Automatic Recognition of Ventricular Arrhythmias Using Temporal Electrogram Analysis

Future antitachycardia devices must be able to deliver a variety of therapies according to the requirements of the underlying arrhythmia. To ensure that appropriate treatment is prescribed the device must use a detection algorithm that is able to discriminate between multiple arrhythmias. Current criteria such as rate, change of rate, duration at high rate, and high rate stability are inadequate for this purpose. Many algorithms that evaluate the morphology of the endocardial electrogram are of too great a complexity to be incorporated in implantable devices that require real-time analysis without undue power consumption. In this study the sensitivity of a simple morphological technique (temporal electrogram analysis) is examined. The method sets threshold 'rails' above and below the isoelectric line and classifies ECG complexes according to the sequence and duration of rail excursions. A total of 27 ventricular tachyarrhythmias were induced in 25 patients (17 with a history of recurrent arrhythmias and eight undergoing risk stratification postmyocardial infarction). Temporal electrogram analysis (TEA), initially detected the onset of the ventricular arrhythmia in all patients whose surface ECG showed polymorphic or right bundle branch block pattern tachycardia, in 5/8 of cases with left bundle branch block pattern and in 4/5 of patients with concordant complexes across the precordial leads. After minor modifications the overall sensitivity of the method was improved to 95% (26/27 arrhythmias detected). TEA is a technique of low computational demands, which in this study, reliably discriminated between resting sinus rhythm and ventricular arrhythmias.     

A CASE OF ''ESSENTIAL'' HYPERNATRAEMIA DUE TO RESETTING OF THE OSMOSTAT

We describe a 24-year-old short, obese girl who has bizarre episodic neurological abnormalities related to hyperosmolality due to hypernatraemia. Investigation of osmoregulation by water loading and infusion of hypertonic saline revealed (i) hypodipsia with thirst onset raised to plasma osmolality of 332 mmol/kg and (ii) elevation of the threshold for vasopressin release (plasma osmolality 320 mmol/kg) but normal slope of the plasma vasopressin-plasma osmolality curve. Baroregulated vasopressin release was also grossly subnormal. Other hypothalamo-pituitary investigations showed deficiencies of releasing hormones for gonadotrophins and growth hormone, but prolactin response to combined hypoglycaemia and TRH was blunted She demonstrated other anomalies including hyperlipoproteinaemia and defective lymph drainage of the legs. Skull X-rays, together with computerized tomography and nuclear magnetic resonance scans of the hypothalamo-pituitary region and the rest of the brain were normal. We believe that this is the first case of essential hypernatraemia documented with direct evidence of resetting of the osmostat.