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Biomedical subjects

M Wathen

Publications and source records attributed to M Wathen.

11 recordsLinked to original sources
PubMed2001

Functional similarity between electrograms recorded from an implantable cardioverter defibrillator emulator and the surface electrocardiogram.

Clinical use of stored electrogram (EGM) configurations currently used in ICDs is limited. The hypothesis that EGMs recorded from electrodes on the ICD surface may improve diagnostic capabilities of the device was tested in the present study. The Buttons on Active Can Emulator (BACE), an ICD-sized device containing four button electrodes, was temporarily placed into a subcutaneous or submuscular left pectoral pocket in 16 patients during ICD implantation. Simultaneous recordings were obtained from the ECG lead II, bipolar EGMs using BACE electrodes, and a bipolar atrial EGM during sinus rhythm (SR), ventricular pacing (VP) at cycle lengths of 500 and 400 ms, and VT. Visible P waves were present in all patients during SR (n = 15), in 5 (33%) of 15 patients during VP, and none of the patients during VT (n = 4) using BACE EGMs and lead II. P and QRS amplitudes and the P:QRS ratio during SR in BACE EGMs were significantly lower than those in lead II. BACE EGMs showed prominent changes in QRS morphology and duration during VP and VT compared to SR, and the magnitude of QRS prolongation during VP was similar to that in lead II. Measurements of PR, QRS, and QT duration during SR showed good agreement between BACE EGMs and lead II. In conclusion, EGMs recorded from electrodes embedded on the ICD housing may potentially improve visual discrimination between supraventricular and ventricular arrhythmias. They also may be useful as a surrogate of the ECG for analysis and monitoring of different components of P-QRS-T complex.

Defibrillators, Implantable↗
PubMed2001

Lead- and device-related complications in the antiarrhythmics versus implantable defibrillators trial.

BACKGROUND: Implantation of transvenous implantable cardioverter defibrillators (ICDs) by use of a nonthoracotomy approach has become routine therapy for survivors of life-threatening tachyarrhythmias. The purpose of this study was to identify and prospectively characterize the frequency of lead- and ICD-related complications from the Antiarrhythmics versus Implantable Defibrillators (AVID) Trial. METHODS AND RESULTS: Between June 1, 1993, and April 7, 1997, 539 patients received nonthoracotomy ICDs either as initial treatment assignment (477) or as crossover from medical management (62). A total of 62 first complications occurred. The subclavian route of insertion resulted in more complications than the cephalic vein route, 46 of 339 (14%) versus 6 of 135 (4%), P = .005, as did the abdominal versus pectoral generator site, 31 of 238 (13%) versus 17 of 291 (6%), P<.02. Most dislodgements and system infections tended to occur in the 3 months after implantation, whereas lead fractures continued to occur throughout follow-up. Failure to use perioperative antibiotics was a predictor of system infection (P = .001). CONCLUSIONS: These data suggest that cephalic vein access and pectoral generator site may result in fewer complications. The continued occurrence of lead fractures and the need for premature system revision supports the practice of close routine ICD system surveillance.

Anti-Arrhythmia Agents↗
PubMed2000

The neuropathic postural tachycardia syndrome.

BACKGROUND: The postural tachycardia syndrome is a common disorder that is characterized by chronic orthostatic symptoms and a dramatic increase in heart rate on standing, but that does not involve orthostatic hypotension. Several lines of evidence indicate that this disorder may result from sympathetic denervation of the legs. METHODS: We measured norepinephrine spillover (the rate of entry of norepinephrine into the venous circulation) in the arms and legs both before and in response to exposure to three stimuli (the cold pressor test, sodium nitroprusside infusion, and tyramine infusion) in 10 patients with the postural tachycardia syndrome and in 8 age- and sex-matched normal subjects. RESULTS: At base line, the mean (+/-SD) plasma norepinephrine concentration in the femoral vein was lower in the patients with the postural tachycardia syndrome than in the normal subjects (135+/-30 vs. 215+/-55 pg per milliliter [0.80+/-0.18 vs. 1.27+/-0.32 nmol per liter], P=0.001). Norepinephrine spillover in the arms increased to a similar extent in the two groups in response to each of the three stimuli, but the increases in the legs were smaller in the patients with the postural tachycardia syndrome than in the normal subjects (0.001+/-0.09 vs. 0.12+/-0.12 ng per minute per deciliter of tissue [0.006+/-0.53 vs. 0.71+/-0.71 nmol per minute per deciliter] with the cold pressor test, P=0.02; 0.02+/-0.07 vs. 0.23+/-0.17 ng per minute per deciliter [0.12+/-0.41 vs. 1.36+/-1.00 nmol per minute per deciliter] with nitroprusside infusion, P=0.01; and 0.008+/-0.09 vs. 0.19+/-0.25 ng per minute per deciliter [0.05+/-0.53 vs. 1.12+/-1.47 nmol per minute per deciliter] with tyramine infusion, P=0.04). CONCLUSIONS: The neuropathic postural tachycardia syndrome results from partial sympathetic denervation, especially in the legs.

