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Biomedical subjects

R N Hauer

Publications and source records attributed to R N Hauer.

At least 19 recordsLinked to original sources
PubMed2001

Activation delay after premature stimulation in chronically diseased human myocardium relates to the architecture of interstitial fibrosis.

BACKGROUND: Progressive activation delay starting at long coupling intervals of premature stimuli has been shown to correlate with sudden cardiac death in patients with hypertrophic cardiomyopathy. The purpose of this study was to elucidate the mechanism of increased activation delay in chronically diseased myocardium. METHODS AND RESULTS: High-resolution unipolar mapping (105, 208, or 247 recording sites with interelectrode distances of 0.8, 0.5, or 0.3 mm, respectively) of epicardial electrical activity was carried out during premature stimulation in 11 explanted human hearts. The hearts came from patients who underwent heart transplantation and were in the end stage of heart failure (coronary artery disease, 4; hypertrophic cardiomyopathy, 1; and dilated cardiomyopathy, 6). Eight hearts were Langendorff-perfused. Epicardial sheets were taken from the remaining hearts and studied in a tissue bath. Activation maps and conduction curves were constructed and correlated with histology. Conduction curves revealing prominent increase of activation delay were associated with zones of dense, patchy fibrosis with long fibrotic strands. Dense, diffuse fibrosis with short fibrotic strands only marginally affected conduction curves. The course of conduction curves in patchy fibrotic areas greatly depended on the direction of propagation relative to fiber direction. CONCLUSIONS: The study demonstrates that in chronically diseased human myocardium, nonuniform anisotropic characteristics imposed by long fibrotic strands cause a progressive increase of activation delay, starting at long coupling intervals of premature stimuli. The increase strongly depends on the direction of the wave front with respect to fiber direction and the architecture of fibrosis.

Adult↗
PubMed2001

Increased dispersion and shortened refractoriness caused by verapamil in chronic atrial fibrillation.

OBJECTIVES: The objective was to assess the effect ofverapamil on atrial fibrillation (AF) cycle length and spatial dispersion of refractoriness in patients with chronic AF. BACKGROUND: Previous studies have suggested that verapamil prevents acute remodeling by AF. The effects of verapamil in chronic AF are unknown. METHODS: During electrophysiologic study in 15 patients with chronic AF (duration >1 year), 12 unipolar electrograms were recorded from right atrial free wall, right atrial appendage and coronary sinus, along with monophasic action potential recordings from the right atrial appendage. The mean fibrillatory interval at each atrial recording site was used as an index for local refractoriness. Dispersion of refractoriness was calculated as the standard deviation of all local mean fibrillatory intervals expressed as a percentage of the overall mean fibrillatory interval. After baseline measurements, verapamil (0.075 mg/kg intravenous in 10 min) was infused and the measurements were repeated. RESULTS: After administration ofverapamil, mean fibrillatory intervals shortened by a mean of 16.6 +/- 3.3 ms (p < 0.001) at the right free wall, 15.0 +/- 3.5 ms (p < 0.001) at the appendage and 17.1 +/- 3.2 ms (p < 0.01) in the coronary sinus. Monophasic action potential duration decreased by 15.9 +/- 4.0 ms (p < 0.01). Dispersion of refractoriness increased in all patients from 3.8 +/- 0.8 to 5.1 +/- 1.8 (p < 0.001). A strong correlation between mean fibrillatory intervals and action potential duration was found, both before and after verapamil. CONCLUSIONS: Verapamil caused shortening of refractoriness and increase in spatial dispersion of refractoriness in patients with chronic AF. This implies that verapamil is not useful in reversing the remodeling process in these patients.

Aged↗
PubMed2001

Sequential map-guided endocardial resection for ventricular tachycardia improves outcome.

