Impact of timing of urgent coronary artery bypass grafting following coronary angiography on acute kidney injury.

OBJECTIVES: Prior studies have examined the association between timing of cardiac surgery after coronary angiography with risk of acute kidney injury, but this remains controversial. The purpose of this study was to investigate the association between interval from coronary angiography to urgent coronary artery bypass grafting with acute kidney injury, and to examine this possible effect in patients with preexisting kidney disease. METHODS: Patients from a single institution undergoing urgent, isolated coronary artery bypass grafting within 7 days of coronary angiography were included. Patients were subdivided by chronic kidney disease stage and angiography-to-surgery interval. Locally estimated scatterplot smoothing was used to evaluate the functional relationship of the probability of acute kidney injury and time interval. Adjusted odds ratios were calculated for each time interval group compared against the Day 0 to 1 interval group, controlling for multiple covariates. Analyses were repeated for each chronic kidney disease subgroup. RESULTS: A total of 2249 patients were included in this study. There were 271 (12.0%) patients with postoperative acute kidney injury. Plots demonstrated a decreasing risk of kidney injury from Day 0 to 1 to Day 3 following coronary angiography. Adjusted odds ratios also showed a significant decrease in risk of kidney injury on Day 3 compared with Day 0 to 1. Analyses repeated for each chronic kidney disease stage showed similar trends. CONCLUSIONS: For patients undergoing urgent coronary artery bypass grafting, there is a decreased risk of kidney injury in those having surgery on day 3 after coronary angiography compared with those having surgery on Day 0 to 1, regardless of preexisting kidney disease.

A Genotype-Phenotype Analysis of Glutathione Peroxidase 4 in Human Atrial Myocardium and Its Association with Postoperative Atrial Fibrillation.

Heterogeneity in the incidence of postoperative atrial fibrillation (POAF) following heart surgery implies that underlying genetic and/or physiological factors impart a higher risk of this complication to certain patients. Glutathione peroxidase-4 (GPx4) is a vital selenoenzyme responsible for neutralizing lipid peroxides, mediators of oxidative stress known to contribute to postoperative arrhythmogenesis. Here, we sought to determine whether GPX4 single nucleotide variants are associated with POAF, and whether any of these variants are linked with altered GPX4 enzyme content or activity in myocardial tissue. Sequencing analysis was performed across the GPX4 coding region within chromosome 19 from a cohort of patients (N = 189) undergoing elective coronary artery bypass graft (−/+ valve) surgery. GPx4 enzyme content and activity were also analyzed in matching samples of atrial myocardium from these patients. Incidence of POAF was 25% in this cohort. Five GPX4 variants were associated with POAF risk (permutated p ≤ 0.05), and eight variants associated with altered myocardial GPx4 content and activity (p < 0.05). One of these variants (rs713041) is a well-known modifier of cardiovascular disease risk. Collectively, these findings suggest GPX4 variants are potential risk modifiers and/or predictors of POAF. Moreover, they illustrate a genotype−phenotype link with this selenoenzyme, which will inform future mechanistic studies.

Thromboelastography-Platelet Mapping Allows Safe and Earlier Urgent Coronary Artery Bypass Grafting.

