Search PubMed⌕ Search

Biomedical subjects

D Baumgart

Publications and source records attributed to D Baumgart.

At least 19 recordsLinked to original sources
PubMed1995

[Electron beam tomography in coronary disease. Prevalence and distribution of coronary calcifications and their relationship with coronary risk factors in 650 patients].

OBJECTIVE: The extent of coronary calcification demonstrated by electron beam tomography was correlated with the individual cardiac risk profile. PATIENTS AND METHODS: The possible presence of coronary calcifications was studied by electron beam tomography (EBT) in 650 patients (526 men, 124 women; mean age 54 +/- 10 [28-81] years) with known or suspected coronary heart disease. Depending on the degree of density and the size of the lesion a score was calculated according to an international standard. RESULTS: No calcification was shown to be present in 202 patients (score of 0). A score of more than 0 was calculated in 73.8% of men and 48.4% of women. The average score was 227.8 +/- 24.8 in men, compared with 65.3 +/- 26.5 in women (P < 0.001). There were significantly more calcifications in older patients: Men aged 71-75 years had the highest score, 859.4, while the lowest, 9.6, was in those aged 36 to 40 years. The most important variables for the presence of calcification were age (relative risk per age group: 1.6), male sex (relative risk: 4.3), hypertension (relative risk: 2.4) and nicotine consumption (relative risk: 1.8). The median point score in patients without known risk factors was 1.3, with one known factor it was 7.2, and with three it was 48.0. The vessel segment most affected with calcification was the anterior interventricular branch with an average score of 84. CONCLUSION: Together with an evaluation of the risk profile EBT provided a better assessment of individual risk than conventional examination.

Adult↗
PubMed1995

Intravascular ultrasound approach to the diagnosis of coronary artery aneurysms.

Coronary artery aneurysms are usually diagnosed by contrast coronary angiography, which portrays the silhouette of the lumen but cannot distinguish true and false aneurysms. To differentiate true and false aneurysms and to study the morphologic changes of the vessel wall, intravascular ultrasound (IVUS) was performed in patients with angiographic signs of coronary artery aneurysms. We used a 4.8F or 3.5F, 20 MHz IVUS catheter for ultrasound examination. Fourteen patients (12 men and two women ranging in age from 43 to 73 years) with angiographic signs of coronary aneurysm were enrolled. IVUS imaging was optimally obtained in all patients. The vessel area, lumen area, and plaque area of the aneurysm segment and of the proximal and distal segments were determined. IVUS showed that both the proximal and distal reference segments were severely affected by atherosclerotic lesions in all the patients and by calcium deposits in six patients. The percent stenoses were 63.0% +/- 13.7% and 60.9% +/- 17.8% in the proximal and distal reference segments, respectively. In nine patients the walls of the aneurysms showed signs of atherosclerosis. Three angiographically indicated aneurysms were found to be plaque ruptures. Although the lumen and the vessel areas of the aneurysm segments were larger than those of the proximal and distal segments (p < 0.01 and (p < 0.001), no significant differences in plaque area and plaque composition were found between the aneurysm segment and adjacent vessel segments (p > 0.05). In conclusion, IVUS allows detailed characterization of coronary aneurysms. Atherosclerosis seems to play an important role in the formation of acquired coronary aneurysms.

Adult↗
PubMed1995

Cholinergic and alpha-adrenergic coronary vasomotion [corrected] with increasing ischemia-reperfusion injury.

