Biomedical subjects
Publications and source records attributed to Gerhard Steinbeck.
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BACKGROUND: Randomized clinical trials have demonstrated that the use of statins in heart transplant patients lowers cholesterol levels and significantly reduces mortality and the development of transplant vasculopathy. The aim of the present study was to test these effects and the safety of statin therapy over an 8-year period. METHODS AND RESULTS: In 1991, a prospective, randomized, unmasked study was initiated to compare the efficacy of simvastatin, started on the fourth postoperative day (n=35), with that of dietary therapy alone (n=37). Because of significantly improved survival and a lower incidence of transplant vasculopathy, most patients in both groups received statins as open-label prescriptions after 4 years. After 8 years, the Kaplan-Meier survival rate was 88.6% in the simvastatin group versus 59.5% in the control group (P<0.006 by log rank; hazard ratio, 0.24; 95% CI, 0.08 to 0.71). Deaths in the simvastatin and control groups were due to transplant vasculopathy (1 versus 4; P<0.2), severe transplant rejection (1 versus 5; P<0.1), malignancies (0 versus 3; P<0.1), and other causes (2 versus 3; P<0.7). The incidence of transplant vasculopathy confirmed by angiography was 24.4% in the simvastatin group versus 54.7% in the control group (P<0.02 by log rank). There was no difference in organ function between the 2 groups. No severe adverse effects of the therapy were observed up to the end of the 8-year observation period. CONCLUSIONS: Simvastatin therapy initiated early after heart transplantation leads to significantly better 8-year survival rates and a significantly lower incidence of transplant vasculopathy without impairment of organ function or severe adverse effects.
AIMS: The aim of this pilot study was to evaluate provocative sotalol testing to unmask abnormal repolarization due to altered myocardial electrical properties as the key feature in acquired Long-QT-Syndrome. Reliable diagnosis and risk stratification for the individual patient are complicated by the multitude of mechanisms involved in acquired QT-prolongation. The combined influence of all components determines susceptibility to arrhythmias related to QT-prolongation. METHODS: Twenty consecutive patients who had experienced torsades de pointes in association with QT-prolonging drugs were tested with i.v. D,L-sotalol (2mg/kg) with 24-h intensive care monitoring to evaluate the repolarization process by determining QT- and QTc-prolongations. Results were compared to age and sex matched controls. RESULTS: At baseline, no differences between control and study population with regard to QT and QTc were detected. After sotalol infusion, QTc increased from 422+/-17 to 450+/-22ms in controls and from 434+/-20 to 541+/-37ms in the study population. Torsades de pointes occurred in three out of 20 patients (15%) in the study population but in none of the control patients following i.v. sotalol testing. CONCLUSIONS: Controlled exposure to sotalol successfully identifies patients with normal QTc intervals but altered myocardial repolarization. This may be useful for clarifying diagnosis and pathogenesis of acquired Long-QT-Syndrome.
Arrhythmogenic right ventricular dysplasia is a structural heart disease characterized by fibrofatty degeneration of right ventricular myocardium and arrhythmias of right ventricular origin. The aim of this study was to characterize endocardial right ventricular activation by electroanatomic mapping as a guide for catheter ablation in patients with arrhythmogenic right ventricular dysplasia. Electroanatomic mapping and entrainment procedures were performed in 5 patients with arrhythmogenic right ventricular dysplasia. Endocardial mapping during ventricular tachycardia demonstrated a focal activation pattern with radial spreading of activation from a site of earliest ventricular activation in all directions. Right ventricular activation time (127 +/- 34 ms) was markedly shorter than tachycardia cycle length (415 +/- 92 ms). The site of earliest ventricular activation was found in an aneurysmal outflow tract (n = 2), at the border of aneurysms near the tricuspid annulus (n = 2), and at the apex of the right ventricle (n = 1). Entrainment mapping criteria of these areas of earliest endocardial activity were consistent with exit sites of a reentrant circuit in an area of abnormal myocardium. Fractionated potentials were found 61 +/- 29 ms before the onset of the QRS complex at these sites. Catheter ablation rendered the "clinical" ventricular tachycardia noninducible in four patients but "nonclinical" faster ventricular tachycardias were inducible in three patients. During the follow-up of 7 +/- 3 months after ablation, the frequency of therapies in 4 patients with an implantable cardioverter defibrillator decreased from 49 +/- 61 episodes per month before ablation, to 0.3 +/- 0.5 episodes per month after ablation (P < 0.05). Electroanatomic mapping during ventricular tachycardia facilitates localization of exit sites in relation to aneurysms in diseased right ventricle and may guide catheter ablation in patients with arrhythmogenic right ventricular dysplasia.
