Wolff-Parkinson-White syndrome associated with persistent left superior vena cava.
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Biomedical subjects
Publications and source records attributed to H Gülker.
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BACKGROUND: Impaired glucose regulation (IGR) and diabetes mellitus (DM) are amongst the main risk factors for developing coronary heart disease (CHD). The aim of this study was to investigate previously unknown glucose metabolism disorder in patients scheduled for an elective coronary angiography. METHODS: A total of 141 patients scheduled for coronary angiography without signs of acute myocardial ischemia or previous history of a glucose metabolism disorder were prospectively included in the study. An oral glucose tolerance test (OGTT) was performed in each patient. RESULTS: IGR was diagnosed in 40.4% (95% confidence interval 32.3-49.0) and undetected DM in 22.7% (16.1-30.5) of patients undergoing an elective coronary angiography. Depending on the severity of CHD, the percentage of IGR and DM increased up to 45.3% (34.6-56.5) and 26.7% (17.8-37.4) in the subgroup with the need of percutaneous angioplasty, while the corresponding proportions in the group without CHD were 30.3% (15.6-48.7) and 12.1% (3.4-28.2). The percentage of undiagnosed DM increased with the number of epicardial vessels involved. Using the recommended fasting plasma glucose value of > or = 126 mg/dl for the diagnosis of DM, we would have missed 71.9% of the patients with undiagnosed DM. If all patients with a fasting plasma glucose of > or = 90 mg/dl had been subjected to OGTT, 93.8% of DM would have been identified. CONCLUSIONS: Prevalences of DM and IGR are higher than expected in patients with CHD. An OGTT should be considered for all patients with a fasting plasma glucose > or = 90 mg/dl undergoing a coronary angiography.
Inflammation contributes to the development of atherosclerosis and cardiovascular events. Counteracting pro- and anti-inflammatory responses of serum cytokines have been reported, but the relevance of TNF-alpha, TGF-beta and IL-6 gene expression in peripheral blood leukocytes and their contribution to systemic inflammation in atherosclerosis, especially after acute myocardial infarction (AMI), has not been investigated yet. Using quantitative RT-PCR, we determined temporal cytokine mRNA expression alterations in blood cells from patients with AMI (n = 51). Serum cytokine concentrations were analyzed in parallel using the ELISA technique. TNF-alpha mRNA expression rates and serum concentrations were significantly elevated in AMI patients compared to controls (n = 77), while mRNA expression and serum content of TGF-beta were decreased. Interestingly, we found no statistically significant correlation between transcript and protein levels, indicating that gene expression in leukocytes may be an independent sign for systemic inflammation. While IL-6 was significantly increased in serum from AMI patients with positive correlation to left ventricular dysfunction and negative correlation to ejection fraction, IL-6 mRNA levels did not differ between patients and controls. Gene expression alterations indicate a sophisticated regulation of counteracting TNF-alpha and TGF-beta cytokine expression in peripheral blood leukocytes after AMI with bias towards a pro-inflammatory situation.
HISTORY: A 38 year old man suffered from exercise-induced reproducible dizziness and syncopes. INVESTIGATIONS AND DIAGNOSIS: During exercise testing a ventricular tachycardia at a rate of 300 beats/min was identified as the cause of the symptoms. Because of the ventricular morphology with inferior axis, left bunde branch block and the typical monomorphic repetitive characteristics, idiopathic adenosine-sensitive ventricular tachycardia was diagnosed. TREATMENT AND CLINICAL COURSE: Curative catheter ablation of the arrhythmogenic focus in the right ventricular outflow tract was performed. The patient has now been free of symptoms for more than two years. The characteristics of idiopathic ventricular tachycardia and the electrophysiological techniques are described. CONCLUSION: Idiopathic ventricular tachycardia is a rare cause of syncope in young patients without underlying heart disease and can be cured by catheter ablation. Exclusion of cardiac diseases, especially arrhythmogenic right ventricular cardiomyopathy, is of prognostic value.
