In-situ left-sided bilateral internal thoracic artery: elevated hemidiaphragm.

Background Procurement of the internal thoracic artery risks ipsilateral phrenic nerve injury and elevated hemidiaphragm. Anatomical variations increase the risk on the right side. Patients receiving left-sided in-situ right internal thoracic artery configurations appear to be at greatest risk. Methods From 2014 to 2016, 432 patients undergoing left-sided in-situ bilateral internal thoracic artery grafting were grouped according to right internal thoracic artery configuration: retroaortic via transverse sinus (77%) or ante-aortic (23%); targets were the circumflex and left anterior descending artery territories, respectively. Elevated hemidiaphragm was assessed by serial chest radiographs and categorized by side, complete (≥2 intercostal spaces) versus partial, and permanent versus transient. Results Right elevated hemidiaphragm occurred in 4.2% of patients. The incidence of radiological complete right elevated hemidiaphragm was 2.8% (12/432); 8 cases were transient with recovery in 3.5 ± 0.3 weeks. Permanent right elevated hemidiaphragm occurred in 0.9% (retroaortic group only). Permanent left elevated hemidiaphragm occurred in 0.9% and was significantly higher in the ante-aortic group (3/99 vs. 1/333, p = 0.039). No bilateral hemidiaphragm elevation was documented. Partial right elevated hemidiaphragm occurred in 1.4% and was not associated with adverse early or late respiratory outcomes. Conclusions Despite susceptible right phrenic nerve-internal thoracic artery anatomy, the incidence of permanent right elevated hemidiaphragm is low and no higher than left-sided in prone bilateral internal thoracic artery subsets. This reflects skeletonized internal thoracic artery procurement. Although statistical significance was not achieved, a retroaortic right internal thoracic artery configuration may constitute a higher risk of right phrenic nerve injury.

Blood-Brain Barrier Disruption After Cardiopulmonary Bypass: Diagnosis and Correlation to Cognition.

BACKGROUND: Cardiopulmonary bypass (CPB) elicits a systemic inflammatory response that may impair blood-brain barrier (BBB) integrity. BBB disruption can currently be detected by dynamic contrast enhancement magnetic resonance imaging (MRI), reflected by an increase in the permeability constant (Ktrans). We aimed to determine (1) whether CPB induces BBB disruption, (2) duration until BBB disruption resolution, and (3) the obtainable correlation between BBB injury (location and intensity) and neurocognitive dysfunction. METHODS: Seven patients undergoing CPB with coronary artery bypass grafting (CABG) were assigned to serial cerebral designated MRI evaluations, preoperatively and on postoperative day (POD) 1 and 5. Examinations were analyzed for BBB disruption and microemboli using dynamic contrast enhancement MRI and diffusion-weighted imaging methods, respectively. Neuropsychologic tests were performed 1 day preoperatively and on POD 5. RESULTS: A significant local Ktrans increase (0.03 min-1 vs 0.07 min-1, p = 0.033) compatible with BBB disruption was evident in 5 patients (71%) on POD 1. Resolution was observed by POD 5 (mean, 0.012 min-1). The location of the disruption was most prominent in the frontal lobes (400% vs 150% Ktrans levels upsurge, p = 0.05). MRI evidence of microembolization was demonstrated in only 1 patient (14%). The postoperative global cognitive score was reduced in all patients (98.2 ± 12 vs 95.1 ± 11, p = 0.032), predominantly in executive and attention (frontal lobe-related) functions (91.8 ± 13 vs 86.9 ± 12, p = 0.042). The intensity of the dynamic contrast enhancement MRI BBB impairment correlated with the magnitude of cognition reduction (r = 0.69, p = 0.04). CONCLUSIONS: BBB disruption was evident in most patients, primarily in the frontal lobes. The location and intensity of the BBB disruption, rather than the microembolic load, correlated with postoperative neurocognitive dysfunction.

Correlation between atrial ZnT-1 expression and atrial fibrillation in humans: a pilot study.

BACKGROUND: Until recently, the membrane protein ZnT-1 was studied mainly in the context of zinc homeostasis. However, new findings indicate that it acts as an inhibitor of L-type calcium channels. We recently found that acute rapid pacing of the rat atria in vivo augments the expression of ZnT-1, while knockdown of ZnT-1 in culture can oppose the inhibition of L-type calcium channels following rapid pacing. This pilot study, the first to assess cardiac ZnT-1 in humans, was designed to look for possible correlation between the atrial expression of ZnT-1 and atrial fibrillation. METHODS: Right atrial appendage tissue was collected from 39 patients (27 with sinus rhythm and 12 with atrial fibrillation; 6-permanent, 6- paroxysmal or persistent) undergoing open-heart surgery. The expression of ZnT-1 was analyzed by Western blot utilizing beta-actin as an internal loading control and a standard rat heart sample (STD) for inter-blot comparison. RESULTS: Overall atrial fibrillation patients (n = 12) had median ZnT-1/beta-actin of 1.80 STD (inter-quartile range 1.26 to 2.85) versus 0.73 STD (0.24 to 1.64) in the sinus rhythm group (P = 0.002). No association was found between ZnT-1 level and most other clinical parameters tested. Multivariate analysis determined that atrial fibrillation and increased body mass index were the only independent variables clearly associated with higher ZnT-1 levels (Standardized coefficients Beta = 0.62, 0.31; P = 0.002, P = 0.04, respectively). CONCLUSIONS: This pilot study provides evidence for increased ZnT-1 expression in the atria of patients with atrial fibrillation.