Biomedical subjects
Publications and source records attributed to Thomas Schimpf.
Mitral valve prolapse usually has a good prognosis. However, an association between mitral valve prolapse and atrial and ventricular arrhythmias has been described. This case presents a patient who was admitted after cardiac resuscitation due to ventricular fibrillation. A severe mitral valve prolapse was the only pathology found.
BACKGROUND: Left ventricular lead implantation for cardiac resynchronization therapy (CRT) usually requires a pre- or intraprocedural occlusion contrast venography of the coronary sinus (CS) in order to identify tributaries to the lateral wall. As many patients undergo a preprocedural coronary angiogram, we investigated the diagnostic accuracy of venous phase imaging of the CS in patients prior to CRT implantation. The aim of this study was to assess the quality of venous phase coronary sinus angiography. METHODS: In 24 CRT patients retrograde occlusion venography and venous phase coronary sinus angiography obtained during coronary angiography were compared with respect to image quality, vessel diameters and the ability to identify a coronary sinus side branch suitable for left ventricular lead placement. RESULTS: Suitable target vessels for left ventricular lead implantation were identified in all patients irrespective of the method (retrograde occlusion venography or venous phase coronary sinus angiography). There was a high concordance in vessel diameters between venous phase and retrograde angiography. Visibility was superior in retrograde venography. CONCLUSIONS: In heart failure patients who are scheduled for coronary angiograms venous phase coronary sinus angiography is a time-saving and easy to perform alternative imaging modality. Radiation exposure and the amount of contrast medium needed is reduced as compared to coronary sinus occlusion angiography. The information obtained thereby may be used to plan subsequent CRT implantation without the need for retrograde coronary sinus angiography.
Explore the source record for details and available documents.
BACKGROUND: Pre-interventional three-dimensional (3D) reconstruction of the heart by CT or MRI provides important information on cardiac anatomy for electrophysiological interventions. However, updates of 3D-imaging modalities with high soft-tissue contrast are not available during ablation procedures. OBJECTIVE: We describe the development and first clinical testing of a close to real-time visualization of cardiac anatomy by intracardiac echocardiography (ICE). METHODS: An electronic phased-array 5-10 MHz ICE-catheter (AcuNav/Siemens/64 elements) was inserted via a straightened femoral vein sheath (12F) and placed in the right atrium in 5 pigs. A custom-made prototype stepper motor allowed automatic rotation around the longitudinal axis from 90 degrees to 360 degrees in 2-5 degrees steps. For every plane 2D images of a complete cardiac cycle were acquired, triggered by respiration and ECG. The ultrasound images were digitized and 3D-reconstruction was performed by a prototype software. After experimental validation the system was tested in 6 patients during electrophysiological studies. RESULTS: From a single location in the right atrium, 3D-acquisition and reconstruction of both atria and ventricles with good image quality were achieved within 3-5 minutes. Doppler-mode facilitated identification of the great vessels including the pulmonary veins and their entry into the heart. 3D-visualization of ablation catheters was also possible in all patients and pigs. CONCLUSION: Semi-automated 3D intracardiac echocardiography from a single site inside the right atrium provides the electrophysiologist with a detailed image of both atria and ventricles with repeated updates of the cardiac anatomy.
Explore the source record for details and available documents.
Access to the intrinsic cardiac autonomic nervous system can now be achieved via percutaneous catheter stimulation techniques. Thereby, cardiac functions like atrioventricular nodal conduction, sinus cycle length and ventricular inotropy can be dynamically regulated. The present article provides examples of this new technique in acute and chronic models but also first human applications.
INTRODUCTION: Because of the proximity of the esophagus to the heart, transesophageal defibrillation might increase defibrillation success. We assessed the defibrillation threshold (DFT) of transesophageal defibrillation compared with standard transthoracic defibrillation. METHODS: Defibrillation success and DFTs were determined in 22 female pigs with high (68+/-4 kg, n=12) or low body weight (39+/-1 kg, n=10). After induction of ventricular fibrillation, biphasic shocks were delivered between two cutaneous patch electrodes (sternal and apical position) or between an esophageal and two cutaneous patch electrodes in a sternal and apical position. The esophageal electrode was integrated into a latex sheath covering a standard transesophageal echocardiography probe. RESULTS: In 5 of 12 pigs with high body weight, external defibrillation failed despite 3 consecutive 200-J shocks, whereas subsequent transesophageal defibrillation was successful with the first shock. In the remaining 7 pigs, a more than 50% reduction in DFT was obtained with transesophageal defibrillation compared with standard biphasic external defibrillation (67+/-27 vs 164+/-23 J, P<.001). Pigs with lower body weight were successfully defibrillated by both transthoracic and transesophageal shocks. The DFT in pigs with low body weight was significantly lower using transesophageal defibrillation compared with transthoracic shocks (65+/-15 vs 99+/-38 J, P<.05). CONCLUSIONS: In this animal model, nonresponders to standard external defibrillation could successfully be defibrillated via an esophageal-cutaneous electrode configuration. Overall, an almost 50% DFT reduction was achieved by transesophageal defibrillation. Transesophageal defibrillation may provide an additional tool for terminating VF, which is refractory to external defibrillation, eg, in patients with very high body weight.
