Incidental findings in CT imaging of coronary artery bypass grafts: results from a Canadian multicenter prospective cohort.

OBJECTIVE: To assess the prevalence and clinical significance of incidental findings identified during computed tomography imaging of coronary artery bypass grafts. RESULTS: This prospective study includes 144 patients undergoing coronary graft patency assessment using computed tomography. Incidental findings were classified as significant if they were considered to need an immediate action or treatment, short-term work-up or follow-up, or minor. A total of 211 incidental findings were present in 109 (75.7%) patients. Seventy-one incidental findings (33.6%) were cardiac and 140 (66.4%) were extracardiac. Most common cardiac incidental findings were atrial dilatation [39 patients, 48 incidental findings (67.6%)] and aortic valve calcifications (7 patients, 9.9%). Among the 140 extracardiac incidental findings, the most common were lung nodules (51 patients, 54 nodules, 38.6%), and emphysema (21 patients, 15%). Thirty-six (25.7%) extracardiac incidental findings were significant and notably, 23 (63.9%) were lung nodules. Follow-up was recommended in 37 cases, among which all patients with significant lung nodules (23 patients, 62.2%). In conclusion, most common computed tomography incidental findings in patients with coronary grafts were lung nodules and emphysema.

Endothelin receptor blockade improves endothelial function in human internal mammary arteries.

OBJECTIVE: Endothelial dysfunction, specifically endothelium-derived contracting factors have been implicated in the development of arterial conduit vasospasm. The potent vasoconstrictor endothelin-1 (ET-1) has received much attention in this regard. The present study was designed to evaluate the role of ET-1 in the development of endothelial dysfunction in human internal mammary arteries (IMA). To this aim, we examined the effects of specific and non-specific ET-receptor antagonists on endothelial function (assessed using acetylcholine (ACh)-induced vasodilation) in segments of IMA obtained during coronary artery bypass graft (CABG) surgery. METHODS: Vascular segments of IMA were obtained from 51 patients undergoing elective coronary artery bypass graft (CABG) surgery and in vitro endothelium-dependent and -independent responses to ACh and sodium nitroprusside (SNP) were assessed. Isometric dose response curves (DRC) to ACh and SNP were constructed in pre-contracted rings in the presence and absence of bosentan (ET(A/B) receptor antagonist, 3 microM), BQ-123 (ET(A) antagonist, 1 microM) and BQ-788 (ET(B) antagonist, 1 microM) using the isolated organ bath apparatus. Percent maximum relaxation (%E(max)) and sensitivity (pEC(50)) were compared between interventions. RESULTS: ACh caused dose-dependent endothelium-mediated relaxation in IMA (%E(max) 43+/-4, pEC(50) 6. 74+/-0.12). In the presence of bosentan, BQ-123 and BQ-788 ACh-induced relaxation was significantly augmented (%E(max) bosentan 60+/-3, BQ-123 56+/-4, BQ-788 53+/-5 vs. control 43+/-4, P<0.05) without affecting sensitivity. The effects of these antagonists were endothelium-specific since endothelium-independent responses to SNP remained unaltered. Furthermore, the beneficial effects were independently and maximally mediated by ET(A) and ET(B) receptors (%E(max) BQ-123 56+/-4 vs. BQ-788 53+/-5 vs. bosentan 60+/-3, P>0. 05). CONCLUSIONS: These data uncover, for the first time, beneficial effects of ET receptor blockade on endothelial-dependent vasorelaxation in human IMA.

Tetrahydrobiopterin improves endothelial function in human saphenous veins.

