Abstract

Obesity is associated with an elevated risk of cardiovascular disease, metabolic disease, and cardiac mortality. Reactive oxygen species and inflammation in an obese individuals are among a number of suspected driving forces behind obesity’s detrimental health effects. These factors can elevate cardiovascular risk by causing impairments in cardiovascular structure and function. It is hypothesized that gastric bypass surgery will lead to near immediate reversal of metabolic deviations and rapid weight reduction, in addition to remodeling and improvements in arterial function as weight is lost. Patients that meet protocol inclusion criteria are invited to join the study during their 1 week pre-operative clinical appointment. At this time patients are consented and instructed to lie supine for 10 minutes of quite relaxation. Patients then begin a sequence of non-invasive examinations starting with a 12-lead electrocardiogram, followed by an echocardiogram, carotid artery ultrasound, radial applanation tonometry, and endothelial function analysis using EndoPAT technology. Upon completion of the non-invasive procedures a blood sample is taken for analysis. Preliminary results on 12 study subjects suggests the following. As hypothesized, body weight had decreased (pre: 131.8 ±5.6 to post: 125 ±5.2 kg) along with BMI (pre: 45.2 ±2.3 to post: 42.9 ± 2.2) and waist circumference (pre: 122.1 ±5.0 to post: 111.9 ± 3.2 cm) at the 1-week time point. Decrease in body size and weight was aided by a reduction in low-density lipoprotein (pre: 127 ±6.2 to post: 113 ±4.5 mg/dL). In addition, a number of improvements to the cardiovascular system were also marked at the 1-week time point. Estimated left ventricular end systolic pressure and direct measure of left ventricular end systolic volume (pre: 66 ±4 to post: 55 ±3 mmHg) declined post-GBS. This is in consort with an increase in contraction rate (dP/dt pre: 672 ±54 post: 737 ±46, p<0.01), a reduction in LV ejection time (pre: 291 ±10 to post: 211 ± 30ms), and a decrease in myocardial oxygen demand (PTIs pre: 2346 ±120 post: 2194 ±107 area/min, p<0.05). Similar improvements in augmentation index can be seen in assessments of peripheral vessels. Independent of brachial artery blood pressure, central systolic blood pressure (pre: 112 ± 4 to post: 105 ±2 mmHg, p=0.08), augmentation index (pre: 16 ±3 to post: 8 ±3, p=0.06), an indirect measure of arterial stiffness, and central augmentation pressure (pre: 4.9 ±1.1 to post: 2.5 ±0.9 mmHg, p=0.06) tended to decrease 1-week post GBS. The data suggests that vascular changes are happening in the early stages of recovery, prior to dramatic weight loss, thus suggesting vascular changes are a result of an alternate surgical benefit. In conclusion, the preliminary results of this study suggest noteworthy cardiovascular improvements post-gastric bypass surgery, yet prior to significant weight loss.

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