Replacement of ascending aorta and aortic valve.
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Biomedical subjects
Publications and source records attributed to H G Borst.
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Clinical cardioplegic arrest may coincide with a washout of cardioplegic agents by varying amounts of extracoronary collateral blood flow. This may shorten the duration of electromechanical arrest. Furthermore, even in the absence of electromechanical cardiac activity, washout may influence the cardioprotective properties of cardioplegic methods. The present study was designed to quantify the effects of cardioplegic washout. In a standardized isolated paracorporeal dog heart model, the St. Thomas's Hospital solution (ST-CP) and the Bretschneider histidine buffered solution (B-CP) were compared under the condition of washout by arterial blood. An inverse relationship was found between the amount of blood flowing through the coronary system and the duration of electromechanical arrest. Flow rates compatible with a 100 min period of complete electromechanical arrest were less than 0.41 ml/100 gr heart weight . min in ST-CP arrest and less than 0.21 ml/100 gr . min in B-CP arrest. This would indicate a greater safety against washout-induced re-excitation in ST-CP arrest. Postarrest myocardial function after 2 hours of complete electromechanical arrest at 20 degrees C was distinctly influenced by washout with arterial blood (20 degrees C) even in the absence of cardiac activity. A 100-min period of 0.2 ml/100 gr . min blood flow during arrest improved postarrest recovery of left ventricular developed pressure by 10% (76% versus 66%) after ST-CP arrest. By contrast, after B-CP arrest at equal rates of washout, recovery was diminished by 20% (79% versus 99%). It is concluded, that ST-CP, as compared to B-CP, provides longer periods of electromechanical arrest under the same washout conditions. Whereas postarrest recovery in the B-CP group is clearly superior to ST-CP in totally ischemic hearts, i.e. in hearts without collateral blood supply (99% versus 66%), this advantage may vanish in the presence of cardioplegic washout.
Out of 75 consecutive patients with left main coronary artery (LMCA) obstruction who underwent coronary revascularization between January and October 1980, 3 patients had total occlusion of the LMCA. All 3 patients were suffering from severe angina pectoris preoperatively. On cardiac catheterization they had shown extensive collaterals from the right coronary artery and relatively well-preserved left ventricular function. In addition to intercoronary anastomoses a relatively high extracoronary collateral blood flow was measured at operation. Postoperatively the 3 patients remained free of angina (class I NYHA) at 5, 20 and 50 months after uneventful surgery. It is concluded that patients with adequate intercoronary and extracoronary collaterals may well survive complete occlusion of the LMCA. Surgery appears to carry a low risk no greater than that involved in conservative treatment of LMCA stenosis and the postoperative clinical status of the patients continues to be satisfactory.
Vascular prostheses of different porosity (Cooley Very Soft; Miliknit Lo-Por; Microvel; Sparks Mandril) were pretreated with fibrin glue and the permeability was assessed both in vitro and in 12 dog experiments by descending aorta replacement under full systemic heparinization. It was found that all types of prostheses were completely sealed after the pretreatment. In 28 patients undergoing descending or abdominal aorta replacement under systemic heparinization high porosity knitted Dacron grafts were pretreated with the fibrin glue only. There was no blood loss across the prosthetic wall. It is concluded that graft-pretreatment with fibrin glue allows for combining full heparinization and the use of high porosity vascular grafts.
From 1973 through December 1980, 41 children with total anomalous pulmonary venous connection (TAPVC) were seen in our hospital, and 35 underwent surgery. The supracardiac type of TAPVC was found in 19 cases (46%), the intracardiac type in 6 infants (15%), the infracardiac type in 15 cases (37%), and the mixed type in one child (2%). Clinical and cardiac catheterization data demonstrated that children with the infracardiac type of TAPVC were referred very early in life and had the highest pulmonary artery pressures. Operation was performed in 35 cases, 15 of supracardiac, 6 of cardiac, 13 of infracardiac, and 1 of mixed type of TAPVC. Total in-hospital mortality was 39%, and was 28% in the operated children. The initial operative mortality of 71% in the years 1973 to 1975 has decreased to 18% in the last 5 years. Twelve of the surviving infants underwent re-catheterization showing excellent results. Only in one case, with additional aplasia of the left lung, did half-systemic pulmonary artery pressure persist. Corrective surgery offers the only chance of survival in most children with TAPVC. The operative risk can be reduced by increased surgical experience supported by optimal medical preparation of the patient. After adequate surgical correction long-term results appear to be excellent.
