Postoperative atrial fibrillation: The role of the inflammatory response

OBJECTIVE: Abnormal atrial conduction has been shown to be a substrate for postoperative atrial fibrillation (POAF). This study aimed to determine the relationship between the location of the atrial reentry responsible for POAF, and degree of atrial inflammation. METHODS: Normal mongrel dogs (n = 18) were divided into 3 groups: anesthesia alone (anesthesia), lateral right atriotomy (atriotomy), and lateral right atriotomy with anti-inflammatory therapy (steroid). Conduction properties of the right and left atria (RA and LA) were examined 3 days postoperatively by mapping. Activation was observed during burst pacing-induced AF. The RA and LA myeloperoxidase activity was measured to quantitate the degree of inflammation. RESULTS: Sustained AF (\u3e2 minutes) was induced in 5 of 6 animals in the atriotomy group, but in none in the anesthesia or steroid groups. All sustained AF originated from around the RA incision. Three of these animals had an incisional reentrant tachycardia around the right atriotomy and 2 had a focal activation arising from the RA during AF. The LA activations in these animals were passive from the RA activation. The RA activation of the atriotomy group was more inhomogeneous than that of the anesthesia group (inhomogeneity index: 2.0 ± 0.2 vs 1.0 ± 0.1, P \u3c .01). Steroid therapy significantly normalized the RA activation after the atriotomy (1.2 ± 0.1, P \u3c .01). The inhomogeneity of the atrial conduction correlated with the myeloperoxidase activity (r = 0.774, P \u3c .001). CONCLUSIONS: Reentrant circuits responsible for POAF are dependent on the degree of inflammation and rotate around the atriotomy. Anti-inflammatory therapy decreased the risk of postoperative AF

The persistent problem of new-onset postoperative atrial fibrillation: A single-institution experience over two decades

ObjectivePostoperative atrial fibrillation is the most common complication after cardiac surgery. A variety of postoperative atrial fibrillation risk factors have been reported, but study results have been inconsistent or contradictory, particularly in patients with preexisting atrial fibrillation. The incidence of postoperative atrial fibrillation was evaluated in a group of 10,390 patients undergoing cardiac surgery among a comprehensive range of risk factors to identify reliable predictors of postoperative atrial fibrillation.MethodsThis 20-year retrospective study examined the relationship between postoperative atrial fibrillation and demographic factors, preoperative health conditions and medications, operative procedures, and postoperative complications. Multivariate logistic regression models were used to evaluate potential predictors of postoperative atrial fibrillation.ResultsIncreasing age, mitral valve surgery (odds ratio = 1.91), left ventricular aneurysm repair (odds ratio = 1.57), aortic valve surgery (odds ratio = 1.52), race (Caucasian) (odds ratio = 1.51), use of cardioplegia (odds ratio = 1.36), use of an intraaortic balloon pump (odds ratio = 1.28), previous congestive heart failure (odds ratio = 1.28), and hypertension (odds ratio = 1.15) were significantly associated with postoperative atrial fibrillation. The non-linear relationship between age and postoperative atrial fibrillation revealed the acceleration of postoperative atrial fibrillation risk in patients aged 55 years or more. In patients undergoing coronary artery bypass grafting, increasing age and previous congestive heart failure were the only factors associated with a higher risk of postoperative atrial fibrillation. There was no trend in incidence of postoperative atrial fibrillation over time. No protective factors against postoperative atrial fibrillation were detected, including commonly prescribed categories of medications.ConclusionsThe persistence of the problem of postoperative atrial fibrillation and the modest predictability using common risk factors suggest that limited progress has been made in understanding its cause and treatment

How I do it: Minimally invasive Cox-Maze IV procedure

Clinical vignette Our patient is a 66-year-old female with a 2-year history of atrial fibrillation (AF) and mitral valve prolapse who presented with dyspnea on exertion. She was found to be in AF upon her admission electrocardiogram. A transthoracic echocardiogram was performed demonstrating moderate-to-severe mitral regurgitation (MR) with a left atrial (LA) diameter of 5.1 cm and normal left ventricular (LV) function. After completion of her workup, it was decided that the patient would best be treated by a minimally invasive Cox-Maze IV (CMIV) and concomitant mitral valve procedure given her significant MR and symptoms. This article and accompanying video will discuss how the minimally invasive CMIV procedure is performed. Surgical technique

Management of severe tricuspid valve regurgitation due to ruptured papillary muscle in a patient with mediastinitis early after heart transplant

OBJECTIVE: Even though severe tricuspid regurgitation is not uncommon after cardiac transplantation, primary severe tricuspid regurgitation is rare. We present such a case with additional complexities. METHODS: The patient was 44-year-old man with a HeartWare durable left ventricular assist device (Heartware Inc) who received a temporary right ventricular assist device (RVAD) with a ProtekDuo cannula (LivaNova Inc USA) for refractory ventricular fibrillation and underwent a heart transplant as United Network for Organ Sharing Status 1, in the presence of partially compensated cardiogenic shock, renal failure. Given complex re-operative surgery in a volume-overloaded patient with unknown pulmonary vascular resistance, an RVAD cannula was preserved and re- inserted during cardiac transplant. Postoperatively he required hemodialysis, had severe primary tricuspid regurgitation discovered after RVAD removal and developed Enterobacter mediastinitis. He underwent complex tricuspid valve repair for flail tricuspid leaflet due to ruptured papillary muscle likely due to RVAD cannula injury, after multiple mediastinal washouts and was followed by delayed chest reconstruction. RESULTS: The patient is doing well, 6 months after discharge to home, asymptomatic, without re-admissions, on renal recovery path, with no tricuspid regurgitation and good biventricular function. CONCLUSIONS: Replacing the tricuspid valve in presence of hemodialysis catheter, immunosuppression and mediastinitis could be high risk for endocarditis. Even though we have short-term follow-up, tricuspid valve repair can be an effective way of managing primary severe regurgitation especially when there is a desire or need to avoid valve replacement