OBJECTIVES: Diminished production of nitric oxide has been linked to saphenous vein endothelial dysfunction. Tetrahydrobiopterin is an obligate cofactor for the oxidation of L -arginine by nitric oxide synthase in the production of nitric oxide by endothelial cells. The objective of the present study was to examine whether the exogenous addition of tetrahydrobiopterin improves endothelial function in saphenous veins from patients undergoing coronary artery bypass graft operations. METHODS: Vascular segments of saphenous veins were obtained from 17 patients undergoing elective coronary artery bypass grafting, and in vitro endothelium-dependent and endothelium-independent responses to acetylcholine and sodium nitroprusside were assessed. Isometric dose-response curves were constructed in precontracted rings in the presence and absence of tetrahydrobiopterin (0.1 mmol/L) with the use of the organ bath apparatus. The percentages of maximum relaxation and sensitivity were compared between interventions. RESULTS: Acetylcholine caused dose-dependent endothelium-mediated relaxation in saphenous veins. In the presence of tetrahydrobiopterin, acetylcholine-induced relaxation was significantly augmented (percentage maximum relaxation, 16.8% +/- 2.9% vs control 7.5% +/- 1.8%; P =.003) without an effect on agonist sensitivity. These effects were endothelium-specific because endothelium-independent responses to sodium nitroprusside were preserved. CONCLUSIONS: These data uncover beneficial effects of acute tetrahydrobiopterin addition on endothelial function in human vessels. Because endothelial dysfunction has been implicated in the development of graft failure, studies aimed at chronic delivery of tetrahydrobiopterin would be useful in determining the contribution of this cofactor toward saphenous vein atherosclerosis.

Postinspiratory activity of costal and crural diaphragm.

Because the first stage of expiration or "postinspiration" is an active neurorespiratory event, we expect some persistence of diaphragm electromyogram (EMG) after the cessation of inspiratory airflow, as postinspiratory inspiratory activity (PIIA). The costal and crural segments of the mammalian diaphragm have different mechanical and proprioceptive characteristics, so postinspiratory activity of these two portions may be different. In six canines, we implanted chronically EMG electrodes and sonomicrometer transducers and then sampled EMG activity and length of costal and crural diaphragm segments at 4 kHz, 10.2 days after implantation during wakeful, resting breathing. Costal and crural EMG were reviewed on-screen, and duration of PIIA was calculated for each breath. Crural PIIA was present in nearly every breath, with mean duration 16% of expiratory time, compared with costal PIIA with duration -2. 6% of expiratory time (P < 0.002). A linear regression model of crural centroid frequency vs. length, which was computed during the active shortening of inspiration, did not accurately predict crural EMG centroid frequency values at equivalent length during the controlled relaxation of postinspiration. This difference in activation of crural diaphragm in inspiration and postinspiration is consistent with a different pattern of motor unit recruitment during PIIA.

Eliminating ultrasonic interference from respiratory muscle EMG.

Fine wire recordings of the respiratory muscle electromyogram are often employed to represent muscle activity, and recently ultrasound-sonomicrometry has become a common method of measuring length of respiratory muscles in both acute and chronic preparations. Although recording both EMG and sonomicrometry simultaneously has become standard practice, there has not been any consideration of the potential confounding influence of ultrasound noise upon the recorded EMG spectrum. Activation of the sonomicrometry-ultrasound tranducer introduces a high frequency, high amplitude voltage pulse plus harmonics, which can contaminate the EMG spectrum directly, as well as through aliasing when EMG is sampled directly digitally. We describe the use of a new, combined, wing stabilized sonomicrometry- and EMG measurement transducer to characterize exactly the influence of ultrasound upon the crural diaphragm EMG spectrum, and the development of digital filtering techniques which effectively eliminate the ultrasound interference. Two alternative methods of avoiding ultrasound-EMG interference are also considered. The isolation and elimination of ultrasound-sonomicrometry signal interference may be important in studies where EMG and length are measured together.

Diaphragm function during sighs in awake dogs after laparotomy.

