Anthony F. Rickards
University College Hospital
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Featured researches published by Anthony F. Rickards.
Pacing and Clinical Electrophysiology | 1996
Anthony F. Rickards; Toning Bombardini; Giorgio Corbucci; Gianni Plicchi
As the myocardium contracts isometrically, it generates vibrations that are transmitted throughout the heart. These vibrations can be measured with an implantable microaccelerometer located inside the tip of an otherwise conventional unipolar pacing lead. These vibrations are, in their audible component, responsible for the first heart sound. The aim of this study was to evaluate, in man, the clinical feasibility and reliability of intracavity sampling of Peak Endocardial Acceleration (PEA) of the first heart sound vibrations using an implantable tip mounted accelerometer. We used a unidirectional accelerometer located inside the stimulating tip of a standard unipolar pacing lead: the sensor has a frequency response of DC to 1 kHz and a sensitivity of 5 mV/G (G ‐ 9.81 m/s−2). The lead was connected to an external signal amplifier with a frequency range of 0.05–1,000 Hz and to a peak‐to‐peak detector synchronized with the endocardial R wave scanning the isovolumetric contraction phase. Following standard electro‐physiological studies, sensor equipped leads were temporarily inserted in the RV of 15 patients (68 ± 15 years), with normal regional and global ventricular function, to record PEA at rest, during AAI pacing, during VVI pacing, and during dobutamine infusion (up to 20 |mg/kg per min). PEA at baseline was 1.1 G ± 0.5 (heart rate = 75 ± 14 beats/rain) and increased to 1.3 G ± 0.9 (P = NS vs baseline) during AAI pacing (heart rate = 140 beats/min) and to 1.4 G ± 0.5 (P = NS vs baseline) during VVI pacing (heart rate = 140 beats/min). Dobutamine infusion increased PEA to 3.7 G ± 1.1 (P < 0.001 vs baseline), with a heart rate of 121 ± 13 beats/min. In a subset of three patients, simultaneous hemodynamic RV monitoring was performed to obtain RV dP/dtmax, whose changes during dobutamine and pacing were linearly related to changes in PEA (r = 0.9; P < 0.001). In conclusion, the PEA recording can be consistently and safely obtained with an implantable device. Pharmacological inotropic stimulation, but not pacing induced chronotropic stimulation, increases PEA amplitude, in keeping with experimental studies, suggesting that PEA is an index ofmyocardial contractility. Acute variations in PEA are closely paralleled by changes in R V dP/dtmax, but are mainly determined by LV events. The clinical applicability of the method using RV endocardial leads and an implantable device offers potential for diagnostic applications in the long‐term monitoring of myocardial function in man.
Pacing and Clinical Electrophysiology | 1993
Alan D. Bernstein; A. John Camm; John D. Fisher; Ross D. Fletcher; R. Hardwin Mead; Anthony W. Nathan; Victor Parsonnet; Anthony F. Rickards; Nicholas P.D. Smyth; Richard Sutton; Peter P. Tarjan
A new generic code, patterned after and compatible with the NASPE/BPEG Generic Pacemaker Code (NBG Code) was adopted by the NASPE Board of Trustees on January 23. 1993. It was developed by the NASPE Mode Code Committee, including members of the North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Croup (BPEC). It is abbreviated as the NBD (for NASPE/BPEC Defibrillator) Code. It is intended for describing the capabilities and operation of implanted cardioverter defibrillators (ICDs) in conversation, record keeping, and device labeling, and incorporates four positions designating: (1) shock location; (2) antitachycardia pacing location; (3) means of tachycardia detection; and (4) antibradycardia pacing location. An additional Short Form, intended only for use in conversation, was defined as a concise means of distinguishing devices capable of shock alone, shock plus antibradycardia pacing, and shock plus antitachycardia and antibradycardia pacing.
Pacing and Clinical Electrophysiology | 1989
Arif J. Ahsan; David Cunningham; Edward Rowland; Anthony F. Rickards
A new system is described for catheter ablation which comprises a short time capacitive power source and a specially designed catheter. The aim of the new system is to deliver high voltages with minimal or no arcing and thus avoid the risks associated with barotrauma. The performance of the new system was compared in a saline tank with that of the conventional system. The new system allowed significant increases in delivered voltage, current and energy without arcing. This new system should allow safer catheter ablation.
Pacing and Clinical Electrophysiology | 1989
David Cunningham; Arif J. Ahsan; Edward Rowland; Anthony F. Rickards
This study has used high energy ablative shocks in saline and in man to characterize the complex, energy dependent behavior of the impedance at the electrode‐tissue interface. In vitro shocks showed a fall in impedance when an arc was formed, due to formation around the electrode of a vapor globe rendered conductive by the arc. Following arc extinction, this same vapor globe insulates the electrode, and subsequently collapses, forming a shock wave, and allowing current flow to resume. Shocks delivered to tissue specimens exhibited progressively higher impedance and less insulation as contact pressure was increased. In vivo, lesser degrees of insulation during arcing shocks were associated with greater clinical efficacy.
Cardiovascular Research | 1986
Timothy J. Bowker; Paul Edwards; T. Hall; Mark Regel; S. G. Bown; Kim M. Fox; Phillip A Poole-Wilson; Anthony F. Rickards
Pacing and Clinical Electrophysiology | 1989
Anthony F. Rickards
Pacing and Clinical Electrophysiology | 1995
Anthony F. Rickards
Journal of Interventional Cardiology | 1990
John M. Morgan; Tim R. Cripps; Timothy J. Bowker; Anthony F. Rickards
The Lancet | 1986
Graham Jackson; Kim Fox; Anthony F. Rickards
Clinical Science | 1988
A.J. Ahsan; A.D. Cunningham; Edward Rowland; Anthony F. Rickards; Kim Fox