[High frequency surgery in patients with cardiac pacemakers].
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Biomedical subjects
Publications and source records attributed to P Satter.
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This study tests the hypothesis that careful control of the composition of the initial reperfusate and the conditions of the reperfusion during emergency CABG will restore immediate segmental contractility in the previously ischemia area despite ischemic intervals of greater than 2 hours. Between January 1987, and October 1990, 41 consecutive patients with acute coronary occlusion (90% due to PTCA failures) were reperfused during emergency myocardial revascularization according to one of two different protocols: in 25 patients the reperfusate was normal blood given at systemic pressure ("uncontrolled reperfusion"); in 16 patients the ischemic segment was reperfused during the first 20 minutes with a regional blood cardioplegic solution (substrate-enriched, hyperosmotic, hypocalcemic, alkalotic, diltiazem-containing) at 37 degrees C at a pressure of 50 mmHg. Thereafter, total bypass was prolonged for an additional 30 minutes before extracorporeal circulation was discontinued ("controlled reperfusion"). Assessment of regional contractility (echocardiography, radionuclide ventriculography), electrocardiographic evidence of myocardial infarction, release of CK and CK-MB enzymes, and hospital mortality were performed. Quantification of regional contractility was done with a scoring system from 0 (normokinesis) to 4 (dyskinesis). Data are expressed as mean +/- standard error of the mean. Both groups were well matched for age, sex, and the distribution of the occluded artery. In the controlled reperfusion group there was a higher incidence of previous infarctions (50% vs 30%), additional significant stenosis (1.1 +/- 0.2 vs 0.8 +/- 0.1), and cardiogenic shock (38% vs 20%) as compared to uncontrolled reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Improvement of exercise left-ventricular ejection fraction after successful aortocoronary bypass operation and transluminal coronary angioplasty has been demonstrated. The purpose of this study was to investigate in which patients improvement of left-ventricular function at rest can be observed. Radionuclide ventriculography and exercise stress test was carried out in 34 patients before and after successful aortocoronary bypass operation (Group 1), and in 69 patients before and after successful transluminal coronary angioplasty (Group 2). After bypass surgery, mean ejection fraction at rest increased from 42 +/- 11 to 49 +/- 13% (p less than 0.001). Marked improvement (greater than or equal to 5%) was observed in 19 patients (56%) in whom severe myocardial ischemia could be documented during exercise ECG (Group 1.1: Increase of ejection fraction from 40 +/- 14 to 54 +/- 12%, p less than 0.001; ischemia score during exercise test 8.8 +/- 10). In the remaining 15 patients no significant improvement occurred (Group 1.2: 43 +/- 16 vs. 43 +/- 16%, p = n.s.; ischemia score during exercise test 3.2 +/- 2.4, p = 0.02 vs. Group 1.1). After angioplasty, resting left-ventricular ejection fraction increased, on average, from 50 +/- 11 to 52 +/- 12% (p less than 0.001). Comparable to the results observed in patients after surgery, improvement was most pronounced in patients with severe exercise-induced ST-depression (Group 2.1: Increase of ejection fraction from 49 +/- 10 to 58 +/- 10%, p less than 0.001; ischemia score during exercise 2.5 +/- 2.3).(ABSTRACT TRUNCATED AT 250 WORDS)
This study tests the hypothesis that contractile dysfunction that often develops after acute coronary occlusion despite emergency revascularization can be avoided by careful control of the composition of the initial reperfusate and the conditions of the reperfusion. Between January 1987 and May 1989, 31 consecutive patients with acute coronary occlusion (90% resulting from percutaneous transluminal coronary angioplasty failures) were reperfused during emergency myocardial revascularization according to one of two different protocols. In 23 patients the reperfusate was normal blood given at systemic pressure ("uncontrolled reperfusion"); in eight patients the ischemic segment was reperfused during the first 20 minutes with a regional blood cardioplegic solution (substrate-enriched, hyperosmotic, hypocalcemic, alkalotic, diltiazem-containing) at 37 degrees C at a pressure of 50 mm Hg. Thereafter total bypass was prolonged for an additional 30 minutes before extracorporeal circulation was discontinued ("controlled reperfusion"). Assessment of regional contractility (echocardiography, radionuclide ventriculography), electrocardiographic evidence of myocardial infarction, release of creatine kinase and isoenzyme of creatine kinase, and hospital mortality was performed. Regional contractility was quantified with a scoring system from 0 (normokinesis) to 4 (dyskinesis). Data