By F. Silas. Plymouth State University, Plymouth New Hampshire.

Although some authors purchase 75mg imipramine with amex, suggest that termination by ventricular extrastimuli only occurs when a retrograde His bundle is not seen generic imipramine 25mg mastercard, we have not found this to be the case buy imipramine 75mg amex. Ventricular stimulation produces antegrade block in the atriofascicular pathway due to retrograde invasion of the atriofascicular bypass tract and premature atrial activation over the A-V node purchase imipramine 75 mg with visa. The ease of termination of programmed stimulation suggests that an antitachycardia pacemaker may be useful in management of this arrhythmia, but in our experience it is unnecessary. Those tachycardias using atriofascicular pathways respond readily to calcium blockers (Fig. Invariably, in response to beta- blockers or calcium-blockers, the tachycardia slows without any change in the fixed short V-H before block, which must occur above the site of takeoff from the A-V node. These findings also suggest that in cases where slowly conducting atriofascicular bypass tracts are operative, they have A-V nodal-like properties. Sometimes, as with A- V nodal reentry, Type I agents produce retrograde block in the fast pathway and prevent the arrhythmia. We have also found Type I agents to be useful in blocking the bypass tract, a response that may enable one to make the diagnosis of A-V nodal reentry with an innocent bystander bypass tract. As stated earlier, responsiveness to lidocaine is more common in a short decrementally conducting A-V accessory pathway. Note that the tachycardia slowing is related to an increase in the P-R and A-H interval. This suggests that the site of action of verapamil is in the atriofascicular bypass tract. Intermittent conduction of sinus beats over the fast pathway has an H-V of and 0 msec while conduction over the slow pathway proceeds over a nodofascicular bypass tract to the distal His, giving rise to a shorter H-V. Ablation of the slow pathway produces conduction only over the fast pathway with an H-V of 70 msec. Fasciculoventricular Bypass Tracts Fasciculoventricular bypass tracts are believed to be a rare form of preexcitation. In 41 years of practicing electrophysiology I have personally observed 15 cases and have seen less than two dozen others studied by colleagues. Preexcitation should be present with normal P-R and A-H intervals and a short H-V (His-to-delta wave) interval. Atrial pacing prolongs the P-R interval owing to A-V nodal delay but will not change the degree of preexcitation because the fiber takes off from the His–Purkinje system. Junctional rhythms or His extrasystoles should be associated with a similar degree of preexcitation and short H-V interval (Fig. A-V nodal Wenckebach should be associated with loss of preexcitation and A-V conduction (Fig. The degree of preexcitation generally remains fixed, unless delay in the His–Purkinje system below the takeoff of the bypass tract occurs. Theoretically, if delay occurs in a bundle branch proximal to the takeoff of a fasciculoventricular bypass tract, preexcitation will decrease owing to a greater degree of ventricular activation over the contralateral bundle branch (a situation which I have not encountered). Block of conduction in fasciculoventricular bypass tracts can be observed in response to atrial extrastimuli in which case there will be sudden H-V prolongation (to normal) with loss of preexcitation (Fig. Even during atrial flutter and fibrillation rapid ventricular responses are not expected in the presence of a normal A-V node proximal to the bypass tract. When tachycardias are observed in the presence of a fasciculoventricular bypass tract, it functions as an innocent bystander. All my patients manifested either A-V nodal reentry or circus movement tachycardia due to a concealed accessory pathway. Thus, because it is not directly responsible for arrhythmias, this form of preexcitation does not require treatment. Preexcitation (note delta wave) is present with an identical, short H-V interval (30 msec) during both sinus and junctional rhythm. During atrial pacing at a cycle length of 500 msec results in A-V nodal Wenckebach. During atrial pacing (S1-S1) at a cycle length of 400 msec an atrial extrastimulus (S2) is delivered at a coupling interval of 290 msec. During the pacing drive (S1) preexcitation is present with an H-V interval of 20 msec. Following S2, block in the fasciculoventricular bypass tract occurs, which is associated with a prolongation of the H-V interval to 45 msec. Morphology of the human atrioventricular node, with remarks pertinent to its electrophysiology. Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Supraventricular tachycardia in Lown-Ganong-Levine syndrome: atrionodal versus intranodal reentry. Characteristics of the ventricular insertion sites of accessory pathways with anterograde decremental conduction properties. Supraventricular tachycardia in children: clinical features, response to treatment, and long-term follow-up in 217 patients. Familial occurrence of accessory atrioventricular pathways (preexcitation syndrome). Longitudinal clinical and electrophysiological assessment of patients with symptomatic Wolff-Parkinson-White syndrome and atrioventricular node reentrant tachycardia. Wolff-Parkinson-White syndrome and supraventricular tachycardia during infancy: management and follow-up. Identification of a gene responsible for familial Wolff-Parkinson- White syndrome. Danon disease as an underrecognized cause of hypertrophic cardiomyopathy in children. Value of programmed stimulation of the heart in patients with the Wolff- Parkinson-White syndrome. Preexcited reciprocating tachycardia in patients with Wolff- Parkinson-White syndrome: incidence and mechanisms. Observations on the antidromic type of circus movement tachycardia in the Wolff-Parkinson-White syndrome. Onset of atrial fibrillation during antidromic tachycardia: association with sudden cardiac arrest and ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome. Atrial fibrillation in patients with an accessory pathway: importance of the conduction properties of the accessory pathway. Frequency of recurrent atrial fibrillation after catheter ablation of overt accessory pathways. A population study of the natural history of Wolff-Parkinson- White syndrome in Olmsted County, Minnesota, 1953–1989. Supernormal conduction in the accessory pathway of patients with overt or concealed ventricular pre-excitation. Concealed conduction in accessory atrioventricular pathways: an important determinant of the expression of arrhythmias in patients with Wolff-Parkinson-White syndrome. Concealed conduction preventing anterograde preexcitation in Wolff-Parkinson-White syndrome. Electrophysiologic demonstration of concealed conduction in anomalous atrioventricular bypass tracts.

The pathologic substrate for patients with ventricular tachyarrhythmias associated with coronary artery disease is 20 21 22 23 usually a prior myocardial infarction resulting in wall motion abnormalities discount 50 mg imipramine fast delivery. The second group of patients who present with a cardiac arrest are those who have severe coronary artery disease and relatively normal ventricular function; in this group the arrest is most likely due to acute ischemia imipramine 50mg cheap. Our patient population is clearly selected so that we study patients with lower ejection fractions effective 50mg imipramine, recognizing that lower ejection fraction per se places a person at high risk for sudden death discount imipramine 75 mg free shipping. The extent of infarction, and perhaps location involving the septum, may be the two important prognostic factors associated with these 21 24 malignant sustained ventricular arrhythmias. The cycle lengths of the tachycardias occurring early after infarction, however, tend to be faster, and the tachycardia is more poorly tolerated. This may reflect evolving scar formation, which when ultimately completed, may be related to longer tachycardia cycle lengths, owing to abnormalities of conduction with which it is 26 associated (see following discussion). Thus, some components of the anatomic substrate must be relatively fixed once infarction has 27 occurred. This is supported by inducibility at 10 and 100 days in an Ovine infarction model. Moreover the ability of programmed stimulation to predict risk of sudden cardiac arrest and survival postinfarction lead credence to 28 this hypothesis. Attempts to make these correlations are fraught with selection and/or entry bias, which is inherent in selecting patients from catheterization laboratories, coronary care units, or exercise laboratories. Similarly, patients studied following cardiac arrest are a selected group of survivors, and as such may not reflect the timing from infarction to cardiac arrest of nonsurvivors. However, this may indicate some of the characteristics of those patients likely to survive. Of more than 1,100 selected survivors of cardiac arrest associated with coronary artery disease who we have studied, the highest incidence (≈50%) of cardiac arrest occurred in the first 6 to 12 months following infarction. After the first year following infarction, the incidence of cardiac arrest decreases rapidly, such that within 3 years the incidence is low. In the thrombolytic and primary angioplasty era, the timing of these events has not changed, but, as stated above, their frequency has been significantly reduced. The pathophysiologic substrate in disease states other than coronary artery disease is less clear. Electrophysiologic Substrate The clinically measurable electrophysiologic consequences of infarction that are potentially arrhythmogenic include abnormalities of conduction and refractoriness, heterogeneity of conduction and refractoriness, enhanced automaticity, and areas of inexcitability. Unipolar (top) and bipolar (bottom) signals recorded with the Rhythmia mapping system. The bipolar signal removes the large farfield signal recorded in the two unipolar electrograms from which the bipolar signal is derived. We developed criteria for normal, abnormal, and fractionated electrograms using bipolar