The success and safety of standard catheter radiofrequency ablation may be limited for ablation of atrial fibrillation and ventricular tachycardia. The aim of this study was to characterize and compare different cooled and noncooled catheter systems in terms of their specific lesion geometry, incidence of impedance rise, and crater and coagulum formation to facilitate appropriate catheter selection for special indications. The study investigated myocardial lesion generation of three cooled catheter systems (7 Fr, 4-mm tip): two saline irrigation catheters with a showerhead-type electrode tip (sprinkler) and a porous metal tip and an internally cooled catheter. Noncooled catheters (7 Fr) had a large tip electrode (8 mm) and a standard tip electrode (4 mm). RF energy was delivered on isolated porcine myocardium superfused with heparinized pig blood (37 degrees C) at power settings of 10-40 W. Both irrigated systems were characterized by a large lesion depth (8.1 +/- 1.6 mm) and a large lesion diameter (13.8 +/- 1.6 mm). In comparison, internally cooled lesions showed a similar lesion depth (8.0 +/- 1.0 mm), but a significantly smaller lesion diameter (12.3 +/- 1.2 mm,P = 0.04). Large tip lesions had a similar lesion diameter (14.5 +/- 1.6 mm), but a significantly smaller lesion depth (6.3 +/- 1.0 mm,P = 0.002) compared to irrigated lesions. However, lesion volume was not significantly different between the three cooled and the large tip catheter. To induce maximum lesion size, power requirements were three times higher for the irrigation systems and two times higher for the internally cooled and the large tip catheter compared to the standard catheter. Impedance rise was rarest with irrigated and large tip ablation. In case of impedance rise crater formation was a frequent observation (61-93%). Irrigated catheters prevented coagulum formation most effectively. Irrigated rather than internally cooled ablation appears to be most adequate for the induction of deep and long lesions at a low rate of impedance rise and thrombus formation. Large tip ablation may be feasible for the creation of long linear lesions, however, with an increased risk of thrombus formation.
ICDs are the therapy of choice in patients with life-threatening ventricular arrhythmias. Mortality, morbidity, and complication rates including appropriate and inappropriate therapies are unknown when ICDs are used in routine medical care and not in well-defined patients included in multicenter trials. Therefore, the data of 3,344 patients (61.1 +/- 12.1 years; 80.2% men; CAD 64.6%, dilated cardiomyopathy 18.9%; NYHA Class I-III: 19.1%, 54.3%, 20.1%, respectively; LVEF > 0.50: 0.234, LVEF 0.30-0.50: 0.472, LVEF < 0.30: 0.293, respectively) implanted in 62 German hospitals between January 1998 and October 2000 were prospectively collected and analyzed as a part of the European Registry of Implantable Defibrillators (EURID Germany). The 1-year survival rate was 93.5%. Patients in NYHA Class III and aLVEF < 0.30 had a lower survival rate than patients in NYHA Class I and a preserved LVEF (0.852 vs 0.975,P = 0.0001). Including the 1-year follow-up, 49.5% of patients had an intervention by the ICD, 39.8% had appropriate ICD therapies, 16.2% had inappropriate therapies. Overall, 1,691 hospital readmissions were recorded. The main causes for hospital readmissions were ventricular arrhythmias (61.3%) and congestive heart failure symptoms (12.9%). Thus, demographic data and mortality of patients treated with an ICD in conditions of standard medical care seems to be comparable and based on, or congruent with, the large secondary preventions trials. When ICDs are used in standard medical care, the 1-year survival rate is high, especially in patients with NYHA Class I and preserved LVEF. However, nearly half of all patients suffer from ICD intervention.
INTRODUCTION: Patients with implantable cardioverter defibrillators (ICD) critically depend on correct functioning of their system. The aim of this study was to determine the incidence and clinical presentation of transvenous ICD lead failures during long-term follow-up. METHODS AND RESULTS: The study group consisted of 261 consecutive patients who received Medtronic right ventricular polyurethane transvenous leads (models 6884, 6966, 6936) between 1990 and 1998 as part of an abdominal (n = 70) or pectoral (n = 191) ICD system. During mean follow-up of 4.0 +/- 2.6 years, 31 patients (12%) developed a lead-related sensing failure with oversensing of artifacts. All failures except two were compatible with an insulation defect and occurred late after ICD placement (6.0 +/- 1.8 years after implant). Lead survival decreased from 98% at 4-year follow-up to only 62% at 8-year follow-up. Lead survival was not related to patient age, sex, venous lead implantation route, or device implantation site. In 26 (87%) of 31 patients, a sensing defect resulted in inappropriate detection of ventricular fibrillation and subsequent delivery of 3 +/- 3 (range 1-11) inappropriate shocks in 19 (61%) of 31 patients. Device interrogation showed artifacts classified as nonsustained ventricular tachycardia in 21 patients, 40 +/- 43 days before clinically relevant failure of the system. One patient with a subclavian crush syndrome required resuscitation because of undersensing of true ventricular fibrillation. CONCLUSION: Transvenous polyurethane ICD leads showed a high rate of lead insulation failure late after implantation with frequent inappropriate shock deliveries. Close follow-up is mandatory in patients with these leads. Automated device control features with patient alert function integrated into new devices may contribute to early detection of lead failure.