OBJECTIVE: Surgery for ventricular tachycardias late after myocardial infarction is frequently associated with high mortality including sudden death, and arrhythmia recurrences. We examined our results of sequential map-guided endocardial resection at normothermia in patients with ventricular tachyarrhythmias late after myocardial infarction to assess the efficacy of this technique as well as the early and long-term outcome. METHODS: From 1995 to 1999, 22 patients underwent normothermic sequential map-guided endocardial resection for ventricular tachyarrhythmias late after myocardial infarction. Mean age was 61.2+/-6.5 years and left ventricular ejection fraction 32.5+/-8.7%. Adjunctive procedures included endoventricular patch repair of left ventricular aneurysm in 21 patients, coronary artery bypass grafting in 15 patients, and mitral valve replacement in one patient. Inducibility of ventricular tachycardia was evaluated postoperatively and patients were treated with sotalol or defibrillator implantation. RESULTS: The intraoperative number of inducible different ventricular tachycardia morphologies was 4.0+/-2.7. More than one mapping-resection sequence was needed in ten patients. In only one patient, sustained ventricular tachycardia was induced postoperatively, sotalol was not tolerated and a defibrillator was implanted. Five patients with inducible non-sustained ventricular tachycardia became non-inducible while on sotalol. There was one operative death (4.5%). During a median follow-up of 26 (1--62) months, there were neither cardiac deaths nor ventricular tachycardia recurrences. Two patients died from non-cardiac causes. Cumulative probability of survival at 5 years was 0.83+/-0.09. CONCLUSIONS: Sequential map-guided endocardial resection at normothermia was associated with low operative mortality and low postoperative inducibility of sustained ventricular tachycardia. The selected therapeutic approach resulted in freedom of arrhythmia recurrence and cardiac mortality including sudden death, during long-term follow-up.

Aged↗
PubMed2001

Diagnosis and long-term follow-up of the Brugada syndrome in patients with idiopathic ventricular fibrillation.

AIMS: Some patients with idiopathic ventricular fibrillation may suffer from the Brugada syndrome. The diagnostic criteria for the Brugada syndrome are uncertain and arbitrarily set. Therefore, we studied the prevalence of the Brugada syndrome using various diagnostic criteria and long-term follow-up in 37 idiopathic ventricular fibrillation patients. METHODS AND RESULTS: Idiopathic ventricular fibrillation was diagnosed after thorough clinical evaluation in 37 survivors of an out-of-hospital cardiac arrest referred to our institute (UMC Utrecht). Retrospectively, nine patients (24%, group I) were classified as potentially having the Brugada syndrome based on the presence of (in)complete right bundle branch block and ST-segment elevation in leads V(1)-V(3)of > or =1 mm. Only three patients (8%, group II) showed (in)complete right bundle branch block and > or =2 mm ST-segment elevation. With the intermittent presence of these ECG features and/or their (re)appearance with class I antiarrhythmic drugs included as criteria, the percentage of the Brugada syndrome was attenuated in group I (2/37; 5%) and group II (1/37; 3%). Sixteen (43%) of all idiopathic ventricular fibrillation patients (mean follow-up 77+/-41 months) had a recurrent episode of syncope, ventricular tachyarrhythmias or sudden death. Recurrence rate was 3/9 (33%) in Brugada patients group I, 2/3 (66%) in group II and 13/28 (46%) in patients without the Brugada syndrome (P=ns). CONCLUSIONS: Depending on the diagnostic criteria used, the Brugada syndrome was observed in 3% to 24% of patients with idiopathic ventricular fibrillation, underlining the importance of defining the precise diagnostic criteria in these patients. For all idiopathic ventricular fibrillation patients, the ventricular tachyarrhythmia recurrence rate was substantial during an average follow-up of more than 6 years.

Adolescent↗
PubMed2000

Identification of the substrate of atrial vulnerability in patients with idiopathic atrial fibrillation.

BACKGROUND: Experimental studies have shown that atrial fibrillation (AF) causes remodeling, which facilitates AF perpetuation. AF may also, however, occur in patients without remodeling and underlying structural cardiac disease. The substrate for enhanced vulnerability in these patients is unknown. METHODS AND RESULTS: We studied 43 patients without structural heart disease: 18 patients with documented sporadic paroxysmal AF and 25 control patients without AF. In each patient, a decapolar catheter was positioned against the right atrial free wall, and a quadripolar catheter was positioned in the right atrial appendage. Unipolar electrograms were recorded. Atrial vulnerability was assessed according to an increasingly aggressive stimulation protocol. Mean local fibrillatory interval (FI) was used as an index of local refractoriness. Spatial dispersion of refractoriness was assessed through the calculation of the coefficient of dispersion (CD), which was defined as the SD of mean local FI expressed as a percentage of the mean FI. In the AF group, AF was induced with a single extrastimulus in 16 of 18 patients; the CD was 5.4+/-2.6, and the mean FI was 164+/-29 ms. In the control group, AF could be induced only with more aggressive pacing in 23 of the 25 patients; the CD was 1.4+/-0.7 (P<0.0001), and the mean FI was 175+/-26 ms (NS). CONCLUSIONS: Patients with idiopathic AF showed increased dispersion of refractoriness, which may be the substrate for the observed enhanced inducibility and spontaneous occurrence of AF.