Ischemia-reperfusion-induced injury of the coronary vasculature could result in an attenuated vasodilator or increased vasoconstrictor tone that might impact on myocardial recovery and viability. In 30 open-chest dogs the left circumflex coronary artery was occluded for 15 or 60 min and then reperfused, and responses to intracoronary acetylcholine, the alpha 1-adrenergic agonist methoxamine, and the alpha 2-adrenergic agonist BHT-933 (n = 10 each) were measured. In the experiments with 60 min of occlusion, triphenyltetrazolium chloride (TTC) staining was used to distinguish reversibly (TTC+) and irreversibly (TTC-) injured myocardium. After 15 min of occlusion, the vasodilator response to acetylcholine was not altered but was significantly reduced in TTC+ subendocardium and midmyocardium after 60 min of occlusion and was further reduced in TTC- subendocardium, midmyocardium, and also in subepicardium. The vasoconstrictor responses to methoxamine and BHT-933 were not altered after 15 or 60 min of occlusion in both TTC+ and TTC- myocardium. Posterior wall thickening was not affected by acetylcholine, methoxamine, or BHT-933. Thus, in reversibly injured myocardium after 15 min of occlusion, cholinergic and alpha-adrenergic coronary vasomotor responses are unchanged. With increasing duration of ischemia, reversibly and even more so irreversibly injured reperfused myocardium are characterized by an impaired cholinergic coronary vasodilation but not an enhanced alpha-adrenergic coronary vaso-constriction.

Acetylcholine↗
PubMed1995

Initial experience with a steerable intravascular ultrasound catheter in the aorta and pulmonary artery.

The aim of this protocol was to test the feasibility and safety of a prototype steerable intravascular ultrasound (IVUS) catheter (Boston Scientific, Waterton, MA) in comparison with standard IVUS catheters. A 3.5F, 20-MHz mechanical echo transducer was incorporated into a bendable sheath with a blunt tip. The flexible IVUS catheter was compared with a standard IVUS catheter in 13 patients. Seven patients underwent catheterization of the left side of the heart, and six patients had catheterization of the right side of the heart for suspected recurrent pulmonary embolism. In the aorta, three lumen area measurements were made: (1) midway between the aortic arch and the aortic root, (2) at the most cranial part of the aorta, and (3) in the descending aorta at the level of the diaphragm. Evaluation of the accuracy of luminal dimension measurements by both types of catheters in perpendicular positions to the vessel wall was evaluated in a hollow rubber cast of an human aorta and its side branches, representing luminal diameters from 3 to 26 mm. We performed 20 measurements with each type of catheter. The results were compared with ruler measurements, after the cast had been cut in slices. The equation for the standard 3.5F IVUS catheter was: y = 0.89x + 0.15; SE = 0.17; r = .97; for the 4.8F 20-MHz standard IVUS catheter: y = 0.97x + 0.05; SE = 0.18; r = .98; and for the steerable catheter, y = 0.94x + 0.09; SE = 0.12; r = 0.97.(ABSTRACT TRUNCATED AT 250 WORDS)

Aorta↗
PubMed1995

[Reconstruction methods for 3D imaging and quantification of intracoronary ultrasound cross-sectional images using biplanar fluoroscopy. Initial experiences in vitro and in vivo].

In this investigation, we studied the feasibility of 3D-reconstruction from 2D cross-sectional intracoronary ultrasound images. A computer-aided, automated 3D-reconstruction was used to generate cylindrical and sagittal format of vessels in vitro (n = 9) and in vivo (n = 48). Ultrasound 2D-images were acquired with a 20 MHz mechanical intracoronary ultrasound catheter (Boston Scientific). A slow pullback (about 1 mm/s) of the catheter was performed during continuous recording of the ultrasound images. The recorded 2D-images were then fed to an image processing computer. Correction and scaling of the axial vessel dimensions was performed by the assessment of the catheter position in the simultaneously recorded biplane fluoroscopy. Digitized data were then processed to 3D-images with use of voxel space modeling. The 3D-views from any plane can be reconstructed. The in-vitro study demonstrated that the reconstructed images were able to correctly portray the pathological changes of the vessel wall in all specimen as proved by pathologic examination. In the in-vivo study, 3D-reconstruction provided not only a spatial visualization of the coronary arterial disorders (such as coronary aneurysm, coronary dissection, spontaneous plaque rupture etc.) but also provides the potential to quantify the mass of lesions. By combining sagittal and cylindrical views, 3D-reconstruction enables longitudinal and orthogonal imaging of the both the vessel lumen and vessel wall, therefore, it has the advantage of cross-sectional viewing as obtained from intracoronary ultrasound and the longitudinal viewing as derived from coronary angiography. These preliminary results of the study indicate that 3D-reconstruction of coronary segments is a promising technique for studying coronary artery disease. Analysis can be based not only on single or multiple cross-sectional images but also on vessel segments facilitating serial studies as for instance studies assessing the progression and regression of atherosclerosis.