Pulmonary complications after upper abdominal surgery are usually ascribed to temporary postoperative impairment of diaphragm function, which may not originate from intrinsic, structural injury but from reflex inhibition of diaphragm contractility. Spontaneous breathing is interrupted periodically by sighs, even after upper abdominal surgery. If postoperative dysfunction of the diaphragm arises from a reflexic inhibition, then the sigh should temporarily override the inhibition and restore normal diaphragm function. We implanted sonomicrometer and electromyogram transducers chronically in six dogs by laparotomy, then directly measured length, shortening, and electromyogram activity of costal and crural diaphragm segments, parasternal intercostal, and transversus abdominis muscles an average of 8.7 (range, 1-16) d later during resting tidal breathing and sighs. In each animal we analyzed a sequence of breaths, including a sigh, when costal or crural diaphragm contractility was abnormal. With each sigh, the shape and amplitude of costal and crural diaphragm segmental shortening improved abruptly, from 0.9 and 1.4% of baseline length (% LBL) during resting breathing to 12.1 and 11.1% LBL, respectively, during sighs. The sighs were compared to CO2-stimulated breaths of equivalent tidal volume, which did not show either pattern or amplitude of shortening equivalent to sighs. We conclude that diaphragm dysfunction after laparotomy arises from a reflex inhibition, which is overridden abruptly to return diaphragm function briefly to normal during each spontaneous sigh.

Government, university, and community collaboration to develop a cardiac surgery database and report of morbidity and mortality while waiting for open heart surgery.

The Provincial Advisory Committee on Cardiovascular Services was established in January of 1990 to advise concerning these services. One of the first tasks assigned was to monitor waiting times for cardiac surgery. Referring cardiologists categorized their patients into four priorities: emergency, urgent-inpatient, urgent-outpatient, and planned. Data of the southern Alberta centers for the past three years were analyzed for events while waiting for surgery. (Median time to event in days) M1=Myocardial Infarction EM=Emergency D=Day A hierarchy was used to assign the single most serious event for patients having more than one event: death>MI>readmission or change from urgent-inpatient to emergency. Events were frequent and unpredictable, particularly in outpatients. Categorization of patient suitable to wait at home for cardiac surgery is imperfect. The risk of having an event while on the waiting list is much greater for out-patients than in-patients: 12.8% (169/1323) versus 1.9% (19/1002). All adverse events for the in-patients occurred at four days--one day less than the proposed maximum waiting time. In the out-patient population, the median waiting time to experiencing adverse events ranged between 32 and 54 days. Target waiting times set by PACCS for these two categories is 14 and 56 days respectively. Total adverse events occurred to 8% of the patients on the waiting list. Median waiting time to experiencing an adverse event while on the list occurs much earlier than suspected: four days in urgent in-patients and 36 days for out-patients; well below the intended maximum of 56 days. This database proved invaluable for this important critical data collection. It is hoped it will serve as a model for similar future projects.

Right atrial and right ventricular transmural pressures in dogs and humans. Effects of the pericardium.

BACKGROUND: To determine the transmural pressure-dimension relations of the right atrium (RA) and right ventricle (RV) before and after pericardiectomy, six open-chest dogs were instrumented with pericardial balloons placed over the RA and RV free walls. METHODS AND RESULTS: PA appendage dimensions and RV free-wall segment lengths were measured using sonomicrometry. Intact-pericardium RA and RV transmural pressures were calculated by subtracting the pericardial pressures (measured using balloons) from the cavitary pressures. Pooled data from six animals with pericardium intact indicate that at RA and RV cavitary pressures of 5, 10, and 15 mm Hg, RV pericardial pressure was 4.3 +/- 0.3, 8.6 +/- 1.0, and 13.3 +/- 1.5 mm Hg, respectively, and RA pericardial pressure was 4.8 +/- 0.3, 9.6 +/- 0.6, and 14.6 +/- 0.6 mm Hg, respectively (mean +/- SD). With calculated unstressed dimensions, the cavity dimension data were normalized to strain (in percent). We determined that in the dog, RV strain would increase by 14% and RA by 68% to maintain cavitary pressure at 10 mm Hg on pericardiectomy. To compare these results with clinical data, RV (n = 7) and RA (n = 6) transmural pressures were measured using balloons in patients (age, 19 to 76 years) undergoing cardiac surgery. RA transmural pressure of six patients was 1.0 +/- 1.5 mm Hg when central venous pressures (CVPs) ranged from 3 to 16 mm Hg. RV transmural pressure equaled 1.2 +/- 1.9, 2.3 +/- 1.9, and 3.4 +/- 2.0 mm Hg when CVP was 5, 10, and 15 mm Hg, respectively. CONCLUSIONS: Pericardial constraint (as evaluated by the ratio of pericardial to intracavitary pressures when CVP is 10 mm Hg) accounted for 96% of RA cavitary pressure in the dog and 89% in humans and at least 86% of RV cavitary pressure in the dog and 77% in humans.