The aim of surgical therapy for ventricular arrhythmias is to eliminate the areas of diseases myocardium from which ventricular tachycardias originate. According to the results of endocardial mapping a 2 to 3 mm deep endocardial incision is performed around the identified arrhythmogenic area. Within the past 12 months, 19 patients with coronary heart disease and complex ventricular arrhythmias were operated upon. In 16 cases an endocardial incision was performed. In 5 a left ventricular aneurysm was resected as well, 4 patients received one to 4 coronary vein grafts, and in 7 patients aneurysmectomy and bypass grafting were combined. Except for one relapse, no ventricular tachycardia has reappeared since the operation. Ventricular tachycardia could not be initiated by intracardiac stimulation postoperatively in any of the cases restudied. Four patients died from causes unrelated to ventricular arrhythmias. Direct surgical therapy was proven a promising new approach in patients with ventricular tachycardia or complex ventricular arrhythmia refractory to medical treatment. Our technique of endocardial incision appears to be effective and less traumatic to the myocardium than the original transmural encircling incision.
To evaluate computer tomography (CT) for assessment of aorto-coronary bypass graft patency, 45 patients with 85 grafts were studied by non-dynamic CT before and after intravenous bolus injection of 50 ml contrast material. 28 patients had undergone postoperative coronary angiography (37 grafts patent, 11 occluded), while 17 (37 grafts) were studied in the early postoperative period without angiographic confirmation. 60 of 74 grafts (81.1%) which were angiographically patent or not checked by postoperative angiography could be visualized by CT. In patients in whom graft patency was documented by angiography, 32 of 37 grafts (86.5%) were identified correctly, including all 18 grafts (100%) to the left anterior descending branch (LAD). With the exception of one LAD graft which was judged differently by the two evaluators, none of the 11 definitely occluded grafts could be visualized by CT. The results suggest that non-dynamic CT allows correct identification of patent aorto-coronary bypass grafts in a high percentage of cases. So far, however, the method does not allow any deduction as to the functional status of the grafts.
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In 74 mongrel dogs 0.02 ml air/kg of body weight was injected into the left anterior descending coronary artery (LAD). Forty-three dogs were studied without (group I) and 31 with (group II) extracorporeal circulation (ECC). Time course and extent of myocardial ischemia were assessed by continous thermographic measurements as well as by fluorescence techniques. Coronary air embolism resulted in an immediate decrease of myocardial temperature associated with transmural ischemia. In 31 surviving dogs (72%) of group I this phenomenon was fully reversible within 8.7 minutes as compared with 5.4 minutes in 100% of the surviving dogs from group II. No postembolic death occurred in the group II animals. In group II the postembolic temperature decrease was significantly less than that in group I, and, in addition, the myocardial area involved was significantly smaller. The results indicate that the extent of myocardial ischemia following coronary air embolism and its time course can be well-documented by means of thermocardiography; using extracorporeal circulation survival can be improved and myocardial damage minimized.
Extracoronary blood flow to the myocardium was studied in 54 patients during cold cardioplegic arrest. Coronary venous return was measured with the aorta and the pulmonary artery cross-clamped, both venae cavae occlusively snared, and the heart completely drained. Cold St. Thomas' cardioplegic solution was infused into either the aortic root or the coronary ostia. Myocardial septal temperature was continuously monitored. The amount of blood in the right atrial effluent was determined by means of the hematocrit and was considered to be the extracoronary collateral myocardial blood flow (QE), originating from the systemic circulation. QE ranged from 0 to 1470 ml-100 min-1 (x = 241.1 ml-100min-1). The myocardial spontaneous rewarming rate was not significantly correlated to QE. QE was lowest in pure mitral valve stenosis (x = 39.9 ml-100 min-1) and higher in aortic valve disease (x = 165.5 ml-100 min-1). Very high QE values (greater than 800 ml-100 min-1) were only observed in patients with severe three vessel coronary artery disease. Patients with angina at rest appear to have lower QE values than patients with equally severe coronary artery disease suffering from angina under excise only. It is concluded that extracoronary collateral blood flow may unpredictably influence the efficacy of clinical cardioplegia and may to some extent compensate for severe coronary artery disease.