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BACKGROUND AND AIM OF STUDY: The implantable cardioverter defibrillator (ICD) is the therapy of choice for patients with ventricular tachycardia (VT) after myocardial infarction. In some patients frequent ICD shocks occur, often resulting in clinical problems, if antiarrhythmic drugs insufficiently suppress them. Our aim was to describe electro-anatomical mapping and ablation techniques in patients with VTs, in which conventional strategy treatments have failed. PATIENTS AND METHODS: 17 patients (69.5 +/- 8 years, 12 male) were included. During 3 months before ablation the number of ICD shocks was 21 +/- 8 (mean +/- SD). Using an electro-anatomical mapping system (CARTO), activation mapping was performed in 12 patients during hemodynamically tolerable, stable VT. In 5 cases with "non-mappable" VT only voltage mapping during sinus rhythm was obtained. The aim was to characterize the underlying scar tissue precisely in order to modify the substrate with an individual strategic linear lesion, thus preventing re-induction of VT. RESULTS: Procedure time was 184 +/- 9 minutes, fluoroscopy time totalled 19 +/- 9 minutes. Lesion lines were established with 13 +/- 9 ablation pulses. In 15 patients (88 %) acute ablation of the VT was successful. During a follow-up of 8 +/- 7 months, 2 patients had a recurrence of the VT. Two patients developed a VT with a different morphology. In another case ventricular fibrillation occurred. No major complications were observed. CONCLUSION: Electro-anatomical mapping combined with an individual linear ablation strategy is a safe and effective method to prevent symptomatic VT in patients after myocardial infarction.
A female patient without underlying heart disease was highly symptomatic from short runs of atrial ectopy. Sustained atrial tachycardia or atrial fibrillation never occurred. Due to ineffective pharmacological therapy, catheter ablation combined with electroanatomic mapping (CARTO) was performed effectively. Characteristics of ectopic atrial tachycardia and the electrophysiological techniques are described.
Parvovirus B19 (PB19) has been identified as a possible cause of myocarditis and heart failure in both children and adult patients. This study used real time PCR analysis, to determine the frequency and to quantify PB19 viral genomes in endomyocardial tissue samples from 80 adult patients with clinically suspected myocarditis or idiopathic left ventricular dysfunction and from 36 controls. Histological (Dallas classification) and immunohistological analyses were performed to detect myocardial inflammation in the endomyocardial biopsies.PB19 genomic DNA was found in nine of 80 patients (11.2%), 4 out of 31 (12.9%) patients with inflammatory infiltrates detected via immunohistological methods and 5 out of 49 (10.2%) patients with left ventricular dysfunction without myocardial inflammation. The copy numbers for PB19 DNA ranged between 30 and 3900 per microg of cellular DNA. Four patients with clinically suspected myocarditis had copy numbers for PB19 DNA of 70, 740, 3400 and 3900, respectively, per microg of cellular DNA in the endomyocardial biopsy. Five patients with idiopathic left ventricular dysfunction had copy numbers for PB19 DNA of 30, 38, 52, 58 and 90, respectively, per microg of cellular DNA in the endomyocardial biopsy. The amplicon of one of the nine positive PCR fragment was sequenced and was found to be fully identical in the highly conserved sequence of published Parvovirus B19 VP1/VP2 genes (NCBI gene bank). In all patients, acute myocarditis was excluded according to the Dallas classification. All biopsies of 36 controls with no history of myocarditis or recent viral infection were negative for myocardial inflammation and parvovirus B19 genomes. In summary, Parvovirus B19 DNA is present within the myocardium of patients with suspected myocarditis and idiopathic left ventricular dysfunction and can be detected and quantified in endomyocardial specimens via real time PCR.
