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The effects of stroke and delirium on postdischarge cognition and patient-centered health outcomes after surgical aortic valve replacement (SAVR) are not well characterized. Here, we assess the impact of postoperative stroke and delirium on these health outcomes in SAVR patients at 90 days.Patients (N = 383) undergoing SAVR (41% received concomitant coronary artery bypass graft) enrolled in a randomized trial of embolic protection devices underwent serial neurologic and delirium evaluations at postoperative days 1, 3, and 7 and magnetic resonance imaging at day 7. Outcomes included 90-day functional status, neurocognitive decline from presurgical baseline, and quality of life.By postoperative day 7, 25 (6.6%) patients experienced clinical stroke and 103 (28.5%) manifested delirium. During index hospitalization, time to discharge was longer in patients experiencing stroke (hazard ratio, 0.62; 95% confidence interval [CI], 0.42-0.94; P = .02) and patients experiencing delirium (hazard ratio, 0.68; 95% CI, 0.54-0.86; P = .001). At day 90, patients experiencing stroke were more likely to have a modified Rankin score2 (odds ratio [OR], 5.9; 95% CI, 1.7-20.1; P = .01), depression (OR, 5.3; 95% CI, 1.6-17.3; P = .006), a lower 12-Item Short Form Survey physical health score (adjusted mean difference -3.3 ± 1.9; P = .08), and neurocognitive decline (OR, 7.8; 95% CI, 2.3-26.4; P = .001). Delirium was associated with depression (OR, 2.2; 95% CI, 0.9-5.3; P = .08), lower 12-Item Short Form Survey physical health (adjusted mean difference -2.3 ± 1.1; P = .03), and neurocognitive decline (OR, 2.2; 95% CI, 1.2-4.0; P = .01).Stroke and delirium occur more frequently after SAVR than is commonly recognized, and these events are associated with disability, depression, cognitive decline, and poorer quality of life at 90 days postoperatively. These findings support the need for new interventions to reduce these events and improve patient-centered outcomes.

Background Patients at intermediate risk (IR) according to The Society of Thoracic Surgeons risk score are today frequently oriented toward the transfemoral aortic valve replacement (TAVR) option. Our goal was to evaluate the best treatment strategies for IR patients with severe aortic stenosis. Methods Of a consecutive series of 1,144 surgical aortic valve replacements (AVRs) performed in our institution between 2008 and 2014, we reviewed the early and late outcomes of two different groups: a low-risk (LR) group of 470 patients, and an IR group of 620. We eliminated from the analysis 54 high-risk patients who were currently candidates for TAVR. All patients underwent surgical AVR with or without concomitant coronary artery bypass grafting. Social Security database interrogation provided long-term information. Results The early mortality rate (30 days) between LR and IR patients was similar (1.70% vs 2.74%, p = 0.25) and both lower than predicted mortality rates. However, cumulative 5-year survival was significantly higher in LR patients (86.3%) than in IR patients (75.4%; p = 0.0007 by log-rank test), although excellent in IR group. Comparing IR survivors and nonsurvivors, ages at operation were 69.5 ± 12.7 years for survivors vs 75.4 ± 9.6 years for those experiencing late deaths ( p = 0.002). Risk factors for late deaths after multivariate analysis were age, hemodialysis, and chronic lung disease. Conclusions Most IR patients today should undergo surgical AVR, but because of survival rates combined with still unavailable late structural deterioration rates in TAVR valves, patients in the IR group with high Society of Thoracic Surgeons scores and known risk factors may be better served with TAVR as data regarding late percutaneous valve function accrue.

Higher mortality in women than in men after isolated coronary artery bypass graft (CABG) procedures has been historically accepted. We have reviewed our continuous series of isolated CABG performed in a single institution providing all coronary interventions in a geographically isolated region