are expressed as mean +/- standard error of the mean. Both groups were well matched for age, sex, and the distribution of the occluded artery. In the controlled-reperfusion group there was a greater prevalence of previous infarctions (63% versus 43%), additional significant stenosis (1.3 +/- 0.2 versus 0.8 +/- 0.2), and cardiogenic shock (38% versus 17%) compared with the uncontrolled-reperfusion group. Furthermore, the interval between coronary occlusion and reperfusion was significantly longer in the controlled-reperfusion group (4.0 +/- 0.5 versus 2.3 +/- 0.3 hr; p less than 0.05). Regional contractility returned to normal in all patients treated by controlled reperfusion (wall motion score = 0.8 +/- 0.3, normokinesis = 0, slight hypokinesis = 1). In contrast, regional contractility remained severely depressed after uncontrolled reperfusion with normal blood (score 2.5 +/- 0.2; p less than 0.05), with only four of 23 patients with a score less than 2 (2 = severe hypokinesis). Postoperatively enzymes and electrocardiographic changes were similar in both groups. One patient died of mitral insufficiency in the controlled-reperfusion group, despite complete recovery of wall motion in the angioplasty-related artery. Conversely, the four of 23 deaths after uncontrolled reperfusion occurred in patients who sustained infarct in the area of the coronary occlusion (mortality 13% versus 17%). In conclusion, these preliminary clinical results indicate that immediate recovery of segmental contractility can be achieved after acute coronary occlusion if the initial reperfusion is controlled.(ABSTRACT TRUNCATED AT 400 WORDS)
Since 1987 patients have been treated with tantalum stents at our hospital (iliac arteries n:40, femoro/popliteal arterie n:35). Before expanding indication for stent implantation to other more difficult areas and vessel segments, we need to guarantee that a misplaced or not sufficient expanded or only temporary used stent, perhaps after dissections, could be rescued out of the vessel without damage of the vessel wall. Therefore we used cadaveric arteries and a special "retrivel set" To rescue the expanded stent through the introducer sheet without wessel wall damage was possible in all cases (iliac arteries n:5, femoral arteries n:5). In a second attempt, we showed, that even a TEA was possible, using a ringstripper which cut a typical cylinder of the atheriosclerotic vessel wall overpassing and including the stent. In 7 out of ten cases (cadaveric iliac arteries) the retrograde ringstripping-procedure was successful. The other 3 cases required an incision of the vessel with local thrombendarteriectomia. Insofar a stent implantation should not be considered as a contraindication for this surgica treatment else in later history.
Severe vascular complications are an inherent risk of percutaneous transluminal coronary angioplasty (PTCA). Data from 100 emergency aortocoronary bypass operations required after 2850 interventions (3.5%) were retrospectively analysed in order to identify factors that determine postoperative infarct size. Large infarctions were assumed if the patient died of cardiogenic shock (n = 12), if postoperative angiography demonstrated a decrease in left ventricular ejection fraction of more than 20% of if R-waves in the ECG decreased by more than 40% and a QRS-score increased by more than 5. According to these definitions, 29 patients experienced large infarctions, while 71 experienced no or only small infarctions. The following factors differentiated the two groups: age (58 vs 53 years, P = 0.008), pre-PTCA exercise work load (88 vs 118 Watts, P = 0.0001), exercise ischaemia score (2.7 vs 1.9, P = 0.045), degree of pre-PTCA stenosis (83 vs 86%, P = 0.03), coronary multivessel versus single vessel disease (60 vs 38%, P = 0.02), collaterals to the target vessel (10 vs 34%, P = 0.05), total vascular occlusion during PTCA (76 vs 56%, P = 0.035), and long duration of ischaemia after onset of the complication (253 vs 179 min, P = 0.012). Data from patients with large postoperative infarctions who survived ranged between those with no or small infarctions and those who died of cardiogenic shock. Higher age (P = 0.04), reduced exercise tolerance (P = 0.0004), absence of collaterals (P = 0.04), and duration of ischaemia until reperfusion (P = 0.001) were independent predictors of large postoperative myocardial infarctions.(ABSTRACT TRUNCATED AT 250 WORDS)
Three patients developed left main stem stenosis within some months after aortic valve replacement. In all of them diagnosis was confirmed by angiography and bypass surgery was performed successfully. Left main stem stenosis is a rare complication of aortic valve replacement and is due to cannulation and perfusion of the coronary arteries. The mechanism is probably injury of the vessel wall due to the perfusion-catheter, followed by intimal hyperplasia. A similar mechanism is assumed for restenosis after transluminal coronary angioplasty.
