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One hundred twenty-nine patients were prospectively studied after a first myocardial infarction. A first signal-averaged electrocardiogram (SAECG-1) was performed in the acute phase (within 48 hours after onset of symptoms) and a second one (SAECG-2) in the late phase (6 to 18 months after hospital discharge). We studied the influence of nine parameters on the evolution of the signal-averaged electrocardiogram: age, gender, myocardial infarction location, number of diseased coronary vessels, infarct-related coronary artery patency, use of thrombolytic therapy or percutaneous transluminal coronary angioplasty in the acute phase, left ventricular ejection fraction, and recurrence of ischemic events. No follow-up data were available in 15 patients. Of the remaining 114 patients, an ischemic event occurred in 25 (22%). The signal-averaged electrocardiogram remained unchanged in 97 (85%) (remaining normal in 78 and abnormal in 19). It became abnormal in 13 (11.5%) and became normal in 4 (3.5%). In patients with a normal SAECG-1, two factors were associated with the change to an abnormal SAECG-2: (1) an ischemic event occurred in 11 (85%) of 13 patients whose SAECG-2 was abnormal compared with only 13 (17%) of 78 patients whose SAECG-2 remained normal (p < 0.0001), and (2) 100% of patients with an abnormal SAECG-2 had an inferior myocardial infarction compared with 54% of patients with a normal SAECG-2 (p = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)

After angiography, 6 to 24 hours of bedrest is indicated to assure that adequate hemostasis of the femoral artery has been achieved. Recently, a new hemostatic puncture closure device (HPCD) has been developed, which consists of a resorbable polymer anchor, a resorbable suture, a small collagen plug and an 8Fr delivery device. The device is delivered into the femoral artery through the introducer sheath, the anchor is secured against the intraluminal artery wall, and the collagen plug is deployed on the arterial wall. The prototype of the HPCD was used in 20 patients administered heparin. After insertion of the HPCD, hemostasis was achieved in 1.2 +/- 2.1 minutes; in 2 patients a light pressure dressing was applied for 4 hours to stop oozing. No late bleeding occurred. In 1 patient the positioning suture broke, requiring the application of a pressure bandage. Patients were uneventfully mobilized after 6.7 +/- 3.5 hours. In all patients serial duplex scanning of the femoral artery was performed before and after 1, 7, 30 and 90 days after HPCD placement. In 5 patients a small subcutaneous hematoma close to the site of introduction could be detected by ultrasound 1 day after catheterization. All but 1 patient had normalization of the flow patterns in the femoral artery. It is concluded that: (1) the HPCD is an effective device to achieve immediate hemostasis after arterial catheterization despite antithrombotic therapy, (2) early mobilization was uneventful, (3) duplex ultrasound studies demonstrated only transient changes in the punctured femoral artery, and (4) further investigations are needed to establish the efficacy and safety of the device.

One hundred twenty-nine patients were retrospectively analyzed and divided into 3 groups according to (1) the presence of a patent artery obtained either spontaneously or after thrombolytic therapy but without percutaneous transluminal coronary angioplasty (PTCA) (group I, n = 83), (2) the presence of a patent artery after opening by PTCA (group II, n = 29), or (3) absence of reperfusion despite thrombolytic therapy or PTCA (group III, n = 17). Thrombolytic therapy was given within 4 hours after onset of symptoms (mean 2.5 +/- 1.0 hours) and PTCA was performed within 24 hours after the onset of symptoms (mean 6 +/- 6 hours). Signal averaging was performed within 24 hours after cardiac catheterization. An abnormal signal-averaged electrocardiogram was present in 10 of 83 (12%) group I, 9 of 29 (31%) group II and 7 of 17 (41%) group III patients (p0.05 group I vs II, p0.01 group I vs III, no statistical difference group II vs III). Therefore, in contrast to reperfusion by thrombolytic therapy the incidence of abnormalities on the signal-averaged electrocardiogram early after myocardial infarction is not reduced by an early opening of the culprit vessel by PTCA.

Four hundred and one patients with acute myocardial infarction of less than 4 h duration were randomized to receive intravenous thrombolytic treatment with either 80 mg of full length unglycosylated single-chain-urokinase plasminogen activator (INN saruplase) or 1.5 million IU of streptokinase delivered over a 60 min period. Angiographic patency rates were higher at 60 min in saruplase treated patients (71.8% vs 48%; P less than 0.001), but did not differ significantly at 90 min (71.2% vs 63.9%; P = 0.15). Fibrinogen levels dropped markedly in both groups, the decrease being delayed and less pronounced with saruplase. Total fibrin and fibrinogen degradation products and D-dimer values rose earlier and to higher peak values in streptokinase treated patients. In both groups marked plasminogen and alpha 2-antiplasmin consumption was observed. Lower fibrinogen levels, and in particular the faster rate of fibrinogen breakdown, were associated with higher patency rates at 90 min (P less than 0.05). Patients with bleeding complications had lower 'lowest points' and a more rapid decrease in fibrinogen (P less than 0.05). These findings were not related to the drug used. Increased heparin levels at 6 to 12 h were correlated to bleeding complications in streptokinase treated patients. It is concluded that the rate of fibrinogen breakdown during and following thrombolytic treatment for acute myocardial infarction is related to early vessel patency and bleeding complications.