BACKGROUND: The Society of Thoracic Surgeons current (STS) guidelines recommend delaying coronary artery bypass graft surgery (CABG) for several days or performing platelet function testing in stable patients who received P2Y12 inhibitors. Our program routinely uses thromboelastography-platelet mapping (TEG-PM) to expedite CABG in P2Y12 nonresponders. We hypothesize that P2Y12 nonresponders had no difference in length of stay to surgery and blood product transfusion compared with patients undergoing urgent inpatient CABG not treated with a P2Y12 inhibitor. METHODS: A total of 221 patients from 2015 to 2019 were P2Y12 nonresponders based on TEG-PM result of less than 50% adenosine diphosphate inhibition. The control group was 232 consecutive patients who also had urgent inpatient CABG but were not treated preoperatively with a P2Y12 inhibitor. Exclusion criteria were identical between groups. RESULTS: Sixty-seven percent of inpatient CABG patients who were treated preoperatively with a P2Y12 inhibitor were nonresponders. The mean number of days from cardiac surgical consultation to CABG in the TEG-PM nonresponders group was 1.6 ± 0.1 vs 2.1 ± 0.1 in the control group (P < .01). The mean total number of blood product units transfused was 1.6 ± 0.2 in the TEG-PM nonresponders group vs 1.6 ± 0.4 in the control group (P = .91). CONCLUSIONS: Our results demonstrate a very high incidence of P2Y12 nonresponders among patients undergoing urgent CABG at our program. These patients underwent surgery at least 3 days earlier than STS recommendations and common practice with no difference in transfusion requirement. Routine use of TEG-PM to identify P2Y12 nonresponders can safely decrease preoperative hospital length of stay and associated cost and improve resource utilization and patient satisfaction.

Analysis of racial disparities in acute type A aortic dissection repair at a rural tertiary academic medical center.

BACKGROUND: To determine if racial disparities exist between African Americans (AA) and Non-Hispanic Whites (NHW) for patients undergoing repair of acute type A aortic dissection (ATAAD) at a rural tertiary academic medical center. METHODS: There were 215 consecutive AA and NHW patients who underwent ATAAD repair at our institution from 1999 to 2019 included in a retrospective analysis of our Society of Thoracic Surgeons Adult Cardiac Surgery Database. Statistical analysis was performed with a p value of less than .05 considered statistically significant. RESULTS: Patients undergoing ATAAD repair were 47% AA despite comprising only 27% of the total population in our region. AAs were significantly younger (54.0 vs. 61.2 years), were more likely to be hypertensive (94.1% vs. 79.7%), had higher creatinine levels (1.7 vs. 1.1 mg/dL), and higher body mass index (30.8 vs. 28.1 kg/m2 ) (all p values < .006). There were no significant differences in type of repair or intraoperative variables. A logistic regression analysis showed AAs had an increased rate of postoperative acute renal failure not requiring hemodialysis when compared to NHWs (20.8% vs. 10.6%, p value = .042). Thirty-day mortality was not significantly different (15.7% vs. 13.4%) nor was 1-year survival (78% vs. 79%) in AAs and NHWs, respectively. CONCLUSIONS: Despite AAs having more medical comorbidities at presentation, there were no differences in short- and intermediate-term survival. In our catchment of 1.8 million people, AAs appear to undergo ATAAD repair at a disproportionate rate versus NHWs. These findings may alter strategies for surveillance and prevention of aortic disease in this high-risk population.

Enhanced Catecholamine Flux and Impaired Carbonyl Metabolism Disrupt Cardiac Mitochondrial Oxidative Phosphorylation in Diabetes Patients.

Aims: Catecholamine metabolism via monoamine oxidase (MAO) contributes to cardiac injury in models of ischemia and diabetes, but the pathogenic mechanisms involved are unclear. MAO deaminates norepinephrine (NE) and dopamine to produce H2O2 and highly reactive "catecholaldehydes," which may be toxic to mitochondria due to the localization of MAO to the outer mitochondrial membrane. We performed a comprehensive analysis of catecholamine metabolism and its impact on mitochondrial energetics in atrial myocardium obtained from patients with and without type 2 diabetes. Results: Content and maximal activity of MAO-A and MAO-B were higher in the myocardium of patients with diabetes and they were associated with body mass index. Metabolomic analysis of atrial tissue from these patients showed decreased catecholamine levels in the myocardium, supporting an increased flux through MAOs. Catecholaldehyde-modified protein adducts were more abundant in myocardial tissue extracts from patients with diabetes and were confirmed to be MAO dependent. NE treatment suppressed mitochondrial ATP production in permeabilized myofibers from patients with diabetes in an MAO-dependent manner. Aldehyde dehydrogenase (ALDH) activity was substantially decreased in atrial myocardium from these patients, and metabolomics confirmed lower levels of ALDH-catalyzed catecholamine metabolites. Proteomic analysis of catechol-modified proteins in isolated cardiac mitochondria from these patients identified >300 mitochondrial proteins to be potential targets of these unique carbonyls. Innovation and Conclusion: These findings illustrate a unique form of carbonyl toxicity driven by MAO-mediated metabolism of catecholamines, and they reveal pathogenic factors underlying cardiometabolic disease. Importantly, they suggest that pharmacotherapies targeting aldehyde stress and catecholamine metabolism in heart may be beneficial in patients with diabetes and cardiac disease. Antioxid. Redox Signal. 35, 235-251.

