Complete disappearance of PVCs was also confirmed with ILR registration (Fig.
In March 2015, after completely abstaining from melatonin, the patient became free from any symptoms. In September and November 2014, he discontinued melatonin resulting in complete cessation of symptoms. Subsequently, 150 mg of flecainide was given in combination with 2.5 mg of bisoprolol, but without any effect. Computed tomography angiography showed no coronary artery disease with a calcium score of zero. A normal left ventricular function was seen on echocardiogram. An exercise test showed only occasional PVCs, both during exercise and recovery phase, and without symptoms of angina or ST segment alterations.
The dominant morphology of the PVCs was suggestive of an OT origin on a 12-lead electrocardiogram (Fig. Holter tracings revealed more than 2000 multiform PVCs per 24 hours and ILR registration (Medtronic Reveal LINQ) confirmed PVCs as the cause for the palpitations. The patient also used melatonin (1 mg once daily, sublingual) because of problems falling asleep. Other medication used by the patient included sitagliptin (oral antihyperglycaemic), atorvastatin (statin), candesartan (angiotensin II receptor blocker), and metformin (oral antihyperglycaemic). In August 2014, he was referred to our outpatient clinic because of palpitations despite being on beta-blocker therapy. The first patient was a 72-year-old man with an uneventful cardiac history (except for a short episode of paroxysmal supraventricular tachycardia in 1980). As OT arrhythmias represent more than 10% of overall referrals for electrophysiological studies, our present findings highlight the importance of identifying pharmacons that can mediate OT PVC generation because refraining from these drugs is safer and more cost-effective than trying to treat the disease with antiarrhythmic medication or catheter ablation. In our patients, however, we observed a clear association between melatonin use and the occurrence of PVCs from the OT. Based on its pharmacological effect of alleviating sleeping problems, it is rather expected to protect against arrhythmias because of the association between arrhythmias and sleep deprivation. Melatonin is widely used as a prescription/over-the-counter drug to treat sleep disorders. Here, we report on the pineal hormone melatonin (which normally regulates the body's circadian rhythms and sleep–wake cycles) being capable of mediating OT PVCs in the absence of structural heart disease. Although it is well known that triggered activity is the main underlying mechanism of arrhythmogenesis, precipitating factors for this focal activity remain largely undetected. The majority originate in the ventricular outflow tracts (OTs). Even in patients with a structurally normal heart, symptomatic premature ventricular contractions (PVCs) are relatively common.