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Biomedical subjects

Katherine M Kavanagh

Publications and source records attributed to Katherine M Kavanagh.

6 recordsLinked to original sources

Pulmonary edema post-cardioversion: a potential calcium signalling problem.

The present report describes an unusual case of pulmonary edema after adenosine cardioversion of a supraventricular tachycardia. Despite a structurally normal heart, a 52-year-old woman presented with pulmonary edema on two separate occasions, having had her atrioventricular nodal re-entrant tachycardia terminated with 12 mg of intravenous adenosine. A third similar episode of tachycardia that was terminated with verapamil was not complicated by pulmonary edema.

Adenosine↗

Cardiac video analysis using Hodge-Helmholtz field decomposition.

The critical points (also known as phase singularities) in the heart reflect the pathological change of the heart tissue, and hence can be used to describe and analyze the dynamics of the cardiac electrical activity. As a result, the detection of these critical points can lead to correct understanding and effective therapy of the tachycardia. In this paper, we propose a novel approach to address this problem. The proposed approach includes four stages: image smoothing, motion estimation, motion decomposition, and detection of the critical points. In the image smoothing stage, the noisy cardiac optical data are smoothed using anisotropic diffusion equation. The conduction velocity fields of the cardiac electrical patterns can then be estimated from two consecutive smoothed images. Using the recently developed discrete Hodge-Helmholtz motion decomposition technique, the curl-free and divergence-free potential surfaces of an estimated velocity field are extracted. Finally, hierarchically searching the minima and maxima on the potential surfaces, the sources, sinks, and rotational centers are located with high accuracy. Experimental results with four real cardiac videos show that the proposed approach performs satisfactorily, especially for the cardiac electrical patterns with simple propagations.

Algorithms↗

Heart block in mice overexpressing calcineurin but not NF-AT3.

OBJECTIVE: Overexpression of calcineurin causes cardiac hypertrophy and arrhythmic deaths. During disease development, sinus bradycardia followed by high degree atrioventricular (AV) block finally culminating in ventricular asystole has been observed over time in calcineurin hearts. AV block is associated with the development of pleomorphic ventricular tachycardia in mice and downregulation of potassium currents in ventricular myocytes. We tested the hypothesis that the abnormalities of AV block and propensity to ventricular tachycardia relate to overexpression of calcineurin independent of the development of hypertrophy. METHODS: Cardiac electrophysiologic properties were compared in isolated perfused hearts with ventricular hypertrophy due to overexpression of calcineurin or NF-AT3 and in their corresponding wild types at 15 or 30 days of age. RESULTS: Compared to wild-type hearts, significant prolongation of sinus node recovery times was noted in both NF-AT3 and calcineurin hearts. Compared to wild-type hearts, Wenckebach cycle length (WCL) and the left ventricular effective refractory period (LVERP) were significantly prolonged in the calcineurin hearts (p<0.05) but not NF-AT3 hearts. In calcineurin mice, left ventricular effective refractory period impinged on Wenckebach cycle length resulting in a significant correlation between left ventricular effective refractory period and Wenckebach cycle length (r(2)=0.56). No such correlation was observed for wild type or NF-AT3 hearts. At 30 days of development, ventricular tachycardia developed in 70% of calcineurin hearts compared to 0% wild-type hearts (p=0.003), whereas ventricular tachycardia was observed in 33% of NF-AT3 hearts and 10% of corresponding wild-type hearts (p=NS). CONCLUSIONS: The prolonged ventricular refractoriness, seen only in calcineurin hearts, impinges on Wenckebach cycle length resulting in heart block and is associated with propensity to ventricular tachycardia.

Animals↗

In vivo temporal and spatial distribution of depolarization and repolarization and the illusive murine T wave.