Aortic Dissection↗
PubMed1994

Attenuation of myocardial stunning by the ACE inhibitor ramiprilat through a signal cascade of bradykinin and prostaglandins but not nitric oxide.

BACKGROUND: Attenuation of myocardial stunning by several angiotensin-converting enzyme (ACE) inhibitors has been demonstrated. However, the signal cascade mediating such protective effect has not been analyzed in detail so far. METHODS AND RESULTS: In a first protocol, we addressed the role of bradykinin and analyzed the effect of the ACE inhibitor ramiprilat without and with added bradykinin B2 receptor antagonist HOE 140 on regional myocardial blood flow (colored microspheres) and function (sonomicrometry). Thirty-two enflurane/N2O-anesthetized open-chest dogs were subjected to 15 minutes of occlusion of the left circumflex coronary artery (LCx) and 4 hours of subsequent reperfusion. Eight dogs served as placebo controls (group 1), and 8 dogs received ramiprilat (20 micrograms/kg IV) before LCx occlusion (group 2). Eight dogs received a continuous intracoronary infusion of HOE 140 [0.5 ng/(mL.min) IC] during ischemia and reperfusion (group 3), and in 8 dogs HOE 140 was infused continuously during ischemia and reperfusion, starting 45 minutes before the administration of ramiprilat (group 4). Mean aortic pressure was kept constant with an intra-aortic balloon, and heart rate did not change throughout the experimental protocols. Under control conditions and during myocardial ischemia, posterior transmural blood flow (BF) and systolic wall thickening (WT) were not different in the four groups of dogs. However, at 4 hours of reperfusion, WT was still depressed in groups 1 (-10 +/- 20% of control [mean +/- SD]), 3 (-18 +/- 12% of control), and 4 (-12 +/- 21% of control), whereas WT in group 2 had recovered to 55 +/- 20% of control (P < .05 versus group 1). BF at 4 hours of reperfusion was not different in the four groups of dogs. Thus, the beneficial effect of ramiprilat on the functional recovery of stunned myocardium was obviously mediated by bradykinin. Since bradykinin stimulates the formation of both prostaglandins and nitric oxide, we tested in a second protocol which of these mediators was further involved in the beneficial effects of ramiprilat. Twenty-four additional dogs were subjected to 15 minutes of LCx occlusion and 4 hours of reperfusion. Six dogs received the cyclooxygenase inhibitor indomethacin (10 mg/kg IV) (group 5) and 6 dogs a combination of indomethacin with ramiprilat (group 6) before LCx occlusion. Six dogs received the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (20 mg/kg IV) (group 7) and 6 dogs a combination of L-NAME with ramiprilat (group 8) before LCx occlusion. BF and WT before and during myocardial ischemia were not different in groups 5 and 6 and groups 7 and 8. However, at 4 hours of reperfusion, WT was still depressed in groups 5 (-10 +/- 38% of control), 6 (-7 +/- 18% of control), and 7 (-12 +/- 14% of control), whereas WT in group 8 had recovered to 47 +/- 28% of control (P < .05 versus group 7). BF at 4 hours of reperfusion was not different in the four groups of dogs. CONCLUSIONS: In summary, the attenuation of stunning by the ACE inhibitor ramiprilat involves a signal cascade of bradykinin and prostaglandins but not nitric oxide.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

[Therapy of cardiogenic shock in acute myocardial infarct].

