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A Geppert

Publications and source records attributed to A Geppert.

At least 19 recordsLinked to original sources

[Pacemaker dysfunction in the clinical practice].

Lead dysfunction is still the predominant cause of pacemaker dysfunction. Beyond lead dysfunction clinicians might encounter problems resulting from the surgical procedure of pacemaker implantation, from specific programmable pacemaker functions (e.g. undersensing of premature ventricular complexes when autosensing is activated) and from interference with electromagnetic fields. Electromagnetic interference between pacemakers and mobile phones has been demonstrated both in vitro and in vivo, but in daily life pacemaker patients can readily use mobile phones when certain security measures are taken into account. Electromagnetic interference between anti-theft devices and pacemakers can arise from situations where the pacemaker is in close proximity to the anti-theft device, but in daily life these interferences are rare. The electromagnetic fields generated during magnetic resonance imaging (MRI) are considerably stronger than those generated by mobile phones or anti-theft devices, therefore permanent pacemakers are still considered a contraindication for MRI, although several case reports have recently been published that reported on uneventful MRI procedures in pacemaker patients. The present review summarizes the current knowledge on the most frequent pacemaker dysfunctions and electromagnetic interferences that might be relevant in clinical practice.

Cardiac Surgical Procedures↗

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↗

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↗

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↗

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↗

Liver penetration by a duodenal ulcer in a young woman.

Liver penetration is a rare but serious complication of peptic ulcer disease. We report a case of a 33-year-old woman who took large doses of nonsteroidal antiinflammatory drugs and developed a giant duodenal ulcer that penetrated into her liver. The diagnosis was based on histologic examination of endoscopic biopsies. She was initially treated with a proton pump inhibitor, but, within 5 weeks, she developed a symptomatic postbulbar stricture that required surgical correction. We also review 11 other reported cases of endoscopically and histologically diagnosed peptic ulcer penetration into the liver.

Adult↗

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↗

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↗

Transient swallow syncope during periods of hypoxia in a 67-year-old patient after self-extubation.

OBJECTIVE: To describe the case of an adult patient with swallow syncope after bypass surgery, possibly related to hypoxia. DESIGN: Case report. SETTING: University hospital, medical-cardiologic intensive care unit. PATIENT: A 67-yr-old patient after second aortocoronary bypass operation for unstable angina. MAIN RESULTS: After the patient managed to extubate himself, he was in a borderline respiratory condition with an oxygen mask. When drinking for the first time after extubation, asystole was observed coincidentally with interruption of oxygen insufflation. During the next days, similar events occurred during food ingestion or when drinking liquids after a fall of oxygen saturation. The bradyarrhythmia was readily reversible on administration of atropine and ventricular backup pacing via temporary pacing wires. After normalization of gas exchange, no more episodes of swallowing-associated asystole were observed and the patient was discharged without a permanent pacemaker. There was no esophageal or gastrointestinal disease. Pre- and postoperative PR and QRS durations were normal. CONCLUSION: Extrinsic and transient mechanisms, rather than intrinsic conduction system disease, seem to have been operative in this case. It is suggested that hypoxia reinforced the vagal pharyngocardiac reflex as described in pediatric patients.

Adult↗

Soluble selectins and the systemic inflammatory response syndrome after successful cardiopulmonary resuscitation.

OBJECTIVE: Elevated cytokine levels have been reported after ischemia/reperfusion injury and might cause a systemic inflammatory response syndrome (SIRS) after successful cardiopulmonary resuscitation (CPR). It is unknown whether patients with SIRS after CPR exhibit higher levels of soluble adhesion molecules than patients without SIRS and whether SIRS or elevation of adhesion molecules is associated with outcome after CPR. We analyzed the relationships among various CPR-related variables, plasma levels of E- and P-selectin, the occurrence of SIRS after CPR, and the development of sepsis and outcome. DESIGN: Prospective, controlled study. SETTING: Intensive care unit at a university hospital. PATIENTS: A total of 25 patients on the second day after successful CPR and 7 non-critically ill control patients. INTERVENTIONS: Blood sampling for determination of plasma levels of soluble (s) E- and P-selectin. MEASUREMENTS AND MAIN RESULTS: SIRS was a frequent finding after CPR (66% of all patients) unrelated to time until return of spontaneous circulation (SIRS, 17+/-13 mins; no SIRS, 19+/-16 mins; p = .761), epinephrine dose (SIRS, 4+/-5 mg; no SIRS, 5+/-6 mg; p = .906), or serum lactate level after CPR (SIRS, 8.6+/-2.6 mmol/L; no SIRS, 8.7+/-4.0 mmol/L; p = .174). sP-selectin levels were higher in patients with SIRS (291.7+/-227.4 ng/mL) compared with patients without SIRS (113.4+/-88.4 ng/mL; p = .018) or with non-critically ill patients (116.9+/-33.4 ng/mL; p = .031). Compared with non-critically ill control patients (42.8+/-19.4 ng/mL), sE-selectin levels were higher in patients with (96.2+/-47.3 ng/mL; p = .023) and without SIRS (99.5+/-65.7 ng/mL; p = .030). sP-selectin was higher in patients developing sepsis within 1 wk after CPR (n = 9) than in patients without sepsis (350.2+/-233.4 ng/mL vs. 158.5+/-157.8 ng/mL; p = .022) and sE-selectin levels were higher in nonsurvivors (n = 5) than in survivors (144.2+/-62.4 ng/mL vs. 85.7+/-45.3 ng/mL; p = .025) whereas SIRS was unrelated to the development of sepsis (p = .4) and unrelated to survival (p = .4). CONCLUSIONS: SIRS is an unspecific finding after CPR with only minor impact on outcome. Determination of sP- and sE-selectin early after CPR might help to identify patients at a high risk for sepsis or for an adverse outcome, respectively.

