Biomedical subjects
Publications and source records attributed to A N Damato.
This is a report of a patient who develops new onset atrial fibrillation in the postoperative setting which is further complicated by the presence of wide beats in singles, pairs, and short runs. Presented are the differential diagnosis of these wide beats and a simple bedside maneuver to help distinguish their origin.
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Of 104 consecutive patients studied in our laboratory with His bundle electrograms, atrial and ventricular pacing and the atrial and ventricular extrastimulus techniques, 18 patients in whom the existence and utilization of ventriculoatrial (V-A) bypass tracts were excluded demonstrated evidence for fixed and rapid retrograde conduction in the region of the atrioventricular node (A-V) as suggested by the following: (1) short (36 +/- 2 msec [mean +/- standard error of mean]) and constant retrograde H2-A2 intervals during retrograde refractory period studies; (2) significantly (P less than 0.025) better V-A than A-V conduction; (3) significantly (P less than 0.025) shorter retrograde functional refractory period of the V-A conducting system than of the A-V conduction system; and (4) the retrograde effective refractory period of the A=V nodal region was not attainable in any of the 18 patients. Fourteen of the 18 patients (77 percent) had a history of palpitations and 10 (51 percent) had documented paroxysmal supraventricular tachycardia; in 13 (72 percent) single echoes or sustained reentrant supraventricular tachycardia, or both, could be induced during atrial pacing or atrial premature stimulation studies, or both. During tachycardia all these 13 patients had a short (37 +/- 2.4 msec) and constant conduction time in the retrograde limb (H-Ae interval) of the reentrant circuit that was identical to the H2-A2 interval. In conclusion, fixed and rapid retrograde conduction in the region of the A-V node (1) is seen in approximately 17 percent of patients, (2) is associated with a large incidence of reentrant paroxysmal supraventricular tachycardia, and (3) suggests the presence of A-V nodal bypass tracts (intranodal or extranodal functioning in retrograde manner).
In a patient with the Wolff-Parkinson-White Syndrome we observed atrial fibrillation and three distinct paroxysmal re-entrant tachycardias. Intracardiac electrograms obtained during the tachycardias showed the mechanisms to be A-V nodal, accessory pathway and sinus node re-entry. When P wave morphology, R-P relationship and QRS configuration are considered, it is illustrated how these four tachyarrhythmias may be successfully diagnosed on the surface electrocardiogram. The therapeutic implications of multiple arrhythmias with different mechanisms in the Wolff-Parkinson-White Syndrome are discussed.
A patient had multiple bilateral stenoses of the pulmonary artery and its branches with systemic hypertension associated with mild stenoses of the renal arteries. Cardiac catheterization and angiocardiography are important in the evaluation of the degree of stenoses and pulmonary hypertension. This case suggests that in a child or young person with hypertension and a loud precordial murmur, lesions other than coarctation of the aorta may be present. Unexplained systemic hypertension requires further investigative workup which is essential for proper treatment and long-term management of these patients.
Temporal effects on refractoriness within the His-Purkinje system (HPS) were studied in 14 patients in whom effective refractory period (ERP) of HPS could be determined, using His bundle electrograms, incremental atrial pacing, and atrial extrastimulus method. His-Purkinje conduction times (H-V interval) and relative (R), effective (E), and functional (F) refractory periods (RP) of HPS were measured during the control period and repeat measurements were made after a 30 minute interval. H-V intervals were unchanged from control in all patients. Although changes of the magnitude of 5 to 25 msec. in either direction from control values commonly occurred, on the average, no statistically significant changes were seen in RRP, ERP, or FRP of HPS. The results of the present study confirm the stability of refractoriness of HPS over a 30 minute period and provide baseline data for future investigations of cardiovascular drugs which act primarily on the distal part of the A-V conduction system.
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The effects of digitalis on retrograde conduction and refractoriness of the His-Purkinje system, ventricular myocardium and reentry within the His-Purkinje system were studied in 17 patients using the ventricular extrastimulus (V2) technique. Studies were performed, before and 30 minutes after intravenous administration of ouabain, 0.01 mg/kg. After treatment with ouabain, there was a significant decrease in the functional refractory period (266 +/- 19 to 254 +/- 18 msec, P less than 0.001), relative refractory period (253 +/- 17 to 240 +/- 16 msec, P less than 0.001) and effective refractory period (242 +/- 23 to 231 +/- 24 msec, P less than 0.005) of the ventricular muscle. In contrast, there was no significant change in retrograde His-Purkinje conduction and refractoriness. The phenomenon of reentry within the His-Purkinje system characterized by the reentrant beat (V3) at critical retrograde conduction delays in the His-Purkinje system (V2-H2) within a narrow range of V1-V2 intervals was seen in 10 of 17 patients. Ouabain increased and shifted to the left the zone of reentry within the His-Purkinje system in 7 of 10 patients (36 +/- 23 to 55 +/- 23 msec, P less than 0.001) and decreased it by 10 to 30 msec in the remaining 3 patients. The critical V2-H2 (186 +/- 29 to 193 +/- 27 msec, difference not significant [NS]) and V1-V2 (299 +/- 30 to 294 +/- 36 msec, NS) intervals for reentry did not significantly change after ouabain. However, the minimal V1-V2 intervals (266 +/- 26 to 253 +/- 25 msec, P less than 0.025) decreased significantly, whereas the maximal V2-H2 intervals (266 +/- 40 to 239 +/- 37 msec, P less than 0.01) increased significantly. Thus, in the intact human heart, digitalis (1) significantly decreased all measures of ventricular myocardial refractoriness, (2) had no significant effect on retrograde conduction and refractoriness of the His-Purkinje system, and (3) widened the zone of reentry within the His-Purkinje system due to shortening of the functional refractory period of the ventricular muscle with attainment of longer V2-H2 delays.
