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Biomedical subjects

G Heinz

Publications and source records attributed to G Heinz.

At least 19 recordsLinked to original sources
PubMed2006

Improvement of cognitive functions in chronic schizophrenic patients by recombinant human erythropoietin.

Schizophrenia is increasingly recognized as a neurodevelopmental disease with an additional degenerative component, comprising cognitive decline and loss of cortical gray matter. We hypothesized that a neuroprotective/neurotrophic add-on strategy, recombinant human erythropoietin (rhEPO) in addition to stable antipsychotic medication, may be able to improve cognitive function even in chronic schizophrenic patients. Therefore, we designed a double-blind, placebo-controlled, randomized, multicenter, proof-of-principle (phase II) study. This study had a total duration of 2 years and an individual duration of 12 weeks with an additional safety visit at 16 weeks. Chronic schizophrenic men (N=39) with defined cognitive deficit (>or=1 s.d. below normal in the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)), stable medication and disease state, were treated for 3 months with a weekly short (15 min) intravenous infusion of 40,000 IU rhEPO (N=20) or placebo (N=19). Main outcome measure was schizophrenia-relevant cognitive function at week 12. The neuropsychological test set (RBANS subtests delayed memory, language-semantic fluency, attention and Wisconsin Card Sorting Test (WCST-64) - perseverative errors) was applied over 2 days at baseline, 2 weeks, 4 weeks and 12 weeks of study participation. Both placebo and rhEPO patients improved in all evaluated categories. Patients receiving rhEPO showed a significant improvement over placebo patients in schizophrenia-related cognitive performance (RBANS subtests, WCST-64), but no effects on psychopathology or social functioning. Also, a significant decline in serum levels of S100B, a glial damage marker, occurred upon rhEPO. The fact that rhEPO is the first compound to exert a selective and lasting beneficial effect on cognition should encourage new treatment strategies for schizophrenia.

Adult↗
PubMed2003

Target site bacterial killing of cefpirome and fosfomycin in critically ill patients.

We employed an in-vivo pharmacokinetic/in-vitro pharmacodynamic method to simulate bacterial killing in plasma and the interstitium of skeletal muscle tissue after intravenous administration of 2 g of cefpirome and 8 g of fosfomycin alone and in combination to patients with sepsis. Interstitial antimicrobial concentrations were determined by use of in-vivo microdialysis. CFU/ml of Staphylococcus aureus (ATCC 29213) and Pseudomonas aeruginosa (clinical isolate) decreased by approximately 2log(10) for plasma and muscle tissue 6 h after cefpirome and fosfomycin administration compared with the baseline, respectively. The simulation of plasma and tissue pharmacokinetics for the combined administration of these antibiotics resulted in complete eradication of S. aureus within 5 h after drug exposure. No bacterial re-growth occurred in any of the simulations within 6 h. The in-vitro simulation of in-vivo plasma and tissue pharmacokinetics of cefpirome and fosfomycin has shown that both antimicrobial agents kill S. aureus and P. aeruginosa strains effectively after single dose administration. This effect was most pronounced by the combined use of these antimicrobial agents. Therefore, this data corroborates antimicrobial strategies of simultaneous administration of cefpirome and fosfomycin in patients with severe soft tissue infection.

Anti-Bacterial Agents↗
PubMed2003

Hemodynamic effects of a continuous infusion of levosimendan in critically ill patients with cardiogenic shock requiring catecholamines.

BACKGROUND: Levosimendan, a novel inodilator, has been shown to improve hemodynamic function in patients with decompensated heart failure with preserved arterial blood pressure. Data on its use in patients with cardiogenic shock are rare. The present series describes the 24-h hemodynamic effects of levosimendan as add-on therapy in desperately ill patients with cardiogenic shock requiring catecholamines. METHODS: Ten patients with cardiogenic shock received levosimendan as continuous infusion of 0.1 microg kg(-1) min(-1) for 24 h. The patients were otherwise unselected. Hemodynamic measurements were routinely performed at baseline (time 0) and at 1, 8, 16 and 24 h after start of levosimendan (LS) using a Swan-Ganz thermodilution catheter. RESULTS: During the levosimendan infusion there was a significant increase in cardiac index from 1.8 +/- 0.4 to 2.4 +/- 0.6 L*min-1*m-2 (P = 0.023) and a significant decrease in systemic vascular resistance from 1559 +/- 430 to 1109 +/- 202 dyn*s*cm-5 (P = 0.001), respectively. Changes in catecholamine dose, and in systolic and diastolic blood pressure were not significant. Given the individual response to LS, 8/10 patients showed an increase in left ventricular stroke work index under reduced or roughly unchanged preload conditions after 8 h. CONCLUSION: This series shows that a LS infusion is feasible and able to improve hemodynamics in severely compromized, critically ill patients with cardiogenic shock requiring catecholamine therapy. Its potential advantages when compared with other inotropes are unclear. To clarify the potential role of LS in this clinical setting randomized controlled trials on hemodynamic and mortality endpoints are needed.

