Biomedical subjects
Publications and source records attributed to M Dahm.
Development of coronary artery aneurysms is one typical complication of Kawasaki disease and can cause coronary artery disease even in early childhood. Information about course and outcome in adults is rare. Here, we present a 49-year-old man with serious three-vessel coronary artery disease and giant coronary artery aneurysms following suspected Kawasaki disease.
The evaluation of cardiac troponin I (cTnI) on the Dimension RxL-HM analyzer is presented. The one-step enzyme immunoassay is based on two cTnI specific monoclonal antibodies. Performed on a separate module of the analyzer, assay-time is 17 minutes. Using as criterion a between-run impression CV <20% the functional limit of detection was set at 0.1 microg/l. Cutoff level for minor myocardial damage of 0.1 microg/l was found. In Duchenne's dystrophy, patients showed increased cardiac Troponin T (cTnT) but no increased cTnI. In patients with a history of coronary heart disease undergoing chronic hemodialysis, cTnT and cTnI were increased. In different patients with submassive pulmonary embolism, increased cTnI was determined. In coronary artery bypass surgery without perioperative myocardial infarction, patients with extracorporeal circulation showed significantly higher cTnI at 24 h after surgery than those with minimal cardiac surgery. In patients with unstable angina, increased cTnI was found more often than on Stratus analyzer. In conclusion, the new assay is a very sensitive cTnI assay, fast and easy to perform in parallel to enzyme and substrate assays.
BACKGROUND AND AIM OF THE STUDY: The excellent results with atrioventricular valve reconstruction have stimulated surgeons to attempt reconstruction of calcified aortic valves using decalcifying techniques, but long-term results have been disappointing. The aim of this in vitro study was to evaluate the surface structure of decalcified aortic valve tissue and its potential for recalcification. METHODS: Aortic leaflets were removed from 26 patients with aortic stenosis during elective valve replacement and decalcified by meticulous dissection. Representative specimens were prepared for scanning electron microscopy (SEM) and calcium content in the heavily calcified part of the leaflet in both macroscopically non-calcified and decalcified tissue was determined by atomic absorption spectroscopy (AAS). Additional probes of 'non-calcified' and decalcified tissue were incubated for two and four weeks with medium containing a physiological concentration of calcium to determine their potential for recalcification. As a control, 13 specimens from non-calcified valves were incubated according to the same protocol. RESULTS: All calcified specimens contained high calcium levels (142.70+/-53.76 mg/g). Surgical dissection reduced tissue calcium content significantly (10.04+/-13.43 mg/g). Following two weeks' incubation with calcium, these specimens retained significantly higher levels of calcium (2.88+/-5.17 mg/g) than the 'non-calcified' specimens (19.17+/-7.61 versus 13.49+/-6.27 mg/g; p<0.05); after four weeks similar calcium levels were reached (32.00+/-10.27 versus 28.35+/-9.84 mg/g; p = NS). Non-calcified tissue showed the lowest calcium uptake (4.75+/-4.55 mg/g and 12.29+/-9.43 mg/g at two and four weeks; p<0.05). SEM revealed a loss of endothelial coverage in the calcified areas; decalcification led to an irregular fibrillar surface. Only parts of the macroscopically normal tissue contained endothelial cells, whereas the control tissue showed intact cellular coverage. CONCLUSION: Aortic valve decalcification can effectively remove calcifications, but leaves a fibrillar structure that tends rapidly to accumulate calcium. Even normal-appearing tissue from diseased valves has a higher potential for calcification than normal valvular tissue. These data support the observation of only limited clinical benefits being derived after aortic valve decalcification for aortic stenosis.
Intimal sarcoma of the pulmonary artery is an extremely rare type of malignant tumor of the large vessels. Despite systematic diagnostics, distinguishing between pulmonary emboli and tumors is difficult. We report a patient who was referred because of suspected embolic occlusion of the pulmonary artery. The operation was started with the intention of performing a pulmonary artery thromboendarterectomy; however, intraoperative histology revealed a malignant mesenchymal tumor. Therefore, the left lung was resected with the use of extracorporeal circulation, and the pulmonary trunk and right pulmonary artery were reconstructed. A solitary right lung metastasis was resected 3 months later using stapling devices. Complete surgical resection is the treatment of choice for patients with sarcoma of the pulmonary arteries. Surgical therapy often includes extensive reconstructive measures. Since, thromboembolic obstruction cannot be excluded preoperatively, patients with this type of disease should be treated at centers experienced with the broad spectrum of pulmonary artery surgery.
