Severe functional mitral stenosis due to a left atrial myxoma masquerading as asthma.

While cardiac myxomas are the most common primary cardiac tumours, their overall incidence remains rare. Most cases (90%) are sporadic and occur in the third-sixth decades of life with a female predominance and have a specific predilection for the left atrium (75%). While often asymptomatic, clinical presentations depend on the tumour size, architecture and location.

Acute Aortocaval Fistula Secondary to Chronic Type 1 B Abdominal Aortic Aneurysm Endoleak.

Aortocaval fistula (ACF) is a rare complication of abdominal aortic aneurysms (AAA), involving less than 1% of all AAA and is associated with high morbidity and mortality; it is even more uncommon, following endovascular aneurysm repair. The clinical presentation can be variable and making the diagnosis can be difficult. It can present with symptoms and signs of an abdominal emergency or systemic hypoperfusion.

Portal vein thrombosis: What surgeons need to know.

Key Points: (a) The lifetime risk of portal vein thrombosis (PVT) is approximately 1%; (b) The portal vein is formed by the union of the splenic and superior mesenteric veins posterior to the pancreas; (c) Imaging modalities most frequently used to diagnose PVT include sonography, computed tomography, and magnetic resonance imaging; (d) Malignancy, hepatic cirrhosis, surgical trauma, and hypercoagulable conditions are the most common risk factors for the development of PVT; (e) PVT eventually leads to the formation of numerous collateral vessels around the thrombosed portal vein; (f) First-line treatment for PVT is therapeutic anticoagulation-it helps prevent the progression of the thrombotic process; (g) Other therapeutic options include surgery and interventional radiographic procedures including mechanical thrombectomy and thrombolysis; (h) Portal biliopathy is a clinicopathologic entity characterized by biliary abnormalities due to portal hypertension secondary to PVT and appears to be more common in cases of extrahepatic PVT.

Republished With Permission From: Quarrie R, Stawicki SP. Portal vein thrombosis: What surgeons need to know.

Left main coronary artery occlusion in an asymptomatic patient: late complication after arterial switch operation.

Long-term complications of the arterial switch operation for transposition of the great arteries include coronary artery stenosis and occlusion. We present a patient with high-grade left main coronary artery stenosis 18 years following the arterial switch procedure who was successfully treated with a left internal mammary artery to left anterior descending artery bypass.

Mitochondrial uncoupling does not decrease reactive oxygen species production after ischemia-reperfusion.

Cardiac ischemia-reperfusion (IR) leads to myocardial dysfunction by increasing production of reactive oxygen species (ROS). Mitochondrial H(+) leak decreases ROS formation; it has been postulated that increasing H(+) leak may be a mechanism of decreasing ROS production after IR. Ischemic preconditioning (IPC) decreases ROS formation after IR, but the mechanism is unknown.

Ischemic preconditioning preserves mitochondrial membrane potential and limits reactive oxygen species production.

Background: Mitochondrial superoxide radical (O(2)(•¯)) production increases after cardiac ischemia/reperfusion (IR). Ischemic preconditioning (IPC) preserves mitochondrial function and attenuates O(2)(•¯) production, but the mechanism is unknown. Mitochondrial membrane potential (mΔΨ) is known to affect O(2)(•¯) production; mitochondrial depolarization decreases O(2)(•¯) formation.

Ischemic preconditioning decreases mitochondrial proton leak and reactive oxygen species production in the postischemic heart.

Background: Proton leak (H(+) leak) dissipates mitochondrial membrane potential (mΔΨ) through the re-entry of protons into the mitochondrial matrix independent of ATP synthase. Changes in H(+) leak may affect reactive oxygen species (ROS) production. We measured H(+) leak and ROS production during ischemia-reperfusion and ischemic preconditioning (IPC) and examined how changing mitochondrial respiration affected mΔΨ and ROS production.

Ischemic postconditioning does not provide cardioprotection from long-term ischemic injury in isolated male or female rat hearts.

Background: Ischemic postconditioning (PoC) is a cardio-protective strategy in which initial reperfusion is interrupted by episodes of ischemia. It is unclear whether PoC can be achieved in the Langendorff perfused rat heart model. We investigated (1) whether postconditioning occurs in Langendorff perfused rat heart and (2) whether there is a gender-specific response to PoC.