Differentiation between typical and atypical atrial flutter solely based upon surface ECG pattern may be limited. However, successful ablation of atrial flutter depends on the exact identification of the responsible re-entrant circuit and its critical isthmus. Between August 2001 and June 2003, we performed conventional entrainment pacing within the cavotricuspid isthmus in 71 patients with sustained atrial flutter. In patients with positive entrainment we considered the arrhythmia as typical flutter and treated them with conventional ablation of the cavotricuspid isthmus. As a consequence of negative entrainment we performed 3D-electroanatomic activation mapping (CARTO trade mark ). Conventional ablation of the right atrial isthmus was successful in all patients (n = 54) with positive entrainment. We performed electroanatomic mapping in the remaining 17 patients (14 male; age 60.9 +/- 16 years) resulting in the identification of 6 cases with typical and 11 cases with atypical flutter. Therefore, entrainment pacing was able to predict the true presence of typical atrial flutter in 91.5%. Atypical flutter was right sided in 4 patients and left sided in 7 cases. Electrically silent ("low voltage") areas probably demonstrating atrial myopathy were identified in all cases with left sided and in 2 patients with right sided flutter. In these patients targets for ablation lines were located between silent areas and anatomic barriers (inferior pulmonary veins, mitral respectively tricuspid annulus, or vena cava inferior). In 1 patient, the investigation was stopped due to variable ECG pattern and atrial cycle lengths. In the remaining cases, ablation was acutely successful. One patient, after surgical closure of a ventricular septal defect, demonstrated a dual-loop intra-atrial reentry tachycardia dependent on two different isthmuses. This arrhythmia required ablation of those distinct isthmuses to be interrupted. After a mean follow-up of 8.8 +/- 3.4 months, there was one patient with a recurrence of left-sided atrial flutter. Another patient developed permanent atrial fibrillation shortly after the procedure. Mean duration time of the procedure was 235.6 +/- 56.4 min (right atrium: 196 +/- 17.3 min; left atrium: 267.2 +/- 59.5 min), and average fluoroscopy time was 21.8 +/- 11.7 min (right atrium: 9.5 +/- 6 min; left atrium: 28.9 +/- 7 min). There was no incidence of serious complications associated with these procedures. In conclusion, conventional pacing in the cavotricuspid isthmus combined with electroanatomic mapping was an effective method to differentiate between typical and atypical atrial flutter. Electroanatomic mapping was a powerful tool both for identification of different atrial re-entrant circuits including their critical isthmuses as well as for effective application of individual ablation line strategies.
Due to its variable origin success for ablation of ectopic atrial tachycardia (EAT) has been difficult to achieve using conventional mapping and ablation strategies. In contrast, no information in the literature is available about the use of a nonfluoroscopic, 3-dimensional electroanatomic mapping system (CARTO) combined with the cooled ablation technology creating deeper lesions in experimental studies compared to standard catheters. In 20 consecutive patients (15 female; age 52.5 +/- 15.4 years), a single focus responsible for clinical EAT has been mapped. Twelve EATs were located in the right atrium, whereas 8 foci were left sided including 3 origins within a pulmonary vein (PV). Due to the reported development of PV stenosis in the ablative treatment of focal atrial fibrillation, direct ablation applied inside the PV was avoided. Instead, PV-disconnection achieved by the use of a Lasso trade mark catheter in 1 case and by circumferential ablation around the PV in 2 other patients was preferred. In 2 patients, ablation was not attempted because of an origin located directly in the area of the atrioventricular node. In another case, CARTO mapping was stopped due to persistent mechanical termination of the tachycardia with no possibility of reinduction. In the latter, ablation was performed in sinus rhythm at the earliest mapped site before terminating. Three weeks later another episode of EAT was noted in this patient. In the remaining 17 cases, ablation was associated with acute success and no recurrences of sustained tachycardia in all patients. Mean duration time was 192 +/- 53.3 min (right atrium 161 +/- 37.9 min; left atrium 229.6 +/- 46.2 min), and average fluoroscopic time was 22.8 +/- 9.7 min (right atrium 17.1 +/- 6.2 min; left atrium 29.8 +/- 8.9 min). There was no incidence of serious complications associated with this procedure. In conclusions, electroanatomical mapping including cooled ablation was a safe and feasible strategy in treating EATs. The benefit of this technique may imply the combination of both precise localization of the focus and effective applications of radiofrequency pulses, thereby minimizing acute failures or reablation. Due to the time consuming point by point data acquisition, the ability to generate precise maps demonstrating the earliest activation at their exact anatomical location can be limited by transient or persistent termination of the tachycardia.