Combined surgical treatment of symptomatic carotid, coronary and mesenteric occlusive disease.

The surgical management of advanced symptomatic atherosclerotic disease in multiple distributions including the coronary circulation presents unique challenges due to the high risk of perioperative ischemic complications in the setting of coronary artery bypass grafting. We present a novel case of the combined surgical management of symptomatic carotid, coronary and mesenteric ischemic disease. The patient underwent carotid endarterectomy followed by combined coronary and mesenteric revascularization using cardiopulmonary bypass during the same hospital admission. He had an uncomplicated post-operative course and was discharged to home on post-operative day 7 after the combined procedure. Ninety-day follow-up was also unremarkable with the patient having no recurrent symptoms of ischemia. This case demonstrates the feasibility and safety of our approach for this rare clinical presentation.

Regulation of cardiac fibroblast-mediated maladaptive ventricular remodeling by ß-arrestins.

Cardiac fibroblasts (CF) play a critical role in post-infarction remodeling which can ultimately lead to pathological fibrosis and heart failure. Recent evidence demonstrates that remote (non-infarct) territory fibrosis is a major mechanism for ventricular dysfunction and arrhythmogenesis. ß-arrestins are important signaling molecules involved in ß-adrenergic receptor (ß-AR) desensitization and can also mediate signaling in a G protein independent fashion. Recent work has provided evidence that ß-arrestin signaling in the heart may be beneficial, however, these studies have primarily focused on cardiac myocytes and their role in adult CF biology has not been well studied. In this study, we show that ß-arrestins can regulate CF biology and contribute to pathological fibrosis. Adult male rats underwent LAD ligation to induce infarction and were studied by echocardiography. There was a significant decline in LV function at 2-12 weeks post-MI with increased infarct and remote territory fibrosis by histology consistent with maladaptive remodeling. Collagen synthesis was upregulated 2.9-fold in CF isolated at 8 and 12 weeks post-MI and ß-arrestin expression was significantly increased. ß-adrenergic signaling was uncoupled in the post-MI CF and ß-agonist-mediated inhibition of collagen synthesis was lost. Knockdown of ß-arrestin1 or 2 in the post-MI CF inhibited transformation to myofibroblasts as well as basal and TGF-ß-stimulated collagen synthesis. These data suggest that ß-arrestins can regulate CF biology and that targeted inhibition of these signaling molecules may represent a novel approach to prevent post-infarction pathological fibrosis and the transition to HF.

Inhibition of Postinfarction Ventricular Remodeling by High Molecular Weight Polyethylene Glycol.