Cardiogenic shock in acute myocardial infarction patients is the most common cause of in-hospital death. Various studies showed, that 60 to 100% of patients in cardiogenic shock will die, if no early reperfusion of their coronary artery could be established. The incidence of cardiogenic shock has decreased during the last years, most likely due to early thrombolytic therapy and administration of nitroglycerin. Reasons for cardiogenic shock are either necrosis of 40% or more of the left ventricular wall, right heart infarction, or complications which can be treated by the surgeon, like papillary muscle rupture, ventricular septal defect or rupture of the free ventricular wall. Diagnosis is based on clinical criteria, echocardiography, and on hemodynamic monitoring. The hemodynamic criteria for cardiogenic shock are a cardiac index of < 2.2/l, and an increased wedge pressure of > 18 mm Hg; additionally, diuresis is usually < 20 ml/h. Therapy can be divided into the following categories: a) pharmaceutical interventions to increase cardiac output like vasodilators or positive inotrope drugs; b) mechanical support systems; c) acute interventions with the aim of reperfusion; d) acute surgical interventions addressing complications like papillary muscle rupture, ventricular septal defect or rupture of the free ventricular wall. While steps a) and b) are able to stabilize the hemodynamical situation in patients with cardiogenic shock, they are rarely the definitive treatment. Point c), reperfusion of the coronary artery, can be divided in thrombolysis or acute PTCA. Thrombolysis failed to show a beneficial effect in most studies, either after intravenous or intracoronary application. On contrast, acute PTCA showed to be of great benefit in various studies with a technical success rate of 54 to 100% and a survival rate of patients from 58 to 100%. Thus, emergency PTCA is the treatment of choice in cardiogenic shock. Point d), surgical interventions can be divided in acute bypass grafting, which should be reserved for patients with severe multivessel disease, left main involvement, or failed PTCA. Furthermore, acute heart transplantation is effective, but will be possible in a minority of patients only. The last part of surgically manageable complications are surgery of papillary muscle rupture and ventricular septal defect. Results of early surgery in papillary muscle rupture or ventricular septal defects are much better than delayed interventions. Rupture of the free wall is usually a fatal event. In summary, the most successful therapy of cardiogenic shock is early emergency PTCA.(ABSTRACT TRUNCATED AT 400 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1994

Enoximon-echocardiography. A new diagnostic approach for the detection of viable myocardium comparison to dobutamin-echocardiography.

UNLABELLED: Hypo- or akinetic myocardial regions can be identified as viable myocardium through recruitment of inotropic reserve. Both, dobutamine (D) as well as enoximone (E) mediate their inotropic action via an increase in intracellular c-AMP concentration based on a different action. In 10 patients with documented myocardial infarction either D (5 to 40 micrograms/kg/min, increments of 5 micrograms/kg/min every 3 min) or E (1 to 9 micrograms/kg/min, increments of 1 microgram/kg/min every 2 min) was administered intravenously on two consecutive days. Heart rate (HR), systolic and diastolic blood pressure (BP), as well as a wall motion score in 16 segment (WMS) and ejection fraction (EF) with 2D-echocardiography were determined at rest and during each increment. Viability of myocardial regions was assessed with 201thallium-SPECT (Table 1). RESULTS: *p < 0.05 vs. rest, data: mean +/- SD. While E did not cause any side effects, patients complained about rash (n = 10), headache (n = 8), angina pectoris (n = 5), and anxiety (n = 2) during the administration of D. D and E are both able to recruit a potential inotropic reserve in infarcted myocardium, and thus, identify viable myocardium. In contrast to E, D caused an increase in HR and systolic BP. Enoximone-echocardiography seems to be a new, promising tool for the identification of viable myocardium.

Adult↗
PubMed1993

A proischaemic action of nisoldipine: relationship to a decrease in perfusion pressure and comparison to dipyridamole.