We report a 25-year-old female patient with a long history of symptomatic paroxysmal supraventricular tachycardia. Electroanatomic activation mapping demonstrated a focal tachycardia originating in the right upper pulmonary vein, 3 cm distal to the ostium. Due to the recent experiences in the management of focal atrial fibrillation with catheter ablation, direct ablation applied inside the pulmonary vein was avoided. Instead, an electrical disconnection of the pulmonary musculature from the left atrium guided by a circumferential 10-electrode mapping catheter was performed. The patient has since been asymptomatic during follow-up.
We report about a 46 year old male, who survived sudden cardiac death caused by recurrent ventricular tachycardia as the clinical manifestation of a vasospastic right coronary artery. After implantation of an implantable cardioverter defibrillator, the patient did not respond to conservative treatment despite of different drug therapies. Therefore, the vasospastic right coronary artery was treated by a percutaneous transluminal coronary angioplasty and stenting, which could not reduce the occurrence of further tachycardias. Finally, the patient underwent an operative myocardial revascularization combined with sympathectomy. During the whole follow-up of six months no new episodes of ventricular tachyarrhythmias have occurred.
AIM: Evaluating the efficiency of a prescribed concept for atrial lead placement in cases of intraoperative atrial fibrillation (AF). METHODS: Over the period from 11/1998 to 5/2000, we carried out a prospective study on 40 patients with AF. After implantation of the screw electrode into the lateral wall of the atrium, an amplitude of the intracardial ECG of > or = 1.4 mV was arbitrarily defined as tolerable. At amplitudes of < 1.4 mV, atrial overdrive-stimulation occurred at 400 to 800 ppm in order to convert the AF to sinus rhythm (SR). Following successful overdrive-stimulation, the atrial electrode was positioned according to standard values (P-wave > 3 mV, pacing threshold < 0.5 V at 0.5 ms). In the case of unsuccessful intraoperative atrial stimulation, the electrode was repositioned until an amplitude of > or = 1.4 mV was reached. In all cases bipolar atrial screw electrodes (Model 4068, Medtronic Inc., Minneapolis, MN, USA) were implanted. The intraoperative measurements were carried out via the atrial channel of a 5311 PSA (Medtronic Inc., Minneapolis, MN, USA). In follow-up after 6 weeks, the atrial stimulation threshold was measured in [V] at 0.5 ms and the signal amplitude of the P-wave in [mV], or in the case of AF detection with successful mode switch activation. RESULTS: In 31/40 patients (77.5 %) with intraoperative persistent AF, fibrillation amplitudes of 1.4 to 3.1 mV (mean value 1.9 +/- 0.4 mV) were measured. In 9/40 patients (22.5 %) with intraoperative AF, 4 cases of conversion to SR using burst stimulation were documented. Atrial lead placement was performed using standard values. After 6 weeks, 33/40 patients (82.5 %) had SR, while intermittent AF episodes with successful mode switch activation were documented in 21 patients (52.5 %). The P-wave amplitude was 3.63 +/- 0.69 mV (range 1.8 to 4.9 mV), the atrial stimulation threshold was 1.3 +/- 0.4 mV (range 0.4 to 1.9 mV). Atrial lead adjustment due to sensing defects was not required for any patients. CONCLUSION: The results show that all atrial leads implanted in accordance with this concept demonstrate proper sensing at SR as well as under AF, with successful mode switch episodes and acceptable stimulation thresholds.