Aged↗
PubMed2003

Prophylactic anticoagulation with enoxaparin: Is the subcutaneous route appropriate in the critically ill?

BACKGROUND: Subcutaneously administered low-molecular-weight heparins are widely used for prevention of venous thromboembolism. The appropriateness of the subcutaneous route in critically ill patients has never been established. OBJECTIVE: To determine anti-Xa activities in critically ill patients and in noncritically ill patients receiving prophylactic doses of subcutaneous enoxaparin. DESIGN: Prospective, controlled, open-labeled study. SETTING: Tertiary medical-cardiologic-postoperative intensive care unit and a general medical ward at a university hospital. PATIENTS: A total of 16 intensive care unit patients (group 1; age, 61.1 +/- 16 yrs; male/female ratio, 7/9; Acute Physiology and Chronic Health Evaluation II score, 20.9 +/- 7; mechanical ventilation, n = 15; vasopressors, n = 13) and 13 noncritically ill medical patients (group 2; age, 61.7 +/- 9 yrs; male/female ratio, 7/6) were studied. Body mass index (25.7 +/- 5 vs. 24 +/- 6 kg/m2, p = not significant) was comparable and serum creatinine levels (0.83 +/- 0.25 vs. 1.07 +/- 0.3 mg/dL, group 1 vs. 2) were within the normal range in both groups. Patients with impaired renal function, receiving hemofiltration, or requiring therapeutic anticoagulation were not eligible. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Anti-Xa activities were determined at 0, 1, 3, 6, and 12 hrs after a single daily subcutaneous dose of 40 mg enoxaparin on day 1 and at 3 hrs after 40 mg of enoxaparin on days 2-5. Mean anti-Xa levels at 0 to 12 hrs were consistently lower in group 1 compared with group 2 by analysis of variance (p =.001 between groups and over time), as was the area under the curve at 0 to 12 hrs (2.6 +/- 1 vs. 4.2 +/- 1.7 units x mL(-1) x hr(-1), group 1 vs. 2, p =.008). Significant differences in anti-Xa activity were also found on days 2-5 (p =.001). Peak anti-Xa activities at 3 hrs after administration were negatively correlated with the body mass index (r = -.41, p <.03). No correlation was found between the anti-Xa activity at 3 hrs and the dose of norepinephrine (r =.12, p =.7). CONCLUSION: Critically ill patients with normal renal function demonstrated significantly lower anti-Xa levels in response to a single daily dose of subcutaneous enoxaparin when compared with medical patients in the normal ward.

Aged↗
PubMed2003

Relevance of soft-tissue penetration by levofloxacin for target site bacterial killing in patients with sepsis.

Antimicrobial therapy of soft tissue infections in patients with sepsis sometimes lacks efficiency, despite the documented susceptibility of the causative pathogen to the administered antibiotic. In this context, impaired equilibration between the antibiotic concentrations in plasma and those in tissues in critically ill patients has been discussed. To characterize the impact of tissue penetration of anti-infective agents on antimicrobial killing, we used microdialysis to measure the concentration-versus-time profiles of levofloxacin in the interstitial space fluid of skeletal muscle in patients with sepsis. Subsequently, we applied an established dynamic in vivo pharmacokinetic-in vitro pharmacodynamic approach to simulate bacterial killing at the site of infection. The population mean areas under the concentration-time curves (AUCs) for levofloxacin showed that levofloxacin excellently penetrates soft tissues, as indicated by the ratio of the AUC from time zero to 8 h (AUC(0-8)) for muscle tissue (AUC(0-8 muscle)) to the AUC(0-8) for free drug in plasma (AUC(0-8 plasma free)) (AUC(0-8 muscle)/AUC(0-8 plasma free) ratio) of 0.85. The individual values of tissue penetration and maximum concentration (C(max)) in muscle tissue were highly variable. No difference in bacterial killing of a select Staphylococcus aureus strain for which the MIC was 0.5 microg/ml was found between individuals after exposure to dynamically changing concentrations of levofloxacin in plasma and tissue in vitro. In contrast, the decrease in the bacterial counts of Pseudomonas aeruginosa (MIC = 2 microg/ml) varied extensively when the bacteria were exposed to levofloxacin at the concentrations determined from the individual concentration-versus-time profiles obtained in skeletal muscle. The extent of bacterial killing could be predicted by calculating individual C(max)/MIC and AUC(0-8 muscle)/AUC(0-8 plasma free) ratios (R = 0.96 and 0.93, respectively). We have therefore shown in the present study that individual differences in the tissue penetration of levofloxacin may markedly affect target site killing of bacteria for which MICs are close to 2 microg/ml.