OBJECTIVE: The calcium antagonist nisoldipine has recently been reported to induce rather than to attenuate ischaemia in some patients with stable angina. The aim of the study was to investigate the mechanisms underlying this proischaemic effect. METHODS: In 20 anaesthetised dogs systemic haemodynamic variables, regional myocardial blood flow (coloured microspheres), and systolic wall thickening (sonomicrometry) were measured during control conditions and following severe stenosis on the left circumflex coronary artery, before and after intravenous administration of equihypotensive doses of either nisoldipine (group I, n = 10) or dipyridamole (group II, n = 10). Finally, measurements were performed while the drug induced decreases in mean aortic pressure--18 (SD 6) mmHg in group I and 14(6) mm Hg in group II--were reversed by inflation of an intra-aortic balloon. RESULTS: The stenosis decreased posterior wall thickening to 50% of control, and posterior subendocardial blood flow from 1.48(0.27) to 0.61(0.19) ml.min-1.g-1 in group I and from 1.49(0.23) to 0.62(0.18) ml.min-1.g-1 in group II. Subendocardial blood flow was further decreased after administration of either nisoldipine [0.37(0.20) ml.min-1.g-1, p < 0.05 v stenosis] or dipyridamole [0.22(0.11) ml.min-1.g-1, p < 0.05 v stenosis]. Regional myocardial blood flow in the anterior region was increased. The drug induced reduction of subendocardial blood flow decreased posterior wall thickening further from 9.3(2.1) to 6.2(3.9)% (p < 0.05 v stenosis, group I) and from 9.1(1.7) to 4.3(2.4)% (p < 0.05 v stenosis, group II). When the drug induced decrease in aortic pressure was reversed, subendocardial blood flow again increased in group I [0.63(0.19) ml.min-1.g-1, p < 0.05 v stenosis and nisoldipine] whereas in group II it remained decreased [0.40(0.29) ml.min-1.g-1, NS v stenosis and dipyridamole]. There was restoration of posterior wall thickening in group I [10.4(3.8)%, p < 0.05 v stenosis and nisoldipine], but not in group II [5.2(3.5)%, NS v stenosis and dipyridamole]. CONCLUSIONS: Nisoldipine and dipyridamole decrease subendocardial blood flow and contractile function distal to a severe stenosis when aortic pressure is decreased. No aggravation of ischaemia by nisoldipine is seen when hypotension is prevented. In contrast, dipyridamole in the absence of hypotension still induces a redistribution of flow at the expense of the ischaemic region.

Animals↗
PubMed1993

Impact of alpha-adrenergic coronary vasoconstriction on the transmural myocardial blood flow distribution during humoral and neuronal adrenergic activation.

Increased heart rate and left ventricular pressure during humoral and neuronal adrenergic activation act to restrict blood flow preferentially in the subendocardium. The hypothesis was advanced that alpha-adrenergic coronary vasoconstriction preferentially in the subepicardium may counterbalance the enhanced extravascular compression in the subendocardium and serve to maintain blood flow transmurally uniform. In 40 anesthetized dogs, regional myocardial blood flow was determined with colored microspheres; wall function, with sonomicrometry. Humoral adrenergic activation (HAA) was induced by a combination of intravenous atropine, intravenous norepinephrine, and atrial pacing during baseline coronary vasomotor tone (group 1, n = 6) and in the presence of maximal coronary vasodilation with intravenous dipyridamole (group 2, n = 6). In an additional group, HAA was induced by intravenous norepinephrine in the presence of dipyridamole but without atropine and atrial pacing in order to increase end-diastolic left ventricular pressure (group 3, n = 6). Measurements were performed at rest, during HAA, and during ongoing HAA with the intracoronary infusion of the alpha-antagonist phentolamine (Phen). At unchanged mean aortic pressure, Phen improved blood flow particularly to the inner layers as follows: from 1.42 +/- 0.40 (mean +/- SD) to 1.90 +/- 0.40 mL/(min.g) (group 1, P < .05), from 4.99 +/- 2.31 to 5.53 +/- 2.56 mL/(min.g) (group 2, P < .05), and from 6.01 +/- 1.41 to 6.29 +/- 1.27 mL/(min.g) (group 3, P < .05), associated with a decrease in outer layer blood flow in groups 2 and 3. In 16 additional dogs, beta-adrenoceptors were blocked by propranolol and muscarinic receptors by atropine. Neuronal adrenergic activation (NAA) was induced by cardiac sympathetic nerve stimulation (CSNS) during baseline coronary vasomotor tone (group 4, n = 8) and in the presence of maximal vasodilation (group 5, n = 8). Measurements were performed at rest, during a first CSNS, and 20 minutes later during a second CSNS+Phen. The reproducibility of two consecutive episodes of CSNS 20 minutes apart was demonstrated in a separate set of experiments (n = 6). At matched mean aortic pressures, Phen improved blood flow to all myocardial layers in group 4, whereas in group 5, Phen induced a redistribution of myocardial blood flow toward subepicardial layers [from 4.44 +/- 0.96 to 4.81 +/- 0.83 mL/(min.g), P < .05] at the expense of inner layers. With the addition of Phen, there was no change in regional wall function in any group of dogs studied. Thus, during HAA, alpha-adrenergic coronary vasoconstriction does not exert a beneficial effect on transmural blood flow distribution. During NAA, a beneficial effect of alpha-adrenergic coronary vasoconstriction becomes apparent only under conditions of maximal coronary vasodilation.

