Mitral annular calcification (MAC) commonly manifests as an incidental, asymptomatic finding that is associated with several cardiovascular risk factors, atherosclerosis, cardiovascular death, and all-cause mortality. Very rarely, patients with severe MAC can have extensive dystrophic calcification extending into the left atrial wall, termed porcelain left atrium. In this case report, we describe a patient who experienced multiple calcific acute embolic strokes in the setting of severe mitral annular calcification and porcelain left atrium. Our patient presented with multiple, small bilateral acute infarcts scattered throughout the cerebrum and cerebellum confirmed on magnetic resonance imaging (MRI). He was placed on continuous telemetry and underwent multimodal imaging with transthoracic and transesophageal echocardiography, carotid neck ultrasound (US), head and neck computed tomography angiogram (CTA), and cardiac MRI. There were no arrhythmic events detected on telemetry, and all imaging excluded left ventricular thrombi, aortic atheroma, carotid artery stenosis, intracardiac shunting, or large vessel stenosis. Noted on imaging, however, was severe mitral annular calcification with numerous, highly mobile calcific extensions and densely calcified plaque along the posterior left atrial wall, presumed to be the source of this patient's embolic stroke. Cardiac catheterization was significant for severe three-vessel disease requiring coronary artery bypass grafting, and our patient was subsequently discharged to outpatient follow-up on event monitoring and aspirin monotherapy. This case serves to highlight a previously unreported complication of calcific embolic stroke in severe MAC and porcelain left atrium, and highlight the need for further randomized controlled trials to determine the optimum management of these cases.
A 93-year-old female presented with persistent shortness of breath and wheezing since the consumption of a meal. Her past medical history is significant for a clinical diagnosis of asthma at the age of 88 years, without pulmonary function testing, complicated by several prior visits to the emergency department (ED) for recurrent exacerbations. Multiple bronchodilators in the ED provided only minimal improvement in her symptoms. Chest imaging eventually revealed a giant, fluid-filled hiatal hernia exhibiting a compressive effect on the posterior aspect of the left atrium. The etiology of the patient's airway bronchoconstriction was likely multifactorial. We hypothesize that the extrinsic, dynamic compression of the bronchial tree by the peristaltic motion of the hiatal hernia, microaspiration from gastroesophageal reflux, and peribronchial edema from left atrial compression accounted for our patient's unique presentation. An outpatient methacholine challenge test eventually excluded bronchial asthma. Although she was considered a poor surgical candidate, she has had no further recurrences of her symptoms with counseling on conservative lifestyle changes. This case serves to highlight the heterogeneity in presentations of hiatal hernias, particularly in elderly females. Furthermore, it remains prudent to maintain a broad differential for wheezing, as evidenced by our patient who was previously managed for a number of years as poorly controlled asthma.
Hypercalcaemia-induced rhinovirus has only been reported in a single study in children. Here, we report a case of hypercalcaemia in an adult who tested positive for rhinovirus. This patient underwent an extensive evaluation of hypercalcaemia, and it was found to be mediated by an increase in 1,25 hydroxy-vitamin D that could not be attributed to a cause. Their hypercalcaemia responded to standard treatment with intravascular expansion, bisphosphonates and calcitonin. Serum 1,25 OH vitamin D levels returned to normal with recovery from rhinovirus infection.
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