signals recorded with a Bard Josephson catheter (see Fig. Normal electrograms had sharp, biphasic, or triphasic spikes with amplitudes of ≥3 mV, durations of ≤70 msec, and/or an amplitude/duration ratio of ≥0. We defined fractionated electrograms as abnormal electrograms that fell outside the 95% confidence limits of amplitude and duration of all abnormal electrograms. The most common abnormalities were low voltage and increase in electrogram duration, both of which appear to be nonspecific markers of infarction or even poor contact. Multicomponent and fractionated electrograms, isolated late potentials and late electrograms were more closely related to 31 arrhythmogenic sites; but the positive predictive value was only ∼30%. Only 14% of “sites of origin” came from sites that demonstrated normal electrograms. It should be obvious that since mapping catheters have different size electrode (tip and ring), normal and abnormal electrogram characteristics need to be defined for each catheter. Subsequent intraoperative studies using a 20 pole plaque electrode showed that successful surgery was associated with elimination of isolated late potentials and split potentials suggesting mechanistic significance 37 (Fig. The first two complexes are sinus in origin and the left ventricular recordings show markedly abnormal electrograms. Multiple components are present, and the electrogram exceeds 160 msec in duration. We defined total endocardial activation as the time from the earliest local activation to the time of the latest local activation. We used the total endocardial activation time, the duration of the longest electrogram recorded, the presence of late electrograms (including late potentials), and the extent of abnormal P. These abnormalities of activation, whether recorded endocardially in the catheterization laboratory or intraoperatively, occur only in areas of prior infarction and 35 36 38 39 significant wall motion abnormalities. Sites 2, 3, and 4 are the septum, 1 is the apex, 5 and 6 are the mid- and basal inferior wall, 8 is the inferoposterior wall, 9 is the apical anterolateral wall, 10 is the basal lateral wall, 11 is the midanterior wall, and 12 is the basal anterior wall. Endocardial catheter mapping in patients in sinus rhythm: relationship to underlying heart disease and ventricular arrhythmias. Three surface recordings accompanied by three local bipolar electrograms (normal, abnormal, and fractionated and late) recorded from different left ventricular endocardial sites are shown. The arrows show the onset and offset (characterized by the amplification signal decay artifact) of local electrical activity. Endocardial catheter mapping in patients in sinus rhythm: relationship to underlying heart disease and ventricular arrhythmias. Normal values and abnormal electrograms recorded with this plaque are shown on the left. The value of catheter mapping during sinus rhythm to localize site of origin of ventricular tachycardia. In this instance, the pattern of activation is normal but the electrograms are of broader duration and several have multiple components. Rate of tachycardia, and not the location of prior infarction, ejection fraction, or extent of coronary disease is the only factor that determines clinical outcome. Clearly, these fragmented or fractionated electrograms are not an artifact of filtering or motion, because such electrograms can neither be created nor abolished by changing the filtering and can be recorded with uni- or bipolar recordings in fixed pieces of tissue or in nonmoving and infarcted regions during intraoperative 39 40 43 mapping. The extent and location of fibrosis is a critical determinant of the electrogram amplitude, duration, complexity, and timing because of its effect on fiber orientation, curvature, connectivity, and anisotropy, all of which influence conduction. The peak-to-peak bipolar amplitude in mV is plotted 2 against the interelectrode activation time. When the bipolar pair of electrodes are more perpendicular to the tissue, the voltage is lower than when the electrodes are parallel to the surface with rapid activation between electrodes. When the wavefront is transverse to the bipoles, activation is slower and the amplitude of the bipolar electrogram is markedly reduced. Detailed mapping studies with microelectrodes in human tissue and in tissue from experimental canine 29 43 44 46 47 48 50 51 52 53 tachycardia models , , , , , , , , , demonstrate that slow propagation of an impulse through areas from which fractionated electrograms are recorded is associated with relatively normal action potentials of the muscle fibers. Response of these local electrograms to antiarrhythmic agents is also compatible with relatively 54 55 normal action potential characteristics. Thus, anatomic abnormalities can produce functional abnormalities (poor cellular coupling, impedance mismatch, altered curvature, etc. Slow conduction produced by ischemia (low pH), hyperkalemia, or uniform depression of Na channels reduces the peak-to-peak unipolar voltage and duration.

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