OBJECTIVES: This study was designed to develop a technique to selectively increase the sympathetic tone to the heart by cardiac sympathetic nerve stimulation (SNS). BACKGROUND: Access to the cardiac sympathetic neurons may allow modulating the adrenergic tone of the heart while avoiding systemic side effects. METHODS: Cardiac sympathetic nerves course within neural sleeves along the subclavian artery. Because of this proximity, transvascular SNS was attempted with electrode catheters inside the subclavian artery in 16 pigs. RESULTS: Right/left (R-/L-) SNS (20 Hz) during ventricular pacing at 200/min evoked a >100% increase of left ventricular systolic pressure (baseline: 51 +/- 1 mm Hg; L-SNS: 118 +/- 26 mm Hg; R-SNS: 116 +/- 33 mm Hg; p < 0.001) while systemic vascular resistance remained unchanged. There was a sigmoid dose-response curve with rapid on- and offset of the effect during SNS initiation/cessation. Positive inotropic effects persisted for 12 h of continued SNS (n = 4). Besides positive dromotropic effects, L-SNS/R-SNS yielded a 41% and 77% sinus rate increase, respectively. CONCLUSIONS: The neural adrenergic tone to the heart can be selectively increased by catheter stimulation of cardiac efferent sympathetic nerves.
Explore the source record for details and available documents.
The role of anticoagulation in the long-term treatment of atrial fibrillation (AF) has been well established in prospective randomized trials. Less certainty exists on the optimal anticoagulation in the setting of AF cardioversion. Current guidelines advocate anticoagulation for 3-4 weeks before and after cardioversion of AF of >48 hours' duration. Alternatively, early cardioversion may be performed after exclusion of left atrial thrombi by transesophageal echocardiography. However, with conventional anticoagulation, the risk of bleeding has to be considered and, thus, anticoagulation is frequently underused in the clinical setting. Moreover, the role of cardioversion has been questioned by recent trials suggesting no benefit of sinus rhythm restoration over rate control in AF. This article aims to summarize the currently available data on anticoagulation in cardioversion of AF in the context of these new studies and points to some new drugs such as low-molecular weight heparins and oral thrombin inhibitors that may lead to safer anticoagulation for prevention of thromboembolic complications of AF in the future.
Implantable cardioverter defibrillators and pacemakers detect an increasing number of silent episodes of AF. In a porcine model, the study evaluated the contractility of the left atrial appendage (LAA) during AF paroxysms as they may occur in patients. Peak outflow velocity of the LA and mean outflow velocity of the LAA (LAA-V(outmean)) (n = 17) were measured before, during, and after induction of self-terminating AF. LAA-V(outmean) was also measured during incremental pacing from different atrial sites using epicardial Doppler probes (n = 6) and during continuous recordings (n = 5) of 40 minutes of pacing maintained AF. Compared to baseline sinus rhythm, LAA-V(outmean) increased during short AF episodes (41 +/- 3 vs 35 +/- 2 cm/s, P < 0.05). After termination of the AF episodes, LAA-V(outmean) further increased (69 +/- 15 cm/s, P < 0.001 vs baseline). This "postfibrillatory enhancement" maintained after repeated induction of short AF paroxysms. During prolonged AF episodes lasting 40 minutes, an initial hypercontractility (44 +/- 2 vs 38 +/- cm/s, P < 0.01) was followed by a hypocontractility after 20 minutes (29 +/- 12 P < 0.05 vs SR) and a postfibrillatory enhancement after cessation of AF (56 +/- 12 vs 27 +/- 9 cm/s at 40 minutes AF, P < 0.001). L-type Ca channel blockade abolished the initial hypercontractility during AF and the postfibrillatory enhancement. Repetitive AF paroxysms up to 2 minutes did not decrease left atrial contractility. During maintained AF up to 40 minutes an initial hypercontractility and a consecutive hypocontractility, which is overcompensated by a postfibrillatory enhancement of atrial inotropy after cessation of AF, are present. The observed phenomenon seems to be related to an increased Ca(2+) influx through the L-type Ca(2+) channel.
BACKGROUND: Atrial fibrillation is the most common arrhythmias with increasing incidence in the elderly. The increased morbidity associated with atrial fibrillation is mainly caused by cardiac emboli, mostly from the left atrial appendage, that may cause cerebral ischemic infarctions. Although electrical cardioversion of atrial fibrillation has been the standard therapy for restoration of sinus rhythm for many years, questions regarding the optimal anticoagulation for the prevention of thromboembolic complications remain unanswered. CURRENT GUIDELINES: Current guidelines advocate the use of oral anticoagulation (adjusted to an Internal Standardized Ratio [INR] of 2.0-3.0) for at least 3-4 weeks before cardioversion for atrial fibrillation of > 48 h duration. Because of the atrial contractice dysfunction following cardioversion, the so-called "atrial stunning", anticoagulation for another 3-4 weeks after cardioversion is recommended. Alternatively, early cardioversion using high-dose intravenous heparin after exclusion of intraatrial thrombi by transesophageal echocardiography is possible, also followed by 3-4 weeks of oral anticoagulants. Because of the fear of bleeding complications, these anticoagulation schemes are frequently underused in the clinical setting, especially in older patients. Thus, new therapeutic approaches for anticoagulation in the setting of cardioversion are currently being investigated. FUTURE PERSPECTIVES: Low molecular weight heparins allow outpatient therapy because no intravenous therapy initiation is necessary and the need for anticoagulation monitoring is reduced. Whether oral thrombin antagonists may increase the safety of chronic anticoagulation because of their higher therapeutic index compared to warfarin has to be determined in future studies.