50Hz interference and noise in ECG recordings--a review.

In this review paper, a simplified model is used to explain the various ways by which 50Hz interference can disturb electrocardiogram recordings. From the model, noise expressions are also derived which explain sources of noise in recordings. Means of minimising the 50Hz interference and noise with emphasis placed on skin abrasion and right-leg drive circuits are discussed. An add-on circuit which can be used with existing amplifiers to improve their performance is shown. Previous interference analysis has concentrated on 2-input differential amplifiers, however in modern hospitals, a wide variety of amplifier configurations are used. An example is the Wilson Central Terminal which is used to obtain a zero potential in body surface mapping applications. In this review it is shown with an example for an ECG amplifier incorporating a Wilson Central Terminal, how it is easy to extend the interference model to other applications.

A novel approach to the design of a Wilson referenced ECG amplifier.

The Wilson Central Terminal consists of three limb electrodes connected through a resistor network at the inverting input to the ECG amplifier. It is often used as a zero potential reference in ECG recordings. In this paper, the implications of using a Wilson central reference on the overall amplifier's common-mode rejection ratio and noise specifications is analysed. It is shown that the Wilson reference can degrade the overall amplifier specifications. The design of a Wilson referenced amplifier is then described which shows this to be true. A novel approach to the design of a Wilson referenced ECG amplifier is then presented, whereby the reference network is moved from the input to an intermediate stage of the amplifier. An analysis on the improvements achieved over the conventional approach is given. An amplifier design using the new approach is then described. Tests results showed a significant improvement in amplifier common mode rejection ratio and noise specifications when compared to the conventional design.

Increased PAC-1 expression among patients with multiple myeloma on concurrent thalidomide and warfarin.

Treatment with thalidomide is associated with vascular thrombosis. The effect of thalidomide on platelet activation is unclear, although the use of aspirin is justified for thromboprophylaxis. A study on platelet activation markers was done among multiple myeloma patients receiving thalidomide therapy with warfarin as thromboprophylaxis. Strict criteria and procedure were set to avoid misinterpretation of platelet activation other than due to the thalidomide's effect. Blood specimen pre and post thalidomide therapy were used for flow cytometric analysis. Platelet surface P-selectin, CD62P expression and PAC-1 (antibody that recognizes conformational change of the GPIIb/IIIa complex) were examined by using three-colour flowcytometer. Increased expression marker for PAC-1 was observed after 4 weeks of thalidomide treatment (P < 0.05) indicating one aspect of platelet activation activity seen in these patients. The mechanism of thrombosis by thalidomide is probably multifactorial and one of them is likely through platelet activation. Further study on the affected pathway/s in the platelet activation process would confirm the exact mechanism of thalidomide-induced thrombosis and potential extended usage of this drug in future.