Respiratory muscle compensation for unilateral or bilateral hemidiaphragm paralysis in awake canines.

In humans and some animals, the surviving respiratory muscles are able to compensate fully for unilateral, and partially for bilateral, hemidiaphragm paralysis. To examine differential activity of individual respiratory muscles after unilateral or bilateral diaphragm paralysis, length and electromyogram (EMG) of left costal and crural diaphragm segments, parasternal intercostal, and transversus abdominis were measured directly in five awake canines after implantation with sonomicrometry transducers and bipolar EMG electrodes under three conditions: during normal breathing (NOFRZ), after infusion of local anesthetic (bupivacaine) through a cervical phrenic nerve cuff to induce reversible contralateral hemidiaphragm (CNFRZ), and after bilateral diaphragm (BIFRZ) paralysis. From NOFRZ to CNFRZ, costal, crural, parasternal, and transversus abdominis increased shortening and EMG activity to compensate for contralateral diaphragm paralysis, but the increase in activity was not equivalent for each muscle. With BIFRZ, parasternal and transversus abdominis showed further increases in activity, coordinated between both inspiration and expiration. Normalized intrabreath profiles revealed dynamic differences in development of muscle activity within each breath as paralysis worsened. Review of simultaneous muscle activities showed coordinated interactions among the compensating muscles: passive shortening of transversus, and lengthening of costal and crural, coincided with increased active inspiratory shortening of parasternal. We conclude that an integrated strategy of respiratory muscle compensation for unilateral or bilateral diaphragm paralysis occurs among chest wall, abdominal, and diaphragm segmental muscles, with relative contributions of individual muscles adjusted according to the degree of diaphragm dysfunction.

Respiratory muscle function during emesis in awake canines.

Emesis requires a coordinated differential recruitment of gastrointestinal smooth muscle, upper airway muscles, and several muscles involved in respiration. In seven awake intact canines we measured the electrical activity (electromyogram) and shortening of costal and crural diaphragm segments, parasternal intercostal, and transversus abdominis during emesis that was induced by instillation of apomorphine into the lower conjunctival fornix. The process of emesis was tightly coordinated with ventilation and showed four respiratory phases: baseline ventilation (Base), initial preemetic hyperventilation (Hyperv), prodromal ventilation associated with salivation and probable nausea (Prodrome), and finally retching and expulsion (Expel) of gastric contents. Ventilation was suppressed during expulsive events, but a small inspiratory airflow was interjected between expulsions. Resting electromyogram of all four muscles increased during the process of emesis, with costal and crural segments showing a marked decrease in resting length through Prodrome and Expel. To produce an expulsive maneuver, both inspiratory and expiratory muscles were activated synchronously, unlike their usual sequential activation during ventilation, with costal and crural segments and transversus abdominis showing the most shortening. The crural segment showed a biphasic length change with initial shortening and then lengthening to assist esophageal sphincter function during Expel. These results indicate a strong coordinated interaction between brain stem centers responsible for control of respiration and of emesis.

A randomized comparison of a bipolar steroid-eluting electrode and a bipolar microporous platinum electrode: implications for long-term programming.