BACKGROUND: Coronary calcification measured by fast computed tomography techniques is a surrogate marker of coronary atherosclerotic plaque burden. In a cohort study, we prospectively investigated whether lipid-lowering therapy with a cholesterol synthesis enzyme inhibitor reduces the progression of coronary calcification. METHODS AND RESULTS: In 66 patients with coronary calcifications in electron beam tomography (EBT), LDL cholesterol >130 mg/dL, and no lipid-lowering treatment, the EBT scan was repeated after a mean interval of 14 months and treatment with cerivastatin was initiated (0.3 mg/d). After 12 months of treatment, a third EBT scan was performed. Coronary calcifications were quantified using a volumetric score. Cerivastatin therapy lowered the mean LDL cholesterol level from 164+/-30 to 107+/-21 mg/dL. The median calcified volume was 155 mm3 (range, 15 to 1849) at baseline, 201 mm3 (19 to 2486) after 14 months without treatment, and 203 mm3 (15 to 2569) after 12 months of cerivastatin treatment. The median annualized absolute increase in coronary calcium was 25 mm3 during the untreated versus 11 mm3 during the treatment period (P=0.01). The median annual relative increase in coronary calcium was 25% during the untreated versus 8.8% during the treatment period (P<0.0001). In 32 patients with an LDL cholesterol level <100 mg/dL under treatment, the median relative change was 27% during the untreated versus -3.4% during the treatment period (P=0.0001). CONCLUSIONS: Treatment with the cholesterol synthesis enzyme inhibitor cerivastatin significantly reduces coronary calcium progression in patients with LDL cholesterol >130 mg/dL.
Electron-beam Computed Tomography (EBCT) has been used for years to quantify coronary artery calcification as a marker of coronary atherosclerosis. The aim of this study was to determine the diagnostic accuracy of a new scanner, the Multi-slice Spiral CT (MSCT), for the assessment of coronary calcification and to compare this new technique to EBCT. The study population consisted of 99 male patients, aged 60 +/- 10 years with suspected or known coronary artery disease. With EBCT 40 axial slices, ECG-triggered (scan time = 100 ms, slice thickness = 3 mm), were acquired in one breath-hold (35 +/- 5 s). For MSCT simultaneous acquisition of four axial slices (scan time = 250 ms, slice thickness = 2.5 mm), allowed the entire heart (48 slices) to be covered in one breath-hold of 25 +/- 5 s. For quantification of coronary calcium the Volumetric Calcium Score (VCS) was calculated. There was an excellent correlation for the VCS (r = 0.994, p = 0.01, mean difference = 97 +/- 115) between both scanners. Comparison of low (1-100), moderate (101-400), high (401-1000) and very high score values (>1,000) showed no significant differences. The number of calcified lesions and densities were statistically not different. Mean variability of the two scans was 17%. The MSCT scanner is equivalent to EBCT for the determination and quantification of coronary calcium and can therefore be used for calcium screening. With application of the spiral mode technique further improvement in variability can be expected, thus allowing for follow-up studies to determine progression or regression of atherosclerosis with high accuracy.