Background Therapeutic ultrasound as an alternative to the maze procedure was evaluated in this large US experience. Safety and efficacy were assessed at 6-, 12-, and 18-month visits with systematic 24-hour Holter monitoring. Methods From February 2005 to February 2007, 220 patients were prospectively enrolled in a single center study, and among them 129 patients with concomitant cardiac surgery and at least 6-month follow-up were reviewed. Primary procedures were mitral surgery in 50% of the cases, coronary bypass in 32%, and aortic surgery in 16%. Atrial fibrillation was permanent in 66 (51.1%), paroxysmal in 43 (33.3%), and persistent in 20 (15.5%) patients. An epicardial and circumferential left atrial encircling line was created on the beating heart. Routinely a mitral isthmus line was also created from the left atrium epicardium using an ultrasonic handheld device. Results No morbidity or mortality was device-related. There were four (2.33%) early deaths and six late extra-cardiac deaths. Follow-up ranged from 6 to 670 days with a mean follow-up of 358.5 days, median 340 days with two patients lost to follow-up. Freedom from atrial fibrillation or left-sided flutter was 83.2%, 84.4%, and 86.2% at 6, 12, and 18 months, respectively. A pacemaker was implanted in seven patients (5.4%). Male gender and left atrial dimension were significant risk factors for failure. Conclusions The study confirms the excellent safety record of the technology, and the efficacy at the level reported in a previous European multicenter study. Efficacy is also maintained at longer (12 and 18 months) follow-up.

Interest in minimally invasive coronary artery bypass grafting (CABG) continues to grow, and the techniques evolve. Our study examines the technical strategies of port-access (PA) CABG and compares results between PA CABG and conventional CABG.Two hundred and twenty-nine consecutive patients underwent PA CABG from December 1996 through July 1998. Postoperative complications were compared with a matched cohort of conventional access patients. Operative technique and times were reviewed in the PA group.The average Society of Thoracic Surgeons (STS) risk assessment was 1.3 in both groups. Observed mortality was 0.9%. Complications of stroke, perioperative myocardial infarction, and atrial fibrillation were not significantly different between the two groups. Reoperation for bleeding was more likely in the PA group, while infections were more likely in the sternotomy group (p0.05). Transfusion requirements and postoperative length of stay were lower in the PA group (p0.05).Early results were similar between these two low-risk cohort groups. These findings support continued careful use of port-access revascularization in low-risk patients. Close follow-up of outcomes is essential to define the appropriateness of port-access techniques in patients requiring surgical revascularization.

Background— Surgical therapy of atrial fibrillation concomitant to coronary bypass grafting using epicardial Ultrasound technology was assessed after a minimum 6-month follow-up. Methods and Results— A cohort of 98 consecutive patients with a mean age of 72±7.58 years and a primary diagnosis of ischemic heart disease had surgery for structural disease. Coronary artery bypass grafting was isolated (n=51) or associated (n=47) with various combinations of aortic, mitral, tricuspid, and left ventricular restoration surgery. Atrial fibrillation duration ranged from 6 to 360 months (mean 71 months) and was permanent in 47 patients, paroxysmal in 34, and persistent in 17. Left atrial mean diameter was 48±6.71 mm. A circumferential ablation was performed off-pump, before the concomitant procedure, and was always associated with an epicardial mitral line lesion using the same technology. At 3-, 6-, and 12-month visits, patients were routinely evaluated by physical examination, ECG, chest X-ray, and 24-hour Holter. There were 1 early death (1%) and 4 extracardiac late deaths. A pacemaker was implanted in 4 patients. Mean follow-up time was 325 days, 2 patients being lost to follow-up. Freedom from atrial fibrillation and flutter at the 6-month visit was 84% for the entire population, 76% in patients with permanent, and 91% in patients with paroxysmal atrial fibrillation. At the 1-year visit, 85% were free from atrial fibrillation or flutter. Conclusion— Epicardial beating heart ablation using therapeutic ultrasound is safe, reliable, and can easily treat atrial fibrillation in a difficult surgical population of patients with primary ischemic heart disease.

Adenosine is released from the myocardium in response to a decrease in the oxygen supply/demand ratio, as is seen in myocardial ischemia; its protective role is manifested by coronary and collateral vessel vasodilation that increase oxygen supply and by multiple effects that act in concert to decrease myocardial oxygen demand (i.e., negative inotropism, chronotropism, and dromotropism). During periods of oxygen deprivation, adenosine enhances energy production via increased glycolytic flux and can act as a substrate for purine salvage to restore cellular energy charge during reperfusion. Adenosine limits the degree of vascular injury during ischemia and reperfusion by inhibition of oxygen radical release from activated neutrophils, thereby preventing endothelial cell damage, and by inhibition of platelet aggregation. These effects help to preserve endothelial cell function and microvascular perfusion. Long-term exposure to adenosine may also induce coronary angiogenesis.

