First degree AV block 12, 13, 14, 15, 16, mobitz type I second degree AV block 17, 18, and third degree AV block 19, 20, 21 has been reported with cocaine use.Cocaine in healthy hearts has been shown to reduce the ventricular effective refractory period however with no change in the intraventricular conduction or spontaneous or induced ventricular arrhythmias 22. A study on asymptomatic chronic cocaine users reported sinus bradycardia in 21% of the cases 11. Studies have reported bradyarrhythmia in patients who presented with chest pain after acute cocaine use 10. Multiple studies have reported increase in mean heart rate in cocaine users 7, 8, 9. Net effect of cocaine abuse is dependent on sympathomimetic action 2, sino-bradycardic effect 5 and its direct anesthetic properties 6. Cocaine is a neuronal norepinephrine and dopamine reuptake inhibitor and thus acts as a sympathomimetic agent 2. Myocardial infarction, arrhythmias, aortic dissection and cardiomyopathy are among the cardiovascular complications reported with cocaine use 2, 3, 4. Adolescents in the age group of 18 to 25 years of age reported a prevalence of use of 1.4% 1. Cardiac monitoring subsequently revealed normal sinus rhythm on the second day of hospitalization.Ībout 1.5 million people reported cocaine use in the past month in 2014. Transthoracic echocardiogram showed normal ejection fraction with no wall motion abnormalities. Troponin levels were also within normal limit. Thyroid function tests were within normal limits. Urine toxicology was positive for cocaine. EKG revealed mobitz type II heart block (Image 1). Investigations including complete blood count, comprehensive metabolic panel, urine toxicology, thyroid function tests, troponin, brain natriuretic peptide, chest X-ray (CXR) and electrocardiograph (EKG) were obtained. The patient was not on any AV nodal blocking agents. On presentation patient was afebrile, bradycardic at 54 beats per minute, respiratory rate was 16 per minute and blood pressure was 123/58 mm of Hg. Pain was no reproducible on chest palpation. The patient described the pain as 6/10 in intensity, non-radiating, not related to breathing or changes in position. Though rare, physicians should be aware of the possibility of bradyarrhythmias associated with cocaine abuse in order to apply standard therapy such as pacemaker in the event of non-resolution of this serious arrhythmia.Ī 55 year old female with a past medical history of asthma, schizoaffective disorder, presented with a chief complaint of retrosternal chest pain after cocaine use. Electrophysiology studies have previously confirmed cocaine mediated delay in impulse conduction and repolarization. Cocaine is known to inhibit sodium channels and thus has been known to decrease SA node automaticity and conduction via AV node. Patient spontaneously converted to normal sinus rhythm the following day post admission to the hospital. This case occurred in a 55 year old woman who presented with retrosternal chest pressure and tested positive for cocaine abuse as documented by urine toxicology test. While Multiple cases of atrioventricular (AV) conduction blocks including first degree AV block, Mobitz type I and third degree AV blocks have been previously reported, we hereby present the first case report of cocaine- induced Mobitz type II second degree AV block.
However, cocaine also exerts other effects on the conduction system including sympathomimetic, sino-bradycardic as well as local anesthetic properties. Cocaine acts as a sympathomimetic by inhibition of reuptake of neuronal catecholamines, leading mostly to tachyarrhythmias on presentation. The complex effects of cocaine on the conduction system of the human heart has not been completely understood. Cocaine is a commonly abused illicit drug in the United States.
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