It has been suggested that the ECG development (ST segment, QRS score) of acute myocardial infarction (MI) pts with TIMI 2 flow is closer to TIMI 0/1 than to TIMI 3. To study this, 358 acute MI pts treated with thrombolytic therapy were investigated. Sum of ST deviation (SST) and QRS score of the 12 lead ECG were calculated at 3 time points during the first 48 hours: ECG 1: on admission (mean 90 min alter onset of MI), ECG 2: mean 9 hours alter MI, and ECG 3: mean 36 hours after MI. ECG's were related to the TIMI flow determined from the last view of angiography 60 and 90 min after start of thrombolytic therapy. Results ECG TIMI TIMI 2 3 0/1 2/3 N 46 248 64 294 SST 1 16.1 ns 15.5 15.4 ns 15.6 (mm) 2 6.5 ns 5.3 10.2 *** 5.5 3 5.1 ns 4.7 6.1 * 4.8 ORS- 1 2.9 ns 2.9 2.6 ns 2.9 score 2 3.9 ns 4.5 4.5 ns 4.4 3 5.1 ns 5.2 6.3 ** 5.2 * p l 0.05 ** p l 0.01 *** p l 0.0001 Conclusion TIMI 2 patients have significantly less ECG changes at 9 hours and later than patients with TIMI 0/1 flow. Electrocardiographically, patients with TIMI2 flow behave like pts with TIMI 3 flow.

The effect of thrombolysis in acute myocardial infarction on infarct size, left ventricular function, clinical course and patient survival was studied in a randomized trial comparing thrombolysis (269 patients) with conventional treatment (264 control patients). All 533 patients were admitted to the coronary care unit within 4 hours after the onset of symptoms related to the infarction. Baseline characteristics were similar in both groups. Informed consent was requested only of patients allocated to thrombolysis; no angiography was performed in 35. The infarct-related artery was patent in 65 patients and occluded in 169. Recanalization was achieved in 133 patients. The median time to angiographic documentation of vessel patency was 200 minutes after the onset of symptoms.The clinical course in the coronary care unit was more favorable after thrombolysis. Infarct size, estimated from myocardial enzyme release, was 30% lower after thrombolysis. In patients admitted within 1 hour after the onset of symptoms the reduction of infarct size was 51%, in those admitted between 1 and 2 hours it was 31% and in those admitted later than 2 hours it was 13%. Left Myocardial infarction in most patients results from a thrombotic occlusion of a major coronary artery. Recently, Rentrop and other investigators (1-4) have demonstrated that rapid recanalization can be achieved by intracoronary inventricular function measured by radionuclide angiography before hospital discharge was better after thrombolysis (ejection fraction 48 ± 15%) than in control patients (44 ± 15%). Similar improvement was observed in patients with a first infarct only (thrombolysis 50 ± 14%, control subjects 46 ± 15%), in patients with anterior infarction (thrombolysis 44 ± 16%, control subjects 35 ± 14%) and in those with inferior infarction (thrombolysis 52 ± 12%, control subjects 49 ± 12%). Similar results were obtained by contrast angiography.Mortality was lower after thrombolysis. After 28 days 16 patients allocated to thrombolysis and 31 control patients had died. One year survival rates were 91 and 84%, respectively. On the other hand, nonfatal reinfarction occurred more frequently after thrombolysis (36 patients) than in control subjects (16 patients). Early thrombolysis by intracoronary streptokinase leads to a smaller infarct size estimated by enzyine release, preserves left ventricular function at the second week and leads to improved 1 year survival.

