Sinus node dysfunction following bariatric surgery: A case report

Abstract

Sinus node dysfunction is often due to degeneration of the heart’s impulse-generating system. We report a case of a 40-year-old woman with a recent gastric sleeve surgery, who presented with symptomatic sinus bradycardia following significant post-surgical weight loss. Extensive workup excluded common causes such as electrolyte disturbances, hypothyroidism, or cardiomyopathy. We hypothesize that alterations in leptin metabolism due to weight loss triggered increased vagal stimulation, leading to her bradycardia. The patient was treated with theophylline as a noninvasive alternative to pacemaker implantation. Long-term monitoring showed partial improvement in heart rate. This case highlights the need for vigilance in managing bradycardia as a potential side effect of bariatric surgery-induced weight loss, emphasizing the importance of follow-up and the potential role of leptin in heart rate regulation.

Introduction

Sinus node dysfunction is a condition that typically affects the elderly and is most often due to degeneration of the heart’s impulse-generating system. ¹ Occasionally, specific contributing factors can be identified, including electrolyte disturbances (e.g., hyperkalemia), hypothyroidism, negative chronotropic medications (such as beta-blockers, antiarrhythmics, certain eye drops, antipsychotics, and dementia drugs), obstructive sleep apnea syndrome, ischemic heart disease, and infiltrative cardiomyopathies. The indication for treatment is determined by whether the patient is symptomatic. It is important to correlate symptoms with the current bradycardia. If no reversible causes are found, pacemaker implantation may be indicated. ¹ Here we present a case where the patient developed bradycardia after a significant weight loss where the presumed link is a change in the leptin metabolism.

Case report

A woman in her early 40s with a history of psoriatic arthritis, post-traumatic stress disorder, and recent gastric sleeve surgery was admitted to the emergency department due to a heart rate in her 30s.

Clinical examination revealed a normal-weight woman with a body mass index (BMI) of 21 kg/m². Her respiration was unremarkable, and she was clinically well-perfused. Auscultation of the heart and lungs was normal, with no evidence of fluid overload. An electrocardiogram (ECG) revealed sinus bradycardia with a normal PQ interval, no fascicular or bundle branch block (QTc 375 ms), and no indications of structural heart disease (Figure 1). Laboratory tests showed no electrolyte or thyroid abnormalities but did reveal a slightly elevated NT-proBNP level of 257 ng/L (reference <169 ng/L). Her medications included calcium tablets, folic acid, and multivitamins. Echocardiography findings were notable only for a mildly dilated normotrophic left ventricle and a bicuspid aortic valve without stenosis or insufficiency.

Figure 1.

12 lead ECG (speed: 50 mm/s): Sinus bradycardia with a frequency of 40. Normal PQ time, 163 ms.

The patient’s history revealed a weight loss from 183 kg in 2017 to 102 kg before the bariatric surgery occurred on February 1, 2024. At the time of surgery, her recorded pulse was 60 beats per minute (bpm) (Table 1). In the following 7 weeks leading up to her admission, she had lost an additional 49.4 kg, bringing her current weight to 52.6 kg. During this period, she noticed a progressively lower pulse on her fitness watch. Concurrently, she reported increased exertional dyspnea and episodes of nocturnal dyspnea. She denied any syncopal episodes, palpitations, or chest pain. Telemetry showed an average heart rate of 40 bpm, with a range of 23–75 bpm.

Table 1.

The course of the weight and heart rate throughout the case.

Variable	Before weight loss	Preoperative	Admission	Follow up
Weight	183 kg	102 kg	52.6 kg	49 kg
Heart rate	—	60	40	55

The patient was unaware of any family history of premature death, early-onset heart failure, or pacemaker implantation at a young age. In the absence of drug-induced bradycardia, electrolyte imbalances, thyroid disorders, or specific cardiomyopathies, we hypothesized that increased vagal stimulation secondary to alterations in leptin metabolism was the triggering factor. We assumed that the cause of bradycardia was reversible and was thus reluctant to treat her symptoms with pacemaker implantation. Instead, to increase her heart rate, she was given sustained-release theophylline tablets in gradually increasing doses. By the end of her hospital stay, her average heart rate remained the same, with a slight increase in maximum heart rate to 88 bpm. Symptomatically, she reported little change. After a 3-week hospital stay, she was discharged on theophylline sustained-release 300 mg twice daily. Long-term ECG monitoring conducted 6 weeks later showed an increase in the average heart rate to 55 bpm with a range of 34–123 bpm. The QTc interval increased marginally to 393 ms. At the same time, she reported no significant changes in symptoms, whereas her weight had decreased slightly to 49 kg. It should be noted that the patient was very dismissive regarding any advice that would increase her body weight.

Discussion

In Norway, bariatric surgery is currently offered to patients with a BMI >40, or >35 with additional criteria. ² The two most common techniques are gastric sleeve and gastric bypass. These involve resection of the greater curvature of the stomach or bypassing with subsequent anastomosis of a smaller part of the stomach to the small intestine, respectively. In 2022, a total of 1576 such procedures were performed in Norway. ³

Several registry and observational studies described in PubMed suggest an association between bradycardia and bariatric surgery.^4,5 The underlying cause is believed to be changes in leptin levels, which are closely related to BMI. Leptin is a signaling hormone primarily secreted by adipose tissue and the stomach. Leptin levels reflect the amount of fat in the body and promote the sensation of satiety. ⁶ With declining BMI and thus declining leptin levels, an association with the development of bradycardia in humans has been observed. ⁷ The impact of leptin on heart rhythm has been studied by exposing rat hearts to varying concentrations of leptin, showing that low concentrations induce bradycardia, while higher doses produce a biphasic response with initially lower and then higher heart rates with increasing concentrations. ⁸

In our case, it seemed reasonable to assume that the bradycardia contributed to her exertional dyspnea. After adequate investigation, we could not identify any specific factors causing her sinus bradycardia. Considering other known cases, we hypothesized that alterations in leptin metabolism were the underlying cause. There are no randomized studies regarding the treatment of this condition. It is believed that the bradycardia resolves when the weight stabilizes, although this is not certain. Theophylline, a xanthine derivative with chronotropic properties, exerts its effects via phosphodiesterase inhibition. Symptomatic treatment with theophylline rather than pacemaker implantation or neurocardiogenic ablation seemed most appropriate, as this was assumed to be a reversible condition.

Conclusion

Along with some previous reports in the international literature, this case highlights an association between significant weight loss following bariatric surgery and the onset of sinus bradycardia. It underscores the importance of follow-up for these patients and the fact that none of the interventions we perform are without potential side effects. Considering the rapidly growing market for drug-induced weight loss, vigilance regarding adverse effects should be a high priority.