Effect of obesity and weight loss on ventricular repolarization: a systematic review and meta-analysis.

We performed a systematic review and meta-analysis of the effects of obesity ± overweight and weight loss on the corrected QT interval (QTc) and QT or QTc dispersion (indices of ventricular repolarization). Mean difference for both QTc and QT or QTc dispersion with 95% confidence intervals (CIs) was calculated comparing obese ± overweight subjects and normal weight controls and QTc and QT or QTc dispersion before and after weight loss from diet ± exercise or bariatric surgery. A total of 22 studies fulfilled the selection criteria. Compared with normal weight controls, there was a significantly longer QTc in obese ± overweight subjects (mean difference of 21.74 msec, 95% CI: 18.76 to 22.32) and significantly longer QT or QTc dispersion (mean difference of 15.17 msec, 95% CI: 13.59 to 16.74). Weight loss was associated with a significant decrease in QTc (mean difference -25.77 msec, 95% CI: -28.33-23.21) and QT or QTc dispersion (mean difference of -13.46 msec, 95% CI: -15.60 to -11.32 in obese ± overweight subjects. Thus, obesity ± overweight is associated with significant prolongation of QTc and QT or QTC dispersion. Weight loss in obese ± overweight subjects produces significant decreases in these variables. © 2016 World Obesity.

Short-term fluctuations of plasma NT-proBNP levels in patients with new-onset atrial fibrillation: a way to assess time of onset?

OBJECTIVE: The objective of this study was to characterise short-term kinetics of plasma amino-terminal pro-B natriuretic peptide (NT-proBNP) levels in patients with new-onset atrial fibrillation (AF) without heart failure. DESIGN: Prospective cohort study. SETTING: Emergency departments and inpatient services of three large community hospitals. PATIENTS: 31 consecutive patients with new-onset atrial fibrillation (<24 h before presentation) persisting at least 48 h, without evidence of heart failure. MAIN OUTCOME MEASURES: Plasma NT-proBNP levels were obtained at presentation and then 6, 12, 18, and 24 h after presentation. A final sample was obtained 48 h after onset of AF. RESULTS: Mean plasma NT-proBNP levels and 95% CIs (pg/ml) during the 48-h period following onset of AF were: 0-6 h: 636 (395 to 928), 6-12 h: 1364 (951 to 1778), 12-18 h: 1747 (1412 to 2083), 18-24 h: 1901 (1549 to 2253), 24-36 h: 1744 (1423 to 2066) and 36-48 h: 1101 (829 to 1373). Mean time to peak NT-proBNP levels was 16.7 (0.7) h; 29 patients reached their peak levels within 24 h. The mean peak NT-proBNP level was significantly higher than those obtained at 0-6 h and at 36-48 h after onset of AF (p<0.001 for both). There was no correlation between ventricular rate and plasma NT-proBNP levels during any time period after onset of AF. CONCLUSION: In patients with new-onset AF but no clinical or radiographic evidence of heart failure, plasma NT-proBNP levels rise progressively to a peak during the first 24 h and then rapidly fall. This pattern may serve as an aid to assess the time from AF onset.

Dyslipidemia in the metabolic syndrome: clinical implications and management.

Dyslipidemia is an important component of the metabolic syndrome. Dyslipidemia in the metabolic syndrome is characterized by hypertriglyceridemia, low serum levels of high density lipoprotein cholesterol (HDL-C) and an increase in the serum fraction of small dense low density lipoprotein cholesterol (LDL-C) particles. Serum LDL-C elevation is frequently present, but is not a criterion of the metabolic syndrome. A Medline search was conducted using the terms metabolic syndrome, dyslipidemia, hypertriglyceridemia and HDL cholesterol. The metabolic syndrome is a common and important risk factor for cardiovascular disease and progression to type 2 diabetes mellitus. Dyslipidemia is present in most patients with the metabolic syndrome and is treatable with therapeutic lifestyle changes and pharmacotherapy. Aggressive management of atherogenic dyslipidemia is justified by the very high cardiovascular risk associated with this disorder. Atherogenic dyslipidemia is frequently present in patients with the metabolic syndrome and requires aggressive treatment due to the very high risk for cardiovascular disease and progression to type 2 diabetes mellitus.

Obesity and the electrocardiogram.

