Max is a 61-year-old retired police officer whom you've known for the past 4 years. He's never smoked, he watches his diet rigorously, and exercises 5 days a week. The only item of significance in his past medical history is a paroxysmal atrial fibrillation that developed after a routine inguinal hernia operation 6 years ago. Though he had a myocardial perfusion scan with stress test and an echocardiogram at the time, they showed no abnormalities, and no etiology for the arrhythmia was ever found. Initially, Max's cardiologist elected to treat the episodes with propa¡fenone and metoprolol, on an "as needed" basis. Over time, the palpitations became more frequent and the medications lost their effectiveness, so the patient underwent a successful cardiac ablation procedure that restored his rhythm to sinus.
Max presents to your office with a 6-week history of dizziness, hemoptysis, productive cough and shortness of breath. On examination, air entry seems good in all lung fields, with no adventitious sounds. You order a complete blood count and chest x-ray, and diagnose Max with a lower respiratory tract infection for which you start him on moxifloxacin 400 mg daily for 10 days. The white blood cell count comes back at 7.6 x 109/L, the hemoglobin level 116 g/L. The chest x-ray is normal, other than showing old granulomatous disease.
Over the next week, Max takes a significant turn for the worse. Your previously fit patient continues to cough up blood and is now short of breath on minimal exertion. You order an urgent CT scan of the chest, which reveals an "extensive, patchy, ground-glass attenuation and septal thickening of the left upper lobe." You arrange for a respiratory consultation stat, after which Max undergoes a bronchoscopy with bronchoalveolar lavage.
The cytology results of the lavage are negative and there's no growth from cultures, including pneumocystis pneumonia and acid-fast bacilli. The patient continues to decline rapidly. What would you do next?
Why is Max's strength waning?
The consulting respirologist ordered a CT angiogram of Max's chest. This revealed a mediastinal mass over the left pulmonary veins. A subsequent PET scan showed only chronic inflammation and no evidence of a malignant process.
Max was next referred to a thoracic surgeon for a tissue biopsy. Before proceeding, a quantitative lung scan was done. This showed almost complete loss of perfusion of the entire left lung, secondary to stenoses of the left superior and inferior pulmonary veins. The surgeon performed a balloon angioplasty of these vessels, restoring perfusion to the left lung and, almost overnight, Max returned to his old self.
The etiology of Max's pulmonary vein stenoses was felt to be a complication of his previous ablation procedure. Radiofrequency catheter ablation of atrial fibrillation is frequently done by radio waves delivered by a catheter inserted into the pulmonary veins. Although the procedure often cures the arrhythmia, it can also significantly scar the pulmonary veins. In a retrospective study published in 2003 (Saad EB et al. Ann Intern Med 2003;138[8]:634-8), 18 of 335 patients developed pulmonary vein stenosis. Although this is a rare complication of cardiac ablation, physicians should be on the lookout for it.
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