Methods

This was a prospective cohort study. Patients whose body mass indexes (BMIs) were ≥40 kg/m ² and whose blood pressures were <140/90 mm Hg on 3 consecutive clinical encounters separated by ≥1 week were considered for entry into the study. All patient evaluations were conducted in the outpatient setting. Patients with current, previous, or treated hypertension were excluded from the study. Patients with clinical, electrocardiographic, radiographic, or echocardiographic evidence of coronary heart disease, idiopathic or secondary cardiomyopathies, valvular stenosis or moderate to severe valvular regurgitation, pericardial disease, or congenital heart disease were excluded from the study. No patient in this study had heart failure (per the Framingham criteria). Also excluded from the study were patients with cardiac arrhythmias on 12-lead electrocardiography and patients with primary pulmonary disease on the basis of clinical and radiographic assessment and pulmonary function tests. Patients receiving drugs and those with medical disorders that might affect ventricular repolarization were also excluded. Consecutive eligible patients who underwent bariatric surgery (vertical banded gastroplasty) were entered into this study.

A complete medical history and physical examination were performed by a single investigator (M.A.A.) just before bariatric surgery and at the nadir of postoperative weight loss. Blood pressure was measured with a cuff sphygmomanometer in accordance with the recommendations of Russel et al. Body weight was obtained after a 12-hour fast using wheelchair-accessible scales. Weight and height were measured in the upright position with the patient barefoot and wearing a thin, lightweight gown. BMI was calculated from these data. Duration of morbid obesity was estimated from patient report. Anthropometric measurements were recorded just before bariatric surgery and at the nadir of postoperative weight loss.

A standard 12-lead electrocardiogram was recorded for all patients just before bariatric surgery and at the nadir of postoperative weight loss in the supine position using a standard technique with a Hewlett-Packard 1D electrocardiograph (Hewlett-Packard, Andover, Massachusetts) with a filter setting of 100 Hz at a paper speed of 25 mm/s. All electrocardiograms were obtained in the fasting state in a quiet room at room temperature of 20°C to 22°C. QT intervals were measured manually in all 12 leads by a single investigator (M.A.A.), who was blinded to patient identity and to clinical, radiographic, and echocardiographic data. QTc was calculated using Bazett’s formula. QTc dispersion was calculated by subtracting the minimum QTc from the maximum QTc on the standard 12-lead electrocardiogram. Leads in which the interface between the terminal portion of the T wave and the subsequent baseline was indistinct were eliminated from the analysis. The upper limits of normal are 420 ms for QTc and 71 ms for QTc dispersion.

M-mode and 2-dimensional transthoracic echocardiograms were obtained in the left lateral and supine positions using a Hewlett-Packard Sonos 1000 echocardiograph with a 2.25-MHz transducer (Hewlett-Packard, Palo Alto, California), and echocardiographic measurements were performed in accordance with American Society of Echocardiography recommendations. Echocardiograms were obtained just before bariatric surgery and at the nadir of postoperative weight loss. LV mass was calculated using the formula of Devereux et al and was indexed to height ^2.7 (LV mass/height ^2.7 ) and to body surface area (LV mass index). LV hypertrophy was defined as LV mass/height ^2.7 ≥51 g/m ^2.7 (a non-gender-specific cut point). LV geometry was based on LV relative wall thickness (ventricular septal plus LV posterior wall thickness in diastole divided by LV internal dimension in diastole). Concentric LV remodeling and hypertrophy and eccentric LV hypertrophy were defined in accordance with the criteria of Devereux et al. Echocardiograms were interpreted by a single investigator (M.A.A.), who was blinded to patient identity and to clinical, radiographic, and electrocardiographic data.

Serum potassium, magnesium, and calcium levels were obtained in the fasting state on the same day as the electrocardiograms and echocardiograms. These levels were obtained just before bariatric surgery and at the nadir of postoperative weight loss. Posteroanterior and lateral chest x-rays were performed within 2 weeks of the preoperative clinical, electrocardiographic, and echocardiographic assessments.

SPSS version 11 (SPSS, Inc., Chicago, Illinois) and R software (R Project for Statistical Computing, Vienna, Austria) were used for statistical analysis. Mean values for continuous variables in patients with and without LV hypertrophy were compared using Wilcoxon’s rank-sum test or Student’s t test for unpaired data. Student’s t test for paired data was used to compare mean values before and after weight loss. The proportions of categorical variables in patients with and without LV hypertrophy were compared using the chi-square test.

Multivariate regression models of pre–weight loss QTc and QTc dispersion and weight loss–induced changes in QTc and QTc dispersion were developed to explain their relations to selected clinical and echocardiographic variables. For pre–weight loss subgroups, the following predictors were considered: LV mass/height ^2.7 , LV internal dimension in diastole, LV end-systolic wall stress, systolic blood pressure, BMI, and the duration of morbid obesity. For weight loss–induced change subgroups, the aforementioned predictor variables were considered except for the duration of morbid obesity. Variance influence factor calculations were used to identify predictors that were correlated with each other (multicollinearity). Conditional inference trees were used were used to guide the modeling process, including the identification of contributing factors associated with levels of QTc and QTc dispersion. Several models were developed iteratively using multivariate generalized additive models and linear regression. These models were assessed for assumptions and goodness of fit. Models selected are described in association with specific data sets in the “Results” section. A p value <0.05 was required for statistical significance for all the aforementioned tests.