BACKGROUND: The results from studies of coronary angioplasty after failed thrombolysis (rescue-PTCA) in acute myocardial infarction are contradictory. Long-term results were not presented till now. Therefore we analyzed the data from our registry of those patients whose acute and long-term results were available. PATIENTS AND METHODS: Data of 49 patients were analyzed who had been admitted for rescue-PTCA from other hospitals. Thrombolysis had to be started < 6 hours (mean 2.7 hours) from onset of symptoms. Rescue-PTCA had to be completed within < 24 hours (mean 10.5 hours). 37 patients received streptokinase, seven rt-PA, three urokinase and two prourokinase. Electrocardiographic and clinical criteria were used to define failure of thrombolysis. The data of the acute results were from a prospective registry and the long-term results came from clinical follow-up visits and a questionnaire sent to the patients. RESULTS: Mean age of the patients was 48.5 years (38-78 years), 45 male, nine patients in cardiogenic shock (18%), infarct related artery (IRA): RCA 22x, LAD 21x, LCX 5x, CABG 1x, single vessel disease 27x, multiple vessel disease 22x. Acute results: Initial IRA-TIMI flow 0 in 28 patients, 1 in twelve patients, 2 in 9 patients; after rescue-PTCA TIMI flow 1 in one patient, 2 in two patients, 3 in 46 patients (procedural success 94%). Hospital mortality 8.2% (four patients), all in cardiogenic shock. Early reocclusion rate 10%. Bleeding complications 14%, no fatal complications. Long-term results: Observation period 2.5 years in 42 patients (0.5-6.5 years). Three more deaths. Total mortality 14% (7/49). Angiographic follow-up: Ejection fraction initially 50%; 53% after 3 months. Repeat revascularization in 43% (15/35): Re-PTCA in 8/35, surgery in 6/35 patients, 1x transplantation. 80% of the patients were free from angina or heart failure. CONCLUSIONS: Rescue-PTCA in acute myocardial infarction has a high procedural success rate with a low hospital mortality. It is the treatment of choice for patients in cardiogenic shock. Transportation to an interventional center is safe. The reintervention rate is comparably high. The long-term results are good.
The use of the internal thoracic artery (ITA) for myocardial revascularization in coronary artery disease increased because of its relative immunity to atherosclerotic obstruction. This study investigated the distal part of the vessel, the region of anastomosis by means of histology to focus the visualization of this region of interest. The histological examination of arterial segments showed minor intimal thickening in 48 out of 100 patients. Twelve patients demonstrated a severe intimal thickening, the residual patients were without any changes. In 52% the elastic type dominated in the distal part. Hybrid and muscular patterns were found in 22 and 26%, respectively. The media could be classified into three different types: muscular, hybrid and elastic type. There was no correlation concerning the different histological type and the incidence of intimal thickening. No evidence whatsoever of atherosclerotic lesion was encountered in any of the investigated vessels. There is no limitation in the use of the distal part of the ITA for coronary artery revascularization.
OBJECTIVE: The internal thoracic artery is an established arterial graft for myocardial revascularisation, especially of the left anterior descending artery because of a higher patency rate compared to venous grafts. It has never been investigated, whether there are morphological differences in this vessel between patients with or without coronary artery disease or if they are comparable to morphological changes in the common carotid artery. METHODS: We investigated the internal thoracic artery and the common carotid artery of 24 patients (12 with coronary artery disease, 12 without coronary artery disease) with an ultrasonic system on both sides. The intima-media thickness and the diameter of both vessels were estimated. RESULTS: The intima-media-thickness of the internal thoracic artery was comparable in all patients, independent of the presence of a coronary artery disease (0.51+/-0.11 mm with coronary artery disease, 0.50+/-0.17 mm without coronary artery disease, P>0.05). Compared with this the intima-media-thickness of the common carotid artery was thicker in patients with coronary artery disease (0.84+/-0.13 mm with coronary artery disease, 0.73+/-0.07 mm without coronary artery disease, P< or or =0.014). There was no correlation between the thickness of the internal thoracic artery and the common carotid artery (r=0.018, P>0.05). CONCLUSIONS: It could be demonstrated for the first with non-invasive ultrasound, that the intima-media-complex of the internal thoracic artery is protected of the influence of arteriosclerosis. There are no morphological differences like the intima-media-thickness of the common carotid artery. The proven protective mechanism underlines the widespread use of the internal thoracic artery as a coronary artery bypass graft.