Differences in acute and chronic pacing thresholds were compared in patients receiving either the Medtronic Model 4004 steroid-eluting lead or the Medtronic Model 4012 microporous platinum lead. Patients (n = 35) were randomized at the time of implant to receive either a steroid-eluting (n = 17) or a microporous (n = 18) lead. Pacing thresholds were determined within 24 hours and at 2, 4, 6, 12, 24, and 52 weeks postimplant. By 2 weeks postimplant, pacing thresholds measured at 0.8, 1.6, 2.5, 3.3, and 4.2 V were significantly lower in the steroid lead group compared to the microporous lead group (P < 0.05). At 24 weeks, the voltage threshold at 0.3 msec was 0.8 V in 88% of patients with a steroid lead whereas this threshold was only observed in 33% of patients with the microporous lead (P < 0.01). At 52 weeks the pacing energy measured at 1.6 V, twice pulse duration threshold, was significantly lower in the steroid lead group (0.81 +/- 0.59 microJ) compared to the microporous lead group (1.25 +/- 0.60 microJ, P < 0.05). Thirteen patients in the steroid lead group and 9 patients in the microporous lead group have been programmed at a pulse amplitude of 1.6 V since the 24-week follow-up visit. These patients have been followed for a minimum of 6 months without documented failure to capture. This study shows that pacemaker/lead systems with stable chronic low thresholds can be safely programmed to low pulse amplitude settings. This practice will prolong the longevity of pulse generators.

Comparison of biphasic and monophasic shocks for defibrillation using a nonthoracotomy system.

A comparison of defibrillation thresholds was made using biphasic and monophasic shocks delivered by a nonthoracotomy lead system in 2 clinically distinct groups of patients. The first group were patients receiving an implantable cardioverter-defibrillator who were studied before surgery with their chests closed. The second group were patients undergoing coronary artery bypass grafting (CABG) who were studied before surgery with their chests open but reapproximated. Biphasic defibrillation thresholds (stored energy) were significantly (p < 0.001) less than monophasic ones in subjects with the implantable cardioverter-defibrillator (12.3 +/- 5.3 vs 21.1 +/- 9.3 J) or CABG (14.6 +/- 7.1 vs 24.2 +/- 12.6 J). These values are less than were previously reported with a similar nonthoracotomy lead configuration. There were no significant differences between the 2 groups in all measurements derived from corresponding shock waveforms, although impedance tended to be greater in patients with CABG. However, subjects with CABG had greater left ventricular ejection fractions and did not have history of potentially lethal ventricular arrhythmias. Despite these differences, the conclusion that biphasic shocks are more effective would have been made in a study of either group alone. It is concluded that patients with CABG who have not had preceding potentially lethal ventricular arrhythmias may be a potential source of surrogate subjects for defibrillation research such as epicardial mapping, which requires that the chest be open.

Reduction in defibrillator shocks with an implantable device combining antitachycardia pacing and shock therapy.

Implantable defibrillators reduce the risk of sudden death in patients with malignant ventricular arrhythmias, but significant restriction in quality of life can occur as a result of frequent device activation. To determine if a device that provides both antitachycardia pacing and shock therapy can safely reduce the frequency of shocks after implantation, 46 consecutive patients undergoing initial implantation of a defibrillator were studied. In all patients, the implanted device provided antitachycardia pacing and shock therapy. Detected tachycardia characteristics and the results of therapy were stored in the device's memory. There were 42 men and 4 women, aged 26 to 71 years (mean 58.7 +/- 13.5). Left ventricular ejection fraction ranged from 13% to 67% (mean 32.2 +/- 13.4%) and 31 patients had experienced one or more episodes of cardiac arrest. Induced arrhythmias included sustained monomorphic ventricular tachycardia in 38 patients, nonsustained polymorphic ventricular tachycardia in 2 and ventricular fibrillation in 4. Over a total follow-up period of 255 patient-months (range 1 to 13, mean 6.1), 25 patients experienced spontaneous arrhythmic events. In 22 patients, 909 episodes of tachycardia were treated by antitachycardia pacing, which was successful on 840 occasions (92.4%). Acceleration of ventricular tachycardia by pacing therapy was estimated to have occurred 39 times. Syncope occurred once during pacing-induced acceleration of ventricular tachycardia. Forty-four episodes of tachycardia in seven patients were treated directly by shocks because of short tachycardia cycle length; 88% of all detected tachycardias were treated without the need for shocks. Four patients died from cardiorespiratory failure and one patient died suddenly without any detected tachyarrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal aortic ectasia resulting from peripheral traumatic arteriovenous fistulization.