Aged↗
PubMed2001

Soluble selectins in the pulmonary and systemic circulation in acute cardiogenic and non-cardiogenic pulmonary failure.

OBJECTIVE: Pulmonary endothelial activation caused by high pulmonary capillary pressures may be involved in the pathogenesis of cardiogenic pulmonary edema (CPE). We studied soluble selectins and soluble ICAM-1 as markers of cell activation in the systemic and pulmonary circulation of patients with respiratory failure (RF) due to CPE (RFCPE) as compared to patients with RF due to pulmonary infection (RFPI). SETTING: Cardiovascular Intensive Care Unit at a university hospital. PATIENTS: Twenty patients with RFCPE, 20 patients with RFPI and 17 critically ill patients without RF. INTERVENTIONS: Blood samples were obtained from the arterial and the pulmonary capillary circulation and sE-, sL-, and sP-selectin as well as sICAM-1 were determined. To distinguish between systemic and pulmonary endothelial activation, transpulmonary gradients (concentrationarterial blood - concentrationpulmonary capillary blood) were calculated. RESULTS: Systemic concentration of sL-selectin was lower in patients with RFCPE and RFPI than in patients without RF (RFCPE: 719.0 +/- 243.9 ng/ml, RFPI: 528.5 +/- 220.8 ng/ml, no RF: 882.4 +/- 222.6 ng/ml; P < 0.001). Systemic concentrations of ICAM-1, sE- and sP-selectin were not significantly different between the three groups. Transpulmonary gradients in sE- and sL-selectin were predominantly negative in patients with RFCPE (-3.2 +/- 7.8 ng/ml and -55.4 +/- 116.1 ng/ml, respectively) and RFPI (-2.3 +/- 5.8 ng/ml and -17.6 +/- 40.3 ng/ml, respectively) but were predominantly positive in patients without RF (11.6 +/- 7.2 ng/ml and 66.6 +/- 69.6 ng/ml, respectively), which suggests trapping of sE- and sL-selectin in the pulmonary circulation in the majority of patients with RFPI as well as in the majority of patients with RFCPE. CONCLUSION: Pulmonary endothelial activation occurs during both RFCPE and RFPI. This adds evidence that, besides hydrostatic mechanisms, cell activation occurs during CPE.

Acute Disease↗
PubMed2001

Incidence and type of cardiac arrhythmias in critically ill patients: a single center experience in a medical-cardiological ICU.

OBJECTIVE: To determine the frequency and types of significant, sustained arrhythmias in a mixed ICU. DESIGN AND SETTING: Prospective, observational study in a medical-cardiological-postoperative ICU at a university hospital. PATIENTS: 133 consecutive patients with arrhythmias. MEASUREMENTS AND RESULTS: All patients had continuous ECG monitoring and automatic arrhythmia detection. We assessed: (a) sustained (>30 s) tachyarrhythmias; (b) all tachyarrhythmias requiring therapy; (c) bradycardias of fewer than 40 beats/min or requiring intervention. There were 310 arrhythmia episodes: 278 tachyarrhythmias (108 narrow-QRS complex, 168 wide-QRS complex; 179 regular, 97 irregular) and 32 bradycardias. Of the 278 tachycardias in 54 patients, 135 (48.6%) were ventricular. There were 13 episodes of torsade de pointes (4.67%) in five patients. Of the 278 tachycardiac episodes 83 were atrial fibrillation (29.8%, 63 patients), 10 atrial flutter (3.6%, 8 patients), 21 supraventricular tachycardias (7.55%, 7 patients), and 2 ectopic junctional tachycardia (0.72%, 1 patient). The number of patients showing significant arrhythmias was comparable over the years (11-12/1996: 4/28 [14.3], 1997: 52/302 [17.2%], 1998: 55/286 [19.2%], 22/140 [15.7%] 1-7/1999). The ICU stay was significantly longer in arrhythmia patients than in 623 patients without arrhythmias (median 4 vs. 14 days), and there was a trend towards higher mortality (40/133, 30.8%, vs. 132/623, 21.2%, P=0.061, log-rank). CONCLUSION: Only one-fifth of patients in this mixed ICU had significant arrhythmias, taking a contemporary definition of arrhythmias. Ventricular tachycardia and atrial fibrillation were the most frequent arrhythmias.

