchers studied Danish registry data to identify patients aged 40 years or older who were discharged from hospital with a VTE diagnosis from January 1980 through December 2005. They used a civil registry to assign each patient in the VTE cohort to five population controls matched for gender, age, and area of residence, and then compared rates of arterial cardiovascular events in the VTE and control groups until the end of the study or 20 years of follow-up.
The results, published in The Lancet, show that the 25,199 patients with deep vein thrombosis (DVT) had significantly higher rates of myocardial infarction (MI) (0.70% vs 0.46%) and stroke (0.83% vs 0.38%) in the first year after the thrombotic event than their 97,773 population matched controls. These data translated into adjusted relative risks (RRs) for MI of 1.60 and for stroke of 2.19.
The excess risks for MI and stroke were greater in the 16,925 patients with pulmonary embolism (PE). Here, the increased rates of MI (0.85% vs 0.58%) and stroke (0.67% vs 0.36%) relative to the 65,793 population matched controls translated into RRs of 2.60 and 2.93, respectively.
The authors note that the excess risks persisted but were lower after the first year, at roughly 20-40% above risks in the control cohort. They report that the RR for MI or stroke was 1.33 at 1-5 years after the DVT event, falling to 1.14 16-20 years after the event, and that RRs were similar at these times after PE.
Further analysis of the patient groups stratified according to provoked or unprovoked VTE revealed similar RRs that were again lower for DVT than for PE, and highest in the year after thrombotic event and modest long-term.
The authors say it is implausible that VTE in itself causes MI and stroke, but that the association must be due to shared risk factors or etiologic pathways, or both.
In an accompanying editorial, Gordon Lowe (University of Glasgow, UK) said that further studies need to establish the nature and causes of the increased risk for arterial thrombotic events after VTE diagnosis. But he recommended that all patients with VTE should now be assessed for cardiovascular risk factors and given appropriate lifestyle advice and possibly preventive medication.
He wrote: In particular, after completion of a course of anticoagulants, low-dose aspirin might be considered for people with a 10-year risk of 20% or more for congestive heart disease or stroke, because aspirin is effective in primary prevention of venous and arterial thrombotic events in individuals at high risk.