The aim of the study was the assessment of left ventricular (LV) systolic function and left ventricular mass following aortic valve replacement (AVR) due to aortic valve stenosis as well as the influence of regression of LV hypertrophy in patients with normal and impaired LV systolic function prior to surgery. 74 patients with severe aortic valve stenosis (29 female, 45 male, mean age 66 +/- 18 years) were divided into 2 groups according to LV ejection fraction (EF): Group 1 with EF > 50% (n = 40); Group 2 with EF < or = 50% (n = 34). Furthermore, patients were differentiated into a group A without (n = 53) and a group B with aortic regurgitation (< or = II degrees, n = 21). All patients were examined by transthoracic echocardiography before and 1 month after surgery. There was a significant decrease of LV enddiastolic and endsystolic volume indices following AVR in group 2 and group B. Patients with preoperatively lower EF (group 2) showed an increase in LV ejection fraction from 39 +/- 10% before AVR to 47 +/- 11% after AVR (p < 0.001), whereas patients with preoperative normal EF (group 1) showed a significant decrease in EF (from 62 +/- 8% to 57 +/- 10%, p < 0.05). Also patients with combined aortic valve disease before AVR had an increase of EF after surgery (from 45 +/- 14% to 56 +/- 14%, p < 0.03). There were significant decreases of interventricular septum thickness and LV posterior wall thickness in group 1 and group A, whereas a significant decrease of LV enddiastolic diameter index was noted only in group B. Improvement of the NYHA functional class could be demonstrated in group 2 from 2.8 +/- 0.7 before to 2.2 +/- 0.6 after AVR, as well as in group B from 2.9 +/- 0.7 before to 1.9 +/- 0.7 after surgery. In conclusion, patients with impaired LV function or combined aortic valve disease showed a significant improvement of left ventricular systolic function after AVR, while patients with normal LV function presented a slight decrease of EF. There was a significant regression of left ventricular muscle mass in all groups independent of the left ventricular functional status.
The aim of the study was to compare the mean and maximum flow and the flow pattern of coronary vein grafts (SVG) supplying target vessels of the inferior and lateral wall with internal mammary (IMA) grafts to the left anterior descending artery (LAD). In 21 patients 25 bypass grafts (13/25 SVG, 12/25 IMA) were investigated. Using the transit time ultrasound method, flow was measured every 5 ms and the flow data of 60 s were acquired. The flow pattern showed significant differences between both graft types during their cycle. IMA grafts showed only one peak occurring after 22.1+/-12.3% and the second after 63.4+/-15.5% of their cycle. The mean flow was not different in both graft types (IMA: 45.3+/-27.0 ml/min and SVG: 41.8+/-26.7 ml/min, p = n. s.) as it was the case for the maximum flow (IMS: 98. 4+/-45.2 ml/min and SVG: 75.7+/-55.4 ml/min, p = n. s.). In conclusion, there is a different flow pattern for both graft types concerning the number and the occurrence of flow-peaks in the bypass cycle. The mean and peak flow showed no significant difference.