Animals↗
PubMed1991

Primary closure of median sternotomy with interposition of hydroxyapatite blocks. A new approach in pediatric cardiac surgery.

Chest closure after correction of congenital heart disease with subsequent enlargement of the heart has been a problem encountered throughout departments performing pediatric cardiac surgery. Present techniques using Rehbein struts or an open chest with a Gore-Tex patch skin closure have not solved this issue satisfactorily. Between January 1989 and September 1990, median sternotomies could not be closed primarily due to hemodynamic consequences in nine patients age 3 months to 19 years operated upon in our department. In three children, a conduit exchange, in two a Mustard correction, in two a correction of Fallot's tetralogy, in one a prosthetic valve exchange and in one, a new implantation of a homograft was performed. Primary chest closure was achieved by interposing hydroxyapatite blocks (50 mm x 15 mm x 6 mm) without hemodynamic consequences. In a follow-up period of 10 +/- 8 months, all children are alive and well. There was no complication resulting from the implanted blocks. Due to the excellent functional and cosmetic results of this technique and the outstanding histomorphological characters of hydroxyapatite, we regard the implantation of hydroxyapatite blocks as a superb method for primary sternotomy closure especially in pediatric cardiac surgery.

Adolescent↗
PubMed1991

A case of an intramural coronary artery associated with transposition of the great arteries.

One case of an intramural coronary artery in association with transposition of the great arteries is presented. A 16-month-old infant was admitted for the second-stage operation of complete transposition after a subclavian patch plasty for the aortic isthmus stenosis, division of the persisting arterial duct, and pulmonary artery banding had been performed in the first-stage operation soon after birth. The primarily planned arterial switch operation was, however, not performed because of an unusual coronary artery morphology and pattern--a separated origin of both coronary arteries from the posterior, "facing" sinus of Valsalva and an intramural course of the left anterior descending artery. This very rare case of coronary artery variation is presented from the surgical point of view.

Abnormalities, Multiple↗
PubMed1990

[Surgical treatment of Wolff-Parkinson-White syndrome--experiences with 87 surgically treated patients].

Since January 1984, 87 patients (pts) (57 male, 30 female; age 3 to 64 years) with Wolff-Parkinson-White syndrome were operated upon. The indication for surgical treatment was documented recurrent, paroxysmal tachycardia refractory to medical treatment in 85 cases. Eleven pts (13%) had additional heart disease. 87 pts had a total of 103 accessory pathways (AP). AP was localized at the left free wall in 68% (70 AP), at the right free wall in 16% (16 AP), and localized septally in 17% (17 AP). Thirteen pts (15%) had multiple AP (10 pts had two and three pts had three AP). 87 AP were known preoperatively, 96 were localized intraoperatively, and seven were diagnosed during reoperation. Twenty-seven pts were left lateral AP were operated by the epicardial approach and 37 pts by the endocardial approach. Patients with right lateral AP were approached by an epicardial technique in six cases, and by a transmural technique in five. Cryotechnique was applied additionally in 85 pts. Twelve pts suffered recurrences, 11 were reoperated. 101 AP (98%) were dissected successfully, of which 13 (13%) were ablated during reoperation. All pts survived the initial operation. Two pts died after reoperation. One pt is pacemaker-dependent due to a persisting postoperative AV block. We conclude that surgical dissection of accessory pathways can now be offered as an alternative to the non-surgical treatment modes, with low risk and yielding a high success rate.

Adolescent↗