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Although left ventricular aneurysmectomy (LVA) is a common surgical procedure, the late functional and hemodynamic results have not been well defined. This presentation describes our results with LVA in 135 patients operated between 1969 and 1979. Associated procedures were performed in 57 (42%) including coronary bypass grafting in 50, valve replacement in 5, closure of ventricular septal defect in 2, or combinations of these in 3 patients. One hundred four of the 122 hospital survivors were followed from 2 to 107 months (mean = 37 months). There were 13 hospital deaths (9.6%), 12 late deaths (9.8%) and an actuarial 5-year survival rate of 77%. Clinical improvement of preoperative heart failure occurred in 82%, and of angina in 70%. Only 33 patients (30%) returned to normal work. Bicycle exercise testing in 70 patients showed normal working capacity in 41 (59%). Recatheterization in 49 patients showed no significant changes in left ventricular end-diastolic pressure or cardiac index, and a borderline reduction of the total ejection fraction. Ventricular arrhythmias were detected by long-term ECG in 70% of all patients after surgery. Of those with preoperative life-threatening arrhythmias, rhythm improvement was noted in 50%, but only 2 of 13 patients were free of arrhythmias after operation. This study demonstrates a greater frequency of postoperative symptomatic and functional improvement as compared to hemodynamic and ECG improvement. Ventricular tachyarrhythmias originating from post-infarct scars increased intra- and postoperative risk and aneurysmectomy alone is considered insufficient for treatment of these disturbances. Further electrophysiologic investigations are needed and additional surgical measures may be necessary to improve the subset of patients with life-threatening arrhythmias.
Between 1975 and 1980, 9 patients with traumatic rupture of the thoracic aorta were operated at our institution. All patients showed additional multiple limb and internal organ injuries. Leading symptoms of aortic rupture were mediastinal widening (8), left-sided hemothorax (6), and acute aortic coarctation (2). Aortic rupture was proven by angiography in 8 patients and during exploratory thoracotomy in another. The time interval between trauma and operation was one to 48 hours, in 6 patients less than 4 hours. Atrio-femoral bypass was used in 3 patients, TDMAC-heparin shunt in 4 patients and 2 patients were operated without bypass. Prosthesis interposition was required in 3 patients while direct suture was possible in 6 patients. Long-term survival was achieved in 7 patients, one patient died from shock sequelae and another had suffered inoperable multiple rupture along the ascending and transverse aorta. It is concluded that patients with traumatic aortic rupture have a relatively good prognosis if diagnosis is established immediately and if surgery is feasible. The operative result is influenced substantially by the degree of preoperative shock and the presence of additional injuries.
Twenty adult patients with predominant mitral valve disease and variable degrees of tricuspid incompetence (TI) were reinvestigated 6-28 months after mitral valve operation. Postoperatively, 10 of the 20 patients were in sinus rhythm, compared with four of 20 preoperatively. Right ventricula peak systolic pressure decreased from 48 to 33 mm Hg (p less than 0.005), pulmonary vascular resistance declined from 234 to 141 dyn-sec-cm-5 (p less than 0.05), and cardiac index increased from 2.4 to 3.0 l/min/m2 (p less than 0.01) after operation, but right ventricular end-diastolic pressure and right atrial pressure failed to improve. TI, as graded by semiquantitative criteria from right ventricular angiocardiograms taken in the right anterior oblique projection, was decreased unequivocally in only six patients, unchanged in degree in 13 patients, and worse in one. Improvement in TI was associated with an enhancement of systolic shortening of the tricuspid annulus (24 vs 15%, p less than 0.02), whereas in patients with unchanged TI, tricuspid annulus shortening was also unchanged. These data suggest that TI associated with mitral disease is not invariably decreased after mitral surgery, despite improved hemodynamics. A depressed extent of shortening of the tricuspid annulus in systole seems to be important in the pathogenesis of TI.
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