Variations in processes and structures of cardiac surgery practice.

It is hypothesized that variations in the processes and structures of the selection of patients and the conduct of the surgical procedure may influence risk-adjusted outcome in patients undergoing cardiac surgery. For this reason, the results of the pilot phase of this Veterans Affairs cooperative study were reviewed to determine the variation in the operative practices at six pilot institutions. There were large variations in the percentage of elective, urgent, and emergent cases at each institution, ranging from 58% to 96% elective, 3% to 31% urgent, and 1% to 8% emergent. There was also a tenfold increase in the preoperative use of intra-aortic balloon pump for control of unstable angina, varying from 0.8% to 10.6%. Five of the six centers had accredited thoracic surgical residency programs. There was large variation in the preoperative participation of attending surgeons, from 100% participation at three centers to less than 5% in one. The operation was performed by the attending surgeon in 28% of cases, but this varied from 0% to 100%, depending on the hospital. Cold cardioplegia was used almost uniformly (99%) for myocardial protection; the use of retrograde cardioplegia varied from 2% to 89% among hospitals, and the use of blood cardioplegia ranged from 0% to 100%, with an average of 54% of cases. The use of myocardial temperature monitoring varied between hospitals, from 25% to 99%. The use of the cell saving devices to scavenge shed blood varied from 5% to 99%, and the frequency of the use of banked blood varied from 25% to 65%, depending on the institution. The internal mammary artery was used for 67% patients undergoing coronary artery bypass graft, with a variation between hospitals of 39% to 83%. One hospital used a single cross-clamping technique for the performance of proximal anastomoses in 95% of cases, as opposed to all other hospitals, who used this technique in less than 10% of cases. Aortic venting varied from 58% to 98% and left ventricular venting from 1% to 38%. The use of porcine valves varied approximately 15% in three hospitals to 30% to 40% in the other three hospitals. There were tremendous variations in the duration of operative procedure (5.2-7.3 hours), actual operating time (4.0-5.6 hours), total cardiopulmonary bypass duration (102-146 minutes), and ischemic time (50-87 minutes). The use of inotropic support varied from 41% to 91% between hospitals.(ABSTRACT TRUNCATED AT 400 WORDS)

Evaluating anesthesia health care delivery for cardiac surgery. The role of process and structure variables.

Anesthesia care is an integral component of cardiac surgery. Emphasis on cost-effectiveness and decreased hospital stay has prompted reevaluation of anesthesia practice. However, the role of anesthesia process and structure variables in relation to patient outcomes is largely unknown. Processes, Structures and Outcomes of Care in Cardiac Surgery is the first epidemiologic study to collect data on anesthesia processes, such as the pharmacologic components of anesthesia and types of cardiovascular monitors used. Structures of care, such as resident staffing, supervision, completeness of documentation, and training and experience of care providers, are also being assessed. Pilot data collected from September 1992 to September 1993 demonstrate substantial variation between the six study sites in selected processes and structures. Despite the near-universal use of narcotic anesthesia as the primary anesthetic technique, variation in the type of opioid and adjuvant benzodiazepine used was observed. Regarding invasive hemodynamic monitoring, most centers used only one type of catheter. Intraoperative transesophageal echocardiography was used commonly at several centers for valve surgery, whereas other centers did not use it at all. Its use during coronary artery bypass grafting was less common. Assessment of the preoperative anesthesia note revealed that coronary anatomy and ventricular function were noted in nearly all instances. However, a clear notation that risks and benefits of anesthesia were discussed was less frequent. Structures related to anesthesia attending staffing, board certification, and experience revealed variation. Some sites had smaller and/or more experienced attending staffs, whereas others had larger and/or less experienced staffs. These pilot findings appear to validate the authors' hypotheses that variations in anesthesia practice are present within the Veterans Affairs system. They suggest that the variable set is robust enough to relate processes and structures of anesthesia care to patient outcome.

Thromboembolism in patients undergoing thoracotomy.

