Biomedical subjects

C Hagl

Publications and source records attributed to C Hagl.

31 records · Page 2Linked to original sources

PubMed1999

Ascending aortic replacement with aortic valve reimplantation.

BACKGROUND: Reimplantation of the native, structurally intact aortic valve within a Dacron tube graft in patients with aortic root aneurysms corrects annular ectasia and dilatation of the sinotubular junction. The durability of this valve repair with respect to the increased mechanical stress on valve cusps has been discussed, is quite controversial, and is yet unknown. METHODS AND RESULTS: From July 1993 to November 1998, a replacement of the ascending aorta with a repair of the aortic valve was performed in 75 patients (53 men and 22 women aged 50+/-19 years). Twenty-one patients (28%) had Marfan syndrome, and 11 patients (15%) had an aortic dissection, type Stanford A (6 acute, 5 chronic). In 17 patients (23%), concomitant replacement of the aortic arch was necessary. Clinical and echocardiographic follow-up was performed in 6- to 12-month intervals for a cumulative study period of 137 patient-years. No operative deaths occurred. Two patients (3%) died 5 and 20 months postoperatively. One additional patient experienced a transient ischemic attack within the first postoperative week. Three patients (4%) with progressive aortic insufficiency required aortic valve replacement after 9, 11, and 14 months. All other patients had no or mild aortic insufficiency. The repairs have now remained stable for </=65 months (mean, 22+/-20 months). Other valve-related complications did not occur. CONCLUSIONS: Our results demonstrate that this type of aortic valve repair achieves excellent results in selected patients. Perfect coaptation of valve cusps during the repair with no or only trace aortic insufficiency at initial echocardiography seems to be essential for durability.

Adolescent↗

PubMed1999

C1-esterase inhibitor in graft failure after lung transplantation.

Graft failure after lung transplantation may occur immediately after transplantation due to reperfusion injury or later due to rejection and infection. Although the pathological mechanisms are not completely known, the clinical findings are similar to the adult respiratory distress syndrome. In this condition, the blood coagulation contact system and the complement system are activated, leading to a capillary leak syndrome. Activation of the contact as well as the complement system is regulated by a common inhibitor, C1-esterase inhibitor (C1-INH). We report on two patients who received high doses of C1-INH for 2 days during graft failure either due to reperfusion injury immediately after transplantation or due to an acute rejection 2 months after double-lung transplantation. In both cases of graft failure, a capillary leak syndrome occurred with pleural effusions of 7 l to more than 10 l per day. In case 1 disturbance of gas exchange during severe reperfusion injury could not be treated effectively with other treatment modalities like nitric oxide ventilation or surfactant administration. With the use of C1-INH, pleural effusions reduced within 12 h, leading to normal graft function within 4 days. In the second recipient, acute rejection forced the use of extracorporeal membrane oxygenation (ECMO) within 24 h despite immunosuppressive therapy. After administration of C1-INH, pleural effusions reduced from 19 l per day to 300 ml within 3 days of treatment. ECMO was discontinued after C1-INH treatment and the patient extubated 2 weeks later. This experience indicates that C1-INH may play a role in the management of capillary leak syndrome after lung transplantation.

Capillary Leak Syndrome↗

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

Human cytokine responses to coronary artery bypass grafting with and without cardiopulmonary bypass.

BACKGROUND: Coronary artery bypass grafting (CABG) is associated with a systemic inflammatory response. This has been attributed to cytokine release caused by extracorporeal circulation and myocardial ischemia. This study compares the inflammatory response after CABG with cardiopulmonary bypass and after minimally invasive direct coronary artery bypass grafting (MIDCABG) without cardiopulmonary bypass. METHODS: Cytokine release and complement activation (interleukin-6 and interleukin-8, soluble tumor necrosis factor receptors 1 and 2, complement factor C3a, and C1 esterase inhibitor) were determined in 24 patients before and after CABG or MIDCABG. The maximum body temperature, chest drainage, and fluid balance were recorded for 24 hours after operation. RESULTS: Release of interleukin-6, interleukin-8, and tumor necrosis factor receptors 1 and 2 was significantly higher (p < or = 0.005) in the CABG group than the MIDCABG group just after operation. After 24 hours, a significant increase in interleukin-6 was also found in the MIDCABG group (p = 0.001) compared with preoperative value. Body temperature and fluid balance were significantly higher after CABG (p < or = 0.001). CONCLUSIONS: Minimally invasive direct coronary artery bypass grafting represents a less traumatizing technique of surgical revascularization. The reduction in the inflammatory response may be advantageous for patients with a high degree of comorbidity.