BACKGROUND: Myocardial infarction (MI) is a major etiology for the development of heart failure. We have previously shown that high molecular weight polyethylene glycol (PEG) can protect cardiac myocytes from hypoxia-reoxygenation injury in vitro. In this study, we investigated the potential protective effects of 15-20 kD PEG postinfarction without reperfusion. METHODS: One milliliter of PEG 15-20 was delivered intravenously following permanent left anterior descending ligation in adult male rats with phosphate buffer saline (PBS) as control (n = 9 in each group). Echocardiography was performed at baseline and at 8 wk post-MI. Left ventricles (LVs) were harvested to quantify fibrosis, apoptosis, cell survival signaling, regulation of ß-adrenergic signaling, and caveolin (Cav) expression. RESULTS: The PEG group had significant recovery of LV function at 8 wk compared with the PBS group. There was less LV fibrosis in both the infarct and remote territory. Cell survival signaling was upregulated in the PEG group with increased Akt and ERK phosphorylation. PEG inhibited apoptosis as measured by terminal deoxynucleotidyl transferase [TdT]-mediated dUTP nick-end labeling positive nuclei and caspase-3 activity. There was maintenance of Cav-1, Cav-2, and Cav-3 expression following PEG treatment versus a decline in the PBS group. Negative regulators of ß-adrenergic signaling, G protein-coupled receptor kinase-2, and ß-arrestin 1 and 2 were all upregulated in PBS-treated samples compared to normal control; however, PEG treatment led to decreased expression. CONCLUSIONS: These data suggest that PEG 15-20 may have significant protective effects post-MI even in the setting of no acute reperfusion. Upregulation of Cav expression appears to be a key mechanism for the beneficial effects of PEG on ventricular remodeling and function.

Outcomes of surgical aortic valve replacement for mixed aortic valve disease.

BACKGROUND: Mixed aortic valve disease (MAVD) is associated with a poorer natural history compared with isolated lesions. However, clinical and echocardiographic outcomes for aortic valve replacement (AVR) in mixed disease are less well understood. METHODS: Retrospective review of AVRs (n=1,011) from 2000-2016. Isolated AVR, AVR + coronary bypass, and AVR + limited ascending aortic replacement were included. Predominant aortic stenosis (AS) group was stratified into group 1 (n=660) with concomitant mild or less aortic insufficiency (AI), and group 2 (n=197) with accompanying moderate or greater AI. Predominant AI group was stratified using the same schema for concomitant AS into groups 3 (n=143) and 4 (n=53). Median follow-up was 3.1 and 4.4 years respectively for AS and AI groups. RESULTS: For the predominant AS group (n=857) preoperatively, group 2 had a larger preoperative left ventricular end diastolic diameter (LVESD) (51.0±8.4 vs. 48.6±7.2, P=0.02) and lower preoperative left ventricular ejection fraction (LVEF) (57.6% vs. 60.2%, P=0.043). No differences in left ventricular (LV) dimensions, LV or right ventricular (RV) function was evident at follow up (P>0.05). After propensity matching for age, operation, and comorbidities, there was no difference in survival (P=0.19). After propensity matching for the predominant AI group (n=196), survival was lower for group 4 compared to 3 (P=0.02). There were no differences in LV dimensions, LV or RV function preoperatively or on follow-up (P>0.05). CONCLUSIONS: Predominant AS associated with higher AI grades had larger LV dimensions and worse LV function preoperatively. These differences resolve after AVR with equivalent survival. However, predominant AI with more severe AS had reduced survival despite AVR.

Increased risk of atrial fibrillation among patients undergoing coronary artery bypass graft surgery while receiving nitrates and antiplatelet agents.

Background Postoperative atrial fibrillation (POAF) is a frequent complication of coronary artery bypass graft (CABG) surgery. This arrhythmia occurs more frequently among patients who receive perioperative inotropic therapy (PINOT). Administration of nitrates with antiplatelet agents reduces the conversion rate of cyclic guanosine monophosphate to guanosine monophosphate. This process is associated with increased concentrations of free radicals, catecholamines, and blood plasma volume. We hypothesized that patients undergoing CABG surgery who receive PINOT may be more susceptible to POAF when nitrates are administered with antiplatelet agents. Methods Clinical records were examined from a prospectively maintained cohort of 4,124 patients undergoing primary isolated CABG surgery to identify POAF-associated factors. Results POAF risk was increased among patients receiving PINOT, and the greatest effect was observed when nitrates were administered with antiplatelet therapy. Adjustment for comorbidities did not substantively change the study results. Conclusions Administration of nitrates with certain antiplatelet agents was associated with an increased POAF risk among patients undergoing CABG surgery. Additional studies are needed to determine whether preventive strategies such as administration of antioxidants will reduce this risk.