To determine the incidence of thromboembolism in relation to thoracotomy, 77 patients undergoing pulmonary resection were prospectively studied up to 30 days postoperatively for deep venous thrombosis and pulmonary embolism. Overall, 20 of 77 patients (26%) had thromboembolic events during their hospitalization. Four deep venous thromboses and 1 pulmonary embolism were detected in 5 of 77 patients preoperatively for an incidence of 6%. Postoperative thromboembolism was detected in 15 of 77 (19%): deep venous thrombosis in 11 (14%) and pulmonary embolism in 4 (5%). No postoperative thromboembolisms occurred in the 17 patients receiving preoperative aspirin or ibuprofen, whereas they did occur in 25% of the remainder (15/60). Thromboembolism after pulmonary resection was more frequent with bronchogenic carcinoma than with metastatic cancer or benign disease (15/59 [25%] versus 0/18 [0%]; p < 0.01), adenocarcinoma compared with other types of carcinoma (11/25 [44%] versus 4/34 [12%]; p < 0.0004), large primary lung cancer (> 3 cm in diameter) compared with smaller lesions (9/19 [47%] versus 6/40 [15%]; p < 0.0001), stage II compared with stage I (7/14 [50%] versus 7/34 [21%]; p < 0.04), and pneumonectomy or lobectomy compared with segmentectomy and wedge resection (14/49 [29%] versus 1/28 [4%]; p < 0.005). Three of 4 patients with thromboembolism detected preoperatively had operation within the previous year. Postoperative pulmonary embolism was fatal in 1 of 4 (25%) and accounted for the one death. These results suggest patients undergoing thoracotomy for lung cancer, especially adenocarcinoma, should be considered for thromboembolic prophylaxis.

An update of solid organ transplantation at UAMS.

The one year survival for solid organ transplants is 70 to 90%. Encouraged by this success, the University of Arkansas for Medical Sciences is expanding its organ transplant center and will offer renal, pancreas, liver, heart, and lung within a year. The limiting factor in transplants continues to be a shortage of Donor organs and the need for increased referral of potential donors.

Clinical experience with the Novacor ventricular assist system. Bridge to transplantation and the transition to permanent application.

At Stanford University, a Novacor left ventricular assist system (Baxter Healthcare Corporation, Novacor Division, Oakland, Calif.) was placed as a bridge to heart transplantation in 13 patients. During the hospitalization preceding device implantation, all patients were receiving inotropic support for biventricular failure, 11 had pulmonary edema, 6 had life-threatening ventricular arrhythmias, 5 had liver dysfunction with coagulopathy, and 2 had renal failure necessitating artificial support. The mean cardiac index before implantation of the Novacor system was 1.5. All survivors with the Novacor device had a dramatic increase in cardiac output (mean cardiac index = 3.1). One patient with cardiac allograft rejection died during implantation of the left ventricular assist system. Two patients died of pulmonary sepsis and multiorgan failure after the device was implanted. All patients who had the Novacor device implanted for more than 7 days were able to walk and ride stationary bicycles while awaiting transplantation. Ten patients (77%) underwent successful heart transplantation after a mean of 18 days' support with the Novacor device. One patient died of presumed sepsis 2 days after transplantation. Nine patients (90%) are alive 4 months to 6 years after transplantation. In the overall United States experience, 68 patients (as of May 1990) have had a Novacor left ventricular assist device implanted. Five were still being supported, 39 had received a transplant (62%), and 35 patients (90%) survived the transplant hospitalization (1 died later). No instances of device failure have occurred. Overall, the Novacor assist system provided effective bridging to transplantation, with posttransplant survival similar to results after routine transplantation. Modifications and improvements based on this clinical experience have been made in the areas of patient selection, techniques of operative placement, postoperative management, and design of the assist system. Isolated left heart support with a fully implantable left ventricular assist system will be offered as an alternative to heart transplantation for selected patients by 1992.

Electrophysiological effects of left ventricular free wall traction in intact hearts.

Transmural multipolar electrodes, sonomicrometers implanted within the left ventricular wall, and cardiac electrical stimulation techniques were used to examine the effect of transient mechanically applied traction to the left ventricular free wall on local electrophysiological properties. Twenty-five open-chest dogs were atrially paced (cycle length 400 ms) followed by insertion of timed premature extrastimuli at left ventricular epicardial pacing sites either in the vicinity of (traction zone) or remote from (nontraction-control zone) the site of left ventricular free wall traction. Electrophysiological recordings were made before and during intermittent left ventricular free wall traction applied in late diastole (rate 25 cm/s; duration 170 ms). In 22 of 25 dogs, application of traction resulted in early local ventricular activation (mean activation advancement 64 +/- 15 ms), altered QRS morphology of the last conducted atrial drive train beat, and a relative prolongation of ventricular refractoriness in the traction zone. Conversely, in the nontraction-control zone, early activation did not occur and refractoriness was unchanged. Alterations in regional myocardial blood flow (assessed by microsphere technique) did not appear responsible for the observed changes. Furthermore, phenol interruption of local sympathetic or combined sympathetic and parasympathetic innervation or verapamil pretreatment had no impact on the mechanically induced electrophysiological changes. Thus, in normal myocardium in situ, regional abnormalities in wall motion may be associated with alterations of local ventricular activation and refractoriness, factors that in the diseased heart could lead to increased susceptibility to arrhythmias.