This study assessed in vivo temporal and spatial electrophysiological properties of murine hearts and the effect of manipulation of transmural action potential durations (APDs) on T wave morphology. Monophasic action potentials (MAPs) were acquired from multiple left ventricular sites. All MAPs exhibited a plateau phase, with a spike and dome appearance being present in epicardial recordings. Activation occurred from endocardial apex to epicardial apex and apex to base while repolarization occurred from base (shortest 90 eta0 level of repolarization (MAP90), 95.4 +/- 8.9 ms) to apex and epicardium to endocardium (longest MAP90, 110.77 +/- 10.6 ms). The peak of phase 0 of the epicardial base MAP correlated with the return to baseline of the initial and usually dominant waveform of the QRS and the onset of the second usually smaller wave, which clearly occurred in early repolarization, thus establishing where depolarization ended and repolarization began on the murine ECG. This second waveform was similar to the J wave seen in larger animals. Despite temporal and spatial electrophysiological similarities, a T wave is frequently not seen on a murine ECG. There are several determinants of T wave morphology, including transmural activation time, slope of phase 3 repolarization and differences in epicardial, endocardial and M cell APDs. Experimental manipulation of murine transmural gradients by shortening epicardial MAP(90) to 84% of endocardial MAP90 the epicardial/endocardial ratio in larger mammals when a positive T wave is present, resulted in a positive murine T wave. Thus, manipulation of the transmural gradients such that they are similar to larger mammals can result in T waves with similar morphology.

Action Potentials↗

Autoimmune cardiomyopathy and heart block develop spontaneously in HLA-DQ8 transgenic IAbeta knockout NOD mice.

A line of nonobese diabetic (NOD) mice expressing the human diabetes-associated HLA-DQ8 transgene in the absence of mouse IAbeta failed to show spontaneous insulitis or diabetes, but rather developed dilated cardiomyopathy, leading to early death from heart failure. Pathology in these animals results from an organ- and cell-specific autoimmune response against normal cardiomyoctes in the atrial and ventricular walls, as well as against very similar myocytes present in the outermost muscle layer surrounding the pulmonary veins. Progression of the autoimmune process could be followed by serial ECG measurements; irradiation of young animals significantly delayed disease progression, and this effect could be reversed by adoptive transfer of splenocytes taken from older animals with complete heart block. Disease progression could also be blocked by cyclosporin A treatment, but was accelerated by injection of complete Fruend's adjuvant. The constellation of findings of spontaneously arising destructive focal lymphocytic infiltrates within the myocardium, rising titers of circulating anticardiac autoantibodies, dilation of the cardiac chambers, and gradual progression to end-stage heart failure bears a striking resemblance to what is seen in humans with idiopathic dilated cardiomyopathy, a serious and often life-threatening medical condition. This transgenic strain provides a highly relevant animal model for human autoimmune myocarditis and postinflammatory dilated cardiomyopathy.

Animals↗

Multitasking and the technical quality of the electrocardiogram.

BACKGROUND: The electrocardiogram (ECG) is a powerful clinical tool for diagnosing cardiac abnormalities. Proper ECG data acquisition is essential because it allows physicians to interpret ECG results accurately and efficiently. This is especially important for patients with acute myocardial infarction, so that they can receive early treatment. As a result of multitasking, ECGs are acquired by two groups of personnel at the University of Alberta Hospital, Edmonton - ECG technologists and non-ECG technologists. OBJECTIVE: To evaluate the effectiveness and quality of ECG acquisition at the University of Alberta Hospital site. METHODS: All adult ECGs acquired at the University of Alberta Hospital site from January 1 to June 30, 2000 were assessed. An ECG was classified as unacceptable if it lacked demographics identifying the patient, and/or it was of such poor technical quality that the interpretation was compromised. RESULTS: Of 25,509 ECGs acquired during this period, 13,849 (54%) and 11,660 (46%) ECGs were acquired by ECG technologists and non-ECG technologists, respectively. Eleven ECGs (0.08%) acquired by the ECG technologists and 3683 ECGs (32%) acquired by the non-ECG technologists were of unacceptable quality. The technical cost spent on these unacceptable ECGs is approximately $100,000 a year at this institution. CONCLUSIONS: Multitasking has resulted in a high rate of unacceptable ECGs. There is a significant difference in the effectiveness and quality of ECG acquisition performed by ECG technologists and non-ECG technologists. Poorly acquired ECGs impede proper diagnosis for patients, subject the institution to potential medical legal consequences and add an unnecessary burden to the health care budget.

Canada↗