APACHE↗
PubMed2001

Effect of MTHFR genotypes and hyperhomocysteinemia on patient and graft survival in kidney transplant recipients.

BACKGROUND: The total homocysteine (tHcy) plasma level, which is partly determined by the MTHFR 677C-->T genotype, may be associated with vascular disease. We prospectively examined the influence of MTHFR genotypes (677C-->T, 1298A-->C) and tHcy plasma concentration on all cause mortality and graft outcomes of renal transplant recipients. METHODS: Baseline tHcy plasma levels of 189 patients (three groups with either the MTHFR 677CC, CT or TT genotype, including 63 patients in each group, were matched for age, gender, body mass index and creatinine clearance at baseline), were obtained between September 1996 and May 1997. Follow-up data (time until return to dialysis therapy, time and cause of death) were collected from April to June 1999. Kaplan-Meier survival estimations were calculated and plotted, the groups (three MTHFR 677C-->T genotype groups, or three MTHFR 1298A-->C genotype groups, or two groups with tHcy plasma levels above/below 15 micromol/L) were compared by log-rank test. Age, gender, body mass index (BMI), time since transplantation, serum creatinine, creatinine clearance, combined MTHFR 677C-->T/1298A-->C genotypes, tHcy, folate and vitamin B12 plasma levels were evaluated with regard to graft and patient survival in a multivariate Cox-proportional hazard regression model. RESULTS: During the follow-up period of 2.26 +/- 0.66 years, 9 patients died (5 in the TT, 2 in the CT and 2 in the CC genotype group; P = 0.34) and 22 returned to dialysis treatment (7 in the TT, 9 in the CT and 6 in the CC genotype group; P = 0.65). There was also no influence of MTHFR 1298A-->C genotypes (AA genotype, 114 patients; AC genotype, 64 patients; CC genotype, 11 patients) on patient or graft survival (P = 0.7087 and P = 0.1633, respectively). Two of 93 patients with a tHcy plasma level < or = 15 micromol/L died, in contrast to 7 of 96 patients in the tHcy > 15 micromol/L group, P = 0.0778. Two patients in the low tHcy group had to return to dialysis, in contrast to 20 patients in the high tHcy group (P = 0.0001). In the multivariate model there was no significant predictor of patient survival, and the serum creatinine was the only predictor of graft survival (P < 0.0001). CONCLUSIONS: In summary, our study shows that neither MTHFR 677C-->T/1298A-->C genotypes nor hyperhomocysteinemia are independently associated with patient or graft survival following kidney transplantation.

5,10-Methylenetetrahydrofolate Reductase (FADH2)↗
PubMed2001

Association of two MTHFR polymorphisms with total homocysteine plasma levels in dialysis patients.

The effect of the combined 5,10-methylenetetrahydrofolate reductase (MTHFR) 677C-->T and 1298A-->C genotype on total homocysteine (tHcy), folate, and vitamin B(12) plasma levels was investigated in 983 subjects, including 415 hemodialysis patients, 179 peritoneal dialysis patients, and 389 healthy individuals. Mean tHcy plasma concentrations were 27.2 +/- 15.8 micromol/L in hemodialysis patients, 25.4 +/- 19.1 micromol/L in peritoneal dialysis patients, and 8.9 +/- 3.5 micromol/L in healthy individuals. Hyperhomocysteinemia (tHcy > 15 micromol/L) was detected in 81.6% of patients and 2.6% of controls. Multiple stepwise regression analysis showed that the MTHFR 677C-->T/1298A-->C genotype (CC/AA, CC/AC, CC/CC, CT/AA, CT/AC, TT/AA), vitamin use, age, folate and vitamin B(12) plasma level were significant predictors of tHcy plasma levels. Analysis of variance showed that this effect of MTHFR genotypes on tHcy level was caused by significantly greater tHcy levels in 677TT/1298AA hemodialysis and peritoneal dialysis patients versus other genotypes. Compound heterozygous controls (677CT/1298AC genotype) had significantly greater tHcy levels compared with 677CC/1298AA controls. There was no major effect of MTHFR polymorphisms on folate and vitamin B(12) plasma concentrations. This study shows that the MTHFR 677TT/1298AA genotype, but not the 677CT/1298AC genotype, is a significant predictor of tHcy plasma levels in dialysis patients.

