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F X Witkowski

Publications and source records attributed to F X Witkowski.

33 records · Page 2Linked to original sources

Persistent changes in the body surface electrocardiogram following successful coronary angioplasty.

One hundred twenty-lead body surface potential maps (BSPMs) were recorded immediately before and 24 hours after coronary angioplasty (PTCA) in 24 patients with symptomatic coronary artery disease (single-vessel in 21 and two-vessel in 3). All PTCAs were uncomplicated and successful. The modified Gensini score decreased in every patient and the mean score fell from 43 +/- 36 to 21 +/- 28 (p less than 0.001). Resting spatial patterns of QRS, ST-segment, and T wave integral distributions over the torso surface were unchanged from before to after PTCA. Quantitative temporal subtraction maps, however, revealed a large precordial area of decreased T wave integral values after PTCA. The sum (sigma) positive T wave integrals fell from 20,501 +/- 10,544 microV.s before PTCA to 17,647 +/- 10,310 microV.s after PTCA (p less than 0.02). In contrast, the sigma positive QRS (10,115 +/- 4,848 microV.s before PTCA vs. 9,656 +/- 4,556 microV.s after PTCA) and the sigma negative ST integrals (-2,489 +/- 1,467 microV.s before PTCA vs. -2,359 +/- 1,505 microV.s after PTCA) were unchanged (NS). Thus, successful PTCA does not produce any persistent change in depolarization or early repolarization electrocardiographic variables but is associated with a decrease in late repolarization potentials that persists for at least 24 hours after the procedure. The pathophysiology of this persistent change is speculative, but myocardial ischemia during the PTCA procedure is a likely possibility. The clinical significance, including predictive value for subsequent stenosis, and the natural history of T wave effect remain incompletely defined. These data suggest that measures to decrease myocardial ischemia during PTCA are warranted.

Adult↗

A completely automated activation-repolarization interval algorithm for directly coupled unipolar electrograms and its three-dimensional correlation with refractory periods.

Sintered Ag-AgCl needle electrodes were used to record unipolar directly coupled (DC) electrograms transmurally from right and left ventricular myocardium. Direct coupling yields unfiltered low-frequency signal content, preserving repolarization waveform morphology. These electrograms were analyzed using completely automated computer algorithms for the timing of local activation and local repolarization that permit beat-to-beat determinations of these parameters. The local activation to repolarization interval was compared with the refractory period obtained with the extrastimulus technique from the same electrode during varied basic cycle lengths and pacing sequences. Pooling of the activation to refractory period versus activation-to-repolarization data from all sites and pacing sequences produced a correlation coefficient of 0.96, with a standard error of the estimate of 5.1 msec. The results demonstrate that DC-coupled unipolar electrograms may prove useful in direct, three-dimensional local repolarization timing and in simultaneous assessment of the temporal and spatial dispersion of changes in repolarization from multiple sites.

Algorithms↗

A new fabrication technique for directly coupled transmural cardiac electrodes.

Many current attempts at electrophysiological elucidation of cardiac arrhythmia mechanisms have centered around activation sequence mapping. This is most commonly performed with polarized unipolar or bipolar metal electrodes, which, because of unstable direct current (DC) base-line potentials, necessitate alternating current (AC)-coupled amplification. An ideal nonpolarizable unipolar electrode offers unhindered exchange of charge allowing for stable DC recordings of biological electrical activity. In addition to activation information, DC unipolar recordings enable quantitation of systolic and diastolic potentials, other low-frequency phenomena of interest such as repolarization, as well as rapid recovery from such rapid extreme potential shifts such as defibrillation. Previous attempts to apply nonpolarizable electrodes to transmural cardiac investigations required complex wick electrode techniques to prevent mechanical movement of the fluid-metal interface when chlorided silver wire was used. We have developed a technique to fabricate miniature sintered Ag-AgCl electrodes that are mounted at various locations on a 20-gauge stainless steel needle permitting stable transmural DC unipolar electrogram recordings in vivo. The electrodes are low noise, rugged, sterilizable, and reusable and should prove useful in three-dimensional electrophysiological characterization of the heart.

Animals↗

Simultaneous computer mapping to facilitate intraoperative localization of accessory pathways in patients with Wolff-Parkinson-White syndrome.