To determine the value of the admission 12-lead electrocardiogram to predict infarct size limitation by thrombolytic therapy, data were analyzed in 488 of 533 patients with acute myocardial infarction (AMI) from a randomized multicenter study. All patients had typical electrocardiographic changes diagnostic for an AMI and were admitted within 4 hours after the onset of chest pain; 245 patients were allocated to thrombolytic treatment and 243 to conventional treatment. Cumulative 72-hour release into plasma of myocardial alpha-hydroxybutyrate dehydrogenase (HBDH) was used as a measure of infarct size. In general, the amount of infarct limitation due to thrombolytic therapy was proportional to the size of the area at risk. Patients with new Q waves, high QRS score and high ST-segment elevation or depression had the largest enzymatic infarct size in both treatment groups, irrespective of location of the AMI. Compared with conventionally treated patients, patients with anterior AMI treated with streptokinase had significant infarct size limitation (480 U/liter HBDH, 37%), and limitation was most prominent in those with Q waves (820 U/liter HBDH) or high ST elevation (750 U/liter HBDH). Infarct size limitation in inferior AMI was less impressive (330 U/liter HBDH, 33%) and patients with high ST-segment elevation (460 U/liter HBDH) or marked contralateral ST-segment depression (430 U/liter HBDH) had the most notable infarct limitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Data on the correlation of left ventricular segmental wall motion and electrocardiographic findings are, except for Q waves and ST segment elevation, still controversial. Therefore, in addition to Q waves and ST segment elevation, eight features of the electrocardiogram were studied in 265 patients, 61 with normal coronary arteries and 204 with coronary artery disease. Patients with a QRS duration of 0.12 second or greater were excluded.Left ventricular wall motion was assessed in the 30° right anterior oblique and the 60° left anterior oblique projections and analyzed by the Stanford method and a modification of that method, respectively. Asynergy of a particular segment correlated well with the presence of Q waves in the corresponding electrocardiographic lead or leads, but was also found in other segments. There was a significant (p < 0.001) correlation between the number of leads with Q waves and the degree of extension of asynergy. The R/S ratio in lead V1and Q waves in lead V6appeared to be the most informative about the posterior wall. Loss of R wave voltage had a lower predictive value for segmental asynergy than did Q waves in the same lead. Among patients with electrocardiographic findings of an infarct, asynergy was found in 83 to 94%. Patients having Q waves in combination with ST segment elevation manifested more severe asynergy than did patients whose Q waves were not associated with ST elevation. New data are presented for lateral and posterior infarction. Patients having left-axis deviation, low voltage and QRS notching had severe asynergy. ST segment depression and negative T waves gave only limited additional information on wall motion.It is concluded that certain QRS abnormalities correlate highly with asynergy. ST segment elevation is the most important non-QRS abnormality in predicting asynergy.

The incidence, mechanisms and sites of block of spontaneous termination of circus movement tachycardia (CMT) using an atrioventricular accessory pathway (AP) were analyzed in 24 consecutive patients (17 with Wolff-Parkinson-White syndrome and seven with a concealed AP) who were not receiving antiarrhythmic drugs. Spontaneous termination of tachycardia occurred in 10 patients (105 episodes). A reduced "safety margin" of tachycardia was the only factor that was significantly more common in the patients who manifested spontaneous termination (p less than 0.01). The site of spontaneous block was located in the AP in six patients (50 episodes), atrioventricular node (AVN) in six patients (37 episodes) and His-Purkinje system (HPS) in three patients (18 episodes). At least 14 mechanisms leading to block in the tachycardia circuit were identified. Labile conduction during tachycardia occurred at multiple sites (AVN, His bundle, bundle branches, and AP). Analysis of the duration of tachycardia before spontaneous termination showed a characteristic time pattern for block at each site, consistent with the autonomic and electrophysiologic changes that occur after induction of tachycardia. Spontaneous termination of CMT using an AP is a common phenomenon. Many mechanisms are involved, which are often complex and dependent on interplay of the electrophysiologic characteristics of the components of the tachycardia circuit.

Pacing is becoming an accepted form of treatment for reentry tachycardias. The different pacing modalities available and experience with a patient-activated antitachycardia pacemaker are presented in this paper. This system has bidirectional communication between pacemaker and pacemaker-activator and between pacemaker and prescription formulator (which is a sophisticated portable stimulator used for non-invasive electrophysiological evaluation of the system). This pacemaker was implanted in 18 patients with drug-resistant tachycardias. Six patients had ventricular tachycardia, 3 had A-V nodal reentrant tachycardia, 4 had the concealed accessory pathway, and 5 had the WPW syndrome. In the 3 months before implantation the mean number of admissions for termination of tachycardia was 2.1 per patient-month. During a follow-up period of 3–26 months only 6 patients were admitted once for termination of tachycardia (0.02 admissions per patient-month). The reasons for admission of these 6 patients were: defective pacemaker activator in 2 patients, inadequate control of tachycardia in 2 patients, inappropriate use of the device in 1, and inadequate intake of medication in 1. All these problems were solved easily. Eight pacemaker activators required reprogramming, which was done in 5 patients on an out-patient basis. The interval scanning mode was used in 9 patients. Nine patients required more than 2 stimuli for reproducible termination. A step-wise increase in number of stimuli was used in 5 patients. This system has proven to be a safe and effective form of treatment of drug-resistant supraventricular and ventricular tachycardias and has resulted in marked improvement of the quality of life of these patients.