UNLABELLED: Pulmonary vein bigeminy is the pair of a second, late and ectopic pulmonary vein potential following atrial far-field activation and a first passive pulmonary vein potential during sinus rhythm. The aim of this study was to determine the electrophysiological characteristics of pulmonary vein bigeminy and to evaluate its relevance as a trigger for paroxysmal atrial fibrillation. METHODS AND RESULTS: Pulmonary vein bigeminy was recorded in 8 of 45 patients (18%) who underwent mapping of pulmonary veins for ablation of focal atrial fibrillation. The premature ectopic pulmonary vein potentials were conducted to the atria in 5 patients and were not conducted (concealed bigeminy) in 3 patients. The coupling interval of the ectopic pulmonary vein potential to the preceding atrial signal during sinus rhythm was significantly longer in patients with conducted bigeminy (375 +/- 25 ms) than with concealed bigeminy (230 +/- 17 ms). The pulmonary vein bigeminy was driven by coronary sinus pacing with the pacing cycle length at lower stimulation rates and was suppressed by overdrive pacing. Coronary sinus pacing led to a separation of the first pulmonary vein potential from the atrial signal but the interval between the atrial signal and the second pulmonary vein potential remained unchanged. Focal ablation at the site of earliest ectopic pulmonary vein activity in 5 patients induced rapid repetitive firing before elimination of the pulmonary vein bigeminy. Ostial disconnection of the arrhythmogenic pulmonary vein in 3 patients was associated with elimination of the pulmonary vein bigeminy. During the follow-up of 9 +/- 5 months after ablation of the pulmonary vein bigeminy, 5 of the 8 patients (63%) were free of atrial fibrillation without antiarrhythmic medication. CONCLUSIONS: The response of pulmonary vein bigeminy to atrial pacing and ostial ablation suggests that pulmonary vein bigeminy depends on an intact electrophysiological breakthrough between the left atrium and the pulmonary vein. Ablation targeting the pulmonary vein bigeminy is a possible limited approach for this subgroup of patients with paroxysmal atrial fibrillation.
The aim of this study was to evaluate the clinical use of a new three-dimensional mapping system as a guide for catheter ablation of ectopic atrial tachycardia. A series of 42 consecutive patients with drug refractory ectopic atrial tachycardia was studied in a prospective observational trial with the electroanatomic mapping system CARTO. The arrhythmogenic focus was found in the right atrium in 30 patients and in the left atrium in 12 patients. The construction of a complete electroanatomic map of the right or left atrium was possible in 37 of 42 consecutive patients with ectopic atrial tachycardia. Mean activation time of the right atrium, including the proximal coronary sinus, was 94 +/- 25 ms for right atrial tachycardias; left atrial activation time during left atrial tachycardias was 86 +/- 17 ms. Average mapping time was 30 minutes for right atrial tachycardias and 22 minutes for left atrial tachycardias, allowing the collection of 86 +/- 50 and 65 +/- 28 catheter positions, respectively. The size of the area of earliest atrial activation calculated from the electroanatomic map amounted to 0.6 +/- 0.4 cm2 in right atrial tachycardias and 1.0 +/- 0.9 cm2 in left atrial tachycardias. In the right atrium the most common locations of the 33 arrhythmogenic foci in 30 patients were the high or mid-lateral right atrium (n = 10) and the inferoparaseptal region near the coronary sinus ostium (n = 7). Ectopic left atrial foci were most commonly located in an inferior position near the mitral annulus (n = 5) and in proximity to the ostium of the pulmonary veins (n = 4). Biatrial electroanatomic mapping allowed visualization of earliest right atrial activation during left atrial tachycardia at the high interatrial septum or near the coronary sinus ostium. Catheter ablation was successful in 85% of right atrial tachycardias and 82% of left atrial tachycardias. In patients with ectopic atrial tachycardia electroanatomic mapping is a safe and feasible technique that allows three-dimensional visualization of the automatic focus in a precise anatomic reconstruction of the atria. This novel mapping technology facilitates catheter ablation of complex ectopic atrial tachycardia.
Concealed pulmonary vein bigeminy, as a pair of a pulmonary vein spike potential within a fragmented far-field atrial electrogram and a premature ectopic pulmonary vein spike potential with exit block, was continuously recorded in a patient with paroxysmal AF. Atrial pacing suppressed the breakthrough from the left atrium to the pulmonary vein, thus preventing the conducted and the premature ectopic pulmonary vein potentials. Atrial pacing induced conduction block between the left atrium and the arrhythmogenic pulmonary vein might be a possible explanation for the prevention of paroxysmal AF by atrial pacing.
