Obesity and the electrocardiogram

Abstract

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.

Increased epicardial adipose tissue volume is associated with PR interval prolongation

“…Our study results reveal a positive association between PR interval and both BMI and WHR. This is consistent with reports noting PR interval prolongation with increasing obesity [8,31,32]. In particular, increasing obesity marks increasing pro-inflammatory cytokines.…”

Electrocardiographic Abnormalities in Subjects With Overweight, Obesity and Abdominal Obesity.

“…ECG pathology more common in obese patients, which are manifested in the form of lower voltage, left ventricular hypertrophy, extension of left atrial [13]. There is evidence that visceral fat causes the appearance of pathologic ECG due to sympathetic activation, and was described cases of arrhythmia in patients with obesity [14]. In addition, weight loss was accompanied by the elimination of ECG abnormalities [15], which is similar to the results of research Colombia and Italy [16,17].…”

Prevalence of QT interval prolongation in inflammatory bowel disease

“…Underlying factors could be likely associated with sleep apnea or changes in cardiac morphology because of inappropriate left ventricular mass as suggested by the Losartan Intervention for Endpoint Reduction (LIFE) study (47,48). The mechanistic causes in turn have been postulated to be related to defective calcium inactivation and decreased expression of voltage-gated potassium channels leading to altered myocyte action potentials (49,50).…”