The electrophysiological effects of the intravenous administration of a new antiarrhythmic drug, lorcainide, were evaluated by programmed electrical stimulation of the heart in 23 patients with atrioventricular conduction disturbances (four patients), ventricular tachycardia (five patients), and accessory atrioventricular pathway (14 patients). Lorcainide did not affect the refractory period of the atrium, ventricle, atrioventricular node, or the AH interval. It lengthened the duration of the HV interval, the refractory period of the accessory pathway, and the width of the QRS complex. The drug terminated ventricular tachycardia in four of five patients. It is concluded that the drug may be of potential benefit in patients with ventricular tachycardia or accessory atrioventricular pathways (especially those with a short refractory period). Lorcainide is contraindicated in patients with bundle-branch block and prolonged HV interval.

The effect of early myocardial reperfusion (within 4 hours after onset of symptoms) on regional left ventricular function in patients with acute myocardial infarction has been quantitated by analysis of segmental wall motion. Of 533 patients randomized either to conventional coronary care unit therapy or to a reperfusion strategy, in 332 high quality angiograms were obtained 2 to 8 weeks after the onset of myocardial infarction. In those assigned to thrombolytic therapy, angiographic data were also available after acute reperfusion. Analysis on an “intention to treat” basis revealed significant preservation of left ventricular function after thrombolytic therapy (ejection fraction 53%) compared with conventional treatment (ejection fraction 47%). In addition, wall motion analysis showed significant improvement of regional function in the infarct zone in both inferior and anterior infarction. In addition, significant changes occurred in regional function of the remote “noninfarct zone” in the acute as well as the chronic stage. It is concluded that improved regional and global left ventricular function can be achieved with early reperfusion and that this is the likely explanation for the reduction of early and late mortality after thrombolysis observed in this study.

Ajmaline given intravenously produced complete anterograde block in the accessory pathway of 32 of 59 patients with the Wolff-Parkinson-White syndrome. An electrophysiologic investigation performed 1 day later revealed that failure of ajmaline to produce complete anterograde block in the accessory pathway corresponded to a short refractory period of this pathway (less than 270 ms). The use of ajmaline intravenously is advanced as a reliable and rapid procedure for identifying those patients with the Wolff-Parkinson-White syndrome who have a short refractory period of the accessory pathway and are possible at risk of circulatory insufficiency or sudden death if atrial fibrillation supervenes.

Immediate PTCA following thrombolysis with streptokinase was performed in 46 out of 533 patients enrolled in a multicentre randomized trial of early reperfusion in patients with acute myocardial infarction. Additional effects of PTCA in patients with a residual diameter stenosis in the infarct-related coronary artery of 70% or more after thrombolysis were compared with successful thrombolysis alone in a matched pair analysis. Thirty six pairs of patients were formed identical with respect to the infarct related coronary artery, presence or absence of previous myocardial infarction, total ST segment elevation on the ECG at admission to the trial, and delay between onset of symptoms and hospital admission. PTCA after thrombolysis did not lead to additional limitation of infarct size, nor to further preservation of left ventricular function. Infarction rate during the three-year follow-up was 14% after PTCA versus 30% after thrombolysis alone (P = 0.05). Similarly, patients had less angina or heart failure after PTCA, since on average 128 out of 156 weeks follow-up were symptom free, while this was only 102 weeks after thrombolysis alone (P = 0.03). Immediate PTCA after thrombolysis with intracoronary streptokinase seems to prevent recurrent ischemia and reinfarction. Further studies should address the proper indication and timing of PTCA after thrombolysis.

A 30 year old woman with Wolff-Parkinson-White syndrome underwent electrophysiologic study for investigation of circus movement tachycardia utilizing the accessory pathway for retrograde conduction. The accessory pathway was located on the right side. Episodes of circus movement tachycardia with left and right bundle branch block were induced. Some episodes of circus movement tachycardia with left bundle branch block terminated spontaneously. Two episodes of spontaneous termination at the level of the atrioventricular (A-V) node were preceded by prolongation of the H-V interval causing delay in atrial activation. This delayed atrial cycle was then followed paradoxically by spontaneous termination of the tachycardia in the A-V node. A similar phenomenon could be demonstrated reproducibly with single echo beats induced by coronary sinus extrastimuli. It appears that retrograde concealed penetration of the A-V node through the bundle branch system during anterograde left bundle branch block is the most likely mechanism for this phenomenon.

The effect of procainamide, quinidine, ajmaline and amiodarone on the effective refractory period of the accessory pathway in the (A-V) anterograde and retrograde directions was studied in relation to the length of this period before drug administration. All patients had the Wolff-Parkinson-White syndrome and were studied with intracavitary recordings and programmed electrical stimulation of the heart using identical basic cycle lengths and test stimulus intervals before and after drug administration. The patients were separated into two groups, those in whom the effective refractory period of the accessory pathway was 270 ms or greater (Group 1) and those in whom it was less than 270 (Group 2). In the anterograde direction the magnitude of increase in the length of the effective refractory period of the accessory pathway after drug administration was related to its initial length. Only modest lengthening of this period could be accomplished in patients with an initially short period. In evaluating the effect of drugs in patients with the Wolff-Parkinson-White syndrome, the role of the initial length of the effective refractory period of the accessory pathway should be considered.