A 61-year-old World War II fighter pilot sustained a gunshot injury to the right fibula and an arteriovenous fistula subsequently developed. Angiographic examination 44 years later for evaluation of an abdominal aortic aneurysm showed an unusually shaped aneurysm and the right arteriovenous fistula with antegrade dilation of the ipsilateral arterial system in continuity with the aneurysm. We hypothesize that this arteriovenous fistula, which involved the peroneal and anterior tibial arteries of the right leg of 44 years' duration, was responsible for the development of this man's abdominal aortic aneurysm.

Sequential coronary bypass grafts. Long-term follow-up.

Sequential venous coronary bypass grafts have presented problems, mainly because of commonly reported differences between patency of side-to-side and end-to-side vein-coronary anastomoses. Better to define this, we have studied sequential anastomosis grafts done during a 13 year period. We concentrated specifically on 212 "double" grafts with 100% selective angiographic follow-up early, 90% at 1-year, and 44% at 5 years after operation. Four hundred twenty-four control single grafts were studied similarly. We found that patency rates of side-to-side anastomoses were much better than those of end-to-side anastomoses, whether of sequential or control single grafts. Considering specifically diagonal coronary artery-anterior descending coronary artery sequential grafts, the combined patency of all sequential anastomoses theoretically exceeds that of a comparable number of single grafts at all times of study, but the differences are small. Furthermore, there is definite danger of preserving proximal and perhaps limited bypass runoff at the cost of losing distal and perhaps more important myocardial perfusion. On balance, we believe that single vein grafts are to be preferred over sequential grafts unless shortage of conduit material or local aortic wall conditions dictate otherwise.

Cardiac mortality and morbidity after vascular surgery.

To determine the clinical, hemodynamic and pathological features that contribute to major cardiac complications after vascular surgery, six patients with early postoperative cardiogenic shock (group 1) were analysed retrospectively and compared to nine patients without complications (group 2) who were carefully analysed prospectively. Four group 1 patients had elective repair of an abdominal aortic aneurysm, one had repair of a false iliac artery aneurysm and one had a femoropopliteal graft inserted. Four group 2 patients had elective repair of an abdominal aortic aneurysm and five had aortobifemoral reconstruction. The Goldman multifactorial index was similar in both groups and indicated an expected death rate of 2% and a morbidity rate of 5%. In group 1, the earliest sign of cardiovascular compromise was an elevated pulmonary wedge pressure during operation. Postoperatively, electrocardiographic evidence of myocardial ischemia was present in all six patients and preceded cardiogenic shock. Autopsy of the four patients who died demonstrated triple-vessel disease in all but recent occlusion in only one patient. There was evidence of extensive subendocardial infarction in all four. Angiography of the two survivors in group 1 also demonstrated triple-vessel disease. The authors conclude that by using ordinary clinical methods it is difficult to identify patients likely to have major complications postoperatively. Elevated pulmonary wedge pressures or electrocardiographic evidence of myocardial ischemia may be early warning signs of impending cardiac catastrophe and should be treated aggressively. The underlying pathophysiology appears to be perioperative stress in a setting of severe triple-vessel coronary artery disease.