An isolated, isovolumetrically contracting rat heart preparation, perfused at constant flow, was used to test the hypothesis that adenosine treatment (100 μM) throughout the experiment could enhance the repletion of adenosine triphosphate and the recovery of ventricular function following 10 minutes of global, normothermic (37° C) ischemia. Left ventricular developed pressure was measured with an intraventricular balloon, and myocardial adenine nucleotides were measured from freeze-clamped tissues in a parallel series of experiments. The adenosine triphosphate level in the adenosine-treated hearts was not different from that of the untreated control hearts at the end of 30 minutes of equilibration but was significantly (p

The purine precursor AICAR (5-amino-4-imidazolecarboxamide) has been advocated as a substrate for myocardial adenine nucleotide repletion during postischemic reperfusion. The purpose of this study was to investigate the acute effects of this agent on adenine nucleotides, inosine monophosphate, and postischemic ventricular function in an isolated rat heart preparation. The hearts were perfused at constant flow, either continuously for 90 minutes or for a 30 minute period followed by 10 minutes of global normothermic (37° Q ischemia. The ischemic hearts were then reperfused for 15, 30, and 60 minutes. Both groups were treated with AICAR in a concentration of 100 μmol/L throughout the perfusion protocols. In the nonischemic time control group there was no effect on the levels of adenosine nucleotides or developed pressure over 90 minutes of perfusion. In contrast, AICAR treatment increased tissue inosine monophosphate content fourfold and sevenfold at 60 and 90 minutes, respectively (p

Coronary blood flow responds uniquely to changes in myocardial demand, regardless of the stimulus. If adenosine mediates this response, interstitial fluid adenosine concentration should also change in parallel with myocardial oxygen consumption and coronary blood flow during alterations of cardiac work. We tested this hypothesis by measuring coronary blood flow, myocardial oxygen consumption, and the concentration of adenosine in pericardial infusates, an index of interstitial fluid adenosine concentration, during six experimental conditions and control states in anesthetized, open-chest dogs. Significant alterations of myocardial oxygen consumption and coronary blood flow during aortic constriction, vagal stimulation, atrial pacing, or intravenous infusion of calcium chloride, norepinephrine, or isoproterenol were accompanied by significant alterations in pericardial infusate adenosine concentration. Significant linear relationships were determined among myocardial oxygen consumption, coronary blood flow, and pericardial infusate adenosine concentration for each of the experimental stimuli and their paired control values. There were no significant differences among the six different conditions for any of these relationships. In addition, these relationships were not altered by beta-blockade in five dogs subjected to aortic constriction and calcium infusion. Although beta-blockade may alter the effects of a stimulus, myocardial oxygen consumption, coronary blood flow, and adenosine all are affected proportionately. The results suggest that adenosine production responds to alterations of myocardial oxygen consumption independently of the stimulus which produces the change in oxygen demand, and the resultant change in interstitial fluid adenosine concentration may initiate the change in coronary blood flow to maintain the balance between oxygen supply and demand.

Myocardial dysfunction after induced ischemic arrest is an important problem in cardiac surgery. Adenosine-5’-triphosphate content in myocardial tissue remains depressed for days after ischemia, perhaps because of reperfusion washout of diffusable purine substrates. Left ventricular function is also depressed after ischemia, but its relationship to absolute tissue adenosine triphosphate content is unclear. We tested the hypothesis that arresting hearts with a cardioplegic solution containing adenosine, hypoxanthine, and ribose would result in improved tissue adenosine triphosphate content and left ventricular function after 1 hour of normothermic global ischemia in dogs supported by cardiopulmonary bypass. Animals with ischemic arrest initiated with a crystalloid cardioplegic solution containing adenosine 100 μmol/L, hypoxanthine 100 μmol/L, and ribose 2 mmol/L demonstrated significant improvement (p

The hypothesis that endogenously released adenosine plays an important role in maintaining patency of the fetal lamb ductus arteriosus was tested. The design of the study was (1) to determine the effect, if any, of exogenous adenosine on blood flow through the ductus arteriosus and (2) to evaluate the relationship among the partial pressure of oxygen in arterial blood, circulating endogenous plasma adenosine concentration, and the rate of blood flow through the ductus. When exogenous adenosine (5 mumoles) was administered during oxygen-induced ductal constriction, ductal blood flow increased from 101 +/- 6 ml/min to 153 +/- 4 ml/min (p less than 0.01). When fetal blood adenosine concentrations were measured during nonventilation and ventilation with 100% oxygen, endogenous adenosine concentrations fell to less than one-half of the preventilation levels, i.e., from 1.12 +/- 0.17 to 0.49 +/- 0.03 microM (p less than 0.01). Finally, when fetal lambs were ventilated with increasing concentrations of oxygen (0%, 10%, 20%, 60%, and 100%) and measurements obtained simultaneously at each level, there was a significant monoexponential relationship among the rise in PO2, the fall in plasma adenosine concentration, and the decrease in ductal blood flow. These data suggest that: (1) adenosine is a potent vasodilator of the lamb ductus arteriosus during oxygen-induced vasoconstriction; (2) fetal endogenous plasma adenosine levels fall significantly when PO2 is increased; and (3) the fall in adenosine concentrations parallels a decrease in ductal blood flow. The findings suggest that the endogenous vasodilator adenosine plays an important role in maintaining ductal patency in utero.

