Weight Gain Linked to Later Life Incident VTE

Simone A. French, PhD

While weight gain is a known risk factor for cardiovascular disease, it has not been examined extensively in relationship to venous thromboembolism (VTE).

A team, led by Simone A. French, Division of Epidemiology & Community Health, School of Public Health, University of Minnesota, examined the link between weight change over 9 years and subsequent VTE.

In the Atherosclerosis Risk in Communities (ARIC) study, the investigators calculated quintiles of 9-year weight change (visit 4 1996–1998 weight minus visit 1 1987–1989 weight in kg: Quintile 1: ≥−1.81 kg; Quintile 2: <−1.81 to ≤1.36 kg; Quintile 3: >1.36 to ≤4.08 kg; Quintile 4: >4.08 to ≤7.71 kg; Quintile 5: >7.71 kg).

The researchers identified and adjudicated incident VTEs from visit 4 (1996-1998) through 2015 using medical records and calculated hazard ratios (HRs) using Cox models.

Overall, the researchers identified 529 incident cases of VTE during an average of 19 years of follow-up. Compared to Quintile 2, participants in Quintile 5 of weight change had 1.46 times the rate of incident VTE (HR, 1.46; 95% CI, 1.09-1.95), which was adjusted for age, race, sex, income, physical activity, smoking, and prevalent cardiovascular disease.

The HR for Quintile 5 was modestly attenuated to 1.38 (95% CI, 1.03-1.84) when the first visit body mass index (BMI) was included in the model.

After the investigators examined separately, the results were significant for unprovoked VTE, but not for provoked VTE.

For obese patients at visit 1, both weight gain (HR, 1.86; 95% CI, 1.27-2.71) and weight loss (HR, 2.11; 95% CI, 1.39-3.19) were linked to incident VTE when compared with normal-weight participants with no weight change.

“Weight gain later life was associated with increased risk for unprovoked VTE,” the authors wrote. “Among those with obesity, both weight gain and weight loss were associated with increased risk for VTE.”

Recently, investigators found commonly used risk tools for acute pulmonary embolism have adequate estimating ability.

The findings suggested clinicians might need to integrate broad clinical information instead of relying on a single risk assessment tool to estimate mortality risk and determine management for patients with acute pulmonary embolism.

Of the patients evaluated, all-cause death occurred within 7 days for 6% of patients and within 30 days for 12.3% of patients. Seven-day mortality in the low-risk groups ranges from 1.3% (sPESI) to 3.1% (Bova) and the 30-day mortality ranged from 2.6% (PESI) to 10.2% (Bova). The rate was 3.8% for sPESI.

For patients in the highest risk groups, the seven-day mortality ranged from 7% (sPESI) to 16.3% (Bova) and 30-day mortality ranged from 14.4% (sPESI) to 26.3% (PESI).

All risk stratification tools had modest discrimination for seven-day mortality (AUC range, .616-.666) with slightly lower discrimination for 30-day mortality (AUC range, .55-.694). Differences in AUC between different scores were small for seven-day mortality (<.05) and somewhat larger for 30-day mortality. This was especially true in comparing the Bova score with PESI (AUC difference, .13-.14) or sPESI (AUC difference, .09-.11) scores.

The study, “Weight change over 9 years and subsequent risk of venous thromboembolism in the ARIC cohort,” was published online in the International Journal of Obesity.