Adult↗
PubMed2001

Amiodarone versus diltiazem for rate control in critically ill patients with atrial tachyarrhythmias.

OBJECTIVE: To compare the rate-lowering effect of diltiazem and two amiodarone regimens in critically ill patients with recent-onset atrial tachyarrhythmias. DESIGN: Prospective, randomized, controlled study. SETTING: Medical cardiologic intensive care unit in a university hospital. PATIENTS: Sixty critically ill patients (Acute Physiology and Chronic Health Evaluation [APACHE] III score 70 +/- 30, age 67 +/- 10 yrs). INTERVENTIONS: Patients with atrial fibrillation (n = 57), atrial flutter (n = 2), or atrial tachycardia (n = 1, and a heart rate consistently >120 beats/min over 30 mins were randomly assigned to one of three intravenous treatment regimens. Group 1 received diltiazem in a 25-mg bolus followed by a continuous infusion of 20 mg/hr for 24 hrs, group 2 received amiodarone in a 300-mg bolus, and group 3 received amiodarone in a 300-mg bolus followed by 45 mg/hr for 24 hrs. MEASUREMENTS AND MAIN RESULTS: The primary study end point was a >30% rate reduction within 4 hrs. The secondary study end point was a heart rate <120 beats/min (a patient was considered to have uncontrolled tachycardia if heart rate was >120 beats/min 4 hrs after study drug). The primary study end point was achieved in 14/20 (70%), 11/20 (55%), and 15/20 (75%) of patients in groups 1, 2, and 3, respectively (chi2 = 1.95, p =.38). Uncontrolled tachycardia was more frequently observed in group 2 (0/20, 9/29 [55%], and 1/20 [5%] of patients in groups 1, 2, and 3, respectively; chi2 = 17, p =.00016). In patients achieving tachycardia control, diltiazem showed a significantly better rate reduction (p =.0001 group 1 vs. group 3, p =.0001 over time; p =.0001 group 1 vs. group 2, p =.001 over time) when compared with the amiodarone groups. Premature drug discontinuation due to hypotension was required significantly more often in group 1 (6/20 [30%], 0/20, and 1/20 [5%] for groups 1, 2, and 3, respectively; chi2 = 10, p =.01). CONCLUSION: Sufficient rate control can be achieved in critically ill patients with atrial tachyarrhythmias using either diltiazem or amiodarone. Although diltiazem allowed for significantly better 24-hr heart rate control, this effect was offset by a significantly higher incidence of hypotension requiring discontinuation of the drug. Amiodarone may be an alternative in patients with severe hemodynamic compromise.

APACHE↗
PubMed2001

Plasminogen activator inhibitor type 1 and outcome after successful cardiopulmonary resuscitation.