Adult↗

IV milrinone for cardiac output increase and maintenance: comparison in nonhyperdynamic SIRS/sepsis and congestive heart failure.

OBJECTIVE: To characterize the effect of the phosphodiesterase inhibitor (PDEI) milrinone in adult patients with a non-hyperdynamic condition during the course of the systemic inflammatory response syndrome (SIRS) or sepsis when compared with patients with congestive heart failure (CHF). PDEIs are potent inhibitors of cytokine production and expression. We hypothesized that there might be an outstanding beneficial effect of PDEIs in the setting of SIRS/sepsis. DESIGN: Prospective, open labeled, protocol-driven pilot study. PATIENTS: Nine patients with a nonhyperdynamic hemodynamic condition during SIRS/sepsis (group 1) and seven patients with CHF (group 2) requiring inotropic support. All patients were having heart disease. All patients had a combination of various catecholamines at the time of inclusion in the study and had received fluid resuscitation to an extent that left ventricular stroke work index (LVSWI) did not increase further. INTERVENTION: Milrinone infusion at a rate of 0.5 microg/kg per min in addition to preexisting catecholamine therapy. MEASUREMENTS AND RESULTS: Measurements of cardiac index (CI; thermodilution) and calculation of vascular resistance and LVSWI was done every 8 h for at least 40 h during milrinone infusion. CI and LVSWI significantly increased in both groups (p < 0.001 and p = 0.006, respectively). There were no significant differences between groups in these parameters (p > 0.11 and p > 0.13, respectively). The LVSWI increase occurred while there was a decrease in pulmonary capillary wedge pressure, suggesting a true and comparable improvement in cardiac function relatively independent of loading conditions. Preexisting catecholamines had to be increased in both groups (NS). Milrinone had to be discontinued in one patient due to hypotension. CONCLUSION: Milrinone administration is feasible in selected patients with a non-hyperdynamic condition during SIRS/sepsis and with preexisting heart disease. Under the conditions of this study, milrinone was no better in terms of CI and LVSWI maintenance in septic cardiac dysfunction when compared with CHF. These results do not necessarily extend to other cohorts with no preexisting heart disease.

Adult↗

Immunofluorescent analysis of antibodies against neurons in the case of paraneoplastic syndrome.

The authors report clinical and neuropathological findings especially immunofluorescent detection of antineuronal antibodies in the case of paraneoplastic syndrome in course of the small-cell lung carcinoma. The clinical symptoms, observed in 48-year-old woman, covered bilateral pyramidal syndrome, cerebellar syndrome, myasthenic syndrome and impairment of the cranial nerves. Neuropathological investigation revealed paraneoplastic encephalopathy in the form of encephalitis. Immunofluorescent analysis showed brightly fluorescent neurons standing out against a dull background.

Antibodies, Neoplasm↗

Extensive necrotizing fasciitis in a diabetic patient.

Necrotizing fasciitis is a rare but life-threatening infection of the subcutaneous tissue. In addition to Group A streptococci, polymicrobial infection with various aerobic and anaerobic gram positive or gram negative bacteria is frequently observed. The present case illustrates that a high level of clinical suspicion is necessary for early diagnosis of this disease and confirms the value of computed tomography in patients with sepsis of unknown origin. Because of rapid progression of the disease early debridement of necrotic tissue is mandatory for survival.

Anti-Bacterial Agents↗

Concentration of endogenous tPA antigen in coronary artery disease: relation to thrombotic events, aspirin treatment, hyperlipidemia, and multivessel disease.

Tissue plasminogen activator (tPA) is the major plasminogen activator responsible for dissolving blood clots found in blood vessels. However, elevated concentrations of tPA antigen were found to be related to adverse events in patients with coronary artery disease (CAD). Considerable controversy about the significance of these results exists. The goal of this cross-sectional study was to identify independent determinants for tPA antigen concentrations in patients with CAD, to possibly clarify the above paradoxical relationship. The baseline tPA antigen concentrations of 366 patients with angiographic evidence of coronary sclerosis were determined. Univariate analysis showed that age (P=0.013), angiographic extent of disease (P<0.001), presence of angina at rest (P<0.001), diabetes mellitus (P=0.004), hypercholesterolemia (P=0. 045), hypertriglyceridemia (P=0.015), and chronic intake of nitrates (P<0.001) were significantly and positively related to tPA antigen concentration, while the chronic intake of aspirin was inversely related to tPA antigen (P<0.001). In addition, plasminogen activator inhibitor type 1 (PAI-1) activity was found to be significantly and positively associated with tPA antigen concentration (P<0.001). A multivariate analysis identified chronic low-dose aspirin therapy (P<0.001), PAI-1 activity (P<0.001), hypertriglyceridemia (P=0.005), the type of angina (P=0.026), multivessel disease (P=0.041), and hypercholesterolemia (P=0.043) as significant and independent determinants of tPA antigen. While hypertriglyceridemia and hypercholesterolemia both are related to the underlying disease, the type of angina and the number of involved vessels are linked to the severity and extent of disease, and all of them are indicators of a prothrombotic state found during the progression of CAD. In contrary, low-dose aspirin rather would decrease the likelihood of thrombotic events. The relation of tPA antigen to PAI-1 activity furthermore underlines the relation between tPA antigen concentration and a prothrombotic state. Therefore, the positive or-in case of aspirin therapy-negative correlation of these parameters with tPA antigen concentration would indicate that thrombus formation and simultaneous endothelial cell activation might be major determinants for tPA antigen concentration in CAD.

Adult↗