John A. Kastor

Recurrent sustained ventricular tachycardia. 1. Mechanisms.

SUMMARYEndocardial ventricular mapping of 21 ventricular tachyardias (VT) in 17 patients was performed using electrode catheters. Activation at multiple left and right ventricular sites was utilized to determine the site of origin of the VT. Eleven VT had a left bundle branch block pattern (VT-LBBB) and 10 VT had right bundle branch block pattern (VT-RBBB). In all VT-RBBB the earliest site of activation was in the LV or septum. In VT-LBBB the earliest site was RV (4/11), LV (5/11) and septum (2/11). All ventricular tachycardias with QRS < 140 msec arose in the septum. In patients with an aneurysm, the site of origin of ventricular tachycardia was always in the aneurysm. All VT-LBBB arising from the left ventricle originated in an aneurysm involving the septum. QRS changes during ventricular tachycardia were associated with alterations in the pattern of ventricular activation without alteration of the site of origin. In three patients the site of origin predicted by endocardial ventricular mapping was confirmed intraoperatively by epi- and/or endocardial mapping.We conclude that endocardial ventricular mapping demonstrates the limitations of the surface electrocardiogram in localizing the site of origin of ventricular tachycardia. The method may provide important data upon which the surgical therapy of ventricular t-achycardia is based.

Recurrent sustained ventricular tachycardia. 2. Endocardial mapping.

Endocardial ventricular mapping of 21 ventricular tachyardias (VT) in 17 patients was performed using electrode catheters. Activation at multiple left and right ventricular sites was utilized to determine the site of origin of the VT. Eleven VT had a left bundle branch block pattern (VT-LBBB) and 10 VT had right bundle branch block pattern (VT-RBBB). In all VT-RBBB the earliest site of activation was in the LV or septum. In VT-LBBB the earliest site was RV (4/11), LV (5/11) and septum (2/11). All ventricular tachycardias with QRS less than 140 msec arose in the septum. In patients with an aneurysm, the site of origin of ventricular tachycardia was always in the aneursm. All VT-LBBB arising from the left ventricle originated in an aneurysm involving the septum. QRS changes during ventricular tachycardia were associated with alterations in the patterm of ventricular activation without alteration of the site of origin. In three patients the site of origin predicted by endocardial ventricular mapping was confirmed intraoperatively by epi- and/or endocardial mapping. We conclude that endocardial ventricular mapping demonstrates the limitations of the surface electrocardiogram in localizing the site of origin of ventricular tachycardia. The method may provide important data upon which the surgical therapy of ventricular tachycardia is based.

Electrocardiographic left atrial enlargement electrophysiologic, echocardiographic and hemodynamic correlates

The mechanism of the electrocardiographic pattern termed left atrial enlargement was evaluated in 21 patients. Left atrial size and pressure as well as interatrial conduction were correlated with electrocardiographic left atrial enlargement using echocardiography, mean pulmonary capillary wedge pressure and activation time from the P wave to the coronary sinus. In the group as a whole only prolongation of interatrial conduction time was consistently related to the electrocardiographic pattern of left atrial enlargement; left atrial size or pressure was not predictably abnormal in patients with this pattern. Five patients had neither elevation of pulmonary capillary wedge pressure nor echocardiographic evidence of an enlarged left atrium. When the etiologic type of heart disease was analyzed, an enlarged left atrium correlated with electrocardiographic left atrial enlargement only in patients with rheumatic mitral valve disease (eight of nine patients). Elevated pulmonary capillary wedge pressure correlated with electrocardiographic left atrial enlargement in all four patients with cardiomyopathy. In patients with coronary artery disease the electrocardiographic pattern was unrelated to either left atrial pressure or volume overload. Thus, the electrocardiographic pattern termed left atrial enlargement appears to represent an interatrial conduction defect that can be produced by a variety of factors.

Nifedipine in the treatment of Prinzmetal's (variant) angina.

The clinical response to therapy with the calcium-blocking agent nifedipine was assessed in 12 patients with variant angina pectoris who were 44 to 67 years old. Five patients had vasospasm of the left anterior descending coronary artery, and seven had spasm of a dominant right coronary artery. Before nifedipine therapy, the frequency of anginal attacks per 24 hour period ranged from 1 to 12, with ventricular tachycardia accompanying ischemic episodes in 7 of 12 patients and high grade atrioventricular block occurring in 2 patients. After therapy with nifedipine, 11 of 12 patients had initial relief of symptoms, and 7 of the 11 had long-term relief. Withdrawal of nifedipine led to recurrence of angina on six occasions in four patients. Provocative testing in the cardiac catheterization laboratory by means of the cold pressor test in one patient and ergonovine maleate in another before and after nifedipine administration showed that this agent can block both alpha adrenergic- and regonovine-induced vasospasm. Nifedipine may have a significant role in the therapy of angina caused by coronary spasm.

The hemodynamic effects of induced supraventricular tachycardia in man.

SUMMARY The circulatory effects of supraventricular tachycardia (SVT) were studied in eight patients who reported disabling symptoms during paroxysms of the arrhythmia. Supraventricular tachycardia was induced in each patient by rapid atrial pacing or with atrial premature stimuli. Hemodynamic parameters in sinus rhythm and following the initiation of SVT were recorded and compared.The following mean values were observed in sinus rhythm (SR) and SVT. Heart rate (beats/min): SR 79, SVT 183; P-R interval (msec): during SR, 154; during SVT, 256; ratio of mean P-R intervals to mean R-R cycle lengths: SR 20%, SVT 76%; brachial artery pressures (mm Hg): SR 141, SVT 99; cardiac index (L/min/m2): SR 3.6, SVT 2.2; pulmonary artery pressures (mm Hg): SR 18/7, SVT 26/15; peak right atrial pressures (mm Hg): SR 4, SVT 17. Large waves appeared in the right atrium during SVT due to atrial contraction against closed tricuspid valves. Pulsus alternans were observed in each case during SVT. Despite the presence of chest pain during SVT, the coronary arteries were normally patent in four patients who underwent coronary arteriography.