Adult↗
PubMed2000

Ventricular tachycardia as a complication of atrial flutter ablation.

A 61-year-old woman with dilated cardiomyopathy, who previously underwent successful radiofrequency catheter ablation for atrial flutter, developed monomorphic ventricular tachycardia (VT). The site of VT origin was the inferobasal right ventricle adjacent to the previous atrial isthmus ablation area. The most likely mechanism for the VT was scar-related reentry, the scar being the result of previous radiofrequency lesions in the atrial isthmus. The VT was successfully ablated.

Atrial Flutter↗
PubMed1999

Reentrant pathway during ventricular echoes is confined to the atrioventricular node : high-resolution mapping and dissection of the triangle of koch in isolated, perfused canine hearts.

Background-During ventricular echoes, reentrant excitation is supposed to involve 2 functionally distinct pathways in the atrioventricular (AV) nodal area. The exact pathway of reentrant excitation is unknown. The objectives of this study were to analyze electrical activity in the AV nodal area after ventricular stimulation and during ventricular echoes and to assess the role of perinodal atrial tissue in AV nodal reentry. Methods and Results-In 16 isolated, blood-perfused canine hearts, multiterminal electrodes were used to map electrical activity in Koch's triangle after ventricular stimulation and during ventricular echoes. The subendocardial cell layers were chemically destroyed in 3 hearts. Incisions in the posterior approach to the compact node were made in 6 hearts. The apex of the triangle of Koch was surgically dissociated from the perinodal atrial tissue in 5 hearts. Retrograde atrial activation occurred via 2 distinct endocardial exit sites. Ventricular echoes could be induced in all hearts irrespective of the atrial activation pattern. Simultaneous retrograde activation of both exit sites often preceded reciprocation. Ventricular echoes were demonstrable after chemical destruction of the endocardium and after surgical dissociation of the perinodal atrial tissue from the AV node. Conclusions-Our data show that the reentrant pathway during ventricular echoes is confined to the AV node. The tissue that connects the node to the endocardial exit sites has to be excluded from the reentrant circuit responsible for single echoes.

Action Potentials↗
PubMed1999

[Presymptomatic screening after a sudden cardiac death in the family].

Sudden cardiac death without ischaemic heart disease may be due to a hereditary heart disease with an autosomal dominant heredity. The occurrence, if any, of sudden death in such a family is a main indicator for the risk of sudden cardiac death in other family members. Cardiological and/or genetic investigation may reveal a hereditary disease in relatives without symptoms. Of some of these pathological conditions, the corresponding chromosomal localizations and sometimes the gene mutations have been identified. The psychic burden of family investigation and the socio-economic consequences (insurances, occupation, family relationships) are potentially heavy. Prophylactic treatment of asymptomatic persons in whom a gene mutation is established may comprise advice about lifestyle (e.g. avoidance of peak exercise in patients with hypertrophic cardiomyopathy), medication (e.g. beta-receptor blockers in patients with a long QT interval) or implantation of a pacemaker or internal defibrillator (e.g. in asymptomatic persons with the Brugada syndrome, a form of right bundle branch block). Presymptomatic investigation must be performed multidisciplinary.

Cardiovascular Diseases↗
PubMed1999

Clinical application of an integrated 3-phase mapping technique for localization of the site of origin of idiopathic ventricular tachycardia.