OBJECTIVE: Patients after successful cardiopulmonary resuscitation have been shown to exhibit elevated plasma concentrations of plasminogen activator inhibitor (PAI) type 1, the main circulating antifibrinolytic protein. It has been suggested that elevations in PAI-1 contribute to cerebral no-reflow after successful cardiopulmonary resuscitation. We analyzed whether PAI-1 concentrations might predict cerebral outcome after cardiopulmonary resuscitation. DESIGN: Prospective, controlled study. SETTING: Intensive care unit at a university hospital. PATIENTS: Thirty-five patients after successful cardiopulmonary resuscitation and 35 control patients who were not critically ill. INTERVENTIONS: Blood sampling for determination of plasma concentrations of active and total PAI-1 antigen. MEASUREMENTS AND MAIN RESULTS: Plasma concentrations of total and active PAI-1 antigen on the second day after successful cardiopulmonary resuscitation were significantly higher in patients after cardiopulmonary resuscitation than in controls (p <.0001) and were unrelated to duration of cardiopulmonary resuscitation. Both active and total PAI-1 antigen were higher in patients who developed acute renal failure after cardiopulmonary resuscitation. Patients with an unfavorable cerebral outcome after cardiopulmonary resuscitation had higher total PAI-1 antigen concentrations compared with patients with good outcome after cardiopulmonary resuscitation (p =.026). We identified 180 ng/mL as the best cutoff value for total PAI-1 antigen with respect to cerebral outcome (chi-square 11.8, p =.001). In a logistic regression analysis, only systemic inflammatory response syndrome (p =.028), acute renal failure after cardiopulmonary resuscitation (p =.017), and cardiopulmonary resuscitation duration >15 mins (p =.042) were significantly and independently associated with cerebral outcome after cardiopulmonary resuscitation. Total PAI-1 antigen reached only borderline significance (p =.058) but nevertheless slightly improved the correct prediction of cerebral outcome after cardiopulmonary resuscitation. CONCLUSIONS: Acute renal failure after cardiopulmonary resuscitation, systemic inflammatory response syndrome, and cardiopulmonary resuscitation duration are better predictors of cerebral outcome after cardiopulmonary resuscitation than PAI-1 antigen, but determination of total PAI-1 antigen nevertheless might improve the early prediction of cerebral outcome after cardiopulmonary resuscitation. Whether elevated PAI-1 concentrations, possibly via prothrombogenic/antifibrinolytic effects, contribute causally to cerebral no-reflow and acute renal failure after cardiopulmonary resuscitation remains to be clarified.

Acute Kidney Injury↗
PubMed2000

Successful emergency percutaneous cardiopulmonary support during coronary intervention in an 80-year old patient.

In an 80-year old patient with acute coronary syndrome emergency institution of stand-by percutaneous cardiopulmonary support (PCPS; Bio-Medicus; Medtronic Inc, Minneapolis MN) for hemodynamic collapse in the cardiac catheterization laboratory resulted in successful hemodynamic stabilization and enabled safe performance of a complex coronary intervention. Weaning from PCPS was effectuated after 4 hours total extracorporal circulation time. Despite development of a systemic inflammatory response syndrome and prolonged weaning from mechanical ventilation the patient could be discharged from the intensive care unit after 14 days and eventually from hospital another 28 days later with favorable outcome. Although an increased complication rate with prolonged rehabilitation has to be taken into account percutaneous cardiopulmonary support may constitute a live-saving option even in selected elderly patients.

Aged↗
PubMed2000

Elevation of prostate-specific markers after cardiopulmonary resuscitation.

BACKGROUND-Prostate-specific antigen (PSA), acid phosphatase (AP), and prostatic acid phosphatase (PAP) are serum markers for adenocarcinoma of the prostate gland. Previous studies indicated that prostatic ischemia may also produce elevations of PSA. Cardiopulmonary resuscitation (CPR) is frequently associated with profound tissue hypoperfusion. The present study investigated whether PSA, AP, and PAP are influenced by prolonged CPR. METHODS AND RESULTS-PSA, AP, and PAP were assessed immediately, 12 hours, 24 hours, 2 days, 3 days, 5 days, and 7 days after prolonged CPR (>5 minutes) in 14 male and 5 female patients. No changes were noted in women. In men, serum levels increased significantly after CPR and gradually decreased to near baseline values after 7 days. PSA, AP, and PAP values above the normal range were observed in 63%, 71%, and 64% of all patients, respectively. Compared with survivors, nonsurvivors exhibited higher peak serum levels of PSA (98.6+/-14.3 versus 1.1+/-2.2 mcg/L; P<0.03), AP (57.0+/-71 versus 8.6+/-8.8 U/L; P<0.05), and PAP (47.0+/-62 versus 5.7+/-8.0 U/L; P=NS). Patients with poor neurological outcome exhibited higher peak serum levels of PSA (86.4+/-135.5 versus 12.0+/-23.8 mcg/L; P<0.05), AP (50.9+/-68.1 versus 8.7+/-9.6 U/L; P=NS), and PAP (41.6+/-59.5 versus 5.8+/-8.8 U/L; P=NS) than patients with good neurological outcome. CONCLUSIONS-Prolonged CPR is frequently associated with increases of PSA, AP, and PAP serum levels. Therefore, PSA cannot be used for diagnosis of adenocarcinoma of the prostate during the first weeks after CPR. Further evaluation of these parameters as additional prognostic markers after CPR is warranted.

