We report a patient with transient advanced atrioventricular (AV) block induced by obstructive sleep apnea (OSA). This 54-year-old man was diagnosed as having severe OSA and AV block with ventricular asystole for more than 6 s during overnight polysomnography, which occurred just from the onset of OSA before oxygen desaturation had occurred. An electrophysiological study revealed normal AV conduction system function and normal His-Purkinje system function. The resolution of OSA with continuous positive airway pressure therapy improved the advanced AV block. Therefore, the bradyarrhythmia was determined to be an OSA-induced AV block that occurred before oxygen desaturation.
A 67-year-old man with overt hypothyroidism and medically controlled hypertension was admitted for coronary angiography because of exertional angina. His triiodothyronine (T3) and thyroxine (T4) levels had been low for 4 years. Although signs and symptoms of hypothyroidism were apparent, his hypercholesterolemia was mild. Coronary angiography revealed an eccentric stenosis in the distal portion of the right coronary artery and it was decided to perform angioplasty because his angina had continued in spite of medication. The dissection appeared at the lesion site after the first nominal inflation, and a subsequent image disclosed a spiral dissection from the dilated site to the aortic sinus and peripheral coronary artery. Although emergency stenting could not prevent the extension near the origin of the brachiocephalic artery, the false lumen thrombosed and then diminished with conservative therapy. Aorto-coronary dissection is potentially life-threatening and has been recently reported as a complication during cardiac catheterization procedures. Chronic hypothyroid insufficiency may be one of the risk factors for this complication.
Anomalous left main coronary artery (LMCA) originating from the right coronary sinus and running between the aorta and pulmonary trunk is a rare congenital condition. Although this disease is known to be associated with myocardial infarction and sudden death, the precise mechanism is uncertain. A 14-year-old male with this anomaly developed myocardial infarction during exercise complicated by primary antiphospholipid syndrome. He was admitted to hospital with persistent chest pain and sudden cardiac collapse that occurred while he was running. Cardiac catheterization demonstrated a narrowed segment in the LMCA and impaired blood flow, prompting a diagnosis of extensive anterior myocardial infarction. Emergency bypass surgery was performed using a single saphenous vein graft to the left anterior descending artery. Postoperative angiography showed the presence of an anomalous LMCA arising from the right sinus of Valsalva and running between the great vessels. The aortic samples were pathologically normal. He was discovered to also have primary antiphospholipid syndrome and was discharged without symptoms after warfarin therapy. Complicated primary antiphospholipid syndrome may trigger myocardial infarction in asymptomatic patients with this type of coronary anomaly.
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