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C Nibley

Publications and source records attributed to C Nibley.

3 recordsLinked to original sources

Transient data stream dissociation in computerized data acquisition system masquerading as a sensing abnormality.

During testing of a CPI model 1715 ICD, an apparent sensing abnormality was noted following shock delivery for VF. Close inspection of the recording prior to the defibrillation attempt revealed that the surface leads spontaneously lost 848 ms of data while the event marker was unaffected. Computer simulations revealed that an inadequate buffer size for the amplified (surface ECG) data was the likely source of data loss. It is important to recognize that a discordance between surface leads and event marker may represent an abnormality in the data acquisition system and simulate an ICD or lead malfunction.

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Ventricular tachycardias with left bundle branch block morphology.

The differential diagnosis of VTs with LBBB morphology includes several well-defined syndromes. Although the majority of cases are attributable to acquired structural heart disease, including ischemia, prior infarction, or dilated cardiomyopathy, consideration of specific right ventricular processes is essential to proper evaluation and treatment. The approach to older patients or those with evidence for heart disease should begin with an evaluation for coronary artery disease and an assessment of biventricular function. Careful evaluation for bundle branch reentry should be performed during electrophysiological study, especially when there is underlying conduction system disease. Younger patients, those without overt heart disease, or those with isolated right ventricular disease, should receive a complete noninvasive evaluation of right and left ventricular size and function. An abnormal SAECG or identification of intracardiac late potentials suggest right ventricular dysplasia or cardiomyopathy, whereas responsiveness to adenosine and absence of detectable heart disease support the diagnosis of idiopathic right VT. Newer techniques, including MRI, show promise in identifying subtle right ventricular disease not otherwise detectable even in the setting of presumed idiopathic right VT. Following surgical repair of selected congenital heart defects, particularly tetralogy of Fallot, symptoms of recurrent palpitations, near syncope, syncope, or aborted sudden death may be attributable to recurrent VT, and diagnostic electrophysiological study should be considered for these patients. Finally, SVTs with LBBB morphology, particularly cases associated with right-sided or septal accessory pathways, should always be considered in this differential diagnosis.

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Polymorphous ventricular tachycardia associated with acute myocardial infarction.

BACKGROUND: During a 2.9-year period, 11 patients developed polymorphous ventricular tachycardia 1-13 days after acute anterior (seven patients) or inferior (four patients) myocardial infarction. None of the 11 patients had sinus bradycardia (mean heart rate, 90 +/- 23 beats/min), but three had a sinus pause immediately before the onset of polymorphous ventricular tachycardia. In all 11 patients, the QT interval and corrected QT interval (QTc) were normal or minimally prolonged (QT, 385 +/- 34 msec; QTc, 442 +/- 40 msec). None had significant hypokalemia (mean serum potassium concentration, 4.3 +/- 0.5 meq/l) or a grossly abnormal serum magnesium or calcium concentration (2.1 +/- 0.4 and 8.9 +/- 0.7 mg/dl, respectively). METHODS AND RESULTS: Immediately before the onset of polymorphous ventricular tachycardia, symptoms and/or electrocardiographic changes consistent with recurrent myocardial ischemia occurred in nine of 11 patients. One patient died before drug therapy could be initiated. Lidocaine was used in 10 patients and proved to be effective in only one. Intravenous procainamide was used in six patients: one improved, and five had recurrence of polymorphous ventricular tachycardia. Bretylium was used in five patients and was ineffective in all cases. Overdrive pacing was used in four patients and failed to suppress recurrent arrhythmias in all cases. Four patients with persistent polymorphous ventricular tachycardia unresponsive to lidocaine, procainamide, or bretylium responded to intravenous amiodarone. One patient with polymorphous ventricular tachycardia that was consistently preceded by ST segment elevation responded to intravenous nitroglycerin. Two patients with persistent polymorphous ventricular tachycardia and obvious recurrent ischemia unresponsive to pharmacological intervention responded to emergency coronary revascularization. A third patient who experienced recurrent angina and polymorphous tachycardia was initially stabilized with pharmacological therapy but subsequently underwent elective revascularization and has remained stable without antiarrhythmic therapy. CONCLUSIONS: Post-myocardial infarction polymorphous ventricular tachycardia is not consistently related to an abnormally long QT interval, sinus bradycardia, preceding sinus pauses, or electrolyte abnormalities. This arrhythmia has a variable response to class I antiarrhythmics but may be suppressed by intravenous amiodarone therapy. It is often associated with signs or symptoms of recurrent myocardial ischemia. Furthermore, coronary revascularization appears to be effective in preventing the recurrence of polymorphous ventricular tachycardia when associated with recurrent postinfarction angina.

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