Sixteen patients with the Wolff-Parkinson-White syndrome underwent simultaneous intraoperative computer mapping from multiple sites before surgical division of the accessory pathways. A 16-bipolar electrode band was positioned around the atrioventricular groove. Ventricular epicardial electrograms from single beats were recorded simultaneously during atrial pacing, resulting in maximal preexcitation, and atrial electrograms were recorded during orthodromic supraventricular tachycardia. Four-level transmural plunge needle electrodes were used concomitantly in 3 patients. Electrograms were processed separately using a guarded signal conditioner that isolates, amplifies, filters and analog-to-digitally converts synchronously at 2 kHz with 12-bit accuracy. Digital data were transmitted by fiber optics to a high-density digital recorder and processed with a computer having rapid interactive graphics. Results in the 16 patients revealed 20 distinct Kent bundles. Two patients had only nonsustained supraventricular tachycardia induced intraoperatively and 1 patient manifested intermittent anterograde ventricular preexcitation. Multiple pathways were identified in 4 patients. This simultaneous multiple electrode mapping procedure facilitates intraoperative mapping by requiring only a single beat for analysis of anterograde and retrograde activation times, decreases cardiac manipulation during mapping and obviates the need for cardiopulmonary bypass, and permits analysis of transmural activation patterns. This approach decreases markedly the time required for mapping and permits accurate study of nonsustained arrhythmias as well as rapid identification of multiple accessory pathways.

Adolescent↗

Intramural reentry as a mechanism of ventricular tachycardia during evolving canine myocardial infarction.

We evaluated the contribution of intramural electrical events in initiation and maintenance of ventricular tachycardia in 15 dogs 3-8 days after either permanent (n = 2) or transient (n = 13) coronary artery occlusion. Seven of the dogs (47%) demonstrated eight distinct monomorphic ventricular tachycardia patterns which were mapped by means of a recently designed computerized system capable of simultaneously detecting, storing, and assessing information from 232 individual cardiac sites. Using both epicardial and intramural electrodes, we found definitive evidence for intramural reentry in seven of the eight monomorphic tachycardias analyzed. Furthermore, five of these animals (71%) demonstrated microreentry, in which small epicardial conduction loops exited intermittently into nonrefractory subendocardium to initiate succeeding beats, while, in the remaining two dogs, ventricular tachycardia was due to macroreentry, during which the broad subendocardial wavefronts depolarizing the ventricle constituted the proximal (fast) reentry limbs. Detailed anatomical analysis of the resultant infarcts demonstrated the thin surviving epicardial tissue rim to be the site of conduction delay necessary for reentry, whereas "preferred pathways" of exit into the subendocardial plane occurred at the infarct borders and were of variable configuration. Successful interruption of these rhythms should accompany interference with the process of exit into nonrefractory subendocardial tissue.

Animals↗

An automated simultaneous transmural cardiac mapping system.

The origin and propagation sequence of cardiac depolarization in situ requires accurate simultaneous three-dimensional information from multiple sites. Likewise, the mechanism underlying an arrhythmia can often be elucidated by determining the course of impulse propagation through the heart, particularly if information can be obtained from multiple sites simultaneously, allowing analysis of transient or rapidly occurring events. The most significant problem with obtaining such detailed continuous information is the large amount of data storage required as well as the need for rapid analysis. In the present system these problems are overcome by immediate conversion of all electrograms from analog to digital for all subsequent storage and processing. The bipolar electrogram information is acquired from 240 cardiac sites simultaneously at a sampling rate of 2 kHz with continuous and total data storage of up to 60 min. Rapid two-dimensional isochronic maps at multiple depths (effective 3-dimensional information) are presented via computer-generated interactive graphics. System design permits easy expansion to almost 2,000 simultaneous sites. Surgical electrophysiological intraoperative studies in humans are performed at an operating room located 2,000 ft from the computer facility with all communications carried by a fiber-optic link. The system allows both experimental and clinical cardiac mapping from multiple sites from a single cardiac depolarization, minimal redundancy of costly hardware, and direct rapid visualization of all original electrogram data.

Arrhythmias, Cardiac↗

Fast-Fourier transform analysis of signal-averaged electrocardiograms for identification of patients prone to sustained ventricular tachycardia.