In patients admitted to the hospital because of unstable angina, a subgroup can be recognized that is at high risk for the development of an extensive anterior wall myocardial infarction. These patients, who show characteristic ST-T segment changes in the precordial leads on or shortly after admission, have a critical stenosis high in the left anterior descending coronary artery. Of 145 patients consecutively admitted because of unstable angina, 26 (18%) showing this ECG pattern, suggesting that this finding is not rare. In spite of symptom control by nitroglycerin and beta blockade, 12 of 16 patients (75%) who were not operated on developed an usually extensive beta blockade, 12 of 16 patients (75%) who were not operated on developed a usually extensive anterior wall infarction within a few weeks after admission. In view of these observations, urgent coronary angiography and, when possible, coronary revascularization should be done in patients with unstable angina who show this ECG pattern.

One hundred eighty-seven patients with clinically documented supraventricular tachycardia with a narrow QRS complex were admitted for electrophysiologic study. The diagnoses after this study were circus movement tachycardia using an accessory pathway in 50 patients, atrioventricular nodal tachycardia in 50 patients, atrial flutter in 50 patients, atrial tachycardia in 27 patients and an incessant tachycardia retrogradely using a slowly conducting accessory pathway in 10 patients. On retrospective analysis, 5 criteria on the 12-lead electrocardiogram during tachycardia were analyzed for their value in making the diagnosis of site of origin. These criteria were P-wave location, axis of the P wave, atrial rate, alternation of the QRS complex and atrioventricular relation. Fifty-seven patients with a narrow QRS tachycardia were prospectively studied using the 5 criteria. A correct diagnosis was made in 48 of the 57 patients (84%). Thus, in most patients with a narrow QRS tachycardia, information from the 12-lead electrocardiogram is adequate for diagnosis.

Termination of atriovontricular nodal (A VN) re-entrant tachycardia by one or two induced premature beats generally occurs within one tachycardia cycle from the last premature beat. Two cases are described in which programmed stimulation during sustained re-entrant AVN tachycardia caused delayed termination in the second or third tachycardia cycle following the extrastimuli. The site of block was the antegrade pathway in one case and the retrograde pathway in the other. The most likely mechanism was induced second degree block in one limb of the tachycardia circuit. Delayed termination provided evidence for concealed penetration of the tachycardia circuit in one case. We conclude that delayed termination of tachycardia is not an indicator of the underlying mechanism of tachycardia. Delayed termination may reveal concealed penetration of the tachycardia circuit. Lastly, in unusual cases programmed stimulation may fail to cause immediate termination of re-entrant tachycardia but may perturb the tachycardia circuit enough to cause termination in subsequent tachycardia cycles.

Different mechanisms of block of impulse propagation in several re-entrant circuits resulted in a major discordance between the "echo-zone" and the "tachycardia-zone" in a patient with intermittent Wolff-Parkinson-White syndrome, dual atrioventricular nodal pathways, and bundle branch re-entry. This case illustrates the delicate balance in electrophysiological properties required between the tissues incorporated in a re-entrant circuit to initiate and sustain the arrhythmia. It also shows how the presence of several reentrant pathways can lead to refractoriness in the circuit responsible for the circus movement tachycardia.

In 18 consecutive patients with the Wolff-Parkinson-White syndrome undergoing electrophysiologic study, the ventriculo-atrial conduction time of right ventricular apical extrasystoles which advanced atrial activation during circus movement tachycardia was studied in relation to accessory pathway location. Accessory pathway location was determined by delta wave morphology during maximal pre-excitation, mapping of atrial activation during circus movement tachycardia and ventricular pacing, the effect of bundle branch block on ventriculo-atrial conduction time during circus movement tachycardia, and the effect of pacing from different sites in the atria on the stimulus-to-delta wave interval. In 7 patients with septal accessory pathways, ventriculo-atrial conduction time was similar during circus movement tachycardia and following right ventricular apical extrasystoles (mean difference 0 +/- 6 ms, range -5 to +10 ms). In contrast, in 11 patients with a left free wall accessory pathway, ventriculo-atrial conduction time increased by 46 +/- 15 ms (range 15 to 65 ms) following right ventricular apical extrasystoles. Therefore, measurement of the ventriculo-atrial conduction time of right ventricular extrasystoles during circus movement tachycardia provides an easy way to distinguish between septal and left free wall accessory pathways. This finding may be of particular use in determining the location of concealed bypass tracts.