In the past years the number of patients with combined treatment of the heart valves and coronary arteries rised as well as the patients age did. In 1980-1987 the rate of patients with aortic valve replacement and simultaneous aorto-coronary bypass was 10.9% in those who underwent aortic valve replacement and 2.9% in those who had aorto-coronary bypass operation. Since 1988 the ratios changed to 18.2% and 4.9%. For the calculation of the operative risk of the combined operative treatment (AVR + CABG, MVR + CABG) we compared these groups with those patients with isolated operations (MVR, AVR, CABG). We studied all patients during 1980 and July 1989. The hospital mortality of combined procedures was significantly increased. The mortality among female patients was higher as compared to the male group. The age of patients treated by the combined procedures was higher as compared to the isolated procedures. The mean age of the patients which died was severely increased as compared to the isolated procedures. However, in the combined procedures this increase was not as pronounced as in the isolated groups. Patients with combined procedures had a higher NYHA class. The risk factors of the combined procedures were comparable to isolated CABG.
Left ventricular systolic and diastolic performance was evaluated by radionuclide angiography in 17 patients following cardiac transplantation and compared with normal persons. Both groups performed supine bicycle exercise during the investigation, the control group at 102 +/- 73 W and the transplanted patients at 61.2 +/- 15 W. The ejection fraction increased in the normal persons from 61 +/- 8 to 69 +/- 10% whereas in the transplanted patients it did not increase significantly. There were no relevant changes in systolic parameters during exercise in the transplant recipients. The changes in diastolic parameters were significantly smaller in transplant patients than in normals. After correction for heart rate-induced changes a significantly different time course of the systolic-diastolic sequence during the cardiac cycle became evident in the transplanted group at rest. During exercise the systolic-diastolic sequence during the cardiac cycle became similar in both groups. It is concluded that the reduced exercise capacity of patients in the late phase after cardiac transplantation is partially due to the absence of an EF increase and a limitation of diastolic reserve during exercise.
The concentrations of isosorbide dinitrate (ISDN), isosorbide-5-mononitrate (IS-5-MN) and isosorbide-2-mononitrate (IS-2-MN) were determined in plasma (PL), saphenous vein wall (SV) and pectoral muscle (PM) from 8 patients undergoing coronary bypass surgery. The patients were pretreated for 2 days with ISDN 240 mg per day (standard release formulation) in 4 doses of 40 mg and one dose of 80 mg. The plasma and tissue samples were obtained during the operation, 10-12 h after the last dose. Isosorbide-2-mononitrate and isosorbide-5-mononitrate were present in plasma and tissues in the same concentration ranges with molar concentration ratios of 0.88 (IS-2-MN: PM/PL), 0.85 (IS-5-MN: PM/PL), 0.99 (IS-2-MN: SV/PL) and 1.06 (IS-5-MN: SV/PL). Mean ISDN concentrations in tissue were considerably higher than in plasma; the molar concentration ratios were 4.9 (SM/PL) and 7.21 (SV/PL). The accumulation of ISDN in vessel walls may contribute to its greater vascular action compared to the mononitrates, but it may also facilitate the development of tolerance during long-term treatment.
This study evaluated the mechanism of valvular area expansion during single- and double-balloon valvuloplasty in fibrotic and calcific mitral valves. Special interest was focused on the morphological features of the valves treated. Mitral valves that appeared unsuitable for commissurotomy were excised in toto at the time of mitral valve replacement in 15 patients. The excised valves were mounted in a fluid-filled chamber with a window for photographic evaluation. The chamber was perfused continuously to ensure maximal valvular opening. The valve was photographed, and the orifice area was measured before and after balloon expansion. In addition, the specimens were examined macroscopically and radiographically with regard to calcium content and degree and localization of fibrosis. These data were correlated with splitting of commissures and with rupture of leaflets. Nine valves were fibrotic, and six were calcific. Dilatation was performed first with a single-balloon catheter (diameter, 2 cm) and then with a double-balloon catheter (diameter, 2 and 1.5 cm). After dilatation with one balloon, the average mitral valve area increased from 0.79 to 1.09 cm2, and with two balloons, average area increased to 1.59 cm2. The single-balloon technique caused commissural splitting in nine valves, stretching in three, partial leaflet rupture in one, and no change in two. After the double-balloon technique, commissural splitting occurred in 12 valves and three leaflets were ruptured where severe fibrosis and calcification were mainly located within the commissures. As a rule, after dilatation with the single-balloon technique, the remaining stenosis was still severe, and after dilatation with the double-balloon technique, the remaining stenosis was moderate.(ABSTRACT TRUNCATED AT 250 WORDS)
Elective operations of chronic thoracic aortic aneurysms (TAA) can be performed with low risk. In contrast, emergency repair of TAA in symptomatic patients including those with rupture is associated with a high mortality. The worst results were obtained (a) in patients who were in shock preoperatively, (b) with palliative procedures during acute dissection and (c) in patients older than 70. The results may be improved by early diagnosis and better operative technique and perioperative management.