Allopurinol, a competitive inhibitor of xanthine oxidase, has been shown to have a protective effect on ischemic myocardium, but its mechanism of action remains controversial. We used an isolated rat heart preparation to test the hypothesis that allopurinol could restore adenosine triphosphate (ATP) levels and improve the recovery of left ventricular function after global myocardial ischemia. Hearts were equilibrated for 30 min, subjected to 10 min of global, normothermic (37 degrees C) ischemia, and reperfused for 15, 30, and 60 min. Hearts treated with allopurinol (100 microM) exhibited greater ATP levels and improved function during reperfusion than did untreated control hearts. Hearts treated with hypoxanthine (100 microM), the substrate for xanthine oxidase, also showed increased ATP and functional recovery compared with controls. These results suggest that allopurinol may protect the globally ischemic myocardium by enhancing the salvage of hypoxanthine for reincorporation into adenine nucleotides.

It has been demonstrated that resting coronary vascular resistance is elevated with chronic hypertension and concomitant cardiac hypertrophy. The present study employed a model of 6-week, one-kidney, one wrapped Page hypertension to determine if the ability of the heart to match an increase in oxygen demand with an increase in oxygen supply (coronary blood flow) is impaired, and to determine if these vasoregulatory abnormalities are attributable to inadequate adenosine release. Studies were performed in a pentobarbital anesthetized, open-chest canine preparation using a pericardial infusate method to determine adenosine release. Results showed that dobutamine (a beta-receptor agonist) induced increases in myocardial oxygen consumption (MVO2) over a physiological range (8-30 ml O2 X min-1 X 100 g-1) that were accompanied by an increase in coronary blood flow (CBF) with no change in oxygen extraction. The relationship between MVO2 and CBF was not different between the normotensive (NTC) and hypertensive (RHT) animals. Pericardial infusate adenosine (PI ADO) concentrations were not different for the same MVO2 and CBF, and the relationships for MVO2 vs PI ADO as well as PI ADO vs CBF were unaltered by hypertension. However, the relationship between PI ADO and coronary vascular resistance (CVR) was altered in the RHT group such that a given PI ADO concentration was associated with a significantly higher CVR. These data suggest that, over the range of MVO2 studied, there are no limitations in metabolic regulation of the coronary circulation of RHT animals, and that the higher CVR encountered in the RHT group is not the result of a reduced release of the endogenous vasodilator, adenosine.

1. Eight mongrel dogs were anaesthetized with sodium thiamylal and chloralose-urethane, ventilated, vagotomized and heparinized. Five Poland-China pigs were anaesthetized with sodium thiamylal and nitrous oxide, ventilated, vagotomized and heparinized. 2. Extracorporeal perfusion of the right coronary artery at constant pressure (100 mmHg) was instituted. A lung from a donor animal was interposed in the coronary perfusion circuit to effect changes in CO2 and O2 tensions in the coronary arterial blood while systemic blood gases were maintained at normal levels. 3. Local hypoxia (PO2 range 17-22 mmHg) produced a 25-75% decrease in coronary vascular resistance (P less than 0.05) and a 0-24% (not significant) decrease in right ventricular dP/dt. 4. Local changes in PCO2 over the range 8-105 mmHg were associated with a 17-58% decrease in coronary vascular resistance (P less than 0.05), a 19-24% decrease in right ventricular dP/dt (P less than 0.05) with no change in right ventricular end-diastolic pressure, and a 1-18% (not significant) decrease in heart rate. 5. These studies suggest that local decreases in O2 or increases in CO2 tensions produce decreases in right coronary vascular resistance that are in the opposite direction to those that would be expected from the observed changes in heart rate and contractility (two primary determinants of myocardial oxygen consumption). 6. These data support the hypothesis that CO2 and O2 are locally vasoactive in the coronary circulation.