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. We hypothesize that pharmacologically increasing mitochondrial H(+) leak would decrease ROS production after IR. We further hypothesize that IPC would be associated with an increase in the rate of H(+) leak. Isolated male Sprague-Dawley rat hearts were subjected to either control or IPC. Mitochondria were isolated at end equilibration, end ischemia, and end reperfusion. Mitochondrial membrane potential (mΔΨ) was measured using a tetraphenylphosphonium electrode. Mitochondrial uncoupling was achieved by adding increasing concentrations of FCCP. Mitochondrial ROS production was measured by fluorometry using Amplex-Red. Pyridine dinucleotide levels were measured using HPLC. Before IR, increasing H(+) leak decreased mitochondrial ROS production. After IR, ROS production was not affected by increasing H(+) leak. H(+) leak increased at end ischemia in control mitochondria. IPC mitochondria showed no change in the rate of H(+) leak throughout IR. NADPH levels decreased after IR in both IPC and control mitochondria while NADH increased. Pharmacologically, increasing H(+) leak is not a method of decreasing ROS production after IR. Replenishing the NADPH pool may be a means of scavenging the excess ROS thereby attenuating oxidative damage after IR.

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. We examined the relationship between O(2)(•¯) production and mΔΨ during IR and IPC. MATERIALS/METHODS: Rat hearts were subjected to Control or IPC. Mitochondria were isolated at end equilibration (End EQ), end ischemia (End I), and end reperfusion (End RP). mΔΨ was measured using a tetraphenylphosphonium electrode. Mitochondrial O(2)(•¯) production was measured by electron paramagnetic resonance using DMPO spin trap. Cytochrome c levels were measured using high-pressure liquid chromatography. RESULTS: IPC preserved mΔΨ at End I (-156 ± 5 versus -131 ± 6 mV, P < 0.001) and End RP (-168 ± 2 versus -155 ± 2 mV, P < 0.05). At End RP, IPC attenuated O(2)(•¯) production (2527 ± 221 versus 3523 ± 250 AU/mg protein, P < 0.05). IPC preserved cytochrome c levels (351 ± 14 versus 269 ± 16 picomoles/mg protein, P < 0.05) at End RP, and decreased mitochondrial cristae disruption (10% ± 4% versus 33% ± 7%, P < 0.05) and amorphous density formation (18% ± 4% versus 28% ± 1%, P < 0.05). CONCLUSION: We conclude that IPC preserves mΔΨ, possibly by limiting disruption of mitochondrial inner membrane. IPC also decreases mitochondrial O(2)(•¯) production and preserves mitochondrial ultrastructure after IR. While it was previously held that slight decreases in mΔΨ decrease O(2)(•¯) production, our results indicate that preservation of mΔΨ is associated with decreased O(2)(•¯) and preservation of cardiac function in IPC. These findings indicate that the mechanism of IPC may not involve mΔΨ depolarization, but rather preservation of mitochondrial electrochemical potential.

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. MATERIALS AND METHODS: Isolated rat hearts (n = 6/group) were subjected to either control-IR or IPC. Rate pressure product (RPP) was measured. Mitochondria were isolated at end reperfusion. Respiration was measured by polarography and titrated with increasing concentrations of malonate (0.5-2 mM). mΔΨ was measured using a tetraphenylphosphonium electrode. H(+) leak is the respiratory rate required to maintain membrane potential at -150 mV in the presence of oligomycin-A. Mitochondrial complex III ROS production was measured by fluorometry using Amplex-red. RESULTS: IPC improved recovery of RPP at end reperfusion (63% ± 4% versus 21% ± 2% in control-IR, P < 0.05). Ischemia-reperfusion caused increased H(+) leak (94 ± 12 versus 31 ± 1 nmol O/mg protein/min in non-ischemic control, P < 0.05). IPC attenuates these increases (55 ± 9 nmol O/mg protein/min, P < 0.05 versus control-IR). IPC reduced mitochondrial ROS production compared with control-IR (31 ± 2 versus 40 ± 3 nmol/mg protein/min, P < 0.05). As mitochondrial respiration decreased, mΔΨ and mitochondrial ROS production also decreased. ROS production remained lower in IPC than in control-IR for all mΔΨ and respiration rates. CONCLUSIONS: Increasing H(+) leak is not associated with decreased ROS production. IPC decreases both the magnitude of H(+) leak and ROS production after ischemia-reperfusion.

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. MATERIALS AND METHODS: Male/female rat hearts (n = 8/group) were subjected to 30 min of equilibration, 30 min of ischemia, and 120 min of reperfusion (Control). PoC was induced by 6 cycles (PoC 6c10s), 3 cycles (PoC 3c10s), or 2 cycles (PoC 2c10s) of 10 s reperfusion/10 s ischemia. Rate pressure product (RPP) and infarct size were measured. Male rats (n = 7/group) were subjected in vivo to 30 min left coronary ligation followed by 24 h of reperfusion (Control) or PoC 6c10s and 24 h of reperfusion. RESULTS: Recovery of RPP was 18% ± 4% in male Control versus 17% ± 2% for 6c10s, 16% ± 1% for 3c10s, and 15% ± 3% for 2c10s. Female Control hearts recovered 25% ± 3% of their RPP versus 21% ± 2% for 6c10s. Infarct size was 25% ± 3% for male Control versus 26% ± 3% for 6c10s, 30% ± 2% for 3c10s, 28% ± 1% for 2c10s, and 30% ± 2% for female Control versus 29% ± 2% in 6c10s. In vivo infarct size for Control and PoC 6c10s was 44% ± 3% and 28% ± 5%, respectively (P < 0.05). CONCLUSIONS: In the Langendorff perfused rat hearts, none of the PoC protocols improved myocardial tolerance to ischemia reperfusion injury nor decreased infarct size; however, in vivo postconditioning did confer protection. The lack of protection in the isolated hearts was not gender specific.

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. Echocardiography remains the mainstay for diagnostic evaluation. Tumour resection is the only definitive treatment. Histopathology using H&E and immunohistochemical stains, such as calretinin and CD34, confirms the diagnosis. We present a case of a patient with reported history of asthma who presented with recurrent acute on chronic shortness of breath refractory to inhaler therapy, multiple outpatient visits and hospitalisations for 'asthma exacerbations'. After further evaluation, she was diagnosed with a left atrial myxoma attached to the inferior aspect of the intra-atrial septum complicated by severe functional mitral stenosis.

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. The traditional method of repair has been open surgery, which is associated with a high mortality rate. Endovascular repair has become more common, but results are difficult to interpret due to the low incidence of ACF. A high index of suspicion is imperative to avoid delay in diagnosis and care.

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. OPUS 12 Scientist 2008;2(3):30-33.