Echocardiographic assessment of regional systolic left ventricular function is usually performed qualitatively and depends on investigator experience. In this study, we investigated a new method for quantifying regional systolic wall motion based on color kinesis. In this study, regional systolic wall motion velocity (Vsys) was determined by dividing end-systolic color width by systolic time. High regional wall motion velocity (Vhigh) was determined by dividing the width of the widest color by its duration of 40 ms. First, in vitro measurements with an acrylic glass model were obtained; these demonstrated a high correlation between echocardiographically determined and real "wall motion velocities" (R = 0.99, p<0.001, R2 = 0.99). Then, 17 healthy, young persons were examined, and normal values for each left ventricular wall segment (16-segment model) were determined. The mean Vsys and Vhigh of all 272 wall segments were 2.3+/-0.6 and 7.4+/-1.8 cm/s, respectively. Finally, in 12 patients with coronary artery disease and prior myocardial infarction, Vsys and Vhigh of each left ventricular wall segment were determined and compared with conventional echocardiographic wall motion analysis using the usual 4-grade score system. Analysis of data showed that quantitative color kinesis measurements demonstrated significantly lower velocity values in pathologic than in normal wall segments (Mann-Whitney U test, p<0.05). Measurements discriminated between pathologic and normal wall motion, with an accuracy of 89% for Vsys and 83% for Vhigh (chi-square test, p<0.05). To summarize, in this first study, measurements of regional wall motion velocities with color kinesis demonstrated reliable results for the quantification of regional left ventricular systolic function.
BACKGROUND AND OBJECTIVE: Coronary stents are used nowadays not only for the reduction of restenosis and for treating acute vessel occlusions after PTCA but also after acute myocardial infarction. This study was undertaken to determine whether widening the indications has affected the incidence of acute complications and to compare acute cardiac and vascular complications. PATIENTS AND METHODS: The data on 197 consecutive patients (155 men, 42 women; mean age 62 +/- 9 [37-85] years) with coronary stents were analysed retrospectively, divided into 5 groups depending on the indications for the stent implantation: 1) acute or threatened vessel occlusion after elective PTCA ("bail-out"); 2) acute myocardial infarction (AMI); 3) unstable angina with threatened vessel occlusion; 4) suboptimal primary results (angiographically assessed) after PTCA; 5) elective stent implantation to prevent restenosis. Acute or subacute stent thrombosis, side-branch occlusion, intra- and transmural infarction, death and emergency aortocoronary bypass operation were classified as acute cardiac complications. Haemorrhage in the inguinal region requiring blood transfusion, false aneurysm and operative vascular reconstruction were classified as vascular complications. RESULTS: An intended stent implantation was impossible in 18 patients (primary success rate 91%). Independent of indication an acute or chronic stent stenosis occurred in three (1.6%) and seven (3.9%) patients, respectively. Side-branch occlusion was observed in 12 patients (6.7%), transmural infarction in nine (5.6%). No emergency bypass operation had to be performed. Comparing the different indication groups there was a significantly increased rate of "non-Q" infarctions in patients with unstable angina pectoris (P < 0.014). Among acute vascular complications (10 [5%] inguinal haemorrhages requiring transfusion and 5 [2.5%] operative vascular reconstructions), false aneurysm was significantly more common in patients with AMI (P < 0.014). Comparing emergency and elective stent implantations, side-branch occlusions were significantly more common in the former (12% vs. 0%; P < 0.08), as were also "non-Q" infarcts (10% vs. 0%; P < 0.002). CONCLUSION: Coronary stent implantation for these indications, including AMI, can be taken as firmly established. Stent thrombosis was not significantly increased after "bail out". Implantation in an acute ischaemic episode led to a significantly higher incidence of side-branch occlusion and "non-Q" infarction.