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S Hagl

Publications and source records attributed to S Hagl.

At least 19 recordsLinked to original sources
PubMed2001

Systolic and diastolic properties and myocardial blood flow in the heterotopically transplanted rat heart during acute cardiac rejection.

The aim of the study was to characterize the course of systolic and diastolic function, myocardial blood flow, and histologic changes during acute rejection in a model of heterotopic transplantation in rats. For this purpose isogenic Lewis-to-Lewis and allogenic DA (Dark Agouti)-to-Lewis rat cardiac transplants were studied 1 hour and 1, 3, and 5 days, respectively, after heterotopic intraabdominal transplantation. Myocardial tissue blood flow (MBF) was assessed by the hydrogen-clearance method. An implanted balloon was used to measure pressure-volume relations in the transplanted heart. Myocardial water content was determined at the end of the experiments, and histologic examinations were performed. The MBF recovered during the first day postoperatively in both groups and decreased again in the allogenic group after 3 and 5 days (p < 0.05); it remained stable in the isogenic group. Myocardial relaxation was already prolonged in the allogenic group after 3 days and deteriorated further. Left ventricular end-diastolic pressure progressively increased in the allogenic group, whereas it remained unchanged in the isogenic group up to 5 days. After recovery from ischemia, the left ventricular peak systolic pressure was stable in the isogenic group for the entire further observation period, but it significantly decreased in the allogenic group after 5 days (p < 0.05). Myocardial water content showed a significant increase in the allogenic group compared to that in the isogenic group after 5 days. In the allogenic group histologic examination confirmed mild to moderate rejection after 3 days and severe acute rejection after 5 days. Thus, after recovery from ischemia, mild to moderate cardiac rejection was associated with reduced MBF and impaired relaxation. In a typical sequence, generation of edema and impaired diastolic compliance were terminally followed by systolic dysfunction during severe rejection.

Animals↗
PubMed2001

[Thrombolysis of prosthetic heart valve thrombosis using recombinant tissue plasminogen activator (rt-PA) in infancy and childhood].

Thrombotic obstruction of a mechanical cardiac valve prosthesis requires urgent therapy. We report on the treatment of prosthetic valve thrombosis with recombinant tissue plasminogen activator (rt-PA) in three children at the age of 4, 10 and 18 months, in whom a St. Jude Medical prosthesis had been placed at the atrioventricular valve level 2 to 6 weeks earlier. The initial rt-PA dose was 0.4 mg/kg given over 15 min and followed by a continuous daily infusion of 1.6 to 2.0 mg/kg. In addition the patients received heparin (200 U/kg/d). Thrombolytic therapy was administered for a range of 4 to 28 days. The therapy was successful in the first case. The second child had four recurrent events of prosthetic valve thrombosis and the thrombolytic therapy was successful three times. However, the prosthesis had to be finally replaced. In the third case the thrombolytic therapy was only partially successful due to an organized thrombus requiring prosthesis replacement.

Age Factors↗
PubMed2000

Three-dimensional color Doppler reconstruction of intracardiac blood flow in patients with different heart valve diseases.

An improved perception of the magnitude and dynamics of intracardiac flow disturbances has been made possible by the advent of 3-dimensional (3-D) color Doppler, a new diagnostic procedure developed at our institution. This study describes the new insights derived from 3-D reconstruction of color Doppler flow patterns in patients with different heart valve diseases. The color Doppler flow data from 153 multiplanar transesophageal or transthoracic echocardiographic examinations has been obtained from 133 patients with heart valve disease; 73 patients had mitral regurgitation, 15 had mitral stenosis, 18 had aortic regurgitation, 26 had aortic stenosis, and 21 patients had tricuspid regurgitation. Four patients had pulmonary regurgitation associated with mitral valve disease. The 3-D reconstructions of color Doppler flow signals were accomplished by means of the "Heidelberg Raytracing model," developed at our institution. The 3-D color Doppler reconstructions were obtained in all patients. The 3-D images revealed for the first time the complex spatial distribution of the blood flow abnormalities in the heart chambers caused by different heart valve diseases. New patterns of intracardiac blood flow disturbances were observed and classified. Three-dimensional color Doppler provides a unique noninvasive method that can be easily applied for studying intracardiac blood flow disturbances in clinical practice.