Frequency and location of atherosclerotic plaques in the ascending aorta.

Among 97 specimens of ascending aorta from adults with clinical coronary disease, the prevalence of atherosclerotic plaques greater than 8 mm in diameter was 38%. The right side of the ascending aorta was more commonly involved than the left; the sites least commonly involved were the right-posterior, upper right-anterior, and lower posterior locations. Of specimens with plaques at the orifice of the innominate artery, 80% also had plaques in the ascending aorta, and 73% of specimens with plaques at the orifice of the left subclavian artery had plaques in the ascending aorta.

Role of extrastimulus site and tachycardia cycle length in inducibility of atrial preexcitation by premature ventricular stimulation during reciprocating tachycardia.

Preexcitation of the atria during reciprocating tachycardia (RT) by a premature ventricular complex occurring when the His bundle is refractory provides direct evidence of the presence of accessory atrioventricular (AV) connection. The impact of ventricular stimulation site and RT cycle length on inducibility of atrial preexcitation was assessed in 38 patients with RT utilizing a single accessory AV connection (right free wall in 5 patients, left free wall in 21 and posterior septal/paraseptal in 12). Extrastimuli were inserted at right ventricular (RV) apical, left ventricular (LV) septal and LV free wall sites. Inducibility of and magnitude of atrial preexcitation increased as stimulation site approached accessory AV connection site. Thus, for RV free wall connections, RV extrastimuli preexcited the atria in 5 of 5 patients, LV septal in 1 of 5 and LV free wall in 0 of 4. For LV free wall accessory connections, RV extrastimuli preexcited the atria in only 3 of 21 patients, compared with 12 of 17 with LV septal and 20 of 21 with LV free wall stimulation. Additionally, the magnitude of atrial preexcitation achieved was related to RT cycle length, diminishing as cycle length shortened. Finally, in a few instances both RV apical and LV free wall extrastimuli failed to elicit preexcitation in patients with a posterior septal connection. Thus, ventricular pacing site and RT cycle length contribute importantly to induction of atrial preexcitation by ventricular extrastimulation technique and should be considered during evaluation of patients with RT in whom accessory AV connections may be present.

Electrophysiologic properties of the myocardial infarction border zone: effects of transient aortic occlusion.

This study used transmural multipolar electrodes, ventricular pressure monitoring, and cardiac electrical stimulation techniques to examine the effects of transient aortic occlusion on ventricular refractoriness in a canine model of recent myocardial infarction. Six previously instrumented resting awake dogs were atrially paced, followed by timed premature extrastimuli inserted at epicardial pacing sites adjacent to an apical left ventricular (LV) myocardial infarction or in an LV control zone remote from the myocardial infarction. Electrophysiologic and pressure recordings were obtained before and during periods of transient aortic occlusion. Aortic occlusion was applied before the last beat of an eight-beat atrial pacing sequence and resulted in increased peak LV pressure (92.8 +/- 27.7 mm Hg, p = 0.003). Aortic occlusion shortened LV effective refractory period (ERP) recorded from the myocardial infarction border zone in both the subepicardial (-17.0 +/- 11.8 msec, p = 0.019) and subendocardial (-17.7 +/- 10.9 msec, p = 0.011) regions, whereas LVERP of the control zone was unchanged. Conduction latency of premature beats at equivalent coupling intervals and maximum latency observed were unchanged by aortic occlusion. atrioventricular conduction interval shortened in association with aortic occlusion. Thus transient aortic occlusion reduced ventricular refractoriness in the border zone adjacent to the myocardial infarction while control zone refractoriness was minimally or not changed. Heterogeneity of ventricular myocardial refractoriness may result from mechanical dysfunction, potentially increasing susceptibility to arrhythmias.

