Effect of weight loss on ventricular repolarization in normotensive severely obese patients with and without heart failure.

BACKGROUND: Obesity has been reported to be associated with delayed ventricular repolarization. The purpose of this study was to assess ventricular repolarization in normotensive severely obese subjects with and without heart failure (HF) and to assess the effect of weight loss on ventricular repolarization in such patients. METHODS: Twenty-eight patients with and 39 patients without HF (body mass index ≥ 40 kg/m(2)) were studied before and after weight loss from bariatric surgery. Corrected QT interval (QTc) was measured on 12-lead electrocardiograms using Bazett's formula. QTc dispersion was calculated by subtracting the minimum from the maximum QTc on each 12-lead electrocardiogram. Electrocardiograms and transthoracic echocardiograms were performed preoperatively and at the nadir of postoperative weight loss. RESULTS: Mean QTc and QTc dispersion were significantly longer/greater in subjects with HF than in those without HF (P < 0.0001). Weight loss produced significant reductions in mean QTc and QTc dispersion in both subgroups (P < 0.0001). Pre-weight loss left ventricular (LV) mass/height and presence or absence of HF independently predicted pre-weight loss QTc and QTc dispersion (P < 0.0001). Weight loss-induced decrease in LV mass/height independently predicted weight loss-induced decreases in QTc and QTc dispersion (P < 0.0001). CONCLUSIONS: HF independently predicts QTc and QTc dispersion in normotensive severely obese patients. Decrease in the LV mass resulting from weight loss independently predicts reduction in QTc and QTc dispersion in such patients.

Effect of weight loss after bariatric surgery on left ventricular mass and ventricular repolarization in normotensive morbidly obese patients.

To assess the effect of weight loss on ventricular repolarization in morbidly obese patients, 39 normotensive subjects whose baseline body mass indexes were ≥40 kg/m(2) before weight loss from bariatric surgery were studied. All patients were free of underlying organic heart disease, heart failure, and conditions that might affect ventricular repolarization. Twelve-lead electrocardiography and transthoracic echocardiography were performed just before surgery and at the nadir of postoperative weight loss. The corrected QT interval (QTc) was derived using Bazett's formula. QTc dispersion was calculated by subtracting the minimum from the maximum QTc on the 12-lead electrocardiogram. Echocardiographic left ventricular (LV) mass was indexed to height(2.7). The mean body mass index decreased from 42.8 ± 2.1 to 31.9 ± 2.2 kg/m(2) (p <0.0005). For the entire group, weight loss was associated with significant reductions in mean QTc (from 428.7 ± 18.5 to 410.5 ± 11.9 ms, p <0.0001) and mean QTc dispersion (from 44.1 ± 11.2 to 33.2 ± 3.3 ms, p <0.0005). Mean QTc and QTc dispersion decreased significantly with weight loss in patients with LV hypertrophy but not in subjects without LV hypertrophy. Multivariate analysis identified pre-weight loss LV mass/height(2.7) as the most important predictor of pre-weight loss QTc and QTc dispersion and also identified weight loss-induced change in LV mass/height(2.7) as the most important predictor of weight loss-induced changes in QTc and QTc dispersion. In conclusion, LV hypertrophy is a key determinant of QTc and QTc dispersion in normotensive morbidly obese patients. Regression of LV hypertrophy associated with weight loss decreases QTc and QTc dispersion.

Relation of left ventricular mass to QTc in normotensive severely obese patients.

Prolongation of the corrected QT interval (QTc) has been described in obese subjects. This study assesses the relation of left ventricular (LV) mass to QTc in normotensive severely obese subjects. Fifty normotensive patients whose BMI was ≥40 kg/m(2) (mean age: 38 ± 7 years) were studied. QTc was derived using Bazett's formula. LV mass was calculated using the formula of Devereux et al. and was indexed to height(2.7). Mean QTc was 428.8 ± 19.0 ms and was significantly longer in those with than in those without LV hypertrophy (P < 0.01) QTc correlated positively and significantly with BMI (r = 0.392, P < 0.025), LV mass/height(2.7) (r = 0.793, P < 0.0005), systolic blood pressure (r = 0.742, P < 0.001), LV end - systolic wall stress (r = 0.746, P < 0.001) and LV internal dimension in diastole (r = 0.788, P < 0.0005). Among five variables tested, LV mass/height(2.7) was identified as the sole predictor of QTc by multivariate analysis. In conclusion, LV mass and loading conditions that may affect LV mass are important determinants of QTc in normotensive severely obese subjects.

Can paronychia cause a remote necrotizing soft tissue infection?

Remote necrotizing soft tissue infection (NSTI) resulting from paronychia is very unusual but potentially lethal. We report a case of a 39-year-old woman affected by this unusual infection. The paronychia completely resolved in less than 2 weeks, however, a NSTI involved the right chest and flank and the left thigh. The patient required intensive care and multiple surgical debridements. This recent experience and literature data suggest that paronychia can cause a remote NSTI that can rapidly spread and become life-threatening. Broad spectrum antibiotics and aggressive surgical debridement are essential to a successful outcome.

The treatment of obesity.

Obesity is a chronic problem requiring lifelong treatment. Obesity assessment involves measurement of the body mass index, waist circumference, and the identification of other risk factors. Management should include diet and exercise. Selected patients can be offered pharmacotherapy, of which only sibutramine and orlistat are FDA-approved for long-term use. Bariatric surgery is the only option that provides sustained and significant weight loss and should be offered to the severely obese patients.