Electrocardiograms obtained from patients during arrhythmia-free intervals do not identify those prone to sustained ventricular tachycardia (VT) despite the occult delayed activation that is presumably present. To determine whether frequency-domain analysis facilitates detection of this hallmark of predisposition to VT, fast-Fourier transform analysis (FFTA) procedures were developed and tested with a computer-generated mathematical model. The FFTA approach developed allows inherent limitations of high-gain amplification and a priori filtering used commonly for time-domain analysis to be avoided. After demonstrating that FFTA detected low-amplitude oscillatory waveforms in signal-averaged recordings in the frequency domain, the procedure was applied to signal-averaged X, Y, and Z lead recordings from the following three groups of patients: group I, patients with prior myocardial infarction and episodic sustained VT (n = 16); group II, patients with prior myocardial infarction without overt sustained VT (n = 35); and group III, normal control subjects (n = 10). Results of FFTA demonstrated significant (p less than .0001) differences in the decibel drop at 40 Hz and the area under the curve from the fundamental frequency to the frequency at which the spectral amplitude was decreased by 60 dB for both the terminal 40 msec of the QRS and ST segment in patients in group I compared with those in groups II and III, in whom results were similar. Results were independent of QRS duration (r = .2), left ventricular ejection fraction (r = .19), and complexity of spontaneous ventricular ectopy. Thus, patients known to manifest sustained VT also exhibited relatively greater high-frequency content in arrhythmia-free intervals in the terminal QRS and ST segment than those without VT (88%, 15%, and 0% in groups I through III, respectively). FFTA offers promise for the noninvasive detection of patients at risk for the development of sustained VT.

Aged↗

Arrhythmias associated with reperfusion: basic insights and clinical relevance.

Arrhythmias associated with reperfusion of ischemic myocardium may be a major progenitor for sudden cardiac death in man. The electrophysiological basis for arrhythmias associated with reperfusion appears to be heterogeneous electrical recovery, but the precise alterations responsible for malignant versus nonmalignant arrhythmias are unknown. In experimental animals, the highest incidence of malignant arrhythmias after reperfusion occurs after 20 to 30 min of preceding ischemia, a critical time period in which both reversibly and irreversibly injured cells are present, with reperfusion resulting in maximal heterogeneity of recovery of electrical parameters. Although changes in K+, PCO2, and intracellular Ca2+ may be critical in arrhythmogenesis during reperfusion, direct cause-and-effect relationships have not been established. Increases in both alpha-adrenergic responsivity and the density of alpha 1-adrenergic receptors appear to mediate important influences on these malignant arrhythmias, including changes in intracellular calcium. Recent findings also suggest that the accumulation of lysophosphatides in ischemic myocardium may be the responsible moiety for the increase in alpha 1-adrenergic receptors.

Adenosine Triphosphate↗

Potential electrophysiologic mechanisms responsible for dysrhythmias associated with reperfusion of ischemic myocardium.

Dysrhythmia associated with reperfusion may not only play a critical role in sudden cardiac death, but also, the presence of dysrhythmia during intracoronary administration of thrombolytic agents may reflect heterogeneity of recovery of excitability and, hence, salvage of ischemic myocardium. The electrophysiologic basis for these dysrhythmias appears to be heterogeneity of electrical recovery resulting in reentry or enhanced ventricular automaticity. Although the precise mechanisms are unknown, rapid changes in K+, PCO2 and intracellular Ca++ appear to play major roles. In addition, alterations in the regional concentration or tissue compartment localization of amphiphilic lipid metabolites such as lysophosphoglycerides and long-chain acyl carnitines may affect not only the development of dysrhythmia during reperfusion, but also the salvage of ischemic myocardium. Recent experimental evidence in several species also suggests a prominent role of alpha 1-adrenergic stimulation in the evolution of dysrhythmia associated with reperfusion.

Arrhythmias, Cardiac↗

Potential arrhythmogenic electrophysiological derangements in canine Purkinje fibers induced by lysophosphoglycerides.

We have recently detected accumulation of lysophosphoglycerides, catabolites of phospholipids, in ischemic myocardium early after coronary occlusion. In the present study we delineated effects of selected concentrations of albumin-bound lysophosphatidyl choline (LPC) comparable to those accompanying ischemia in vivo on action potentials of isolated canine Purkinje fibers. Lysophosphoglycerides induced concentration-dependent (0.75-3.0 mM) decreases in resting membrane potential, overshoot of phase 0, maximal velocity of upstroke (Vmax) of phase 0, and action potential duration. The highest concentrations (2.0-3.0 mM) induced fractionation of the action potential into several components, unresponsiveness to external stimulation, and enhanced automaticity at normal and reduced membrane potentials. LPC induced a rightward shift in the membrane response curve, a 40-fold prolongation of conduction time, and an increase in the ratio of effective refractory period to action potential duration such that the effective refractory period persisted beyond action potential duration, resulting in postrepolarization refractoriness. These electrophysiological alterations were entirely reversible after 70 minutes of perfusion without LPC, with the exception of a persistent depression in the Vmax of phase 0. Lysophosphatidyl ethanolamine (LPE) elicited alterations in action potentials indentical to those elicited by LPC. Furthermore, LPC (3.0 mM) induced comparable alterations in action potentials recorded from isolated rabbit papillary muscles. Since lysophospholipids accumulate early after myocardial ischemia, and since concentrations equivalent to those occurring in vivo induce electrophysiological alterations resembling those seen in ischemic myocardium in vivo, lysophosphoglycerides may be of major importance as biochemical mediators of malignant dysrhythmia induced by ischemia.