Electrophysiologic effects of papillary muscle traction in the intact heart.

In this study we used transmural multipolar electrodes, sonomicrometers implanted within the left ventricular wall, and cardiac electrical stimulation techniques to examine the effect of transient mechanical posterior papillary muscle traction on local myocardial electrophysiologic characteristics. Nine open-chest dogs were atrially paced (cycle length 400 msec) followed by insertion of timed premature extrastimuli at left ventricular epicardial pacing sites either in the vicinity of (traction zone) or remote from (nontraction zone) the site of papillary muscle traction. Electrophysiologic recordings were made before and during periods of intermittent papillary muscle traction of predetermined timing, application rate (25 cm/sec), and duration (170 msec). Papillary muscle traction was applied in late diastole just before the last beat of each atrial drive train. In seven of nine dogs application of transient papillary muscle traction resulted in significantly earlier local ventricular activation (mean activation advancement 30 +/- 13 msec), altered QRS morphology of the last conducted atrial drive-train beat, and relative prolongation of ventricular functional refractory period in the traction zone. Conversely, in nontraction zones in these seven dogs, early activation did not occur and refractoriness remained unchanged as tested by a locally placed extrastimulus. In two of nine dogs traction failed to induce early activation and changes in refractoriness did not occur. Alterations in regional myocardial blood flow (assessed by radioactive microsphere technique) did not appear responsible for the observed changes, since there was no demonstrable traction-induced difference in regional blood flow between the traction and nontraction zones.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracavitary electrode catheter cardioversion of atrial tachyarrhythmias in the dog.

This study examined factors determining efficacy of intracavitary cardioversion of atrial tachyarrhythmias in closed chest, anesthetized dogs with talc pericarditis. Electrode catheters were positioned transvenously with the cathode in the right atrial appendage. In Group 1 dogs (n = 6), three anode sites (superior and inferior venae cavae ostia and mid-right atrium) were tested with graded energy shocks to determine the lowest effective cardioversion energy at each anode position. In Group 2 dogs (n = 9), multiple cardioversion attempts with energy levels of 0.01 to 5.0 J were used to evaluate reproducibility of energy thresholds. In Group 3 dogs (n = 6) without talc-induced pericarditis, atrial pathologic study was done after five intracavitary shocks (0.5 or 5.0 J). In Group 1, cardioversion was achieved with 0.75 J or less with no significant difference in minimal effective cardioversion energies among the three anode positions tested. In Group 2, 98 (26%) of 372 cardioversion attempts were successful. Intra-animal minimal effective cardioversion energies varied widely, and timing of shocks relative to atrial electrograms did not influence efficacy. Complications were infrequent and included delayed sinus rhythm recovery, transient atrioventricular block and ventricular fibrillation. Ventricular fibrillation occurred in 9 (2.4%) of 372 shocks, and was associated with higher delivered energies (6 of 9 with greater than or equal to 1.0 J) and with shocks delivered 116 to 180 ms after onset of the QRS complex. In Group 3, two dogs had no histologic damage, three dogs had multiple small foci of subendocardial necrosis and in one dog these foci coalesced to involve half the atrial wall thickness. Thus, low energy cardioversion of atrial tachyarrhythmias is feasible using intracavitary electrodes. Synchronization of energy delivery to the QRS complex is important to minimize risk of ventricular fibrillation.

Electrophysiological effects of transient aortic occlusion in intact canine heart.

This study utilized sonomicrometers transmural multipolar electrodes and cardiac electrical stimulation techniques to examine the effect on myocardial electrophysiological characteristics of altering ventricular systolic mechanical properties by transient aortic occlusion. Nine anesthetized open-chest dogs were atrially paced, and timed extrastimuli were inserted during alternate drive-train sequences at right or left ventricular (RV, LV) epicardial sites to measure ventricular effective refractory period (ERP). Sonomicrometer measurements of LV systolic mechanical parameters and both RV and LV electrophysiological findings were determined prior to and during periods of transient aortic occlusion. Aortic occlusion was applied just prior to the last beat of each eight-beat atrial drive train and released immediately following the programmed ventricular extrastimulus. Aortic occlusion increased LV systolic pressure (+42 +/- 26.6 mmHg, P less than 0.01) and diminished segmental stroke shortening (0.100 +/- 0.059 mm, P less than 0.02), shortening fraction (0.086 +/- 0.048, P less than 0.001), mean velocity of stroke shortening (0.444 +/- 0.186 mm/s, P less than 0.001), and stroke work (P less than 0.001). LV epicardial and endocardial ERP were prolonged as a result of aortic occlusion (5 +/- 7.2 and 6 +/- 6.5 ms, respectively, P less than 0.05), whereas RV ERP was unchanged. Latency of premature beats at equivalent coupling intervals was unaltered. ERP prolongation correlated most strongly with reductions of segmental stroke shortening (r = 0.928, P less than 0.001), shortening fraction (r = 0.901, P less than 0.001), and mean shortening velocity (r = 0.819, P less than 0.01). Thus transient aortic occlusion prolonged LV refractoriness, and electrophysiological changes closely paralleled the severity of systolic mechanical disturbance.