OBJECTIVE: In patients with chronic thromboembolic pulmonary hypertension, pulmonary vascular resistance (PVR) can be reduced by pulmonary thromboendarterectomy (PTE). In this study, long-term symptomatic and hemodynamic effects were investigated. METHODS: Twenty-two patients (12 female, 10 male, mean age 40 years, preoperative NYHA functional class II/III/IV: n = 1/12/9) were re-evaluated 48-72 months (mean 60 months) after surgery. In addition to clinical assessment, radiologic, hemodynamic and echocardiographic investigations were performed. RESULTS: All patients reported a marked improvement of their clinical condition. At follow-up, 11 patients were identified as NYHA class I, 10 as NYHA class II and one patient was in class III. PVR and mean pulmonary artery pressure (mPAP) were significantly reduced (preoperative PVR 800+/-274 dynes/s per cm(-5), follow-up PVR 180+/-28.3 dynes/s per cm(-5); P < 0.001; preoperative mPAP 48.5+/-7.4 mmHg, follow-up mPAP 27.5+/-4.9 mmHg; P < 0.001). There was also a significant increase in arterial blood oxygen tension (preoperative PaO2 59+/-10 mmHg; follow-up PaO2 84+/-12 mmHg; P < 0.001). Chest roentgenograms and echocardiographic examinations revealed significantly decreased right heart dimensions and a recovery of right heart function. CONCLUSION: In patients with severe chronic thromboembolic pulmonary hypertension, persistent symptomatic and hemodynamic improvements can be achieved by PTE.
BACKGROUND: The antifibrinolytic efficacy of a high-dose regimen of epsilon-aminocaproic acid (epsilon-ACA) was compared with aprotinin in first-time coronary operations. METHODS: In a prospective, double-blinded, randomized study, 20 patients received high-dose epsilon-ACA (10 g both as a loading and cardiopulmonary bypass priming dose, 2.5 g/h until 4 hours after protamine), and another 20 patients received aprotinin (2 x 10(6) KIU [280 mg] for loading and priming, 0.5 x 10(6) KIU/h [70 mg/h]). Ten untreated patients served as controls. RESULTS: Both agents reduced postoperative levels of thrombin/antithrombin III complexes, D-dimers, fibrin degradation products, free plasma hemoglobin (epsilon-ACA versus aprotinin, p = not significant; p < 0.05 versus controls), and amount of retransfused autologous blood (p < 0.001). Epsilon-ACA increased, aprotinin suppressed antiplasmin-plasmin complex generation (epsilon-ACA versus controls, p < 0.02; epsilon-ACA versus AP, p < 0.0001). For 4 hours after discontinuation, more chest drainage occurred with epsilon-ACA than aprotinin (137 +/- 90 mL versus 62 +/- 29 mL; means +/- standard deviation; p < 0.02). Cumulative 12-hour drainage was similar for aprotinin (391 +/- 220 mL) and epsilon-ACA (582 +/- 274 mL), but higher without inhibitor (1,091 +/- 541 mL; p < 0.001 versus drugs). Postoperatively, aprotinin was associated with the lowest autologous retransfusion incidence and highest hematocrits (p < 0.01 versus epsilon-ACA). Homologous transfusion exposures did not differ. CONCLUSIONS: In first-time coronary operations, higher postoperative hematocrit and less shed blood retransfusion constitute only subtle advantages of aprotinin over high-dose epsilon-ACA.
BACKGROUND: Degeneration remains the major drawback of bioprostheses. Among various concepts to mitigate degeneration, the use of autologous pericardium for intraoperative construction of aortic valves (ATCV) was revived recently. Based on in-vivo studies the problem of tissue failure was claimed to be oversome by short immersion in glutaraldehyde. METHODS: Two often ATCV implanted 1994-1996 had to be replaced because of valvular insufficiency due to leaflet shrinkage or tearing. Pathophysiology of failure was evaluated by light microscopy and immune histology, scanning electron microscopy (SEM) and determination of tissue calcium content (AAS). RESULTS: AAS revealed high calcium levels in the shrunken and low levels in the torn leaflets. Histology demonstrated extensive fiber degeneration without inflammation in the destructed and moderate degeneration in the intact leaflets. SEM showed smooth surfaces in the 'normal' and exposure of collagen in the degenerated leaflet associated with calcification. Tears occurred close to the stents. CONCLUSIONS: Failure of ATCV is characterised by either shrinkage and calcification despite a short tanning or by tearing related to the stent design. Clinical use of ATCV cannot be recommended at present.