Electrophysiologic characteristics of Ebstein's anomaly of the tricuspid valve.

Electrophysiologic characteristics of five patients with Ebsteins anomaly of the tricuspid valve were defined with studies using luminal intracardiac electrode catheters. The diagnosis was made in each case from clinical data and confirmed at cardiac catheterization by the presence of an atrialized right ventricular chamber with atrial mechanical activity and ventricular electrical activity. In three cases intra-right atrial conduction was prolonged (P-A intervals of 50, 50, and 65 msec), a finding which reflected the presence of a characteristically large right atrium. The bundle of His electrogram was recorded in its usual anatomical location. Atrioventricular nodal conduction was prolonged in only one case. Intra-His delay was observed in two cases (bundle of His duration of 30 and 30 msec). Infranodal conduction was prolonged in four cases with H-V intervals of 60, 65, 65, and 80 msec. The anatomical abnormalities were least severe in the only patient with a normal H-V interval (50 msec). The prolonged H-V interval was thought to result from stretching of the conduction system over the atrialized right ventricle (ARV). The late depolarization during the splintered R of the electrocardiogram found during intracardiac mapping of the ARV in three patients confirms the theory that the ARV produces the second QRS typically seen in this anomaly. The ARV was particularly irritable, and ventricular fibrillation was produced in two patients during catheter manipulation in this area. In one case the ARV had a shorter refractory period than the body of the right ventricle. Reentrant supraventricular tachycardia was induced in the only patient with Wolff-Parkinson-White syndrome. In addition to the previously recognized electrophysiologic features reconfirmed here, patients with Ebsteins anomaly of the tricuspid valve usually have: normal position of the bundle of His, prolonged intraright atrial conduction, prolonged infranodal conduction, and irritable ARV with delayed activation.

Atrial endocardial activation in man electrode catheter technique for endocardial mapping

The sequence of antegrade atrial endocardial activation was evaluated in 49 patients: 24 with a normal P wave configuration, 15 with electrocardiographic criteria for left atrial enlargement and 14 with a variety of supraventricular arrhythmias. In 17 patients, 6 with and 11 without evidence of the Wolff-Parkinson-White syndrome, retrograde atrial activation sequence was analyzed during ventricular premature beats, junctional rhythm or supraventricular tachycardia. The recording sites included the high mid- and low right atrium the right atrioventricular (A-V) junction and the distal coronary sinus or the left atrium. In patients with normal P waves atrial activation began at either the high or the mid-right atrium and proceeded to the low right atrium and A-V junction and then the coronary sinus. A similar sequence of activation was noted In patients with left atrial enlargement, but activation at the coronary sinus was markedly delayed (77 ± 8 [mean ± standard deviation] versus 112 ± 14 msec, P

Relationship of atrial fibrillatory wave amplitude to left atrial size and etiology of heart disease

It is commonly stated that coarse f waves in atrial fibrillation suggest the presence of rheumatic heart disease and large left atrial size, whereas fine f waves indicate non-rheumatic disease and small left atrial size. Using echocardiography as a more reliable indicator of left atrial size, 37 consecutive patients with chronic atrial fibrillation were evaluated. The correlation coefficients between left atrial size and maximum f wave amplitude was -0.12 and -0.07, using average f wave amplitude. Only 53 per cent (9 of 17) of patients with rheumatic heart disease had f wave greater than 1 mm. and 56 per cent (10 of 18) of patients with f wave size less than or equal to 1 mm. had non-rheumatic disease. This study refutes the contention that the f wave amplitude in atrial fibrillation is correlated with either left atrial size or etiology of heart disease. It is possible that an intra-atrial conduction defect is responsible for coarse f wave morphology.

The effects of coronary artery disease on the ventricular fibrillation threshold in man.

The ventricular fibrillation threshold (VFT) was measured in 28 patients at the time of cardiac surgery. The VFT was measured with a 100 Hz train of 24 rectangular pulses positioned across the ST segment and T wave. Current was applied to the epicardial surface of either ventricle with a bipolar electrode probe. In six patients, the normal right VFT was 24.3 ± 5.2 mA, and in 10 patients the normal left VFT was 33.6 ± 9.5 mA (p < 0.05). In 12 patients with > 75% obstruction of the left anterior descending coronary artery, the left VFT was 18.6 ± 6.9 mA. This value was significantly less than the left VFT in patients without coronary artery disease (p < 0.001). This study shows that the VFT can be measured in man and that coronary artery disease reduces this parameter.

Fascicular conduction disturbances after coronary bypass surgery

Abstract Two hundred patients undergoing coronary bypass graft surgery were studied to determine the frequency and significance of new fascicular conduction disturbances. The follow-up period ranged from 13 to 39 months. New disturbances developed in 39 patients (20 percent). Isolated right bundle branch block (6 percent) and left anterior hemiblock (6 percent) were the most common disturbances. Right bundle branch block was usually transient and was not associated with further complications in the follow-up period. However, patients with either transient or persistent left bundle branch block or left anterior hemiblock, or both, had (1) increased late mortality compared with patients without new fascicular conduction disturbances (5 of 26 versus 11 of 161; P P