Electrophysiologic effects of flecainide acetate and its major metabolites in the canine heart.

Flecainide acetate, an investigational class 1 antiarrhythmic agent, undergoes biotransformation in man with production of 2 major metabolites: meta-O-dealkylated flecainide (S-24623) and the meta-O-dealkylated lactam of flecainide (S-26191). This study compared the effects of flecainide, S-24623 and S-26191 on cardiac electrophysiologic characteristics in the anesthetized dog. Each dog received 2 dose levels of 1 of the 3 test compounds after control measurements. Flecainide (2 and 4 mg/kg in 8 dogs), S-24623 (4 and 8 mg/kg in 8 dogs) and S-26191 (4 and 10 mg/kg in 7 dogs) were administered intravenously in dilute solution. Of the 3 compounds, only flecainide significantly prolonged sinus cycle length (p less than 0.01). However, both flecainide and S-24623 significantly prolonged minimum atrial paced cycle length with 1:1 atrioventricular conduction, atrioventricular nodal effective and functional refractory periods, and right ventricular effective refractory period. Metabolite S-26191 exhibited qualitatively similar but much weaker electrophysiologic actions. The maximal electrophysiologic effects of flecainide and S-24623 were approximately equivalent, but the metabolite was about one-half as potent on a milligram-permilligram basis, and lacked marked effects on infranodal (HV interval) conduction. S-26191 was less than one-tenth as potent as flecainide. Therefore, since both flecainide metabolites occur primarily in the conjugated form in plasma (i.e., free metabolite concentrations are low), it is unlikely that these compounds either potentiate flecainide's antiarrhythmic action or increase susceptibility to drug toxicity in the clinical setting.

Bromocriptine treatment of digitalis-induced ventricular tachyarrhythmias: studies in a canine model.

Ventricular tachyarrhythmias associated with digitalis toxicity are believed to be due, in part, to cardiac glycoside-mediated increased central sympathetic neural activity. Because dopaminergic receptor agonists reduce sympathetic outflow, this study assessed effectiveness of the available dopaminergic agonist, bromocriptine, in slowing or terminating ouabain-induced ventricular tachycardia in anesthetized dogs. In all experiments, ouabain was administered intravenously (20 micrograms/kg body weight bolus injection, followed by 2.5 micrograms/kg per min infusion) until the onset of stable ventricular tachycardia. Of seven untreated dogs (Group 1), ouabain-induced ventricular tachyarrhythmias resulted in ventricular fibrillation in three, while in four dogs tachycardia persisted without significant change in rate until the study was terminated. Fourteen dogs (Group 2) received bromocriptine, either 30 micrograms/kg (Group 2A) or 50 micrograms/kg (Group 2B), after the onset of ventricular tachycardia. Tachycardia slowed in all 14 dogs and terminated with resumption of sinus rhythm in 8 of the 14. In all six dogs pretreated with the peripheral dopaminergic antagonist domperidone (Group 3), bromocriptine, 50 micrograms/kg, slowed ventricular tachycardia and in three of the six, tachycardia terminated. In contrast, of five dogs pretreated with haloperidol, a central and peripheral dopaminergic receptor antagonist (Group 4), bromocriptine, 50 micrograms/kg, failed to slow ventricular tachycardia in three, and two of the three developed ventricular fibrillation. In summary, the dopaminergic receptor agonist, bromocriptine, presumably acting at central dopaminergic receptor sites, consistently slowed and in most cases reversed ouabain-induced ventricular tachycardia in a canine model.