Acid Phosphatase↗
PubMed2000

Prospective randomised cross-over comparison of three LDL-apheresis systems in statin pretreated patients with familial hypercholesterolaemia.

Various LDL-apheresis systems have gained wider clinical acceptance in recent years to treat patients with severe familial hypercholesterolaemia, in particular in patients with coronary artery disease. For each single device data on efficacy have been provided, but up to now no comparative analysis including the novel direct adsorption of lipoproteins from whole blood has been reported. This prospectively designed cross-over comparison of three commercially available LDL-apheresis systems (immunoadsorption, IMAL; dextran sulphate adsorption, DSA; direct adsorption of lipoproteins, DALI) was performed in eight patients with homozygous (n = 3) and heterozygous (n = 5) familial hypercholesterolaemia. Removal of atherogenic lipoproteins was highly effective in all systems, for LDL-cholesterol in particular: DSA: - 84.3 +/- 6.2%; IMAL: -82.1 +/- 8.3%; DALI: -76.6 +/- 7.2% (P < 0.05 as compared DALI versus IMAL and DSA). A reduction in Lp(a) of about 63% was achieved by each device. Loss in HDL-cholesterol was highest with IMAL (-21.3 +/- 4.9%, P < 0.05) as compared to the other two treatment modalities. DSA decreased HDL-cholesterol by - 10.4 +/- 6.1% and the DALI system by -12.7 +/- 5.0%. Remarkable differences were found for the removal of fibrinogen (DSA: -29.8 +/- 14.7%, (P < 0.05 versus DALI/IMAL); IMAL: -21.4 +/- 10.1% (P < 0.05 versus DALI); DALI: -14.8 +/- 8.0%). The shortest duration for treatment was achieved by the DALI system (135 +/- 20 min, P < 0.05 versus IMAL (195 +/- 20 min) and DSA (187 +/- 29 min)). No side effects were recorded in the total of 96 treatments performed during the study. Long-term observations have yet to prove whether these differences in efficacy may be of clinical relevance.

Adsorption↗
PubMed2000

Milrinone therapy in catecholamine-dependent critically ill patients with heart failure.

BACKGROUND: Treatment with the PDE-III inhibitor milrinone improves hemodynamics in patients with heart failure. We examined whether therapy with milrinone is safe and effective in critically ill patients with catecholamine-dependent heart failure and whether treatment with milrinone facilitates weaning from prolonged catecholamine therapy. METHODS: Twenty adult patients with reduced left ventricular function and prolonged (7+/-4 days) catecholamine therapy in whom attempts at catecholamine weaning had failed were examined. Patients were prospectively randomised either to group A (addition of a fixed dose of 0.5 microg x kg(-1) x min(-1) milrinone to catecholamine therapy) or to group B (continued catecholamine therapy without milrinone). Dobutamine and norepinephrine treatment and fluid intake were titrated according to predefined hemodynamic goals. Hemodynamic parameters, fluid requirements and catecholamine dose were monitored. RESULTS: After 24 h of study treatment goup A showed a significant increase in cardiac index (2.2+/-0.4 1 min(-1) x m(-2) to 2.7+/-0.51 min(-1) x m(-2); P<0.005), a decrease in systemic vascular resistance (1,427+/-609 dyn x s x cm(-5) to 951+/-184 dyn x s x cm(-5); P<0.005), required lower doses of dobutamine (5.9+/-4.2 microg x kg(-1) x min(-1) to 2.2+/-3.3 microg x kg(-1) x min(-1); P<0.02), but showed a tendency for higher vasoconstrictor (0.14+/-0.16 microg x kg(-1) x min(-1) to 0.29+/-0.43 microg x kg(-1) x min(-1); P=n.s.) and fluid requirements (+1,404+/-2,257 ml/24 h to +2,508+/-1,873 ml/ 24 h; P=n.s.). No significant changes occurred in group B. Weaning from catecholamine therapy was more often achieved in group A and more milrinone treated patients were discharged alive from the ICU (80% vs. 30%; P<0.05). CONCLUSIONS: Milrinone improves central hemodynamics and may facilitate weaning from prolonged catecholamine support in critically ill patients with heart failure. Its administration in this subset of critically ill patients is safe, but eventually is associated with additional vasoconstrictor and fluid requirements.

Aged↗