Results

A total of 68 patients were referred from the bariatric surgery clinic for consideration for entry into the study. A total of 39 patients qualified for inclusion. Reasons for exclusion were failure to qualify for or agree to bariatric surgery in 11; current, previous, or treated hypertension in 10; heart failure in 3; moderate to severe mitral regurgitation in 3; and atrial fibrillation in 2.

The study population consisted of 31 women and 8 men (mean age 37 ± 8 years). There were 11 patients with diabetes mellitus and 12 cigarette smokers. The mean baseline BMI was 43.8 ± 2.3 kg/m ² . Table 1 lists selected baseline clinical, electrocardiographic, and echocardiographic characteristics for the group as a whole (n = 39). QTc ranged from 397 to 469 ms before weight loss and exceeded 420 ms in 27 patients. Pre–weight loss QTc dispersion values ranged from 24 to 70 ms. Post–weight loss QTc and QTc dispersion ranged from 379 to 442 ms and from 25 to 38 ms, respectively. Table 1 also lists selected baseline clinical, electrocardiographic, and echocardiographic characteristics in patients with LV hypertrophy (n = 25) and without LV hypertrophy (n = 14). Patients with and without LV hypertrophy on the basis of LV mass/height ^2.7 were identical to those with and without LV hypertrophy on the basis of LV mass index. Baseline LV mass index values were 111.0 ± 32.1 g/m ² for the group as a whole, 132.3 ± 24.5 g/m ² for those with LV hypertrophy, and 73.0 ± 7.2 g/m ² for those without LV hypertrophy. There were no significant differences in the proportion of men, women, diabetics, and cigarette smokers between subgroups with and without LV hypertrophy.

Table 1

Effect of weight loss on selected clinical, electrocardiographic, and echocardiographic variables in patients with and without left ventricular hypertrophy (n = 39)

Patients	BMI (kg/m 2 )	Heart Rate (beats/min)	QTc (ms)	QTc Dispersion (ms)	Systolic Blood Pressure (mm Hg)	LV End-Systolic Wall Stress (kdyne/cm 2 )	LV Internal Dimension in Diastole (cm)	LV Mass/Height 2.7 (g/m 2.7 )	Relative Wall Thickness
Before weight loss	42.8 ± 2.1	78.4 ± 2.7	428.7 ± 18.5	44.1 ± 11.2	128.4 ± 5.6	164.5 ± 49.2	5.69 ± 0.75	73.1 ± 24.2	0.39 ± 0.03
After weight loss	31.9 ± 2.2	77.6 ± 2.3	410.3 ± 11.9	32.2 ± 3.3	124.3 ± 4.3	128.1 ± 24.4	5.14 ± 0.62	52.2 ± 13.8	0.42 ± 0.03
Δ	−10 ± 2.7	−0.8 ± 2.0	−18.2 ± 10.6	−12.4 ± 9.9	−4.0 ± 4.0	−36.4 ± 32.5	−0.55 ± 0.45	−20.9 ± 12.9	0.03 ± 0.01
p	<0.0005	NS	<0.0001	<0.0005	<0.001	<0.0001	<0.0005	0.0001	NS
LV hypertrophy present (n = 25)
Before weight loss	43.0 ± 2.4	78.4 ± 2.7	440.3 ± 10.9	50.8 ± 4.1	131.80 ± 4.52	192.04 ± 33.61	6.18 ± 0.39	88.3 ± 16.0	0.40 ± 0.03
After weight loss	30.6 ± 1.2	77.6 ± 2.2	416.9 ± 12.1	32.2 ± 4.3	126.36 ± 3.84	144.48 ± 20.22	5.58 ± 0.37	58.8 ± 12.7	0.44 ± 0.02
Δ	−12.4 ± 2.1	−0.8 ± 1.4	−23.1 ± 13.9	−17.7 ± 8.1	−5.50 ± 2.51	−47.56 ± 31.3	−0.60 ± 0.10	−29.5 ± 5.7	0.04 ± 0.01
p	<0.0001	NS	0.0001	0.0001	0.01	<0.0001	<0.001	<0.0001	<0.01
LV hypertrophy absent (n = 14)
Before weight loss	42.6 ± 2.0	78.4 ± 2.6	407.57 ± 10.81	32.1 ± 4.3	122.29 ± 3.01	115.4 ± 12.6	4.82 ± 0.26	45.9 ± 4.3	0.35 ± 0.03
After weight loss	34.3 ± 1.4	77.5 ± 2.4	394.13 ± 25.07	31.2 ± 4.1	120.7 ± 1.94	106.5 ± 13.5	4.52 ± 0.27	40.4 ± 5.0	0.36 ± 0.02
Δ	−8.3 ± 1.9	−0.9 ± 1.3	−13.44 ± 5.32 ⁎	−0.86 ± 1.5 †	−1.58 ± 1.83 ⁎	−8.9 ± 4.0 †	−0.30 ± 0.10 †	−5.5 ± 5.8 ‡	0.01 ± 0.01 ⁎
p	<0.001	NS	NS	NS	NS	NS	NS	NS	NS

Data are expressed as mean ± SD.

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