Aortic Valve Insufficiency↗
PubMed2000

[Volumetric analysis and visualization of cardiologic ultrasound data].

BACKGROUND: Echocardiography is a standard imaging technique for the assessment of heart valve disease. The good spatial and temporal resolution is the basis for different methods which provide information about the severity of such defects. Dynamic colour visualisation and volumetric measurements of regurgitant jets are a new evaluating tool for the assessment of heart valve insufficiencies. METHODS: The regurgitant jet volume of 58 patients was evaluated on an external work-station after segmentation of the left atrium and compared to regurgitant volume; the correlation was good. This result is valid for central jets as well as for eccentric jets. CONCLUSIONS: Measurement of regurgitant jet volume is a method which considers the three-dimensional shape of the examined volume. Real-time visualisation techniques which support the interactive clipping of morphological structures provide dynamic visualisation of intracardiac flow during the heart cycle. Dynamic colour visualisation of jets together with myocardial structures allows the assignment of intracardiac flow to morphological structures.

Computer Graphics↗
PubMed2000

Dynamic cardiomyoplasty in a growing organism.

BACKGROUND: Until now cardiomyoplasty has been a treatment option for adults only. However, there may be a demand for cardiomyoplasty in children. The purpose of this study was to investigate the possibility of applying the method of cardiomyoplasty before growth is completed. METHODS: The latissimus dorsi muscle (LD) was wrapped around the heart of 20 Göttinger Minipigs (9.1 +/- 1.2 kg body weight). The LD was fixed to the pericardium in group 1 (n = 11) and to the epimyocardium in group 2 (n = 9) and stimulated with burst impulses. After 5.6 +/- 1.8 months hemodynamic and histologic follow-up-examinations were carried out in 13 surviving animals (weight 32.4 +/- 5.3 kg). RESULTS: In group 1 (n = 6) only the left ventricle was covered by the LD. In 4 animals the LD contracted strongly; in 2, the outer border of the muscle was atrophied. In group 2 (n = 7) both ventricles were covered by the LD in all animals and showed strong contractions. In 2 animals the outer border of the muscle was atrophied. In both groups the contracting parts of the LD showed an intact muscle structure, but compared with the contralateral LD, there was a higher percentage of interstitial fat and connective tissue. Hemodynamic measurements and the well-being of the animals suggest that restriction of cardiac chamber diameter did not occur. The electrical stimulation of the LD caused a minimal increase of left ventricular pressure and aortic peak flow in group 2. CONCLUSIONS: Cardiomyoplasty can be applied in a growing organism. There is growth of the LD with the heart. The muscle structure remains intact. To prevent dislocation of the LD, it seems to be important to fix the LD directly onto the epimyocardium.

Adult↗
PubMed2000

The endogenous pathway is a major route for deep sternal wound infection.

OBJECTIVE: Deep wound infections pose an increasing problem in cardiac surgery patients. Prospective infection monitoring is thus a means of identifying possible risk factors. METHODS: Within a period of 5 months, a total of 376 adult patients, 260 men and 116 women, with a mean age of 62.6 years (range 18-88), underwent coronary bypass grafting (n=281) or other cardiac surgery procedures (n=95). Nasal cultures were taken preoperatively from every patient, as well as cultures of the wound during surgery and when dressings were changed thereafter. In addition, nasal cultures were taken from all the medical and nursing staff. To differentiate endogenous and exogenous infection pathways, DNA fingerprint analysis was performed. RESULTS: A total of 38 patients (10.1%) developed a wound infection, in 14 patients this happened to be a deep wound infection, in 24 patients a superficial one. Five sternal wound infections were associated with mediastinitis (1.3%). The occurrence of a wound infection overall resulted in prolonged hospitalization (29.4+/-24 vs. 11.9+/-6.9 days, P=0.001), but not in increased hospital mortality (4.4% vs. 3.9%). Obesity, diabetes mellitus and nasal carriage of Staphylococcus aureus proved to be independent risk factors with an odds ratio of 2.07, 2.26 and 2.28, respectively. In all but one of the sternal colonizations with S. aureus, DNA fingerprint analysis demonstrated an identical pattern of S. aureus from the patient's nose and sternum, indicating an endogenous infection pathway. CONCLUSIONS: The determination of the endogenous pathway for severe wound infection makes prevention possible by means of preoperative local S. aureus eradication.