INTRODUCTION: Noninvasive postinfarction risk assessment for sudden cardiac death is limited. Standard analysis of the signal-averaged QRS complex can identify patients at risk for monomorphic ventricular tachycardia, but its value for discriminating patients at risk for sudden death is low. METHODS AND RESULTS: The aim of this study was to prospectively investigate repeated late potential analysis of digital Holter ECG and compare it with standard analysis of the signal-averaged QRS complex within a short ECG period and with common clinical risk factors for sudden cardiac death in 756 consecutive patients after acute myocardial infarction. Digital Holter ECG were subdivided into 5-minute segments, and late potential analysis was performed on each 5-minute segment. During follow-up of 32 +/- 15 months, 35 patients died of sudden cardiac death and 50 patients died of nonsudden cardiac death. Sudden cardiac death was associated with ejection fraction < 40%, nonsustained ventricular tachycardia, creatine kinase > 1,000 IU/L, and late potentials in > 75% of analyzed Holter ECGs (abnormal LP75), but not with late potentials determined by only a short ECG period. According to multivariate analysis, the best independent significant predictor of sudden cardiac death was abnormal LP75 (P = 0.002, sensitivity 29%, specificity 96%, positive predictive value 40%, negative predictive value 97%). Nonsudden cardiac death was associated with ejection fraction < 40% (P = 0.001). CONCLUSIONS: Late potential analysis of digital Holter ECG is a powerful tool that can be used to determine postinfarction patients at risk for sudden cardiac death and is optimized when combined with determination of ejection fraction.
INTRODUCTION: The rate of implantation of implantable cardioverter defibrillators (ICD) is growing much faster in the United States than in western Europe. Among several factors, education and awareness of the problem of sudden cardiac death might account for this discrepancy. METHODS AND RESULTS: Guidelines for ICD implantation developed in the United States and various European countries are compared, including the one recently published by the Working Groups on Arrhythmias and Cardiac Pacing of the European Society of Cardiology. Although all guidelines fully concur in their recommendations for patients after cardiac arrest due to ventricular fibrillation and ventricular tachycardia, small but noticeable differences in opinion can be traced for patients with sustained ventricular tachycardia or syncope, and for primary prevention. In general, European guidelines are more restrictive for the latter indications. Whereas U.S. guidelines were quickly updated over the years, this process took much longer in Europe, and several countries only recently adopted their first guidelines. CONCLUSION: Although different in details, the recent release of ICD guidelines in major western European countries will undoubtedly lead to a pronounced increase of patients protected by this form of therapy in Europe in the coming years.
OBJECTIVE: To evaluate the diagnostic power of contrast-enhanced multidetector-row computed tomography (MDCT) in assessing the presence, age, and size of myocardial infarctions. METHODS: One hundred six patients underwent standard MDCT coronary angiography without additional changes in the protocol. In all patients, a complete patient history and left heart catheterization with biplane contrast ventriculography were available. The MDCT images were reviewed for the presence and age of myocardial infarctions in a blinded fashion. Infarct areas were detected as regions of reduced uptake of contrast in the early arterial phase and/or regional wall thinning. Reviewing the computed tomography (CT) images, CT density values (Hounsfield units [HU]) were measured at the site of infarcted and noninfarcted myocardium, and a volumetric assessment of the infarct size was performed. RESULTS: In 27 of 106 patients, myocardial infarctions were present. Multidetector-row computed tomography detected 23 of 27 infarctions (sensitivity of 85%, specificity of 91%, and accuracy of 90%). Comparing the HU of infarcted versus noninfarcted myocardium, the mean HU of infarcted areas was 54 +/- 19 HU versus 117 +/- 28 HU for noninfarcted myocardium (P < 0.01). Multidetector-row computed tomography was able to differentiate between recent and chronic infarctions. The infarct volumes of recent infarctions (6.3 +/- 3.6 cm) showed a negative correlation to the ejection fraction (EF) according to contrast ventriculography (ie, the larger the infarct volumes as measured using MDCT, the worse was the EF [r = -0.72, P < 0.01]). CONCLUSIONS: Performing standard MDCT coronary angiography, areas of infarcted myocardium can be identified with moderate to high sensitivity, without additional scanning or contrast administration. Infarct localization can be assessed accurately as compared with cineventriculography. To some degree, infarct age and infarct volume can be estimated.
The authors report the first case of a patient with a hypereosinophilic syndrome associated with heterozygous factor V gene mutation, resulting in an acute coronary syndrome and recurrent cerebral stroke despite effective anticoagulation. A 40-year-old man presented with an acute coronary syndrome accompanied by a brachiofacial right-sided hemiparesis and dysarthria. Diagnosis of a hypereosinophilic syndrome was established by blood testing, myocardial biopsy, and bone marrow analysis. Eosinophilic infiltration was present in the myocardium, accompanied by proliferation in the endomyocardium and a pneumonic infiltrate. Although effective anticoagulation with heparin was administered, a recurrent stroke occurred while blood eosinophils were being normalized by corticosteroid treatment. A coexisting heterozygosity of the factor V mutation was demonstrated, and it is hypothesized that this might have contributed to the recurrent thromboembolic episodes. In patients with hypereosinophilic syndrome and recurrent thromboembolic episodes, other thrombophilic diseases, including factor V mutations, should be considered, and long-term coagulation should be contemplated.