Aged↗

PubMed1999

Replacement of ascending aorta with aortic valve reimplantation: midterm results.

OBJECTIVE: Aneurysms of the aortic root lead to aortic valve incompetence due to dilatation of the sinotubular junction and annuloaortic ectasia. Reimplantation of the native, structurally intact aortic valve within a Dacron tube graft corrects annular ectasia as well as dilatation of sinotubular junction and aortic sinuses. Durability of this valve repair with respect to increased mechanical stress on valve cusps is discussed controversially and is yet unknown. METHODS: Since 7/93, replacement of the ascending aorta with repair of the aortic valve was performed in 48 patients (34 male, 14 female; 47+/-20 years) with aortic insufficiency and aneurysm of the aortic root. Fifteen patients (31%) had Marfan's syndrome and five patients (10%) had an aortic dissection type A (two acute, three chronic). In 11 patients (23%), concomitant replacement of the aortic arch was necessary utilizing elephant trunk technique in two patients. Additionally, one patient required mitral valve repair and two other patients coronary artery bypass grafts. Clinical and echocardiographic follow-up was performed in 6-12 month intervals for a cumulative study period of 100 patient years. RESULTS: There were no operative deaths. Two patients (4%) died 5 and 20 months postoperatively. One additional patient experienced a TIA within the first postoperative week. Three patients (6%) with an early postoperative aortic insufficiency (AI) > 1 required aortic valve replacement after 9, 11, and 14 months due to progressive AI. In these patients, distortion of the aortic root geometry led to valve incompetence. All other patients have no or mild aortic insufficiency. The repair now remains stable for up to 63 months (mean 25+/-18 months). Other valve related complications did not occur. CONCLUSIONS: Our results demonstrate that this type of aortic valve repair achieves excellent results in selected patients. Perfect coaptation of valve cusps during the repair with no or only trace AI at initial echocardiography seems to be essential for durability.

Adolescent↗

PubMed1999

Site of pleural drain insertion and early postoperative pulmonary function following coronary artery bypass grafting with internal mammary artery.

STUDY OBJECTIVES: Coronary artery bypass graft (CABG) surgery using the left internal mammary artery (LIMA) impairs postoperative pulmonary function. We studied the changes in pulmonary function and subjective pain relative to the site of chest tube insertion. DESIGN: Thirty patients undergoing CABG surgery using the LIMA were randomized into two groups. Group A (n = 15) received a left chest tube inserted from the midline (subxyphoid). Group B (n = 15) had a tube placed in the sixth intercostal space at the anterior axillary line. All of the patients underwent bedside pulmonary function testing preoperatively and on postoperative days (PODs) 1, 3, and 5. Pain sensation was quantified by a standardized score (1 to 10). RESULTS: A significant impairment of pulmonary function parameters was observed in both groups until POD 5. For group A, the decline in percent predicted (+/-SD) in the vital capacity (VC) from before surgery to POD 5 was, respectively, 92.3+/-30.6% to 56.9+/-12.6% (p < 0.001). For group B, the decline in the VC was from 88.0+/-18.2% to 55.5+/-14.8% (p < 0.001). The FEV1 declined concomitantly in group A from 86.2+/-18.2% to 50.8+/-12.1%, and in group B from 83.5+/-16.4% to 53.9+/-12.5% (p < 0.001). On POD 1, a significantly lower decrease in the VC was measured in group A than in group B, respectively: 45.3+/-15.5% vs 28.6+/-8.7% (p < 0.001). A significantly lower decrease in the FEV1 was also seen in group A than in group B, respectively: 36.9+/-12.9% vs 28.0+/-10.6% (p < 0.05). Pain experienced during deep inspiration was also significantly less in group A than in group B, respectively: 1.2+/-1.1 vs 2.5+/-0.9 (p < 0.01). CONCLUSIONS: Subxyphoid insertion of the pleural drain leads to a significantly lower impairment of pulmonary function and less subjective pain than insertion at the intercostal position. The drainage of the left pleural space is equally effective with both techniques.

Aged↗

PubMed1998

Right ventricular function after brain death: response to an increased afterload.