Adult↗
PubMed2000

Role of neural and humoral factors in hyperdynamic reaction and cardiac dysfunction following brain death.

BACKGROUND: Although hemodynamic instability and cardiac dysfunction after brain death are reported in the potential organ donor, the underlying mechanisms, for example, neurohumoral changes, myocardial injury, and altered loading conditions, have not been differentiated in clinical and experimental settings. In the present study, we performed a load-independent analysis of cardiac function, focusing on the influence of brain death-associated neural and humoral factors. METHODS: In a canine in situ cross-circulated heart model, brain death was induced by inflation of a subdural balloon catheter. Preload, afterload, and coronary perfusion pressure were kept identical in all hearts throughout the experiment. In Group H (humoral factors), the hearts of healthy dogs were perfused with blood from brain-dead support dogs (n = 6). In Group N (neural factors), the hearts of brain-dead dogs were perfused with blood from healthy support dogs (n = 6). In Group H + N (humoral and neural factors), the hearts of brain-dead dogs were perfused parabiotically in situ with the animals' own blood (n = 6). Systolic and diastolic pressure-volume relationships and coronary blood flow were measured. RESULTS: Induction of brain death led to a significant hyperdynamic response in all groups, with a maximal reaction in Group H + N followed by Group H and Group N. After the initial hyperdynamic phase, cardiac function returned to baseline within 15 minutes and remained stable in all groups for the 2-hour observation period. CONCLUSIONS: (1) Both neural and humoral factors contribute to the initial hyperdynamic reaction after brain death, and only in combination do they cause a maximal hemodynamic effect. (2) If loading conditions and perfusion pressure are kept constant, no cardiac dysfunction occurs after brain death. This indicates that poor cardiac function in the potential donor may reflect altered loading conditions and impaired coronary perfusion rather than neurohumorally mediated direct myocardial injury.

Animals↗
PubMed2000

Acute triiodothyronine administration does not reverse depressed contractile performance following catecholamine exposure in isolated rat cardiomyocytes.

BACKGROUND: It has been previously suggested that triiodothyronine (T3) may reverse depressed cardiac contractile performance occurring after excessive catecholamine stimulation. We therefore investigated the effects of T3 on intracellular calcium transients and contractile performance in isolated ventricular rat myocytes. METHODS: Isolated rat myocytes were loaded with the calcium indicator FURA-2/AM (50 micromol/L) and superfused with Krebs-Henseleit solution (pH 7.4). Cells were illuminated by ultraviolet light and fluorescent images obtained with a target camera at 340 nm and 380 nm excitation wavelengths (ratio method). Simultaneous measurements of calcium transients and cell shortening (35 degrees C, electrical field stimulation: 0.5 Hz) were done. At steady state conditions, FURA-2 loaded myocytes were superfused for 60 min with epinephrine (0.1 micromol/L). After 60 min the effect of T3 (10 micromol/L) on calcium transients and shortening were measured. As control, only the effect of 10 micromol/L T3 was analyzed. RESULTS: Epinephrine significantly increased cell shortening and FURA-2 signals to 148.6+/-8.8% and 109.5+/-3.1% (p < 0.01: n = 21; 5 min) respectively. With longer epinephrine exposure, the increase in cell shortening continuously declined to 134.6+/-7.9% with no change in FURA-2 fluorescence. Acute administration of T3 after epinephrine exposure lowered contractile performance from 136.2 +/- 15.5% to 102 +/- 8.2 %, after 10 minutes. In control experiments acute administration of T3 increased basal contractile response from 100% to 115.8+/-3.3% (p<0.01; n = 8; 5 min). CONCLUSIONS: This study confirms previous reports of impaired cardiac function after high catecholamine exposure. High catecholamine exposure is associated with a desensitization of contractile proteins for calcium. Acute T3 administration increased contractility in untreated myocytes, but further depressed myocyte shortening in epinephrine-treated cells. Our results show that T3 is ineffective at restoring myocardial contractility after excessive catecholamine stimulation.

