Biomedical subjects

Ursula Ravens

Publications and source records attributed to Ursula Ravens.

57 records · Page 4Linked to original sources

PubMed2002

Rate-adaptive pacing using intracardiac impedance shows no evidence for positive feedback during dobutamine stress test.

BACKGROUND: The Inos2 DDDR pacemaker senses unipolar intracardiac impedance signals for adapting heart rate to meet the haemodynamic needs of physical activity. Theoretically, such pacing devices could be limited by positive feedback since increase in beating frequency per se enhances contractility. We have addressed this problem in patients with chronotropic incompetence who were subjected to a pharmacological stress test. METHODS AND RESULTS: Twelve patients with chronically implanted Inos2 DDDR pacemakers were studied using the standard protocol of stress echocardiography. Most of the patients reached the programmable maximum closed-loop rate during the incremental dobutamine challenge. The time courses for increase in as well as for recovery of heart rate were not different from control patients receiving routine diagnostic stress echocardiography. CONCLUSIONS: In patients implanted with the Inos2 DDDR pacemaker acute stimulation with intravenous dobutamine leads to a robust increase in paced heart rate without any evidence of positive feedback.

Cardiac Pacing, Artificial↗

PubMedDate not supplied

Cardiac mechano-electric feedback: past, present, and prospect.

Mechanical effects on heart rhythm have been known to the clinical community for well over a century, and documented cases include both arrhythmogenic and pro-rhythmic consequences of mechanical stimulation. The intracardiac pathway that leads from changes in the cardiac mechanical environment to altered electrical activity is referred to as mechano-electric feedback (MEF). Fundamental research into the mechanisms underlying cardiac MEF is 'engineering-intensive', and much of the current insight would have been impossible without the introduction of novel techniques for the study of isolated cardiac cells. Clinical and basic research into MEF have developed over different time scales, often uninformed of each other, and utilizing disparate concepts and terminology. Bridging the gap between the two domains is not straightforward, as physicians and scientists tend to publish in different journals and attend different meetings. There is, however, a growing interest in 're-uniting' the clinic and basic MEF research, as witnessed by an increasing number of dedicated journal issues and international meetings, including events hosted by major European and American professional organisations such as the ESC and NASPE. Last year alone saw an international workshop on Cardiac MEF & Arrhythmias at Oxford, as well as dedicated sessions at NASPE's 23rd annual meeting in San Diego, CardioStim 2002 in Nice, and the UK Physiological Society meeting in Leeds. This volume of Progress in Biophysics and Molecular Biology incorporates clinical and basic science results, and it is fitting that its publication coincides with a special session on cardiac MEF at the 2003 meeting of NASPE.

Animals↗

PubMedDate not supplied

Mechano-electric feedback and arrhythmias.

The mechanical state of the heart feeds back to modify cardiac rate and rhythm. Mechanical stretch of myocardial tissue causes immediate and chronic responses that lead to the common end point of arrhythmia. This review provides a brief summary of the author's personal choice of contributions that she considers have fostered our understanding of the role of mechano-electric feedback in arrhythmogenesis. Acute mechanical stretch reversibly depolarises the cell membrane and shortens the action potential duration. These electrophysiological changes are related to the activation of mechano-sensitive ion channels. Several different ion channels are involved in the sensing of stretch, among them K(+)-selective, Cl(-)-selective, non-selective, and ATP-sensitive K(+) channels. Sodium and Ca(2+) entering the cells via non-selective ion channels are thought to contribute to the genesis of stretch-induced arrhythmia. Mechano-sensitive channels have been cloned from non-vertebrate and vertebrate species. Chronic stress on the heart activates gene expression in cardiomyocytes and non-myocytes. The signal transduction involves atrial natriuretic peptides and growth factors that initiate remodelling processes leading to hypertrophy which in turn may contribute to the electrical instability of the heart by increasing the responsiveness of mechano-sensitive channels. Selective block of these channels could provide some new form of treatment of mechanically induced arrhythmias, although at present there are no drugs available with sufficient selectivity. Detailed understanding of how mechanical strain on myocardial cells is translated into channel activation will allow to identify new targets for putative antiarrhythmic drugs.

Action Potentials↗