Hein J. J. Wellens

Electrical Stimulation of the Heart in Patients with Ventricular Tachycardia

The initiation and termination of tachycardias were studied in five patients who suffered from recurrent attacks of ventricular tachycardia. In four, coronary artery disease with old myocardial infarction was present. A ventricular tachycardia could be initiated in all patients by a single right ventricular premature beat given during regular driving of the right ventricle. The tachycardia could be terminated by a single right ventricular premature beat, or two right ventricular premature beats given in close succession. In four of our patients an early right ventricular premature beat was followed by the next QRS complex of the tachycardia after an interval shorter than compensatory. Our results favor reentry as the causal mechanism for the tachycardias in our patients. Possible pathways for circus reentry leading to ventricular tachycardia can theoretically be composed of (1) the bundle branches, (2) Purkinje fibers with or without adjacent ventricular myocardium, (3) infarcted or fibrotic ventricular tissue, and (4) combinations of (1), (2), and (3).

The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex.

To determine the value of the electrocardiogram for differentiating aberrant conduction from ventricular ectopy, findings were retrospectively reviewed from patients with a widened QRS complex during tachycardia in whom the site of origin of tachycardia was determined by His bundle electrography. Seventy episodes of sustained ventricular tachycardia from 62 patients and 70 episodes of aberrant conduction during supraventricular tachycardia from 60 patients were available for study. Findings suggesting a ventricular origin of tachycardia were (1) QRS width over 0.14 sec, (2) left axis deviation, (3) certain configurational characteristics of QRS and (4) atrioventricular (A-V) dissociation. Capture or fusion beats resulting from A-V conduction of dissociated atrial complexes during ventricular tachycardia were seen during only four of 33 episodes of sustained tachycardia.

The Role of Premature Beats in the Initiation and the Termination of Supraventricular Tachycardia in the Wolff-Parkinson-White Syndrome

In four patients with WPW syndrome atrial and ventricular premature beats were induced and the changes in form of the ventricular and atrial complexes were studied. Results indicate that, depending upon the timing of the premature atrial beat and the state of refractoriness of the His and Kent bundles, excitation of the ventricles occurs predominantly through the atrioventricular nodal system, predominantly through the Kent bundle or exclusively through one or both conduction systems. With short delays conduction through the Kent bundle may be blocked and only normal excitation of the ventricles occurs. In one patient with a history of attacks of tachycardia these normal QRS complexes were followed by retrograde activation of the atria by the Kent bundle, and attacks of supraventricular tachycardia of shorter or larger duration occurred. They stopped spontaneously, sometimes by delay or block, either of retrograde Kent conduction or of antegrade A-V nodal conduction, making it possible for the sinus node to capture the ventricles. They also could be terminated by induced atrial premature beats.In two patients tachycardias could be induced by appropriately timed ventricular premature beats during regular driving of the right ventricle. In one of these patients a circus movement, involving the Kent bundle, is probably present. By appropriate stimulation of the atria or ventricles during an attack of supraventricular tachycardia in this patient, one cycle length could be shortened without changing those of the following beats. These results suggest that a circus movement involving the atria, the normal atrioventricular conduction system and the Kent bundle is present. In the other patient, not fulfilling the WPW criteria, ventricular or atrial premature beats did not interfere with the basic rhythm of the tachycardia. Two hypotheses for this tachycardia are given: nodal tachycardia caused by rapid firing of the A-V node or a nodal tachycardia caused by a reciprocal mechanism in the A-V junction. The attacks could be blocked too by appropriately timed atrial and ventricular premature beats. No ventricular type of tachycardia could be demonstrated.

Value and limitations of thallium-201 scintigraphy in the acute phase of myocardial infarction

We examined the diagnostic usefulness of thallium-201 scintigraphy in 200 patients with acute myocardial infarction. The scintiscans showed a defect, suggesting infarction in 165. In all 44 patients studied iwthin six hours after onset of symptoms the scintiscans indicated a defect. Frequency of positive scans was significantly higher (90 of 96) in patients studied within 24 hours after onset than in those (75 of 104) studied later (p less than 0.01).

The anatomical substrates of wolff-parkinson-white syndrome. A clinicopathologic correlation in seven patients.