Adult↗
PubMed1999

Congenital long-QT syndrome caused by a novel mutation in a conserved acidic domain of the cardiac Na+ channel.

BACKGROUND: Congenital long-QT syndrome (LQTS) is an inherited condition of abnormal cardiac excitability characterized clinically by an increased risk of ventricular tachyarrhythmias. One form, LQT3, is caused by mutations in the cardiac voltage-dependent sodium channel gene, SCN5A. Only 5 SCN5A mutations have been associated with LQTS, and more work is needed to improve correlations between SCN5A genotypes and associated clinical syndromes. METHODS AND RESULTS: We researched a 3-generation white family with autosomal dominant LQTS who exhibited a wide clinical spectrum from mild bradycardia to sudden death. Molecular genetic studies revealed a single nucleotide substitution in SCN5A exon 28 that caused the substitution of Glu1784 by Lys (E1784K). The mutation occurs in a highly conserved domain within the C-terminus of the cardiac sodium channel containing multiple, negatively charged amino acids. Two-electrode voltage-clamp recordings of a recombinant E1784K mutant channel expressed in Xenopus oocytes revealed a defect in fast inactivation characterized by a small, persistent current during long membrane depolarizations. Coexpression of the mutant with the human sodium channel beta1-subunit did not affect the persistent current, even though we did observe shifts in the voltage dependence of steady-state inactivation. Neutralizing multiple, negatively charged residues in the same region of the sodium channel C-terminus did not cause a more severe functional defect. CONCLUSIONS: We characterized the genetics and molecular pathophysiology of a novel SCN5A sodium channel mutation, E1784K. The functional defect exhibited by the mutant channel causes delayed myocardial repolarization, and our data on the effects of multiple charge neutralizations in this region of the C-terminus suggest that the molecular mechanism of channel dysfunction involves an allosteric rather than a direct effect on channel gating.

Adolescent↗
PubMed1993

Initiation of atrial fibrillation in the Wolff-Parkinson-White syndrome: the importance of the accessory pathway.

Atrial fibrillation in the Wolff-Parkinson-White syndrome may be related to microreentry in the accessory pathway. If such is the case, catheter ablation of the accessory pathway should eliminate atrial fibrillation. Among 95 patients undergoing catheter ablation, 20 had atrial fibrillation during standard electrophysiologic study (atrial vulnerability) before ablation. There were 16 women and four men with a mean age of 32 years. Before ablation six patients required electrical cardioversion. Thirty minutes after ablation, 11 continued to have inducible atrial fibrillation. Atrial fibrillation terminated spontaneously in every patient after ablation. A control group of 20 patients with accessory pathway ablation had no inducible atrial fibrillation before or after ablation. Catheter ablation had no effect on atrial properties including functional refractory period (227 +/- 37 vs 215 +/- 29 msec before versus after ablation, mean +/- SD) or wavelength (7.4 +/- 3.2 vs 7.2 +/- 2.7 before versus after ablation). These data suggest that an intact accessory pathway is not necessary for initiation of atrial fibrillation in most patients with Wolff-Parkinson-White syndrome. A rapid ventricular response over the accessory pathway may facilitate the perpetuation of atrial fibrillation in persons prone to this arrhythmia.

Adult↗
PubMed1993

Comparative atrioventricular node properties after radiofrequency ablation and operative therapy of atrioventricular node reentry.

The anatomical substrate for atrioventricular (AV) node reentry is unclear. To gain insights into the mechanism of cure of AV node reentry by nonpharmacological techniques, we compared AV node properties in 53 patients undergoing operative therapy (perinodal dissection) and 43 undergoing radiofrequency ablation (28 posterior approach, 15 anterior approach). Anterior radiofrequency ablation was associated with significant AH prolongation (62 +/- 18 msec vs 136 +/- 64 msec, P < 0.0001), loss of "fast" pathway physiology, and no change in the anterograde refractory period of the AV node (273 +/- 24 msec vs 268 +/- 28 msec, P = NS). Posterior radiofrequency ablation did not change the AH interval (67 +/- 17 msec vs 68 +/- 17 msec, P = NS), prolonged AV node effective refractory period (275 +/- 48 msec vs 320 +/- 55 msec, P < 0.0001), and was associated with loss of "slow pathway" physiology. Operative treatment prolonged the AH interval (66 +/- 18 msec vs 83 +/- 37 msec, P < 0.0001) and the AV node effective refractory period (264 +/- 52 msec vs 364 +/- 112 msec, P < 0.0001), and affected dual pathway physiology inconsistently. These data support the view that the "fast" and "slow" pathways are distinct perinodal entities that can be selectively ablated. The operative approach causes more diffuse and variable injury to the AV node region.