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To determine if electromagnetically generated shock-wave lithotripsy has potential application for treatment of stenotic, calcified aortic valves, 38 cusps of surgically excised human aortic valves were studied. Valves were weighed, photographed, and calcium deposition was determined by x-ray. Stiffness was determined by palpation and by measuring the pressure gradient generated in a perfusion system. Valves were exposed to shock waves at 16 or 18 kV with 200 or 400 impulses each. Twenty valves reacted to exposure to shock waves with a reduction in pressure gradient of 1.9 +/- 2 cm H2O. Calcified valve area was reduced by 3.5 +/- 1.3 mm2. Valves without changes in pressure gradient showed a reduction of 7.1 +/- 2 mm2 of calcified valve area. There was no significant difference in weight loss. Using a small focus (4 mm) there was a significant reduction in pressure gradient and calcified valve area, but not in weight; with a large focus (8 mm) reduction in calcified valve area, gradient, and weight was significant (p less than 0.05). Changes in valve stiffness were independent of weight loss and reduction in calcified valve area. In conclusion, shock-wave lithotripsy is capable of reducing stiffness of calcified aortic valves, presumably by fragmentation of tissue calcium deposits.
We performed percutaneous balloon valvuloplasty of the pulmonary valve in 24 patients (aged 17 to 72 years) and in two juvenile patients. There were no major complications. In almost all the patients the procedure resulted in a successful pressure gradient reduction from a mean of 92 +/- 36 mmHg to 43 +/- 19 mmHg (P less than 0.01). In seven patients there was a residual pressure gradient greater than 50 mmHg which, however, decreased in all patients within the following 3-12 months due to a decrease in subvalvular muscular hypertrophy (from a mean of 70 to 35 mmHg). No restenosis was observed. Only one patient, who had calcified valve leaflets, developed pulmonary insufficiency and this was of only minor haemodynamic importance. Balloon dilatation of the pulmonary valve can be considered a technique with a high success rate and low complication rate even in the elderly. Good long-term results support this approach as the first choice in the treatment of pulmonary valve stenosis.
The hypothesis was tested, if the addition of 2-mercaptopropionylglycine (MPG, Thiola) to a crystalloid cardioplegic solution provides superior myocardial protection as assessed by biochemical and morphological parameters. Five mongrel dogs underwent a 60-min hypothermic cardioplegic arrest (untreated group). In six dogs, MPG (1.5 mmol/l) was added to the crystalloid cardioplegic solution (treated group). Thereafter a reperfusion phase of 60 min was established. At the end of the reperfusion phase samples for mitochondrial respiration parameters and for mitochondrial energization were collected. Samples for ultrastructure and negative staining were taken at the end of ischemia, and after 15, 30 and 60 min of reperfusion. Hearts which were treated with the MPG-enriched cardioplegic solution showed a better ultrastructure (1 (1/1) vs 2 (2/2), p less than 0.001) and superior preservation of the mitochondrial ATPases (2.4 +/- 2.0 versus 8.4 +/- 2.7, p less than 0.05) as compared to the untreated group at the end of ischemia. At the end of reperfusion, mitochondrial respiration, and energization of the mitochondria was improved significantly with the addition of MPG as compared to the untreated group.
Concentration-dependent relaxation (6-70%) of segments of human saphenous veins under isometric conditions could be demonstrated with cumulative concentrations of isosorbide dinitrate (ISDN) and Glycerol trinitrate GTN (10(-9)-10(-5) M). Vein segments were obtained during coronary by-pass surgery. Nitrate (GTN)-induced relaxation was accompanied by a 2- to 3-fold increase of cyclic GMP content in the vessel walls. However, no change of concentrations in the vessel walls could be determined for the metabolites of prostaglandines: (PG E2, PG F2 alpha, TX B2, 6-keto-PGF1 alpha). Pretreatment of patients with 40 mg ISDN (standard release formulation) 4 times daily for 1 week prior to surgery with the last dose 1 hour before harvesting the vein segments did not influence relaxation. by ISDN. Immersion of vein segments for 1 hour in buffer solution containing 10(-6) M ISDN (= therapeutic concentration) prior to relaxation with cumulative concentrations of ISDN did not influence relaxation either. Induction of in vitro tolerance required ISDN concentrations which exceeded the range achieved under therapeutic conditions: 4.4 x 10(-4) M. This in vitro tolerance could be widely reversed by 10 mM N-Acetylcysteine (NAC) suggesting involvement of sulfhydril (SH) groups. Since tolerance in this experimental model was not seen under concentrations achieved in patients it seems likely that clinical tolerance is caused by activation of counterregulatory forces.