Clinicopathological correlations were made on the hearts from seven patients known to have exhibited electrocardiographic evidence of the Wolff-Parkinson-White syndrome. In each case, clinical and pathological investigations were conducted independently, neither group of investigators having knowledge of the others results. In all seven hearts, the entire atrioventricular junctions were serially sectioned. Accessory atrioventricular connections were predicted in all seven cases following electrocardiographic investigation. Connections were identified histopathologically in four hearts in the predicted site. In another case two connections were identified, one being considered responsible for the pre-excitation. In the sixth case a right lateral connection was anticipated, but only accessory nodo-ventricular fibers were identified following histopathologic studies. In the final case, a posterior septal connection was predicted but the entire septum had fibrosed following previous operation. These findings...

Observations on patients with primary ventricular fibrillation complicating acute myocardial infarction.

In order to evaluate the events preceding primary ventricular fibrillation (PVF), continuous tape recording was performed in 262 patients consecutively admitted to the hospital within six hours of infarction in whom antiarrhythmic therapy was withheld. Warning arrhythmias (defined as ventricular ectopic beats occurring with a frequency of more than five beats per minute, in runs, falling in the vulnerable phase of the cardiac cycle or being multiformed) were registered in an equal percentage in patients who did or did not develop PVF. Immediately prior to PVF seven patients showed sinus tachycardia, 10 a sinus rate ranging from 60 to 100 beats per minute and two bradycardia due to complete atrioventricular block. The ventricular ectopic beat initiating PVF had a late coupling interval (QR′/QT ≥ 0.85) in 11 patients and a left bundle branch block configuration as frequent as a right bundle branch block. Conclusions: 1) Warning arrhythmias are not considered good criteria for institution of antiarrhythmic therapy in order to prevent PVF. 2) In patients with sinus rhythm there may be an association between heart rate and onset of PVF. 3) The malignancy of a ventricular ectopic beat is not determined by its coupling interval or its configuration.

Location and size of acute transmural myocardial infarction estimated from thallium-201 scintiscans. A clinicopathological study.

A clinicopathological study was performed in 23 patients who died from acute transmural myocardial infarction and who had been studied with thallium-201 during the acute phase. Twenty patients died within five days and three later than five days after scintigraphy. The scintigraphic location and the estimated size of infarction in vivo were correlated with postmortem findings. There was good agreement in 91%percnt; between scintigraphic and postmortem location of infarction and in 70%percnt; between the ECG and postmortem find- ings. The size of infarction as determined from computer-processed schematic drawings of postmortem slices of the heart correlated well with the size determined from processed schematic drawings of the scintiscans (r = 0.91 for anterior infarction, r = 0.97 for inferior infarction, r = 0.86 for anterior-inferior infarction). It is concluded that thallium-201 scintigraphy provided more precise location of infarction than the ECG and that the size of the scintigraphically abnormal area reflected the extent of necrotic myocardium.

Ventricular Fibrillation Occurring on Arousal from Sleep by Auditory Stimuli

A patient is described having syncopal attacks on being awakened from sleep by auditory stimuli. The electrocardiogram registered during these episodes showed Q-T-segment changes followed by ectopic ventricular activity and spontaneously ending attacks of ventricular fibrillation. Aside from the attacks, her ECG only showed abnormalities of the S-T segment with marked U waves. Hemodynamic and electrophysiologic studies showed no abnormalities. Coronary angiograms were normal. Following therapy with propranolol and diphenylhydantoin she has been free from syncopal episodes for the past 11 months. The mechanism responsible for the Q-T-segment changes and ventricular tachyarrhythmias is not understood.

Quinidine-induced ventricular flutter and fibrillation without digitalis therapy

Three cases are described with documented ventricular flutter and fibrillation during quinidine medication without concomitant digitalis therapy. In all three patients the arrhythmia developed while they were receiving moderate doses of quinidine. Although no changes in QRS width were observed after administration of quinidine, there was marked prolongation of the Q-T interval. The mechanism of development of ventricular flutter and fibrillation in patients taking quinidine may be similar to that in patients with the Q-T prolongation syndrome.

Second degree block during reciprocal atrioventricular nodal tachycardia.

Of 67 patients with reciprocal atrioventricular (A-V) nodal tachycardia consecutively studied by programmed electrical stimulation of the heart, nine patients showed second degree block toward the ventricle and one patient toward the atrium during tachycardia. In four patients the occurrence of block was critically related to the prematurity of the test stimulus initiating the tachycardia. In three patients block developed following increase in rate of tachycardia. In two patients block could be elicited by introducing premature ventricular stimuli during tachycardia. Our observations indicate that different mechanisms may be responsible for second degree block during reciprocal supraventricular tachycardia. The finding of second degree block during reciprocal supraventricular tachycardia excludes a tachycardia with A-V conduction over the A-V node - His pathway and V-A conduction over an accessory A-V pathway.