Cardiac Surgery Outcomes in Abdominal Solid Organ Transplant Recipients.

BACKGROUND: Cardiovascular disease is a cause of morbidity and mortality in organ transplant recipients. Cardiac surgery after organ transplantation is not uncommon in this population. We evaluated 30-day outcomes and long-term survival of abdominal transplant recipients undergoing cardiac surgery at our institution. METHODS: In all, 138 patients with previous kidney, kidney-pancreas, and liver transplants underwent cardiac surgery from 2000 to 2016. Propensity score (ratio 1:3) matched 115 abdominal transplant with 345 patients undergoing cardiac surgery without a history of abdominal transplant. They were matched for type and year of cardiac surgery, age, sex, body mass index, history of diabetes mellitus, and creatinine level before cardiac surgery. RESULTS: Median time from abdominal transplant to cardiac surgery was 7 years (interquartile range, 3 to 12 years). Perioperative variables, including surgery and cardiopulmonary bypass time, aortic cross-clamp and intubation time, and intensive care unit stay did not differ between the groups. Hospital length of stay and rate of 30-day hospital readmissions did not differ between the groups. Patients with abdominal transplants had more strokes (4% versus 0.6%; p = 0.005) within 30 days after surgery. There were no differences in renal failure, bleeding, site infections, atrial fibrillation, and pneumonia between the groups. Five patients (4%) died within 30 days after surgery in the abdominal transplant group (4 kidneys, 1 liver, 0 kidney-pancreas), and 7 patients (2%) died in the nontransplanted group (p = 0.24). CONCLUSIONS: Previous history of abdominal transplant is associated with an increased 30-day incidence of stroke after cardiac surgery. Abdominal transplant does not affect 30-day mortality after cardiac surgery, whereas long-term survival is significantly reduced. Regular patient follow-up and prevention and early treatment of postoperative complications are key to patient survival.

Natural history of the proximal aorta in patients with descending thoracic aortic disease.

OBJECTIVE: This study investigated the growth and behavior of the ascending aorta in patients with descending thoracic aortic disease. METHODS: We examined 200 patients with descending thoracic aortic disease including acute type B dissection (n = 95), chronic type B dissection (n = 38), intramural hematoma (n = 23), and thoracoabdominal aortic aneurysms (n = 44). Images from computed tomography and magnetic resonance imaging were evaluated after three-dimensional reconstruction to examine the growth rate in those with >1 year of imaging follow-up (n = 108). Survival data were derived from all 200 patients in this study. RESULTS: Average proximal aortic dimensions at the index image were relatively small, measuring 3.65 ± 0.51 cm in the root, 3.67 ± 0.48 cm in the ascending aorta, and 3.50 ± 0.44 cm in the proximal arch. Average growth rate was low for the aortic root, ascending aorta, and proximal arch at 0.36 ± 0.64 mm/y, 0.26 ± 0.44 mm/y, and 0.25 ± 0.44 mm/y, respectively. There was no difference in baseline proximal aortic dimensions and growth rate between the four subgroups. An index aortic diameter ≥4.1 cm grew faster than those <4.1 cm at the ascending aorta (P = .028) and proximal arch (P = .019). There was no difference in aortic growth rates at the aortic root (P = .887). After the index scan, five patients underwent six ascending aortic replacement procedures, leading to a 3% ascending aortic intervention rate. Overall median life expectancy was 86.15 years. CONCLUSIONS: Native ascending aortic growth in patients with descending thoracic aortic disease is slow. We suggest regular follow-up for index ascending aorta ≥4.1 cm because of its larger initial size and more rapid growth.

Cluster analysis of acute ascending aortic dissection provides novel insight into mechanisms of distal progression.