The hypothesis that production of ischemia or cooling of an arrhythmogenic area or pathway could interrupt tachycardias was tested by subselective catheterization of the coronary artery supplying the site of origin of ventricular tachycardia (9 patients), the accessory pathway (2 patients) and the site of origin of atrial tachycardia (1 patient). Ventricular tachycardia was reproducibly terminated and reinduction temporarily prevented in 8 of the 9 patients by occlusion of the artery or administration of iced isotonic saline. Block in the accessory pathway was obtained in 1 of the 2 patients with Wolff-Parkinson-White syndrome. Selective cooling through the atrioventricular nodal artery in 1 patient terminated his circus movement tachycardia. Reproducible termination of a continuous atrial tachycardia was obtained by cooling of the atrial branch supplying the site of origin of the arrhythmia. These data demonstrate the feasibility of identification and selective catheterization of the coronary artery branch supplying blood to an arrhythmogenic area or pathway and suggest a new possibility for treatment of tachycardias by permanently blocking the blood supply to the site of origin or pathway of a tachycardia.

The case of a patient suffering from incessont supraventricular tachycardia is presented. The electrophysiological sludy showed the presence of an accessory atrioventricular (A-V) bundle with nodal-like properties and long conduction times. This structure was used as the retrograde arm of the tachycardia circuit. Tachycardia was intermittent at rest, but had a sustained character during slight exercise. Administration of atropine and isoproterenol failed to sustain the arrhythmia and spontaneous initiation during sinus rhythra was no longer observed. During handgrip exercise a sustained tachycardia developed immediately. During ventricular stimulation a duol atrial response to a single paced ventricular premature beat was repeatedly observed, proving the avoilability of two separate A-V pathways for retrograde conduction. The case illustrates the labile nature of this type of accessory pathway, and suggests that autonomic changes can play an important roJe in the initiation. mainlenance, termination. or even spontaneous cure of tachycardia in patients with this anomaly.

The morphologic characteristics at coronary arteriography of systolic narrowing of the left anterior descending coronary artery (LAD) were evaluated in 14 patients. Six patients had systolic narrowing of the LAD not associated with other cardiac abnormalities (group A) and eight patients had systolic narrowing of the LAD associated with hypertrophic cardiomyopathy (group B). Patients in group A showed a smooth and progressive constriction of the vessel up to the point of maximal stenosis, giving it a "rat-tail" appearance. There was no systolic narrowing of septal branches or of other epicardial vessels in this group. In patients of group B, systolic narrowing of the LAD had a "saw-fish" appearance. Seven patients had systolic narrowing of the septal branches, and five had systolic narrowing of other epicardial vessels. These data indicate that systolic narrowing of the LAD in patients with hypertrophic cardiomyopathy differs angiographically from systolic narrowing due to an intramural course of a part of the vessel (as in group A patients). We postulate that in patients with hypertropic cardiomyopathy, fiber hypertrophy and disarray in the vicinity of the coronary vessels is responsible for the morphology and the widespread distribution of systolic narrowing.

Three patients with reentrant tachycardia are described who had an accessory pathway with a very long conduction time that was incorporated in the tachycardia circuit. The accessory pathway was able to conduct in one direction only, in retrograde manner in two patients and in anteriograde manner in the remaining patient. Evidence is presented that reveals that in the first two patients the accessory pathway was septally located, had completely bypassed the normal atrioventricular (A-V) conduction system, had properties of decremental conduction, and had an atrial exit close to the coronary sinus and a ventricular exit relatively far from the atrioventricular A-V ring. In the third patient, who manifested wide QRS complex during tachycardia, the ventricular end of the accessory pathway seemed to be located close to the right ventricular apex. The atrial end of the pathway could not be localized exactly.

The possible role of the atrioventricular nodal (AVN) function curve during tachycardia as a cause of cycle length alternation was investigated using a computer model of circus movement tachycardia utilizing an atrioventricular accessory pathway. Two types of AVN function curves during tachycardia were entered into the computer: straight lines of various gradients and representative examples of patient-based AVN function curves obtained during clinical electrophysiologic studies. Perturbations of the tachycardia model were induced by introducing a short cycle, by suddenly prolonging a conduction interval, or by moving the AVN function curve relative to that in stable tachycardia. Using the straight line AVN function curves, stable, sustained cycle length alternation could be induced by perturbation of the tachycardia cycle if the gradient of the line was -1 (slope = 45 degrees). If the gradient was more than -1 (slope less than 45 degrees), the perturbation was damped. If the gradient was less than -1 (slope greater than 45 degrees), the perturbation was amplified, leading to termination of tachycardia by block in the AVN. Similar but more complex responses to perturbation of tachycardia were found using patient-based AVN function curves. Thus, sustained cycle length alternation and amplification or damping of perturbation could be produced. Using physiologic AVN function curves, the response to perturbation of tachycardia depended on the interrelationship of the shape of the AVN function curve, the location of the cycle length of tachycardia on the curve, the magnitude and direction of the perturbation, and the AVN effective refractory period. We conclude that cycle length alternation during tachycardia may be explained by the characteristics of a single antegrade AVN function curve without postulating the presence of additional AVN pathways. The stability of circus movement tachycardias depends on the interaction of several variables.