OBJECTIVE: A major cause of early postoperative morbidity and mortality after cardiac transplantation is right ventricular (RV) failure which is attributed to the inability of the donor's RV to acutely compensate for the recipient's elevated pulmonary vascular resistance. This study was performed to determine: (1) the acute effects of brain death on the RV function; and (2) the adaptation potential of the RV to a progressive increase in RV afterload. METHODS: In 13 anesthetized, open-chest dogs (eight with brain death vs. five control with sham operation), brain death was induced by inflation of a subdural balloon catheter. Heart rate, RV systolic and end-diastolic pressure (RVSP, RVEDP), pulmonary arterial pressure (PAP), and cardiac output (CO), and pressure-length loops (sonomicrometry) were recorded. Afterload increase was induced 2 h after brain death induction by constriction of the pulmonary artery with an increase in RVP from 25 to 50 mmHg in 5 mmHg steps. RESULTS: Cushing phenomenon occurred within a few minutes after brain death induction, with a significant increase of HR (229 +/- 10 vs. 89 +/- 6 min(-1), P < 0.001), CO (3.2 +/- 0.2 vs. 1.7 +/- 0.1 l/min, P < 0.001), PAP (30.4 +/- 2.5 vs. 15.5 +/- 1.3 mmHg, P < 0.01) RVSP (55 +/- 5 vs. 23 +/- 2 mmHg, P < 0.001) and RVEDP (7.4 +/- 0.9 vs. 3.3 +/- 0.6 mmHg, P < 0.001). All these values were also significantly (P < 0.01) higher than the time corresponding values of the control group. The analysis of the pressure-length loops showed a hypercontractile state. Within 15-60 min, all parameters turned to baseline and remained stable for up to 2 h. When afterload was increased progressively, RVEDP increased markedly in the brain death and slightly in the control group (9.4 +/- 0.7 vs. 4.2 +/- 1.1 mmHg, P < 0.01, at RVSP = 50 mmHg). On the other hand, the increase of peak positive dP/dt was significantly higher in the control group (430 +/- 37 vs. 644 +/- 55 mmHg/s, P < 0.01, at RVP = 50 mmHg). However, global RV pump function characterized by CO and stroke work was similar in both groups. While regional RV contractility remained unchanged in the brain death group in terms of pressure-length relationships, RV contractility significantly increased in the control group. CONCLUSION: (1) Brain death per se does not result in an acute impairment of RV function. (2) While control animals adapt to an increased afterload by the homeometric, as well as the heterometric regulation, after brain death, an increase in RV preload follows elevations in RV afterload by the Frank-Starling mechanism subserving the increased stroke work required to ensure unchanged pump function.

Adaptation, Physiological↗

PubMed1998

Effects of brain death on myocardial function and ischemic tolerance of potential donor hearts.

BACKGROUND: An increasing number of experimental and clinical studies reports hemodynamic instability in the donor organism after brain death. However, the relative importance of brain death-related cardiac dysfunction on posttransplantation cardiac function and the reversibility of the observed changes remain controversial. In this study a load-independent analysis of cardiac function after brain death was performed. Special interest was focused on a possible interactive influence of brain death and cardiac preservation on postischemic cardiac function. METHODS: In 12 anesthetized dogs, brain death was induced by inflation of a subdural balloon; 12 sham-operated animals served as control subjects. After a 2-hour observation in situ, the hearts were explanted and perfused parabiotically either immediately or after hypothermic ischemic preservation (4 hours, 4 degrees C). Heart rate, cardiac output, left ventricular pressure, the maximum of left ventricular pressure development and aortic pressure were measured in situ. In addition, the slope of the end-systolic pressure-volume relationship, coronary blood flow, and myocardial oxygen consumption were estimated in the cross-circulated hearts. RESULTS: In spite of a brain death-associated hemodynamic deterioration in situ (expressed as low mean aortic pressure and significant decrease of maximal dP/dt), myocardial function was similar to control after explantation, if assessed ex vivo. Furthermore, after hypothermic ischemic preservation and reperfusion, complete functional recovery of control and brain-dead hearts could be observed. CONCLUSIONS: These data indicate that hemodynamic instability after brain death may rather reflect altered loading conditions than irreversible myocardial damage or primary cardiac dysfunction. Furthermore, there is no evidence for a brain death-related impairment of ischemic tolerance.

Animals↗

PubMed1997

Is the brain death related endocrine dysfunction an indication for hormonal substitution therapy in the early period ?