Action Potentials↗

Mechanisms contributing to malignant dysrhythmias induced by ischemia in the cat.

Continuously recorded bipolar electrograms were obtained simultaneously from epi-, endo-, and mid-myocardial regions of the ischemic and normal zones of cat left ventricle in vivo after coronary occlusion, analyzed by computer, and compared to regional cyclic AMP levels. Regional cyclic AMP content was used as an index of the combined local effects of: (a) efferent sympathetic nerve discharge; (b) release of myocardial catecholamines due to ischemia; and (c) circulating catecholamines. Ischemia resulted in a progressive increase in pulse width and rise time and a decrease in rate of rise of voltage (dV/dt) of the local electrograms from ischemic zones reaching a maximum within 2.4+/-0.3 min (mean+/-SE) at the time of onset of severe ventricular dysrhythmias, all of which returned toward control before the cessation of the dysrhythmia (33.5+/-1.5 min after coronary occlusion). Increases in cyclic AMP in ischemic zones preceded corresponding increases in the frequency of premature ventricular complexes (PVCs). Propranolol inhibited the increases in cyclic AMP and reduced the frequency of PVCs in animals without ventricular fibrillation. In animals with ventricular fibrillation, cyclic AMP was significantly elevated in normal and ischemic zones compared to animals with PVCs only. Electrical induction of PVCs or ventricular fibrillation in ischemic and nonischemic hearts failed to increase cyclic AMP. The results suggest that the changes in regional adrenergic stimulation of the heart may contribute to perpetuation of ventricular dysrhythmia and the genesis of ventricular fibrillation early after the onset of myocardial ischemia.

Animals↗

Accumulation of lysophosphoglycerides with arrhythmogenic properties in ischemic myocardium.

Lysophosphoglycerides, products of membrane phospholipid catabolism known to influence membrane function in several systems, appeared in the effluents of anoxic isolated rabbit hearts perfused at low flow and accumulated in perfused hearts and myocardium rendered ischemic in situ. Comparable concentrations of lysophosphoglycerides bound to albumin markedly and reversibly altered action potentials of isolated canine Purkinje fibers in vitro. Changes induced included diminution of the maximum diastolic potential, peak dV/dt of phase zero, amplitude, and action potential duration--alterations resembling those seen in ischemic myocardium in vivo. These electrophysiological alterations are compatible with changes implicated in predisposing to dysrhythmia dependent on reentry, a phenomenon potentiated by the presence of zones of decreased conduction. Thus, accumulation of lysophosphoglycerides induced by ischemia may contribute to the genesis of malignant dysrhythmia early after its onset.

Action Potentials↗

A new technique for three-dimensional localization of transmural electrodes.

Simultaneous multichannel cardiac mapping is used to investigate mechanisms of arrhythmia. Transmural cardiac interrogation is useful in the study of ventricular arrhythmias. The construction of needle electrodes capable of transmural recording, although labor-intensive, is relatively straightforward. The three-dimensional localization of these electrodes within the myocardium and the subsequent depiction of the data obtained have customarily been performed manually. A simple technique for automated recording of site registration and subsequent fully automatic data presentation of three-dimensional data, for use in experimental animals, is presented. It entails replacing each recording needle electrode prior to fixation of the heart with a marker needle electrode that is radiographically coded to permit both three-dimensional recording site localization and unique electrode identification. The fixed and excised heart may then be sectioned with the marker needles in place and an x-ray obtained. The needle identification, electrode locations, and actual tissue outlines are then digitized, allowing for completely automated subsequent assignment of relevant data obtained from these recording sites to morphologically correct anatomic locations. This approach should facilitate transmural studies aimed at elucidating electrophysiologic mechanisms.

Animals↗