BACKGROUND: Whether primary tear size impacts extent of type A dissection is unclear. Using statistical groupings based on dissection morphology, we examined its relationship to primary tear area. METHODS: We retrospectively reviewed 108 patients who underwent acute ascending dissection repair from 2000-2016. Dissection morphology was characterized using 3-dimensional (3D) reconstructions of computed tomography (CT) scan images. Two-step cluster analysis was performed to group the dissections by examining the true lumen area as a fraction of the total aortic area at various levels. RESULTS: Cluster analysis defined two distinct categories. This first grouping corresponds to DeBakey type I (n=71, 65.7%) with a dissection extending from the ascending aorta to the aortic bifurcation. The second grouping conforms more closely to DeBakey type II dissection (n=37, 34.3%). It differs however from the classic type II definition as the dissection may extend up to the distal arch from the ascending aorta. Compared to type I, this "extended" DeBakey type II had no malperfusion (P<0.05), a larger primary tear area (6.6 vs. 3.7 cm2, P=0.009), and a greater burden of atherosclerotic coronary artery disease (P<0.05). A smaller aortic valve annulus (P=0.025) and a smaller root false lumen area (P=0.017) may explain less aortic valve insufficiency (P<0.05) in extended type II dissections. No differences in complications or survival were seen. CONCLUSIONS: In this series, limited distal extension of DeBakey type II dissections appears to be related to a larger primary tear area and greater atherosclerotic disease burden. It is also associated with less malperfusion and aortic valve insufficiency.

Coronary bypass in left ventricular dysfunction and differential cardiac recovery.

Background We aimed to examine the efficacy of surgical revascularization with respect to improvement in ventricular function and survival in patients with ischemic cardiomyopathy and poor left ventricular function. Methods We retrospectively analyzed the data of 429 patients (median age 64.6 years, 81.1% male) with ejection fractions <40% undergoing isolated primary coronary artery bypass grafting from 2000 to 2016. Techniques included on-pump cardioplegic arrest ( n = 312), off-pump ( n = 75), and on-pump beating heart ( n = 42). Propensity matching was performed to compare the cardioplegic arrest group ( n = 114) with the combined off-pump and beating heart groups ( n = 114). Results Postoperatively, ejection fraction increased by 10.1% ± 13.1% (from 31.4% ± 7.1% to 41.6% ± 13.6%; p < 0.001) and mitral regurgitation grade improved ( p < 0.001) but right ventricular function on echocardiographic assessment worsened over time ( p = 0.04). No difference in ejection fraction improvement was seen in the time periods <1 (9.8% ± 11.2%), 1-5 (11.6% ± 14.5%), and >5 (8.8% ± 14.2%) years ( p = 0.442). Following propensity matching, there was no significant difference between the combined off-pump/beating heart and cardioplegic arrest groups with respect to survival or postoperative complications. Conclusions Patients with moderate to severe left ventricular dysfunction experience long-term improvement in left ventricular ejection fraction after coronary artery bypass. However, right ventricular function often continues to decline, contributing to persistent or worsening heart failure symptoms and late mortality. No difference in survival was seen between the 2 techniques.

Acute retrograde type A aortic dissection: morphologic analysis and clinical implications.

BACKGROUND: This study compares the morphology and outcomes of acute retrograde type A dissections (RTADs) with acute antegrade type A dissections (ATADs), and acute type B dissections. MATERIALS AND METHODS: From 2000 to 2016, there were 12 acute RTADs, 96 ATADs, and 92 type B dissections with available imaging. Dissections were characterized using computerized tomography angiography images. We examined clinical features, tear characteristics, and various morphologic measurements. RESULTS: Compared with acute type B dissections, RTAD primary tears were more common in the distal arch (75% versus 43%, P = 0.04), and the false-to-true lumen contrast intensity ratio at the mid-descending thoracic aorta was lower (0.46 versus 0.71, P = 0.020). RTAD had less false lumen decompression because there were fewer aortic branch vessels distal to the subclavian that were perfused through the false lumen (0.40 versus 2.19, P < 0.001). Compared with ATAD, RTAD had less root involvement where root true-to-total lumen area ratio was higher (0.88 versus 0.76, P = 0.081). Furthermore, RTAD had a lower false-to-true lumen contrast intensity ratio at the root (0.25 versus 0.57, P < 0.05), ascending aorta (0.25 versus 0.72, P < 0.001), and proximal arch (0.39 versus 0.67, P < 0.05). RTAD were more likely to undergo aortic valve resuspension (100% versus 74%, P = 0.044). CONCLUSIONS: RTAD tends to occur when primary tears occur in close proximity to the aortic arch and when false lumen decompression through the distal aortic branches are less effective. Compared with ATAD, RTAD has less root involvement, and successful aortic valve resuspension is more likely.