Experimental studies in animals have suggested that brain death (BD) -- related endocrinological dysregulations lead to a significant depression of cardiac pump and muscle function, however, the discussion about the relative extent of this influence remains controversal. The aim of the present study was to assess in an open chest animal model the short time course (5 hours) of hormonal (epinephrine, norepinephrine, T3, T4, ACTH, cortisol, insuline) and metabolic (glucose, lactate) changes in 10 brain dead dogs with special respect to the hemodynamic stability and myocardial pump function. After the onset of BD the concentrations of all hormonal parameters showed a significant decrease. Despite these changes, and in contrast to other studies, an adequate pump function (filling pressures, cardiac output) and muscle function (LVdp/dt) could be maintained by exclusive volume substitution without the use of hormonal or pressor agents. We conclude that in the present model a sufficient pump and muscle function can be maintained by adequate volume substitution, exclusively. The significant fall in adrenal and thyroid hormones had no direct effects on heart functional parameters in the first 5 hours after experimental BD induction.

Animals↗

PubMed1995

Cardiocirculatory effects of acutely increased intracranial pressure and subsequent brain death.

Hemodynamic instability and functional impairment of the donor heart are currently reported problems in organ transplantation. Actual shortage of potential donor hearts continues to raise controversial discussion about adequate donor management with regard to graft quality. In an experimental open chest model, physiopathologic effects of acutely induced, irreversible intracranial hypertension (AIIHT) were investigated in situ with respect to hemodynamics, cardiac pump and muscle function, and hormonal parameters. Acutely induced irreversible intracranial hypertension was induced by rapid inflation of a subdural balloon catheter in 10 anesthetized dogs, four animals serving as controls. The observation period in both groups was 300 min. Cardiocirculatory stability was maintained by continuous crystalloid volume substitution without the use of inotropic or pressor agents. After AIIHT, three characteristic hemodynamic response phases have been observed: 1) The "acute hyperdynamic phase" lasting up to 15 min with marked increases of heart rate (HR), left ventricular pressure (LVP), cardiac output (CO) and myocardial contractility indices, 2) At the end of the "early restabilization phase", (60 min), these parameters returned close to control levels, except HR (+50%) and systemic vascular resistance (SVR) (-40%), 3) During the "late restabilization phase", filling pressures, LVP and CO remained within control limits at low SVR, contractility indices showed a decreasing tendency. All assessed plasmatic hormones (Catecholamines, triiodothyronine (T3), thyroxine (T4), adrenocorticotropic hormone (ACTH), cortisol and anti-diuretic hormone (ADH) showed a continuous fall to levels significantly below control over the phases of restabilization. Acutely induced irreversible intracranial hypertension leads to multifactorial hemodynamic and hormonal changes. At low SVR, cardiac pump function was preserved exclusively by continuous volume substitution, while myocardial contractility indicated a slight decrease. From this observed hemodynamic and functional state within the donor organism, no reliable prediction on graft functional capacity can be made.

Animals↗

PubMed1995

"Cardioplegia on the contractile apparatus level": evaluation of a new concept for myocardial preservation in perfused pig hearts.

UNLABELLED: The concept of a reversible desensitization of the myocardial contractile apparatus for calcium by 2,3 Butanedione Monoxime (BDM) as a method to improve the myocardium's tolerance to cold ischemia was evaluated in normal pig hearts (n = 14). The results were compared to those obtained after application of Bretschneider's HTK cardioplegic solution. METHODS: Series I) After BDM treatment (concentrations: 0-30 mmol/L) the isometric force output and the intracellular calcium transients (measured using the FURA-2 ratio method) of electrically driven (1 Hz) isolated left-ventricular muscle strips excised from beating pig hearts (n = 14) were recorded simultaneously in order to analyse the mode of action of BDM; Series II) The cardioprotective effects of BDM (30 mmol/L) and Bretschneider's cardioplegic solution (HTK) were compared in a large-animal model: after "in situ perfusion" of pig hearts with either 2000 ml ice-cold BDM solution (30 mmol/L) (n = 7) or 2000 ml HTK (n = 7) the hearts were explanted and stored at 4 degrees C in the same solutions for up to 42 h. The contractile properties of muscle fibres, excised after storage periods of 8, 24, and 42 h from these hearts were analyzed in terms of isometric force development and isotonic shortening. 280 muscle fibres from 14 pigs were used for measurements. RESULTS: Series I) In pig myocardium a dose-dependent reduction of isometric force development was found after BDM application. The shape and the amplitude of the intracellular calcium transient were also affected by BDM. At 30 mmol/L BDM no force development could be elicited despite the presence of an intracellular calcium transient (amplitude < 70% of the control). Series II) Shortening, calcium transient, and force of left-ventricular muscle strips of pig myocardium excised after storage periods for up to 42 h showed complete recovery when BDM was applied. In contrast HTK perfusion allowed complete recovery of these parameters when the storage period did not exceed 6 hours. CONCLUSION: Under the given experimental conditions reversible desensitization of the contractile apparatus for calcium results in a considerable prolongation of the tolerance to cold ischemia in explanted pig hearts. The present study shows that the protective effects of BDM are not only present when isolate muscle fibres were stored (and the extracellular space is large) but also after storage of complete hearts in a solution in a solution containing BDM. Thus BDM may become a useful agent to enlarge the storage period of donor hearts in heart transplatation considerably.

