Aortic pericardial heterograft obstruction from endocarditis.
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Biomedical subjects
Publications and source records attributed to S Levitsky.
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In an attempt to arbitrate the reputed clinical efficacy of pulsatile flow during reperfusion in minimizing ischemic injury, 32 mongrel dogs supported by normothermic cardiopulmonary bypass were subjected to 30 minutes (Groups IC and IP) or 60 minutes (Groups IIC and IIP) of global myocardial ischemia. The effect of pulsatile flow (P) initiated during 30 minutes of reperfusion on the recovery of myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) stores, coronary blood flow, and myocardial water content (MWC) was compared to the effect of linear reperfusion (C) in another group of animals. ATP stores, which significantly decreased to 43% and 53% of preischemic levels (Groups IC and IP, respectively, p less than 0.01) and 36% and 31% of control values (Groups IIC and IIP, respectively. p less than 0.001), did not increase with either pulsatile or linear reperfusion. CP stores, depleted 97% during ischemia in all groups, returned to preischemic levels regardless of the mode of reperfusion flow. Coronary blood flow measured 30 minutes after aortic unclamping was not significantly different from control flow in any group. MWC significantly decreased during ischemia from 80.5% +/- 0.8% to 76.5% +/- 1.1% in Group IC and from 81.8% +/- 1.2% to 76.8% +/- 0.8% in Groups IP (p less than 0.05) and returned to preischemic levels with reperfusion. However, following 60 minutes of ischemia, pulsatile reperfusion prevented the significant increase in MWC that accrued after linear reperfusion (80.7% +/- 1.5% to 84.0% +/- 0.7%, p less than 0.05). These data indicate that pulsatile reperfusion initiated after an ischemic injury that results in a 50% or greater depletion of myocardial ATP stores does not restore myocardial nucleotide levels or enhance coronary blood flow, although the pathological increase in MWC may be avoided.
We studied 37 consecutive patients, all drug addicts, who underwent 48 valve operations from 1976 through 1981. GN bacteria were the major organisms in 25 patients (64%), compared with a previous reported incidence of 10%. Operative indications were uncontrolled sepsis in 49%, embolism in 27% and heart failure in 24% of the patients. Primary operations included nine tricuspid valvectomies and 14 aortic, 10 mitral and four aortic/mitral valve replacements. Early (30-day) mortality was 2.7% (one of 37 patients); five of nine patients who had 11 reoperations survived. Long-term follow-up revealed a late mortality of 39% (11 of 28) in patients with left-sided disease; eight of the 11 patients who died had GN infection with perivalvular abscess. Thus, the subgroup with GN sepsis and left-sided disease had a combined early and late mortality of 50%, with all deaths occurring within 8 months postoperatively. We conclude that valve replacement in the presence of active sepsis can be safely performed, but GN sepsis in addicts increases the risk of early reinfection and late mortality.
Simultaneous measurements of pulmonary capillary wedge pressure (PCWP) and left atrial pressure (LAP) were obtained before and after cardiopulmonary bypass and for a period of 16 hours postoperatively in 20 consecutive patients undergoing electric cardiac operations. In contrast to several previous reports that PCWP accurately reflects left-sided hemodynamics, we found that the PCWP significantly exceeded the LAP in the early postbypass period and was most significantly in error at 4, 8, and 12 hours after operation (p less than .02) (95% confidence limit). The magnitude of this discrepancy differed in individual patients; however, it was consistent for each patient for the time period studied and independent of the procedure performed. The disparity between PCWP and LAP may be due to an increase in lung interstitial water as a result of hemodilution, or it may be related to the differing effects of afterload reducing agents on the pulmonary versus the systemic circulation. We conclude from these data that LAP more accurately reflects left ventricular filling and performance in the early postoperative period and should be used instead of PCWP to monitor the hemodynamics of postsurgical patients.