Obesity is associated with a wide variety of electrocardiographic (ECG) abnormalities. Most of these reflect alterations in cardiac morphology. Some serve as markers of risk for sudden death. Key ECG abnormalities or alterations occurring with disproportionately high frequency in obese subjects include: leftward shifts of the P wave QRS and T wave axes, various changes in P wave morphology, low QRS voltage, various markers of left ventricular hypertrophy (particularly the Cornell voltage and product), T wave flattening in the inferior and lateral leads, lengthening of the corrected QT interval and prolonged QT interval duration. Alterations in the signal-averaged ECG and in heart rate variability may be arrhythmogenic. Cardiac arrhythmias have been described in obese subjects, but are often accompanied by left ventricular hypertrophy or the sleep apnea syndrome. Many of these ECG abnormalities are reversible with substantial weight loss. Thus, obesity is associated with a wide variety of ECG abnormalities, many of which are corrected by weight loss.

Reflections of depression in acoustic measures of the patient's speech.

BACKGROUND: The literature on acoustic measures of voice in depression is reviewed. Authors have separated results derived from studies of automatic speech, such as counting or reading, from free speech. Free speech requires cognitive activity such as word finding and discourse planning in addition to the motor activity of automatic speech. Also, results have been less ambiguous if homogeneous groups of agitated or retarded depressed patients were examined. METHODS: These distinctions are applied to the results of a 12-week double-blind treatment trial that compared response to nortriptyline (25-100 mg/day) with sertraline (50-150 mg/day). Twelve male and ten female elderly depressed patients and an age-matched normal control group (n=19) were studied. Patients were divided into retarded or agitated groups on the basis of ratings. Results from measures of fluency (speech productivity and pausing) and prosody (emphasis and inflection) are described. RESULTS: Depressed patients showed less prosody than the normal subjects. Improvement in the retarded group was reflected in briefer pauses but not longer utterances. There was a trend in the agitated group for improvement to be reflected in the utterance but not the pause measure. CONCLUSIONS: Clinical impressions are substantially related to acoustic parameters. Temporal changes associated with depression appear to reflect the depressed state whereas prosodic features seem to reflect a depressed trait. Acoustic measures of the patient's speech may provide objective procedures to aid in the evaluation of depression. Limitations of the study are discussed.

Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome.

Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/ obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death.

Management of obesity cardiomyopathy.

Therapy of acute exacerbations of congestive heart failure associated with obesity cardiomyopathy consists of dietary salt restriction, inspired oxygen, diuretics, and angiotensin-converting enzyme inhibitors or, if left ventricular systolic dysfunction is present, hydralazine/isosorbide dinitrate. Digitalis may be indicated in selected cases. These measures may also be useful chronically in association with weight loss. Substantial weight loss is capable of reversing all of the hemodynamic abnormalities associated with obesity except elevation of left ventricular filling pressure. Substantial weight loss may also reduce left ventricular mass and improve left ventricular diastolic filling in those with left ventricular hypertrophy before weight loss. Left ventricular systolic function also improves after weight loss in those with impaired pre-weight-loss systolic function. These beneficial effects of weight loss occur partly because of favorable alterations in left ventricular loading conditions. Substantial weight loss in patients with congestive heart failure associated with obesity cardiomyopathy produces a reversal of many of the clinical manifestations of cardiac decompensation and improves New York Heart Association functional class in most patients.

Cardiovascular complications of weight reduction diets.

Weight reduction diets may reduce the severity of risk factors for coronary heart disease such as diabetes mellitus, hypertension, and dyslipidemia. Several case reports and small studies of patients receiving starvation diets have reported hypotension and sudden cardiac death. Myofibrillar damage was documented in 1 case. Very-low-calorie diets are generally safe and well-tolerated. However, low QRS voltage, QT interval prolongation, and both nonsustained ventricular arrhythmias and sudden cardiac death have been described in subjects treated with such diets. Orthostatic hypotension may complicate very-low-calorie protein diets because of sodium depletion and depressed sympathetic nervous system activity. Bariatric surgery is associated with disproportionately high mortality rates in both the perioperative and postoperative periods.

Comparative efficacy of primary angioplasty with stent implantation and thrombolysis in restoring basal coronary artery flow in acute ST segment elevation myocardial infarction: quantitative assessment using the corrected TIMI frame count.