BACKGROUND: Radiofrequency (RF) catheter ablation provides curative treatment for idiopathic ventricular tachycardia (VT). METHODS AND RESULTS: Nineteen consecutive patients with an idiopathic VT underwent RF catheter ablation. An integrated 3-phase mapping approach was used, consisting of the successive application of online 62-lead body surface QRS integral mapping, directed regional paced body surface QRS integral mapping, and local activation sequence mapping. Mapping phase 1 was localization of the segment of VT origin by comparing the VT QRS integral map with a database of mean paced QRS integral maps. Mapping phase 2 was body surface pace mapping during sinus rhythm in the segment localized in phase 1 until the site at which the paced QRS integral map matched the VT QRS integral map was identified (ie, VT exit site). Mapping phase 3 was local activation sequence mapping at the circumscribed area identified in phase 2 to identify the site with the earliest local endocardial activation (ie, site of VT origin). This site became the ablation target. Ten VTs were ablated in the right ventricular outflow tract, 2 at the basal LV septum, and 7 at the midapical posterior left ventricle. A high long-term ablation success (mean follow-up duration, 14+/-9 months) was achieved in 17 of the 19 patients (89%) with a low number of RF pulses (mean, 3.3+/-2.2 pulses per patient). CONCLUSIONS: This prospective study shows that integrated 3-phase mapping for localization of the site of origin of idiopathic VT offers efficient and accurate localization of the target site for RF catheter ablation.

Adult↗
PubMed1999

LocaLisa: new technique for real-time 3-dimensional localization of regular intracardiac electrodes.

BACKGROUND: Estimation of the 3-dimensional (3D) position of ablation electrodes from fluoroscopic images is inadequate if a systematic lesion pattern is required in the treatment of complex arrhythmogenic substrates. METHODS AND RESULTS: We developed a new technique for online 3D localization of intracardiac electrodes. Regular catheter electrodes are used as sensors for a high-frequency transthoracic electrical field, which is applied via standard skin electrodes. We investigated localization accuracy within the right atrium, right ventricle, and left ventricle by comparing measured and true interelectrode distances of a decapolar catheter. Long-term stability was analyzed by localization of the most proximal His bundle before and after slow pathway ablation. Electrogram recordings were unaffected by the applied electrical field. Localization data from 3 catheter positions, widely distributed within the right atrium, right ventricle, or left ventricle, were analyzed in 10 patients per group. The relationship between measured and true electrode positions was highly linear, with an average correlation coefficient of 0.996, 0.997, and 0.999 for the right atrium, right ventricle, and left ventricle, respectively. Localization accuracy was better than 2 mm, with an additional scaling error of 8% to 14%. After 2 hours, localization of the proximal His bundle was reproducible within 1.4+/-1.1 mm. CONCLUSIONS: This new technique enables accurate and reproducible real-time localization of electrode positions in cardiac mapping and ablation procedures. Its application does not distort the quality of electrograms and can be applied to any electrode catheter.

Bundle of His↗
PubMed1999

Genetic and molecular basis of cardiac arrhythmias: impact on clinical management parts I and II.

Genetic approaches have succeeded in defining the molecular basis of an increasing array of heart diseases, such as hypertrophic cardiomyopathy and the long-QT syndromes, associated with serious arrhythmias. Importantly, the way in which this new knowledge can be applied to managing patients and to the development of syndrome-specific antiarrhythmic strategies is evolving rapidly because of these recent advances. In addition, the extent to which new knowledge represents a purely research tool versus the extent to which it can be applied clinically is also evolving. The present article represents a consensus report of a meeting of the European Working Group on Arrhythmias. The current state of the art of the molecular and genetic basis of inherited arrhythmias is first reviewed, followed by practical advice on the role of genetic testing in these and other syndromes and the way in which new findings have influenced current understanding of the molecular and biophysical basis of arrhythmogenesis.

Arrhythmias, Cardiac↗
PubMed1999

Accuracy of the LocaLisa system in catheter ablation procedures.

Estimation of the 3-dimensional (3D) position of ablation electrodes from fluoroscopic images is inadequate in the ablation of complex arrhythmogenic substrates. We developed a new technique for real-time 3D localization of intracardiac electrodes. Regular catheter electrodes are used as sensors for a high-frequency transthoracic electrical field, which is applied via standard skin electrodes. We investigated localization accuracy by comparing measured and true interelectrode distances between the tip and the 10th electrode of a decapolar catheter, and the tip and the 4th electrode of a quadripolar catheter during catheter ablation procedures. Long-term stability was analyzed by localization of the proximal His bundle before and after slow pathway ablation. Accuracy achieved with the 54-mm distance between the two outer electrodes of the decapolar catheters was 101% +/- 15%, 95% +/- 10%, and 97% +/- 8% in the right atrium, right ventricle, and left ventricle, respectively. During catheter ablation procedures, the measured distance between the tip and 4th electrode of the mapping catheter was 100% +/- 15% in atrial flutter, 100% +/- 12% in slow pathway ablation, and 100% +/- 14% in ablations for left ventricular tachycardia. After 2 hours, localization of the proximal His bundle was reproducible within 1.4 +/- 1.1 mm. The LocaLisa technique allows for reproducible, real-time nonfluoroscopic 3D visualization of standard mapping and ablation catheters and is sufficiently accurate for the creation of linear radiofrequency lesions. The freedom of catheter choice makes the LocaLisa system an invaluable tool in catheter mapping and ablation procedures.