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The effect of therapeutic doses of digitalis on functional (F), relative (R) and effective (E) refractory periods (RP) of the His-Purkinje system (HPS) was studied in 12 open-chested, innervated adult mongrel dogs (10-20 kg) during control and 15, 30 and 45-60 min after 0.016 mg/kg of intravenous ouabain. To determine the stability of the preparation and to assess time-dependent changes in His-Purkinje refractoriness, another six dogs (Group II) had similar studies, but without drug administration. In all dogs, the His bundle was paced by using the plunge wire technique at a predetermined cycle length (CL) and a premature stimulus (S2) to the His bundle was introduced at decreasing S1 S2 intervals. Following ouabain, in Group I dogs, at the longest Cls tested (458 +/- 125 msec; +/- SD) there was significant increase in the FRP (+4.34%; P less than 0.05), RRP (S2 V2 (+6.57%, P less than 0.05), RRP (Ab) (+6%, P less than 0.05) and ERP (52%, P less than 0.05) of the HPS. These significant changes were generally observed 30 minutes after drug administration. Changes in RPs were of greater magnitude at longer CLs (greater than 400 msec), but insignificant at shorter CLs (less than 400 msec). The H-V interval during sinus rhythm and the S1 V1 interval during His bundle pacing at all CLs did not change after ouabain. In Group II dogs there were no significant change in His-Purkinje refractoriness over 60 minutes. These findings suggest that therapeutic doses of digitalis 1) tend to increase refractoriness within the HPS to a very small degree, 2) have no appreciable effect on His-Purkinje conduction, and 3) affect CL-dependent changes in refractoriness. The His bundle extrastimulus method is useful in studying the HPS in the intact heart.
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To determine the effect of abnormal ventricular activation on ventricular septal motion, left ventricular endocardial motion and left ventricular dimensions, 12 patients with normal motion were studied with echocardiography during incremental pacing of the right ventricular apex, outflow and inflow regions. Three types of abnormal ventricular septal motion were seen: The type I pattern was characterized by an early rapid preejection posterior ventricular septal motion followed by another posterior systolic motion that lasted throughout ejection, both of which were associated with septal thickening. In the type II pattern an early rapid preejection posterior ventricular septal motion was followed by an anterior ejection motion; the latter was not accompanied by septal thickening. The type III pattern consisted of an early preejection posterior ventricular septal motion followed by a mid and late systolic posterior motion: the latter motion extended through diastole. During right ventricular apical pacing, 8 of 11 patients showed a type 1 pattern, 1 a type II pattern and 2 a normal septal motion. During right ventricular outflow pacing,seven of nine patients showed a type II pattern, one a type III pattern and one a type I pattern. During right ventricular inflow pacing, eight of nine patients showed a type II pattern and one a type III pattern. At faster pacing rates patterns of types I and III changed to a type II pattern (five patients). End-diastolic dimensions decreased significantly during incremental right ventricular pacing when compared with those during sinus rhythm. End-systolic dimensions decreased significantly only during right ventricular apical and outflow pacing at maximal rates. In the seven patients who had pacing from all three sites, the decrease in left ventricular dimensions did not significantly differ when the three pacing sites were compared. These findings suggest that (1) abnormal ventricular septal motion during right ventricular pacing (induced left bundle branch block patterns) is dependent on the sequence of ventricular activation; (2) ventricular septal motion during right ventricular outflow and inflow pacing is similar to that seen in spontaneous left bundle branch block, whereas the pattern of septal motion during right ventricular apical pacing is different from that of spontaneous left bundle branch block; and (3) changes in left ventricular dimension are dependent on ventricular pacing rate but independent of pacing site.
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Atrial flutter has never been satisfactorily defined. The 'common' pattern of flutter was originally described by Lewis in 1913. Less frequently observed forms of flutter are termed 'uncommon'. Sixteen cases of the 'common' and 6 of the 'uncommon' type have been studied using isolated P loop vectorcardiography. All patients had some degree of atrioventricular block but none had evidence of digitalis excess. The atrial rates were regular and were in a range between 250 and 330/minute. Vagal manoeuvres increased AV block in each instance. All those with the 'common' type of flutter had P loops with a caudad-cephalad orientation and fifteen of the sixteen had forces which descended over the right atrium and ascended over the left atrium. The 6 cases of the uncommon type of flutter had rates which ranged between 250 and 300/minute and did not fulfil both of the criteria for 'common' flutter; namely continuous baselineu ndulation and prominent negative P deflections in the inferior leads. The cases with the 'uncommon' type of flutter had a variety of loop patterns. The most frequent type was oriented inferior slightly to the right and anterior. One patient satisfied criteria for left atrial flutter. In another the loop was oriented inferior leftward and anterior. The vectorcardiogram provides a rich source of descriptive data but does not identify the underlying mechanism(s) of flutter.