Animals↗

PubMed1994

Reversible desensitization of the myocardial contractile apparatus for calcium. A new concept for improving tolerance to cold ischemia in human myocardium?

UNLABELLED: The influence of 2,3-Butanedione monoxime (BDM) on the human myocardium's tolerance to cold ischemia was analyzed in two experimental series. METHODS: I) Left ventricular human muscle fibers (0.6 x 4.0 mm) were obtained from recipient hearts (n = 10) and loaded with the fluorescent dye Fura-2. Simultaneous measurements of intracellular calcium transients ("ratio-method"; excitation wave lengths: 340 nm and 380 nm) and isometric force development of electrically driven (1 Hz) muscle fibers were carried out at BDM concentrations ranging from 0 to 30 mM at a bath temperature of 37 degrees C; II) Left ventricular human muscle strips were obtained from beating recipient hearts (n = 10), and right atrial fibers from patients operated upon for aortic valve stenosis or combined mitral valve disease (n = 14). Muscle strips of these hearts were incubated for parallel measurements in the following solutions: a) a 37 degrees C oxygenated Krebs-Henseleit solution (KHS), b) a 4 degrees C Bretschneider's cardioplegic solution (HTK) without oxygenation and c) a 4 degrees C KHS containing 30 mM BDM without oxygenation (BDM solution). After standardized time intervals the muscle fibers were removed from the storage solutions, reperfused in KHS solution at 37 degrees C and stretched to optimal length (supramaximal electrical stimulation). After obtaining a steady state of force development, the contractile behavior under isometric and isotonic measurement conditions was measured. The influence of the incubation periods and the incubation solution was analyzed. RESULTS: I) BDM reduced the isometric force development of the electrically driven isolated human myocardial muscle strip in a dose-dependent way.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗

PubMedDate not supplied

Delayed chronic type A dissection following CABG: implications for evolving techniques of revascularization.

BACKGROUND: Postoperative dissection in some patients is related to manipulation of the aorta and accounts for 3% to 5% of deaths after cardiac surgery. METHODS: Between 1987 and 1999, 109 patients with previous cardiac operations were treated for chronic type A dissection. In 31 of the patients, the etiology was related to aortic manipulation. Twenty-one patients (17 men, 4 women; 67+/-13 years of age) had isolated coronary artery bypass grafting (CABG) as their first operation and were reviewed. The interval between operations was 52.9+/-47.3 months. RESULTS: Reoperation was elective in 11 patients, urgent in 10 patients. Median maximal aortic diameter was 6.8+/-2.1 cm; 9 patients had major aortic insufficiency. The intimal tear was at the partial occlusion clamp site in 12 patients (57.1%), at the cross-clamping site in 4 patients (19.1%), and at the proximal anastomosis in 1 patient (4.8%); 4 patients (19.1%) had multiple tears at several sites. Cystic media necrosis was present in 9.5% of the patients, severe atherosclerosis in 47.6% of the patients, and 42.9% of the patients had both. Nine patients (42.9%) underwent a modified Bentall procedure, 12 patients (57.1%) underwent a supracoronary anastomosis, and all had open distal anastomosis. There were two (9.5%) hospital deaths and three (14.3%) postoperative strokes. Freedom from cardiac or aorta-related mortality was 85.7% at a mean follow-up of 49.3 months. CONCLUSIONS: In patients who develop type A dissection of the aorta after previous CABG, the intimal tear most often is at partial occlusion clamp site. This complication is associated with morbidity and mortality. It remains to be seen whether the use of partial occlusion clamps on the pulsating and often diseased aorta during off-pump coronary artery bypass (OPCAB) will increase the risk of delayed iatrogenic dissections.

Aged↗