Animals↗
PubMed2000

Vascular tracheobronchial compression syndromes-- experience in surgical treatment and literature review.

Between January 1988 and December 1997 a total of 22 patients (age: 8 days-46 years) were operated for vascular airway compression syndromes with respiratory insufficiency. Vascular anomalies in tracheal compression were double aortic arch in 7 patients, (2 previously operated elsewhere), right aortic arch + left ligamentum arteriosum in 1, and pulmonary artery sling in 3. Three of these patients had secondary long-segment tracheomalacia. Compression of trachea and a main bronchus existed in 2 patients with right aortic arch + left ligamentum. Isolated main bronchus obstruction was present in 9 patients (abnormal insertion of ligamentum arteriosum in 1, status post (s.p.) previous operation for PDA in 4, s. p. surgery for coarctation in 1, right aortic arch + left ligamentum arteriosum in 2, and right lung aplasia + left ligamentum in 1). 3 of these cases had secondary long-segment bronchomalacia. All patients had a complex respiratory anamnesis [long-term intubation in 7, s.p. tracheostomy in 2 (over 3 months - 3 years), and progressive respiratory insufficiency in 13). In tracheal compression, surgical correction included transsection of the underlying ring or sling components (with additional anterior aortic arch translocation in 5 patients resection-reimplantation of left pulmonary artery in 3, segmental tracheal resection in 1, and external tracheal suspension in 2). In the 2 cases with compression of the trachea and a main bronchus, aortic "extension" by a prosthetic tube was necessary. In isolated main bronchus obstruction, surgical decompression basically consisted of transsection of the ligamentum arteriosum or resection of its scarry remnant forming the "corner point" of a compression between aorta and pulmonary artery. In 3 patients with secondary long-segment malacia, additional external bronchus suspension was performed. Effective decompression and re-expansion of the airway segment concerned was achieved, and was demonstrated by intraoperative endoscopy in all patients. There were 3 postoperative deaths (sepsis 2; massive, irreversible edema of the tracheal mucosa 1). Of the 19 surviving patients 16 could be extubated between the 1st and 17th (mean = 7.5) postoperative day. In 1 case the preoperative long-term tracheostomy had to be left in place for inoperable additional laryngeal stricture. 2 patients had to be reoperated (segmental cervical tracheal resection after 5 months for primary long-term intubation-related subglottic stenosis in 1, esophageal decompression for residual dysphagia after 57 months related to a traction phenomenon at the right descending aorta in the other), both with gratifying results. In all other patients clinical, endoscopic, and radiographic examinations (follow-up = 2 months - 6 years) demonstrate good results.

Adolescent↗
PubMed2000

Sepsis and catecholamine support are the major risk factors for critical illness polyneuropathy after open heart surgery'.