The effect of amiodarone in the Wolff-Parkinson-White syndrome was studied with programmed electrical stimulation of the heart in 15 patients. All 15 patients had circus movement tachycardias; 7 also had atrial fibrillation. Programmed electrical stimulation was performed before and after 14 days of oral administration of amiodarone. The effective refractory period of the accessory pathway lengthened in an atrioventricular direction in all patients and in a ventriculoatrial direction in eight patients. The effective refractory period of the atrium and ventricle lengthened in 14 and 12 patients, respectively. After administration of amiodarone, circus movement tachycardia could no longer be initiated in five patients. The zone of tachycardia narrowed in four patients, did not change in two and increased in seven. The effect of amiodarone on initiation of circus movement tachycardia could be related to differences in effect of the drug and in the mechanism of tachycardia in individual patients. In all patients in whom tachycardias could still be initiated after treatment with amiodarone the heart rate during tachycardia was slower than before treatment. This slowing was caused by a decrease in conduction velocity of the circulatory wave in different parts of the tachycardia circuit. The effect of amiodarone in prolonging the refractory period of the accessory pathway makes this drug especially useful in patients with the Wolff-Parkinson-White syndrome and atrial fibrillation.

In 1981 we initiated a randomized trial at the Thoraxcenter in Rotterdam which was later extended to include four other hospitals cooperating in the Netherlands Interuniversity Cardiology Institute: the Zuiderziekenhuis in Rotterdam, the Free University in Amsterdam, the St. Annadal Hospital in Maastricht and the Leiden University Hospital. Since the global results of the study have been published in the Lancet (4) and in other journals (3, 5) we present a summary of the findings and discuss the clinical consequences of the trial.

Three cases of pacemaker interactive tachycardia are presented. The first two are [artificial] circus movement tachycardias. In the first one the retrograde arm of the tachycardia circuit was provided by the A-V node and the antegrade arm by an atrial synchronous pulse generator. In the second case, the A-V node and, coincidentally, an A-V sequential pulse generator alternately provided the antegrade arm while the retrograde arm was by way of an accessory pathway. In the third case ventricular inhibition during A-V sequential pacing gave the paced atrial events the chance to be conducted to the ventricles with a long A-V interval. This resulted in a tachycardia with a rate of 150 bpm, instead of the programmed rate of 110 bpm.

Unusual mechanisms of spontaneous termination of atrioventricular (A-V) nodal reentrant tachycardia were observed in two patients during programmed electrical stimulation of the heart. In both patients the mechanism of termination was based on the use of another reentrant pathway than the use used during tachycardia. This pathway was located extranodally in one patient and intranodally in the other. The observations illustrate some of the complexities of reentry in the human heart and how they can play a role in spontaneous termination of A-V nodal tachycardia.

To evaluate the effect of beta adrenergic stimulation on the duration of the anterograde refractory period of the accessory pathway, isoproterenol was infused in seven patients with the Wolff-Parkinson-White syndrome. In two patients the effect of isoproterenol was studied during long-term oral amiodarone administration. To avoid rate-related changes induced by isoproterenol, the anterograde refractory period of the accessory pathway was determined using the single test stimulus method at identical basic cycle lengths. Isoproterenol shortened the anterograde refractory period of the accessory pathway in six of the seven patients studied. In two of the three patients with an initial anterograde refractory period of the accessory pathway of equal to or less than 290 ms, shortening measured 30 ms. In three patients having an anterograde refractory period of the accessory pathway of more than 290 ms, isoproterenol abbreviated these values by 30, 60 and 80 ms, respectively. The greatest amount of shortening was observed in patients having the longest initial values for the anterograde refractory period of their accessory pathway. In the two patients receiving oral amiodarone therapy, isoproterenol shortened the anterograde refractory period of the accessory pathway by 180 and 60 ms, respectively, indicating that the effect of isoproterenol can not be prevented by long-term oral amiodarone administration. Our observations may be of importance in patients with the Wolff-Parkinson-White syndrome and atrial fibrillation. They suggest that beta adrenergic stimulation induced by hypotension or anxiety may result in shortening of the anterograde refractory period of the accessory pathway, leading to increased ventricular rates during atrial fibrillation.