Adolescent↗
PubMed1992

An anatomically guided approach to atrioventricular node slow pathway ablation.

Radiofrequency ablation of the "slow" pathway of the atrioventricular (AV) node reentrant circuit may be guided by electrophysiologic ("slow pathway potential") or anatomic landmarks. Experience with a systematic, anatomically guided approach in 25 patients (20 women and 5 men, aged 38 +/- 15 years) with typical AV node reentry is described. The slow pathway is assumed to be the posterior input to the AV node, approaching the nodal region in the corridor between the tricuspid annulus and the orifice of the coronary sinus. A series of radiofrequency lesions are given to interrupt this corridor at its entrance to Koch's triangle. If this is unsuccessful, the series of lesions are repeated progressively at higher levels approaching the AV node. The major end point for success is elimination of the slow pathway as determined by extrastimulus testing. A mean of 1.2 +/- 0.2 ablative sessions (20 +/- 12 applications of energy) achieved clinical success in 24 of 25 patients (96%) at a follow-up of 8.6 +/- 2.2 months. Anterograde Wenckebach cycle length increased from 361 +/- 67 ms to 398 +/- 70 ms (p = 0.01), yet the atrio-Hisian interval in sinus rhythm did not change (69 +/- 17 ms before vs 65 +/- 15 ms after ablation), p = 0.22. Retrograde Wenckebach cycle length was not affected (348 +/- 78 ms before vs 366 +/- 82 ms after ablation). During ablation, transient third-degree AV block occurred in 6 patients with no permanent sequelae. This approach provides a systematic, expedient technique to eliminate slow pathway conduction based on anatomic landmarks.

Adult↗
PubMed1985

Effects of propranolol and diltiazem alone and in combination on the recovery of left ventricular segmental function after temporary coronary occlusion and long-term reperfusion in conscious dogs.

We evaluated the ability of propranolol and diltiazem alone and in combination to enhance the recovery of left ventricular (LV) segmental function during 1 month of reperfusion after two temporary occlusions of the left anterior descending coronary artery (LAD) in conscious dogs instrumented with ultrasonic crystals for the measurement of regional net systolic wall thickening (NET). LV segments were classified according to their contractile function after 1 hr of LAD occlusion: class 1, greater than 67% of preocclusion (control) NET; class 2, 0% to 66.9%; class 3, less than 0% (paradoxical systolic wall thinning). Propranolol (1 mg/kg iv) or diltiazem (20 micrograms/kg/min) was given 65 min after LAD occlusion in dogs that had 2 (group I) or 4 hr (group II) of LAD occlusion. Diltiazem plus propranolol (same doses) were given to another group of dogs that underwent 4 hr (but not 2) of LAD occlusion. Untreated control dogs received 25 ml of saline and underwent 2 or 4 hr of LAD occlusion. The NET of class 2 and 3 segments in group I control dogs increased significantly during 1 month of reperfusion, from 32 +/- 5% and -43 +/- 6% to 66 +/- 9% and 26 +/- 9%, respectively (p less than .05). Neither diltiazem nor propranolol enhanced the long-term recovery of these segments in group I dogs. However, diltiazem prevented further deterioration of contractile dysfunction observed in control dogs immediately after reperfusion in both segment classes. The NET of class 2 segments in group II control dogs after 4 weeks of reperfusion remained at levels observed during LAD occlusion: 30 +/- 4% to 37 +/- 12%. Class 3 NET increased from -33 +/- 5% to 12 +/- 12% with 1 month of reperfusion, but these segments were essentially akinetic. Propranolol or diltiazem alone did not produce significant overall increases in NET, but diltiazem again prevented further declines in NET of class 2 and 3 segments during early reperfusion. However, the combination of diltiazem and propranolol significantly enhanced overall recovery of class 2 NET in group II dogs (44 +/- 3% to 88 +/- 7%) and prevented the worsening of NET associated with early reperfusion. Compared with untreated dogs, propranolol plus diltiazem also significantly decreased the extent of histologic necrosis in class 2 and 3 segments as well as the macrohistochemically determined infarct size in group II dogs.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