Despite meticulous adherence to presently known principles of myocardial preservation, reperfusion after aortic cross-clamping results in a unique injury manifested by decreasing high-energy phosphate levels and increased coronary resistance. We hypothesize that platelet deposition into the coronary microvasculature is a major factor in reperfusion injury. To differentiate platelet deposition due to subendocardial hemorrhage from deposition due to vascular entrapment, we infused 111In-labeled platelets together with 51Cr-labeled erythrocytes into 15 dogs that were on normothermic bypass and subjected to 60 minutes of global ischemia followed by 30 minutes of reperfusion. Platelet deposition is indicated only when the proportion of platelets to erythrocytes in tissue exceeds that measured by peripheral blood. Myocardial biopsy specimens were obtained after 10 minutes of bypass, 120 minutes of continuous bypass (Group I), and at the end of reperfusion after global ischemia (Group II). In five dogs (Group III), dipyridamole (1 mg/kg), an antiplatelet activation agent, was administered in the preischemic period. Platelet deposition was expressed as the number of radioactive-labeled platelets deposited per gram of tissue. Bypass for 120 minutes resulted in only a minimal increase in platelet deposition. However, normothermic ischemia followed by reperfusion resulted in over a twofold increase in platelet deposition compared to controls. Pretreatment with dipyridamole appeared to avoid platelet deposition. These data indicate that platelet deposition in the coronary microcirculation following surgically induced myocardial ischemia may be associated with reperfusion injury and that antiplatelet drugs after this sequence.
The purpose of this study was to investigate the changes in serum and urine potassium before, during, and after the administration of potassium cardioplegia using a solution containing 28 mEq/L of potassium chloride in 20 consecutive patients with acquired heart disease. The data obtained suggest that the concentration of potassium administered does not result in inordinately elevated serum potassium levels (peak, 4.6 +/- 0.18 mEq/L at 2 hours of multidose hypothermic potassium cardioplegia) during or after infusion. Additionally, the urinary excretion of potassium increased during infusion and eventually exceeded the amount of potassium infused. While hypothermic potassium cardioplegia appears to be a safe and efficient method of myocardial protection, continued surveillance of postoperative potassium levels remains necessary to detect obligatory urinary potassium excretion following cardiopulmonary bypass and operation.
Three young children with anomalous origin of the left coronary artery (LCA) from the pulmonary artery were studied by two-dimensional echocardiography. The LCA was shown to be in confluence with the left posterior aspect of th pulmonary artery root in the two patients studied preoperatively. In one of these patients, and in another patient 2 years after surgery, studied after direct surgical implantation of the LCA to the aorta, the LCA was shown to be confluent with the left anterior aspect of the aortic root. In all, the LCA could be followed beyond the branching point. This study demonstrates the feasibility of noninvasive diagnosis of anomalous origin of the LCA from the pulmonary artery by direct visualization with two-dimensional echocardiography.
Acute renal failure (ARF) is an important complication of cardiac surgery in children. The incidence is 8% and mortality ranges from 10-89%. Thus, these infants pose a formidable therapeutic challenge in management. This review is an attempt to present a brief discussion of normal renal functions in neonates and children followed by the discussions of problems of renal failure and management in children undergoing cardiac surgery.
The effect of the coronary vasocilator agents dipyridamole and nifedapine on ischemia-induced changes in cardiac performance and coronary flow was studied in extra-corporeal-circulation supported, open-chest dogs during cardio-pulmonary bypass. Coronary flow and isovolumic cardiac performance were measured prior to clamping the aorta to induce global ischemic for 60 min and again after 30 min of reperfusion. Both agents given prior to ischemia significantly enhanced the coronary flow measured 30 min after reperfusion. Almost complete complete return of pre-ischemic left ventricular dp/dt and diastolic compliance was seen if dipyridamole was administered prior to the onset of ischemia. Dipridamole administered at the end of the ischemic period and prior to reperfusion also prevented the ischemia-induced fall in dp/dt but not the decrease in compliance. Myocardial high energy phosphate compounds decreased markedly during global ischemia and dipyridamole administration had no effect on the rate or extent of their depletion. Nifedapine administration led to even greater post-ischemic coronary vasodilation; however, the ischemia-induced decline in myocardial performance was not prevented.
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A 41-year-old man had chronic, recurrent, drug-resistant paroxysmal right atrial tachycardia. Electrophysiologic studies revealed features suggesting atrial reentrance, including induction and termination of tachycardia with rapid atrial pacing and atrial extrastimuli. Endocardial catheter mapping localized the origin of tachycardia to the right atrial appendage. Intraoperative epicardial mapping refined the localization to the posterolateral rim of the appendage. The appendage was excised and the tachycardia was permanently cured. Microelectrode studies on the excised tissue revealed an inducible rhythm localized to a small area of the atrial endocardium, characterized by rapid pacing induction, rhythmicity generated from a suprathreshold afterdepolarization, low maximum diastolic potential, low overshoot potential and a smooth transition from phase 4 to phase 0, suggesting triggered automaticity. This is the first observation in man of probable triggerable atrial automaticity, which may be a direct counterpart of the clinical arrhythmia. The successful surgical outcome indicates that a focal atrial tachycardia can be excised in selected patients.
