We investigated the prevalence of cardiac arrhythmic events in patients with moderate-severe obesity during cardiopulmonary exercise testing before and after SG. To the best of our knowledge, no previous study analyzed the association between patients affected by severe obesity undergoing SG and exercise-induced cardiac arrhythmias. The main outcomes of this study are:
SG and ECG parameters
Patients affected by obesity present usually higher resting HR compared with subjects with normal weight, probably due to a reduction in parasympathetic activity and relative predominance of sympathetic activity.18 Weight loss after bariatric surgery has been shown to decrease resting HR and affect HR variability.19 Moreover, several studies showed that patients with obesity have a prolonged QT interval, highlighting the effects of bariatric surgery on reducing QTc.20–22 In our study, resting HR and QTc interval were found significantly decreased at six months post SG and further changes are not evident one year after bariatric surgery. The relationship between obesity and prolonged ventricular repolarization is not clearly understood and various hypotheses have been proposed. Typical obesity related comorbidities such as insulin resistance, arterial hypertension and obstructive sleep apnea syndrome could be involved in shortening ventricular repolarization parameters.23–25 All these comorbidities are represented in our study population before SG and their reduction after bariatric surgery could influence the ECG repolarization pattern.
Moreover, patients post SG showed a longer exercise phase when compared to their own pre-SG testing. This data is in accordance with previous study results that showed how patients with severe obesity have a better exercise tolerance six months after bariatric surgery.26 SG has a positive impact on body composition, physical functioning and metabolic parameters, allowing to perform the same workload with less energy expenditure, also due to improved cardiac reserve.27
SG and arrhythmic risk during exercise testing
Our analysis focused on the comparison of arrhythmias during maximal exercise testing before and after SG. It is known that obesity is associated with an increased risk of cardiac arrythmia including AF,28,29 PBs10,16 and sudden cardiac death.30,31 Moreover, several studies showed the importance of weight reduction in patients with obesity for the treatment of AF, while others report little or no effectiveness.11,15,32−34 In our study only one patient presented a short-run AF at six months post-SG and none presented an exercise-induced AF, therefore, it was not possible to analyze the effect of SG on this form of arrhythmia. However, P-wave dispersion and QTc dispersion showed to be attenuated after bariatric surgery, indirectly suggesting a reduction in risk of AF, ventricular arrhythmias, and sudden cardiac death.20–22, 35,36
At six months post-SG, despite a major loss of BMI by all patients, an increase in ventricular arrhythmias, mainly during the recovery phases, was showed. The same phenomenon does not seem to be confirmed for the rest and exercise phases. This behaviour seems to contradict some of the evidence on arrhythmias and obesity since an independent association between BMI and exercise-induced ventricular arrhythmias has already been described in a large cohort of patients.16 Indeed, several hypotheses (anatomical, immunological, hormonal and multifactorial) have attempted to explain why patients with obesity are more prone to arrhythmic onset. Different studies agree that atrial and ventricular ectopy activation could be due to the structural and electrical remodeling that increase the risk of AF and VPBs.37,38 Moreover, the epicardial fat presents a pro-inflammatory profile, promoting chronic inflammation of the adjacent cardiac tissue, which may potentially increase the risk of ventricular arrhythmias.31,39 A further hypothesis involves the possible role of leptin in increasing sympathetic activity and reducing vagal tone.40 This hormone has been demonstrated to correlate with BMI and it has been associated with an increase in mean arterial blood pressure and HR in animal models, due to alterations in the autonomic nervous system.41,42
At twelve months post-SG evaluation, an overall reduction in number of patients presenting VPBs and in VPBs/minute, still primarily during the recovery phase, was observed. The prevalence of arrhythmias seems similar to one month pre-SG evaluation. A possible explanation for this increase and subsequent decrease in arrhythmias during the recovery phase could be due to the imbalance between the circulating catecholamines produced during exercise and the raising of vagal tone, responsible for lowering HR after exercise. An attenuated vagal reactivation might be associated with a minor suppression of ventricular activity and more frequent ventricular arrhythmias during recovery. This was also described as an important and independent predictor of increased mortality risk.43 A previous study conducted by our research group showed that during the recovery phase HR decreases more rapidly in patients at six months after SG, when compared to the pre-surgical evaluation.26 In fact, in these patients there is no difference in the maximum HR reached during exercise testing between evaluations pre and post-SG, while the resting HR appears lower at six months after surgery; therefore, a greater vagal effort is required for the complete recovery after exercise.26 Results of the current study are in line with those already described and provide an implementation of data evaluating also cardiovascular adaptations one year after bariatric surgery. Indeed, at twelve months post-SG, the reduction of arrhythmic events during recovery phase might suggest a restoration of sympathetic-vagal balance related to weight loss maintenance and metabolic equilibrium.
Moreover, a further hypothesis could be related to the nutritional alterations that these patients have to undergo in the first period after SG.44 In fact, bariatric surgery patients are at risk for deficiency of different nutrients, especially of trace elements, despite taking supplements.45,46 The transition from strong catabolism during the first period after bariatric surgery to progressive anabolic recovery can cause nutritional alterations such as micronutrient deficiency (e.g. thiamine), intracellular and extracellular electrolyte disturbances (hypophosphatemia, hypokalaemia, hypomagnesemia), fluid imbalance and salt retention even in the cardiac tissue.47 Thus, these subjects might be exposed to an increased risk of cardiac arrhythmias, in a similar way to those documented in the "refeeding syndrome".48 It is possible that restoring a regular diet and maintaining a stable weight will help to reduce the arrhythmic susceptibility during the first year after surgery.