BACKGROUND AND AIMS OF THE STUDY: The risk of reoperation due to calcific degeneration is the most important drawback of biological heart valves compared with mechanical prostheses. Concepts to mitigate calcification have been tested experimentally and clinically, but none has proven completely to prevent degeneration. METHODS: Renewed interest has involved the use of autologous pericardium for intraoperative construction of autologous aortic valves (ATCV). RESULTS: Of 10 ATCV implanted between 1994 and 1996, one was removed from an 84-year-old female 27 months after implantation because of severe valvular insufficiency. Eight months earlier, a broken spring of the stent system was detected radiographically, with normal valvular competence at echocardiography. Valve dysfunction was due to shrinkage of one leaflet. Measurement of tissue calcium by atomic absorption spectroscopy showed high levels in the shrunken leaflet compared with two intact leaflets (42.82 versus 0.51 and 2.42 mg Ca2+/g). Histology and immunohistology demonstrated extensive fiber degeneration without inflammation or immune reactions in the destroyed leaflet, and moderate fiber degeneration in intact leaflets. Scanning electron microscopy showed smooth surfaces in the normal leaflet and exposure of collagen in the degenerated leaflet in association with calcium deposition. CONCLUSIONS: In contrast to the outcome in animal studies, intraoperative tanning did not prevent tissue shrinkage in this case. Leaflet malfunction was associated with calcification. At present, the clinical use of valves constructed from autologous pericardium can not be recommended.
BACKGROUND AND AIMS OF THE STUDY: Reduction of biomaterial calcification is an important aim in the basic research of biological heart valves. An in vitro model was used to investigate the influence of serum calcium concentration and surface coverage with cells or basal proteins on calcium uptake of bovine pericardium. METHODS: Samples of glutaraldehyde-tanned bovine pericardium, stored in formaldehyde and detoxified with borohydride were incubated for two weeks with cell culture medium containing low (1.0 mmol/l) or physiologic (2.3 mmol Ca/l) calcium concentration. Specimens were either unseeded, completely surface-covered with rat fibrocytes (rf) or fibrin (fi), or incompletely seeded with rabbit cells (re). Quality of surface coverage was assessed by surface scanning electron microscopy and calcium content by atomic absorption spectroscopy. RESULTS: Serum calcium had a significant influence on calcium uptake (low versus physiological (1.58 +/- 2.45 mg/g versus 8.10 +/- 1.73 mg/g wet wt, p < 0.001). This may explain early calcification of bioimplants in children and patients on dialysis. Surface coverage significantly reduces calcium uptake (fi, 1.20 +/- 0.41 mg/g, rf, 4.20 +/- 1.70 mg/g, p < 0.001) but complete coverage is necessary (re, 6.98 +/- 1.64 mg/g, NS). CONCLUSIONS: In vitro testing of calcium uptake has proven to be a valuable tool for evaluation of biomaterial calcification.
BACKGROUND AND AIM OF THE STUDY: The frequent need for re-replacement of tissue valves due to calcification remains their major disadvantage compared with mechanical implants. A variety of anticalcification treatments has been proposed but none has proved to prevent calcific degeneration. The study aim was to evaluate, in vitro, the time course of calcium uptake of procine and bovine biomaterials and the efficacy of anticalcification treatments. METHODS: Samples of glutaraldehyde-tanned biomaterials with (Carpentier-Edwards, Medtronic Intact, Hancock II, MZGTB) or without anticalcification treatment (Mitroflow) were incubated with culture medium containing physiological calcium levels. Specimens were then analyzed at two, four or eight weeks for their calcium content (mg/g wet weight). RESULTS: All specimens calcified over time, though the time courses for each were significantly different. Mitroflow and Intact valves accumulated high calcium levels rapidly during the first two weeks, with small further increases thereafter. Anticalcification treatment reduced calcium uptake of Carpentier-Edwards material during the first two weeks of incubation, but the material gradually attained comparable calcium levels at eight weeks. Hancock valves and the self-customized MZGTB valve showed the lowest calcium levels over the test period. CONCLUSIONS: This in vitro study documented major differences in calcium uptake of different biomaterials. Some anticalcification treatments render the material temporarily less susceptible to calcium binding but none can prevent calcification. In vitro testing has proved to be a valuable instrument for evaluating anticalcification treatments, but should be combined with evaluation of bioprosthesis surface interaction with circulating blood.
