Abnormal Vessel Architecture Persists in the Microvasculature of the Massive Weight-Loss Patient

Purpose

Studies have demonstrated a link between obesity and increased circulating inflammatory cytokines, ultimately leading to changes in the microvasculature of these patients. Massive weight loss (MWL) patients often experience delayed wound healing following body contouring procedures, however no studies exist to explore the inflammatory response of MWL on the microvasculature. This study hypothesizes MWL patients undergoing body contouring procedures maintain persistently elevated inflammatory markers in the microvasculature that delay wound healing.

Methods

Descriptive data were queried from normal weight and MWL patient charts to assess baseline demographics, medical histories, medications, and smoking status. Superficial Inferior Epigastric Artery (SIEA) vessels were harvested during abdominally based free flap surgery and abdominal contouring surgery for normal weight and MWL patients, respectively. Vessels were histologically assessed using immunohistochemistry to quantify anti-interleukin-1 (IL-1), IL-6, and TNFα expression. Trichrome staining was performed to assess vessel architecture between groups. Statistical analyses included independent samples two-tailed t-tests and Fisher's exact test.

Results

All patients (n=23) were female. Mean time of contouring surgery from initial bariatric procedure was 3.11±1.55 years. There were no significant differences in preoperative BMI, smoking status, diabetes mellitus, hypertension, anemia, or thyroid disease between groups, although a greater proportion of MWL patients presented with a history of diabetes (p<0.002). Quantitative analysis of IL-1, IL-6, and TNFα expression revealed no difference between normal weight and MWL patients (figure 1). Trichrome staining demonstrated abnormal vessel architecture in the MWL group with decreased collagen composition of the tunica adventitia (Figure 2 blue stain) and disorganized smooth muscle in the tunica media (Figure 2 dark red stain).

Conclusions

These data suggest that previously obese MWL patients maintain abnormal vessel wall architecture despite normal inflammatory expression. These persisting changes may explain continued delayed wound healing after MWL. Further studies are warranted to determine the safety of the use of these vessels in microvascular reconstruction.

Legends

Figure 1. Quantification of inflammatory cytokine staining between groups. Results are expressed as percentage of stained versus unstained area per artery cross-section

Figure 2. Histologic arterial cross-section using Masson Trichrome from MWL (A) and normal weight patients (B) at 10x magnification. Note aberrant vessel architecture in MWL group (B) with minimal tunica adventitia (blue), altered tunica intima, and tunica media organization (dark red) Keratin/Muscle (red); Collagen (blue); Cytoplasm (light red/pink); Nuclei (black).