BACKGROUND: Critical illness polyneuropathy (CIP) remains a problem after open heart surgery. Recently, we reported about a retrospectively performed study pointing out that sepsis, the application of higher amounts of catecholamines and intervention such as chronic venovenous hemodiafiltration may be involved in the onset of CIP. A prospectively performed study is presented in order to evaluate the significance of risk factors initially after open heart surgery. METHODS: From June 1997 until September 1998, patients undergoing open heart surgery and being ventilated beyond 3 days were prospectively enrolled in the study and underwent a standard protocol of electromyographic investigation in order to determine CIP. Several items were recorded: amount of catecholamines, serum levels of urea, creatinine, albumin, and glucose. The duration of sepsis and chronic venovenous hemodiafiltration were reevaluated. Additionally the age, the left ventricular end-diastolic pressure prior to the operation, the time of ICU stay and the time of ventilatory support were compared. RESULTS: Within the observation period, 37 adult patients could be enrolled in the study, whereas 12 patients did develop CIP and 7 patients did not. Patients developing CIP required significantly different amounts of epinephrine (0.17 +/- 0.02 vs. 0.09 +/- 0.01 mg/kg/day, p < 0.05, t-test) higher amounts of norepinephrine (0.06 +/- 0.02 vs. 0.02 +/- 0.01 mg/kg/day, p<0.05, t-test), and lesser dosages of dobutamine (2.2 +/- 0.5 vs. 4.9 +/- 0.7, p<0.05, t-test). After cardiac surgery, the plasma levels of urea was initially significantly elevated in patients developing CIP (127.4 +/- 10.5 vs 97.3 +/- 18.5, p<0.05, t-test) Patients suffering from CIP stayed significantly longer in the ICU (40.3 +/- 11.7 vs. 19.6 +/- 11.3 days, p < 0.05 t-test) with an extended time of ventilator support. (769.6 +/- 05.0 vs 295.0 +/- 134.0 hours, p<0.05, t-test). Patients of the CIP group were suffering significant longer from sepsis than patients without CIP. CONCLUSIONS: Sepsis and catecholamine support and an increased level of urea were associated with the development of CIP. The prevention of sepsis and a modulation of the catecholamine support in order to improve microcirculatory flow may reduce the onset of CIP in patients undergoing open heart surgery.

Aged↗
PubMed2000

Target, application, and interpretation of scores and alternative methods for risk assessment in cardiac surgery.

BACKGROUND: The more popular the use of different methods for risk adjustment becomes, the more often data are applied without any regard about the primary target and/or about important assumptions. Furthermore, risk adjustment is no longer restricted for quality assurance purposes, but became a "tool" of health policy. Few working groups currently use risk adjustment for the development of new therapeutic concepts. The aim of our study is to clarify possibilities and limitations of popular risk adjustment methods. PATIENTS AND METHODS: 4985 Patients underwent isolated CABG. Statistics was performed by calculating descriptive statistics, Parsonnet, and Higginsscores. Furthermore, the parametric, time-adjusted hazard function by Blackstone was used. RESULTS: Descriptive statistics allows intra-, and interinstitutional comparisons of single items to identify "outlying" results. Risk scores aim to predict preoperatively the risk category of the patient who undergoes cardiac surgery. However, since different scores are based on a score-specific combination of variables, and different definitions of the investigation interval, different results may occur, when different scores are calculated for a single patient. However, the use for example, of scores in patient groups allows description of changing risk structures. Most of the scores derive from univariate analyses and monophasic functions. However, survival curves are predominantly multiphasic and require a consideration of the time-dependency of "risk factors". DISCUSSION: An increasing number of patients with severe comorbidity undergoes cardiac surgery. To evaluate reliably present and futurous therapeutic options, risk adjustment is necessary. Since various tools for risk-adjustment are available, a serious discussion about reliability and application is necessary.

Aged↗
PubMed2000

Three-dimensional color Doppler flow reconstruction and its clinical applications.

The visualization and quantification of intracardiac blood flow have always been a challenging task for the cardiologist. The advent of color Doppler flow imaging substantially enhanced the clinical diagnosis of heart valve disease. Three-dimensional (3-D) color Doppler, a new diagnostic procedure, refines the diagnostic value of color Doppler by providing unique spatial and temporal information about the actual extension, direction, origin, and size of intracardiac flows. Here, we describe the procedure for 3-D color Doppler reconstruction of intracardiac blood flow velocities and reveal the varied findings in different heart pathologies that cause blood flow disturbances. An automated procedure for the segmentation of turbulent and laminar flows, which allows for the measurement of mitral regurgitant jet volumes, is one of the first 3-D quantitative approaches to the clinical assessment of mitral valve regurgitation. The major technical advances of this procedure include the direct use of digital color Doppler velocity data and an automatic voxel count of the turbulent jet flows. Three-dimensional color Doppler not only can disclose the spatial complex geometry of intracardiac blood flow disturbances but also can quantitatively assess the severity of mitral valve regurgitation.