Coronary Events in Patients Presenting for Repair of Acute Type A Aortic Dissection.

BACKGROUND: Preoperative coronary angiography is often not performed in acute Type A dissection. We examined differences in the incidence of pre-existing coronary disease and subsequent coronary events between patients undergoing acute Type A dissection repair and patients undergoing elective proximal aortic aneurysm repair. METHODS: From 2000 to 2015, there were 154 acute Type A dissection repairs and 457 elective proximal aortic aneurysm repairs. We performed a retrospective review to evaluate preoperative coronary disease and postoperative coronary interventions such as percutaneous coronary intervention (PCI) and coronary bypass grafting (CABG). RESULTS: A total of 31 (20%) dissection patients and 123 (27%) elective surgery patients had preoperative evidence of coronary artery disease (p = 0.094). All elective surgery patients but only six (4%) dissection patients had preoperative coronary catheterization. More CABGs were performed in the elective surgery group (19%) than in the dissection group (3%, p < 0.001). There were no differences in the incidence of prior PCI, CABG, or myocardial infarction between groups. Following dissection repair, four patients required coronary interventions. Of these, two (1.3%) experienced chest pain and underwent PCI at 4.7 and 4.3 months postoperatively, respectively, and another two experienced symptoms and required PCI at 5 and 7 years, respectively. The 30-day and 14-year mortality rates after dissection repair were 13% and 24%, respectively. Although the dissection group had poorer survival than the elective surgery group (p < 0.001), there was no difference in conditional survival after aortic-related deaths over the first year were censored (p = 0.104). CONCLUSIONS: Given the low incidence of missed significant coronary disease (1.3%), it is reasonable to perform Type A dissection repair without coronary angiography.

To use or not to use? Amiodarone before heart transplantation.

BACKGROUND: Amiodarone frequently is used in patients with heart failure. Concerns still exist about possible complications related to its lingering effect during and after heart transplantation. METHODS: We selected all consecutive patients who received a heart transplant at our institution between January 2004 and December 2015 (n = 220) and compared the peri- and postoperative outcomes of patients who were taking amiodarone for at least 120 days before heart transplant (n = 127) with patients who did not take amiodarone prior to heart transplant (n = 93). RESULTS: Compared with patients with no amiodarone use prior to transplant, those who had used amiodarone were similar in age, body mass index, sex, cause of cardiomyopathy, prevalence of diabetes, hypertension, presence of defibrillator, and had similar donor ischemic times during transplant (all P > .05). Median operative time, aortic cross clamp time, mechanical ventilation and median hospital duration of stay did not differ between the 2 groups (P > .05). Patients exposed to amiodarone had fewer cellular rejections (5% vs 20%; P = .001) but more primary graft dysfunction (4% vs 0%; P = .025) and post-transplant pneumonia (P = .047) compared with patients not taking amiodarone prior to transplant. Both groups had similar rate of atrial fibrillation, 30-day readmission, and 30-day mortality (P > .05). Even though 1-year survival was not affected by amiodarone use (P = .51), long-term (5-year) survival was significantly less in patients exposed to amiodarone (P = .03). CONCLUSION: Amiodarone use did not affect the incidence of atrial fibrillation nor 30-day and 1-year survival post-transplantation. Nevertheless, post-transplant pulmonary complications were significantly greater and 5-year survival was less among patients treated with amiodarone prior to transplant.