Suspected association of ventricular arrhythmia with air pollution in a motorbike rider: a case report
Suspected association of ventricular arrhythmia with air pollution in a motorbike rider: a case report
Published: April 2009
Introduction
To some extent premature ventricular complexes (PVCs) are a normal finding in healthy individuals and the prevalence increases with age and is more common in men. However, PVCs can occur in association with a variety of stimuli and can be produced by direct mechanical, electrical and chemical stimulation of the myocardium. Often they are noted in patients with false tendons, ischaemic or inflamed myocardium and during infection, hypoxia, anaesthesia or surgery. They can be provoked by a variety of medications, by electrolyte imbalance, by tension states, by myocardial stretch and by excessive use of tobacco, caffeine or alcohol [1]. A cause of PVCs that is not so well known among physicians is the association between air pollution and ventricular arrhythmias.
Case presentation
A 43-year-old previously healthy man, a physician, living in a city of about 150,000 inhabitants, began to use a lightweight motorbike to commute to work, a distance of about 10 km, in heavy traffic in the middle of August 2006. He had previously been travelling in a car fitted with an air pollution filter, and had experienced no previous heart symptoms. He also walked or jogged about 6 km four to five times a week with no problems and was not on any medication. He felt relaxed and did not experience stress while riding the motorbike in heavy traffic. There were numerous traffic lights on his journey to work, which meant that he was forced to stop behind buses and trucks on several occasions where he experienced a strong smell of exhaust fumes.
After commuting to and from work by motorbike for about 2 weeks he began experiencing cardiac extrasystoles, something not previously experienced; on one occasion he was unable to sleep due to palpitations. He sought help and had an electrocardiogram (ECG) the following morning, which showed PVCs in bigeminy. The patient had also sinus tachycardia with a heart rate of about 110 beats per minute.
The patient was admitted to the cardiac intensive care unit and was examined using echocardiography, which was found to be normal, and there were no signs of false tendons. No ischaemia was seen on ECG and there were no signs of infarction. The frequency of PVCs began to decrease about 8 hours after admission. Blood tests showed no indications of infarction or infection, his blood glucose was normal and his lipid status and thyroid status were within normal limits. The patient had no fever. During the night and the next morning only a few PVCs and some premature atrial complexes were observed and the patient was discharged home. The diagnosis was given as myocarditis, although this diagnosis was uncertain.
The patient rested for 2 weeks with no further symptoms before returning to work. For the first few weeks he drove his car to work, but then began to use his motorbike again. Having used it for a few weeks on the same route he again began to experience extrasystoles and therefore contacted his physician, who recommended an exercise test and Holter ECG.
In the few days before the Holter ECG was applied the patient refrained from using his motorbike and began to feel better. Only a few PVCs and premature atrial complexes were found during 24 hours of Holter monitoring. The heart rate variability (HRV) showed a pattern with a somewhat high low-frequency to high-frequency ratio. An exercise test was carried out and the patient performed well, with no chest pain, arrhythmias or signs of ischaemia.
The patient began to believe that there was an association between using his motorbike and his symptoms and decided to stop using it. Since then no symptoms, apart from an occasional single extrasystole, have been noted by the patient.
Discussion
In the present case there was no obvious explanation for the PVCs. Myocarditis was thought to be the underlying cause, even if this diagnosis was uncertain. This is a condition with various clinical presentations, from non-specific symptoms (fever, myalgias, palpitations or exertional dyspnoea) to fulminant haemodynamic collapse and sudden death. Myocarditis is difficult to diagnose and endomyocardial biopsy remains unequivocally the gold standard for establishing the diagnosis [2], although this cannot always be used in clinical practice. Cardiac biomarkers, especially troponin T or I, are now routinely measured by most clinicians when a clinical diagnosis of myocarditis is considered [2]. In the present case, however, the cardiac biomarkers creatine kinase and troponin T were not elevated.
Echocardiography can also help in the diagnosis of myocarditis, often showing left ventricular dysfunction and segment wall abnormalities in patients with biopsy-proven myocarditis [2]; here, however, the echocardiography was also normal. The patient had no obvious signs of ongoing infection and he had normal laboratory findings. Thus, myocarditis was an uncertain diagnosis in this case.
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