Aortic Valve Stenosis↗
PubMed1999

Influence of Bretschneider's cardioplegia on norepinephrine release from isolated perfused guinea-pig hearts.

It was the aim of the present study to investigate the influence of Bretschneider's cardioplegia on norepinephrine (NE) release [determined by high pressure liquid chromatography (HPLC) and electrochemical detection] in isolated perfused guinea-pig hearts. The following resulted were noted. (1) Calcium-dependent exocytotic NE release evoked by electrical field stimulation (12 Hz, 1 min) was completely suppressed after only 3 min of normothermic (37.5 degrees C) Bretschneider's cardioplegia. (2) Stop-flow ischemia is associated with a substantial calcium-independent, non-exocytotic NE release, which is regarded as a sodium-dependent carrier-mediated process. Accordingly, it is inhibited by blockers of the sodium/proton-exchanger (e.g. amiloride) and the neuronal uptake1-carrier (e.g. desipramine). Compared with stop-flow ischemia alone, cardioplegia with 3 min of Bretschneider's histidine-tryptophan-ketoglutarate (HTK)-solution preceding stop-flow enhanced NE release at all stop-flow durations (10-90 min) investigated (e.g. after 30 min of normothermic Bretschneider's cardioplegia: 1070+/-41 pmol/g, n = 45, v stop-flow alone: 764+/-48 pmol/g, n = 27, P<0.05). The NE concentrations determined in the cardiac effluent upon reperfusion followed a typical first order kinetic indicating that the transmitter release had already occurred during stop-flow. Hypothermia reduced NE release in a temperature-dependent manner down to intramyocardial temperatures of 2 7.5 degrees C. NE release evoked by Bretschneider's cardioplegia still exceeded that induced by stop-flow ischemia alone by up to 60%. The NE release evoked by Bretschneider's cardioplegia and stop-flow ischemia was calcium-independent. However, it was significantly reduced by desipramine and amiloride, but both agents had a more pronounced inhibitory effect on NE release evoked by stop-flow ischemia alone. (3) This difference may be due to an intrinsic effect of Bretschneider's HTK-solution, as continuous administration of normothermic Bretschneider's HTK-solution induced a substantial NE release which was neither calcium-dependent nor inhibited by blockade of either uptake1 or sodium/proton-exchange. It is concluded that Bretschneider's cardioplegia is not neuroprotective, as it even augments the stop-flow ischemia-induced nonexocytotic NE release.

Adrenergic Uptake Inhibitors↗
PubMed1999

Influence of brain death and cardiac preservation on systolic and diastolic function and coronary circulation in the cross-circulated canine heart.

Previous studies have demonstrated hemodynamic instability and cardiac dysfunction in the brain-dead organ donor. It remains unclear if primary cardiac dysfunction is responsible for hemodynamic deterioration or decreased cardiac function is secondary to brain death-associated altered loading conditions. Therefore in the present study the effects of brain death on hemodynamics and cardiac function were analyzed in vivo in an open chest model and ex vivo in a cross-circulated heart preparation. In a second protocol, the impact of brain death-associated hemodynamic changes on postischemic graft function was investigated. Brain death was induced injecting saline in a subdural Foley catheter. Induction of brain death led to a hyperdynamic reaction followed by hemodynamic deterioration with a decrease of systemic vascular resistance and myocardial contractility. If the hearts were explanted and assessed ex vivo, no differences were found between control and brain-dead hearts. Furthermore, both control and brain-dead hearts showed full functional recovery after 4 hours of hypothermic ischemic storage. Despite hemodynamic deterioration in situ after brain death, there were no differences between the postischemic function of control and brain-dead hearts. These results indicate that myocardial dysfunction is not irreversible and may be secondary to altered loading conditions, and that the recovery of cardiac function after long-term hypothermic storage is not impaired by the hemodynamic changes observed in situ after brain death induction. These data may also indicate that potential donor hearts might not be excluded from transplantation on the basis of impaired hemodynamic characteristics, especially if they are evaluated by load-dependent parameters.