Following thrombolysis and primary percutaneous transluminal coronary angioplasty (PTCA) for acute ST segment elevation myocardial infarction, basal flow in the culprit artery is known to influence prognosis. The purpose of this study was to determine if differences exist in basal flow in culprit and nonculprit coronary arteries in patients with acute ST segment elevation myocardial infarction who were treated with thrombolysis or primary PTCA with stent implantation. Twenty patients were randomized to thrombolysis (with recombinant tissue plasminogen activator) and 24 to primary PTCA with stent implantation within 3 hours of onset of acute ST segment elevation myocardial infarction. Coronary angiography was performed 90-120 minutes after thrombolysis or immediately after PTCA with stent implantation and again at 18-36 hours after intervention in both groups. Patients who failed to achieve thrombolysis in myocardial infarction (TIMI) grade 2 or 3 flow were excluded. The corrected TIMI frame count was used as the index of basal coronary artery flow. Early after intervention the mean corrected TIMI frame count in the culprit coronary artery was significantly lower in the primary PTCA with stent group (27.4 +/- 7.7 frames) than in the thrombolysis group (39.8 +/- 10 frames, p < 0.001). Eight thrombolysis patients (40%) and 20 primary PTCA patients (83%, p < 0.01) achieved TIMI grade 3 flow early after intervention. By 18-36 hours after intervention there were no significant differences in the mean correct TIMI frame count between the thrombolysis and primary PTCA with stent groups. There were no significant differences in the mean corrected TIMI frame count between these two groups in the nonculprit coronary artery, either early after intervention or at 18-36 hours. In successfully reperfused coronary arteries following acute ST segment elevation myocardial infarction, primary angioplasty with stent implantation reestablished TIMI grade 2 or 3 flow faster and more effectively than thrombolysis did.

Effect of weight loss on the ECG of normotensive morbidly obese patients.

BACKGROUND: Morbid obesity produces a variety of ECG alterations, including leftward shifts of the P-wave, QRS, and T-wave axes; disproportionately high frequencies of low QRS voltage; left ventricular hypertrophy and left atrial abnormality; and a high frequency of T-wave flattening in the inferior and lateral leads. This study was designed to assess the effects of substantial weight loss on the ECG in morbid obesity. METHODS: We performed a resting 12-lead ECG on 60 normotensive patients (48 women and 12 men; mean +/- SD age, 37 +/- 7 years), whose body weight was twice their ideal body weight prior to and at the time of maximum weight loss after bariatric surgery. RESULTS: Mean weight decreased from 136 +/- 7 to 85 +/- 3 kg. Weight loss produced significant decreases in the frequencies of low QRS voltage; Romhilt-Estes point score > or = 5 points; SV(1) + RV(5) or V(6) > 35 mm; RV(5) or V(6) > 26 mm; RaVL > 11 mm; RaVL > or = 7.5 mm; SaVR > 14 mm; P-terminal force more negative than - 0.04 mm.s in lead V(1); and T-wave flattening in the inferior, lateral, and inferolateral leads. Weight loss significantly shifted the mean P-wave, QRS, T-wave axes rightward, and significantly reduced mean RaVL and mean SaVR voltage. CONCLUSION: Substantial weight loss is capable of reversing many of the ECG alterations associated with morbid obesity.

Left ventricular mass and systolic function in human immunodeficiency virus-infected patients after weight loss.

Transthoracic echocardiography was performed on 27 patients with human immunodificiency virus after weight loss and in 20 lean controls. Left ventricular mass index was significantly higher and left ventricular fractional shortening was significantly lower in patients with human immunodificiency virus after weight loss than in lean, normal controls.

Estrogen replacement therapy is underutilized among postmenopausal women at high risk for coronary heart disease.

Observational studies have found that estrogen replacement therapy (ERT) reduces the risk of coronary heart disease (CHD) in postmenopausal women. To determine the frequency of current use of ERT in an economically and racially diverse group of women at high risk for CHD, we examined the medical records of 393 women older than 40 who were admitted to the University of South Alabama Medical Center with symptoms suggestive of angina. Women in the study group were classified as African American or European American and data were examined for significant differences. Use of ERT was lower in African American women (11 of 111, 9.9%) than in European American women (26 of 152, 17.1%, odds ratio 1.9). Compared with the reported utilization of ERT in middle-class European American women, ERT is underutilized in this economically diverse group of women at high risk for coronary heart disease. In our population, European American women were twice as likely to be receiving ERT as African American women.