In an infant with aortic atresia, two surgical procedures resulted in a 45 day postoperative survival. An atrial septectomy was initially performed. This was followed by the insertion of a Dacron graft from the main pulmonary artery to the descending thoracic aorta; the pulmonary artery was handed distal to the graft and the ductus arteriosus was ligated. Prostaglandin E1 was infused from the time of the diagnostic study to the second surgical procedure, 48 hours later. A postoperative cardiac catheterization was performed 3 weeks following the operation. Death occurred at 67 days of age from renal failure and a low cardiac output state.
A successful direct aortic implantation of an anomalous left coronary artery (ALCA) in an infant is reported. Detailed evaluation of postoperative ventricular function, including repeat cardiac catheterization and serial echocardiography, demonstrated progressive enhancement of ventricular contractility and function. Postoperative angiography confirmed vascular patency. These data support the concept that the ALCA should be corrected by direct aortic implantation early in infancy rather than by expectant treatment or graft interposition.
Several techniques have evolved for the cannulation of the ascending aorta for cardiopulmonary bypass. Although the theoretical risk of air embolization related to cannulation of the aorta has been alluded to in the past, studies of this problem have not previously been reported. Using a mock circulatory circuit, we found that cannulation with an empty clamped cannula caused a mean embolization of 0.0435 cc of air per cannulation compared to 0.0142 cc with a saline filled cannula and 0.0045 cc with a vented cannula. The residual amount of air which embolized in the ideally vented cannula was caused by the air pocket found within the aorta above a tangentially applied excluding clamp and could be eliminated completely by not clamping the aorta.
Four patients with coronary artery disease and chronic marked left axis deviation, defined as a frontal QRS axis more negative than -45 degrees, were studied with epicardial mapping during coronary bypass surgery. All patients had normal right ventricular and inferior left ventricular epicardial breakthrough sites and activation sequence. Normal breakthrough in the basal anterolateral left ventricular epicardium was absent in all four patients. Two patients had breakthrough in the apical region of the anterolateral left ventricle. In the other two this region was activated from wave fronts emerging in the right ventricle and inferior left ventricle. The latest site of left ventricular activation was the basal segment of the anterolateral wall, a site never found to be the latest activated in our previously studied patients without conduction defects. This site was activated during or slightly after the terminal portion of the QRS complex. It is concluded that marked left axis deviation in patients with coronary artery disease reflects delayed activation of the basal anterolateral left ventricle, and is consistent with the presence of block or delay in the anterior "fascicle" of the left bundle branch.
Operation for interrupted aortic arch (IAA) was successful in 2 infants during the first week of life. Both had postoperative hemodynamic and angiographic evaluation at one year of age. The first infant had a type A IAA, and prostaglandins were infused to prevent ductal closure prior to the insertion of a graft between the two ends of the interrupted aorta. The second infant had a palliative operation for type B IAA (pulmonary artery banding and graft from main pulmonary artery to descending aorta). These patients represent the ninth and tenth successful operations for IAA in this age group and are reported with long-term reevaluation.
To describe the epicardial ventricular activation sequence in the intact human heart, we obtained epicardial maps from 11 patients with normal QRS undergoing open heart surgery. Epicardial breakthrough (EBT), defined as the emergence of a radially propagating epicardial wavefront, occurred in three to five sites in each patient, and was earliest in the anterior right ventricle, 7--25 msec (mean 17 msec) after the onset of the QRS in all patients. Subsequent EBT occurred in the inferior right ventricle (10 sites in 10 patients), in the anterolateral left ventricle (13 sites in 10 patients), and the inferior left ventricle (eight sites in seven patients). Latest epicardial activation (LEA), defined as the latest site of recordable epicardial activity, occurred in the basal segments in all patients, anteriorly in the right ventricle in five patients, and inferiorly in six patients, four on the right and two on the left. LEA occurred 63--96 msec (mean 77 msec) after the onset of the QRS, and was recorded within 20 msec of the end of the QRS in all patients. Sequence of epicardial activation reflected a fusion process among the wavefronts. This descriptive and quantitative data should provide a suitable basis for comparison of abnormal ventricular activation sequences in patients undergoing surgery for preexcitation or ventricular tachycardia.
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