Myocardial injury after ischemia (I) and reperfusion (R) is related to leukocyte activation with subsequent release of cytokines and oxygen-derived free radicals as well as complement activation. In our study, the cardioprotective effects of exogenous C1 esterase inhibitor (C1 INH) were examined in a rat model of myocardial I + R (i.e., 20 min + 24 hr or 48 hr). The C1 INH (10, 50 and 100 U/kg) administered 2 min before reperfusion significantly attenuated myocardial injury after 24 hr of R compared to vehicle treated rats (P < .001). Further, cardiac myeloperoxidase activity (i.e., a marker of PMN [polymorphonuclear leukocyte] accumulation) in the ischemic area was significantly reduced after C1 INH treatment compared to vehicle treated animals (0.81 +/- 0.1, 0.34 +/- 0.13, 0.13 +/- 0.1 vs. 1.44 +/- 0.3 U/100 mg tissue, P < .001). In addition, C1 INH (100 U/kg) significantly attenuated myocardial injury and neutrophil infiltration even after 48 hr of reperfusion compared to vehicle treatment. Immunohistochemical analysis of ischemic-reperfused myocardial tissue demonstrated activation of classical complement pathway by deposition of C1q on cardiac myocytes and cardiac vessels. In addition, expression of the endothelial adhesion molecules P-selectin and intercellular adhesion molecule 1 (ICAM-1) was observed after reperfusion of the ischemic myocardium. In this regard, C1 INH administration abolished expression of P-selectin and ICAM-1 on the cardiac vasculature after myocardial ischemia and reperfusion. Blocking the classical complement pathway by exogenous C1 INH appears to be an effective means to preserve ischemic myocardium from injury after 24 and 48 hr of reperfusion. The mechanisms of this cardioprotective effect appears to be due to blocking of complement activation and reduced endothelial adhesion molecule expression with subsequent reduced PMN-endothelium interaction, resulting in diminished cardiac necrosis.
In a prospective study, 39 patients following aortic or mitral valve replacement underwent investigation of molecular markers (prothrombin fragment F1+2, Factor II) in the initial phase of oral anticoagulation therapy (OAT). The results demonstrate that, despite INR being in the depicted range, the levels of the molecular markers remained high, indicating an increased risk of thromboembolic events. This leads to the conclusion that molecular markers are superior to INR in the monitoring of the early phase of OAT.
Pulmonary thromboendarterectomy (PTE) is a potentially curative procedure in chronic thromboembolic pulmonary hypertension. From June, 1989, to December, 1994, we performed PTE in 109 consecutive patients. Multiple changes in surgical approach and postoperative management have been implemented since January, 1995. We report the early results of 32 thromboendarterectomies performed from January, 1995, to January, 1997. Thirty-two patients (16 females, 16 males; mean age 55 years) were operated using cardiopulmonary bypass, deep hypothermia and circulatory arrest. Preoperative NYHA functional class was III in 21 and IV in 11 patients. Pulmonary vascular resistance (PVR) and mean pulmonary artery pressure (mPAP) were elevated to 967 +/- 238 dynes.s.cm-5 and 51 +/- 11 mm Hg respectively. The perioperative mortality rate was 9.3% (3 of 32). Twenty-nine survivors were weaned from mechanical ventilation and extubated after a mean of 35 hours (12 to 190 hours). PVR was reduced to 301 +/- 151 dynes.s.cm-5 (p < 0.001) and mPAP was reduced to 28 +/- 10 mm Hg (p < 0.001). Pulmonary thromboendarterectomy is an effective surgical procedure for chronic thromboembolic pulmonary hypertension. By means of modifications in surgical approach and postoperative management, early results can be improved and perioperative mortality can be decreased to less than 10%.
