Prosthetic aortic valve dehiscence is an uncommon complication of prosthetic valve endocarditis that may occur in patients who have undergone aortic valve replacement (AVR). The concurrent presence of aortic root pseudoaneurysm may further complicate the clinical presentation through the external compression of coronary arteries. Thus, patients may present with clinical features of coronary ischemia. Echocardiogram and coronary angiography are useful in establishing diagnosis. Treatment involves a multidisciplinary approach involving cardiologists, infectious disease specialists, and cardiothoracic surgeons. The authors of this study discuss a 51-year-old male who presented with anginal chest pain and was found to have a new left bundle branch block, elevated troponins, and left main coronary artery compression complicating aortic root aneurysm. He ended up requiring a re-do AVR, repair of the pseudoaneurysm, and coronary artery bypass graft.
The implantation of a temporary pacemaker lead is a very common procedure performed in most hospitals and is known to be relatively safe, but there can be serious complications in rare circumstances. Reported complications including arrhythmias, infection, thromboembolic phenomena, and perforation of the vessel or the heart are all extensively described. However, an unusual and life-threatening complication that is not frequently discussed is the formation of intracardiac knots. We present a case of a rare complication of a temporary pacemaker placement with the formation of a knot in the distal lead requiring expert technique for removal.
Cor triatriatum sinister (CTS) is a rare congenital cardiac malformation. In CTS, a fibromuscular membrane subdivides the left atrium into 2 chambers. The communication between the 2 chambers is through 1 or more orifices in the dividing membrane. We present an interesting case of a 2-month-old infant with obstructed CTS membrane who first presented on account of poor feeding and failure to thrive. Echocardiography showed a persistent levoatrial cardinal vein (LACV) connecting the left atrium and the innominate vein. This allowed the proximal left atrial chamber to decompress its blood volume into the innominate vein and subsequently the superior vena cava. There was minimal prograde blood flow across the Cor triatriatum membrane, so the majority of pulmonary venous blood ultimately returned to the heart by way of the decompressing vertical vein into the systemic venous circulation. Surgical repair was performed with an uneventful postoperative course. The specific anatomical variant of Cor triatriatum found in our subject has rarely been reported.
Brugada syndrome is a known cause of dysrhythmias and sudden cardiac death. It is linked to mutations in myocardial sodium channel leading to hyperexcitable cardiac myocytes. The use of this sedative has been linked to the development of inducible Brugada via blockade of sodium currents in cardiac myocytes. Although propofol is usually avoided in patients with known Brugada syndrome, some patients might have undiagnosed Brugada syndrome and thus are at risk for complications. We present a case of propofol induced Brugada in a critically ill patient.
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