Analysis of Variance↗
PubMed1999

[A new concept for treatment of supraventricular tachycardia after heart operations: low energy internal cardioversion using a temporary atrial electrode].

Supraventricular tachycardia (SVT) is a common complication early after cardiac surgery. A novel temporary atrial patch electrode (TAPE) for low energy atrial defibrillation was first implanted for intraoperative testing and subsequently removed during open heart surgery in 10 patients (Phase I). After the intraoperative testing period, the TAPE was implanted in 20 patients for postoperative termination of spontaneous episodes of supraventricular tachycardia (Phase II). In case of supraventricular tachycardia (SVT), biphasic shocks (1.2-5.0 J) were applied, measuring the atrial defibrillation thresholds. Phase I: The mean intraoperative atrial defibrillation threshold was 1.6 +/- 1.4 J with a mean shock-impedance of 64.0 +/- 7.3 Ohms. Phase II: Postoperatively, 6 out of 20 patients (30%) developed 7 episodes of atrial fibrillation (n = 6) and atrial flutter (n = 1). In 5 patients, SVT could be converted to sinus rhythm (n = 5) or junctional rhythm (n = 1). The mean postoperative defibrillation threshold (DFT) was 2.7 +/- 2.1 J with a mean shock-impedance of 50.2 +/- 6.8 Ohms. In conclusion, the TAPE allows low-energy defibrillation of atrial fibrillation. It seems to be a useful alternative in the treatment of supraventricular tachycardia.

Adult↗
PubMed1999

Assessment of mitral regurgitant jets by three-dimensional color Doppler.

BACKGROUND: Color Doppler echocardiography is a standard technique for assessing mitral regurgitation before and after mitral valvuloplasty. Mitral valve prolapse produces complex eccentric jet flows that cannot be visualized and measured by two-dimensional color Doppler echocardiography. The aim of this study was to evaluate the clinical impact of three-dimensional color Doppler echocardiography, a new technique developed at our institution, for assessing mitral regurgitation. METHODS: Forty-five patients with mitral regurgitation underwent intraoperative transesophageal echocardiography and three-dimensional Doppler data acquisition. The grade of mitral regurgitation was assessed by angiography. The jet areas were calculated by planimetry from conventional color Doppler; the jet volumes were obtained by three-dimensional Doppler data. RESULTS: New patterns of mitral regurgitant flows were recognized according to the origin, direction, and spatial spreading into the left atrium. Conventional jet areas failed to separate the groups of patients with different degrees of regurgitation, whereas the jet volumes were able to divide patients with different regurgitation grades. No significant correlation was found between jet area and angiographic grading (r = 0.63, p = NS). Jet volumes were significantly correlated to angiography (r = 0.89, p < 0.001). CONCLUSIONS: Three-dimensional color Doppler echocardiography revealed new patterns of regurgitant flow and allowed a more accurate semiquantitative assessment of complex asymmetrical regurgitant jets.

Blood Flow Velocity↗
PubMed1999

Modulation of coronary perfusion pressure can reverse cardiac dysfunction after brain death.

BACKGROUND: Brain death results in a rapid decline in left ventricular function, which has clinical relevance for organ transplantation. The aim of the present study was to investigate coronary perfusion changes during brain death and their role in cardiac dysfunction. METHODS: In an in situ isolated canine heart model, brain death was induced by inflation of a subdural balloon catheter. The heart was perfused separately with the animal's own blood by a pressure-controlled roller pump that was coupled to the measured aortic pressure. Myocardial contractility was estimated by the slope of the end-systolic pressure-volume relation. RESULTS: Induction of brain death resulted in a transient hyperdynamic response, followed by a significant decrease in systemic vascular resistance, coronary blood flow, and the end-systolic pressure-volume relation (p<0.05). However, if coronary perfusion pressure was decoupled from aortic pressure and elevated to pre-brain death levels, coronary blood flow and the end-systolic pressure-volume relation were also restored to baseline levels. CONCLUSION: Severe impairment of coronary blood flow may contribute to decreased contractility after brain death that can be reversed by modulation of coronary perfusion pressure.

Animals↗