PURPOSE: The present investigation aimed at examining changes in muscle metabolism caused by treatment of arterial occlusive disease, using dynamic 31-phosphorus methods. METHOD: 32 patients with arterial occlusive disease were examined in a 1.5 T apparatus with a 6 cm surface coil before and after treatment. The metabolic changes in the quadriceps muscles were visualised during a 36 s phosphorus spectrum during rest, exercise (isometric and isotonic) and during a period of recovery. RESULTS: Vascular therapy resulted in a significant increase in the duration of both types of exercise during dynamic phosphorus spectroscopy (isometric exercise: 282 s against 199 s: p = 0.002, isotonic exercise: 575 s against 222 s; p = 5 x 10(-6). After treatment, exercise-induced changes in pH (7.00 against 6.94; p = 0.004 and 7.00 against 6.93; p = 0.02) and the ratio Pi/PCr (0.34 against 0.44; p = 0.002 and 0.36 against 0.50; p = 0.009) were significantly smaller than before therapy, using a similar amount of exercise. Recovery time of Pi/PCr (45 s against 82 s; P = 10(-5) and 42 s against 57 s; p = 0.01) and pH value (154 s against 181 s; p = 0.14 and 173 s against 214 s; p = 0.22) showed significant reduction after treatment. CONCLUSIONS: Dynamic 31-phosphorus magnetic resonance spectroscopy indicates increased mitochondrial oxidative capacity in the quadriceps muscles as evidence for increased oxygen supply to muscle tissue following vascular therapy.
Pulmonary thromboendarterectomy is an accepted operative procedure for treatment of pulmonary hypertension due to chronic embolism. Despite its proven value this procedure has been established at very few centers worldwide. In this paper we report our actual operative concept and operative results. Between 8'89 and 4'96 127 patients were operated with use of extracorporeal circulation, deep hypothermia and circulatory arrest. After analysis of the initial high perioperative mortality (26%, 29/108) our operative and postoperative concept changed since 11'94: 1. central incision of both pulmonary arteries, 2. endarterectomy exclusively during circulatory arrest, 3. prolonged reperfusion to 37 degrees C, 4. pressure controlled ventilation, NO-inhalation, early extubation, and 5. modified vasopressor therapy. Preoperatively 12 of the 19 patients were in NYHA class III and 6 in class IV. Mean pulmonary artery pressure was 52(17) mmHg with a calculated pulmonary resistance of 1013(579) dynes.s.cm-5. Mean circulatory arrest time was 37 min (19-57 min) (bypass time 345 min, (240-430 min)). Perioperatively two patients (11%) died (multiorgan failure; rethrombosis of pulmonary artery/right heart failure), all other patients survived (89%). Perioperative complications included reversible renal failure, delirium and postcardiotomy syndrome (1/2/1). Mean pulmonary resistance was postoperatively significantly reduced (362(124) dynes.s.cm-5) (p < 0.01). Early results of pulmonary thromboendarterectomy can be improved by consequent modifications of the intra- and postoperative concept.
OBJECTIVE: To find out whether pulmonary thromboendarterectomy (PTE) can achieve lasting reduction of pulmonary vascular resistance in patients with pulmonary arterial hypertension due to chronic thromboembolism. PATIENTS AND METHODS: 45 patients (25 women, 20 men; mean age 45 +/- 24 [19-67] years) were re-investigated a mean of 21 (13-32) months after successful PTE. Two patients had then been in New York Heart Association (NYHA) stage II, 26 in stage III, and 17 in stage IV. In addition to clinical examination and chest radiogram 36 patients had right heart catheterization, 28 pulmonary angiography and 44 echocardiography. RESULTS: Definite improvement of symptoms had occurred in all. 34 were now in NYHA stage I, nine in stage II, and two in stage III. The pulmonary vascular resistance was significantly lower than before and immediately after PTE (pre-PTE: 1052 +/- 472 dyn.s.cm-5; post-PTE: 293 +/- 175 dyn.s.cm-5; at follow-up: 187 +/- 92 dyn.s.cm-5; P < 0.001 for follow-up vs pre-PTE; P < 0.05 for follow-up vs post-PTE). Correspondingly, cardiac index had significantly increased (3.0 +/- 0.5 vs 2.0 +/- 0.7 l/min.m2; P < 0.001). Radiological and echocardiographic examinations showed a definite decrease in right ventricular dimensions and improvement in right ventricular function. CONCLUSION: In patients with pulmonary arterial hypertension due to chronic pulmonary thromboembolism PTE can achieve a reduction in pulmonary vascular resistance with lasting improvement in right heart function and clinical symptoms.