Atrial Flutter↗
PubMed1999

Auditory stimuli as a trigger for arrhythmic events differentiate HERG-related (LQTS2) patients from KVLQT1-related patients (LQTS1).

OBJECTIVE: This study was performed to identify a possible relationship between genotype and phenotype in the congenital familial long QT syndrome (cLQTS). BACKGROUND: The cLQTS, which occurs as an autosomal dominant or recessive trait, is characterized by QT-interval prolongation on the electrocardiogram and torsade de pointes arrhythmias, which may give rise to recurrent syncope or sudden cardiac death. Precipitators for cardiac events are exercise or emotion and occasionally acoustic stimuli. METHODS: The trigger for cardiac events (syncope, documented cardiac arrhythmias, sudden cardiac death) was analyzed in 11 families with a familial LQTS and a determined genotype. RESULTS: The families were subdivided in KVLQT1-related families (LQTS1, n = 5) and HERG (human ether-a-gogo-related gene)-related families (LQTS2, n = 6) based on single-strand conformation polymorphism analysis and sequencing. Whereas exercise-related cardiac events dominate the clinical picture of LQTS1 patients, auditory stimuli as a trigger for arrhythmic events were only seen in LQTS2 patients. CONCLUSIONS: Arrhythmic events triggered by auditory stimuli may differentiate LQTS2 from LQTS1 patients.

Acoustic Stimulation↗
PubMed1998

Effects of intracavitary blood flow and electrode-target distance on radiofrequency power required for transient conduction block in a Langendorff-perfused canine model.

OBJECTIVES: We sought to quantify the effects of electrode-target distance and intracavitary blood flow on radiofrequency (RF) power required to induce transient conduction block, using a Langendorff-perfused canine ablation model. BACKGROUND: Given the thermally mediated nature of RF catheter ablation, cooling effects of intracavitary blood flow and electrode-target distance will influence lesion extension and geometry and electrophysiologic effects. METHODS: In eight Langendorff-perfused canine hearts, the right ventricular free wall was opened, and the right bundle branch (RBB) carefully localized by multielectrode activation mapping. The right atrium was paced at cycle length of 500 ms. Proximal and distal electrodes were attached at the endocardial aspect of the RBB, and the perfused heart was submerged in heparinized blood at 37 degrees C. A standard 4-mm tip ablation electrode was positioned at a constant contact pressure of 5 g between the two electrodes at the site of maximal RBB potential (0 mm) and 2 and 4 mm distant from this site along a line perpendicular to the RBB. RF pulses (500 kHz) were delivered for 30 s at 0.5-W increments until transient bundle branch block. In four hearts, intracavitary flow was simulated by directing a 30-cm/s jet of blood parallel to the septum at the ablation site, and the protocol was repeated to assess the effects on power required for block. In one heart, the effect of variable flow was assessed (0, 15 and 30 cm/s). RESULTS: An exponential distance-related increase was seen in power required for block, from 1.8 +/- 0.9 W (mean +/- SD) at 0 mm to 5.4 +/- 1.1 W at 4 mm. In the presence of 30-cm/s flow, an increase to 3.9 +/- 0.8 W at 0 mm and 13.1 +/- 2.4 W at 2 mm was seen. At 4 mm, coagulum formation invariably occurred before block could be induced. For 15-cm/s flow, less power was required: 3 and 7 W at 0 and 2 mm, respectively. CONCLUSIONS: Increasing the ablation electrode-target distance causes an exponential increase in power required for conduction block; this relation is profoundly influenced by intracavitary flow. Given the geometry of endomyocardial RF lesions, these findings are particularly relevant for directly subendocardial ablation targets.

Animals↗