The effects of early intracoronary streptokinase (SK) on enzymatic infarct size and rate of enzyme release were studied in a randomized multicenter trial. A total of 533 patients with acute myocardial infarction (AMI) were allocated to either the SK treatment group (n = 269) or the conventional (control) treatment group (n = 264). Enzymatic infarct size was represented by the cumulative quantity of alpha-hydroxybutyrate dehydrogenase (HBDH) released by the heart per liter of plasma in the first 72 hours. Rate of enzyme release was represented by the ratio of HBDH quantities released in 24 hours and 72 hours. On an "intention to treat" basis, the SK group had a smaller (by 30%; p = 0.0001) median enzymatic infarct size and a higher (by 35%; p = 0.0001) median rate of enzyme release than the control group. Limitation of infarct size was less apparent in patients treated with intracoronary SK only (25%) than in patients treated with intravenous plus intracoronary SK (34%). Compared to the control group, the enzyme release rate in patients treated with intracoronary SK only was slightly less (34%) than that in patients treated with intravenous plus intracoronary SK (38%). Patients with a patent infarct-related coronary artery at acute angiography had a median infarct size which was 55% (p = 0.0001) smaller than the median infarct size of the control group, and the median rate of enzyme release was 38% (p = 0.001) higher than the median release rate of the control group. Patients with successful recanalization during intracoronary SK infusion had a median infarct size which was 31% (p = 0.002) smaller than the median infarct size of the control group and a median rate of enzyme release which was 42% (p = 0.0001) higher than the median release rate of the control group. Patients with persistent coronary occlusion in spite of thrombolytic therapy had a median infarct size which was 11% (NS) higher than the median infarct size of the control group, although the median rate of enzyme release was still 23% (p = 0.02) higher than the median release rate of the control group. It is concluded that thrombolysis in the early phase of AMI limits infarct size and that intracoronary SK treatment itself accelerates the process of enzyme release from infarcted myocardium, independent of the angiographic result.

The effect of short-term intravenous administration of procainamide (12 patients), propranolol (4 patients) and verapamil (4 patients) was studied in 12 patients with chronic recurrent sustained ventricular tachycardia. In all patients tachycardia could reproducibly be initiated and terminated with programmed electrical stimulation of the heart. Procainamide (1) lengthened the effective refractory period of the right ventricle, (2) affected the tachycardia zone, (3) reduced ventricular rate during tachycardia, and (4) lengthened the interval between the tachycardia-initiating premature ventricular beat and the first QRS complex of tachycardia. No effect on the refractory period of the right ventricle or the mechanism of tachycardia was seen after administration of propranolol or verapamil. Apart from their therapeutic implications these data suggest that it may be possible to use drugs to study mechanisms of ventricular tachycardia in the human heart.

Programmed electrical stimulation of the heart was performed in a 47 year old man with prior myocardial infarction and recurrent sustained ventricular tachycardia that was refractory to standard medical therapy. The tachycardia could be provoked by regular atrial pacing at a rate of 100/min, regular ventricular pacing at the same rate and regular atrial pacing at a rate of 200/min in the presence of 2:1 atrioventricular block. All three techniques resulted in an interval of approximately 600 ms between successive ventricular depolarizations. Single interpolated ventricular premature depolarizations delivered during sinus rhythm were followed by a postextrasystolic conducted sinus beat that initiated ventricular tachycardia. However, when the same interpolated ventricular premature depolarization was followed by a ventricular fusion beat no tachycardia ensued. This study therefore emphasizes the importance of heart rate and the pattern of ventricular activation in determining whether ventricular tachycardia can be provoked by programmed electrical stimulation of the heart.

Several recent articles have called attention to the role of accessory atrioventricular pathways, only conducting in ventriculo-atrial direction, in patients suffering from paroxysmal reciprocal tachycardia [1–8]. In this chapter we will review our results of studies in patients with concealed accessory pathways. It will be shown that two types of concealed accessory pathways exist, resulting in two types of supraventricular tachycardia that differ in their clinical behaviour and electrocardiographic morphology. Participation of a concealed accessory pathway should be suspected in any patient presenting with a regular supraventricular tachycardia. Diagnosis, incidence and management of tachycardias using concealed accessory pathways will be discussed successively.

In a randomized study on early intracoronary thrombolytic therapy in patients with acute myocardial infarction (AMI), serial plasma enzyme activities were measured to analyze the rate of enzyme appearance in plasma with reference to treatment allocation, area at risk, and infarct size. Cumulative activities of alpha-hydroxybutyrate dehydrogenase (HBDH) appearing in plasma in the first 24 hours (Q24), 48 hours (Q48), and 72 hours (Q72) were calculated to obtain infarct size (= Q72) and rate of HBDH appearance in plasma (= Q24/Q72). Analyzed on the basis of "intention to treat" in 448 patients with AMI, the mean Q24/Q72 value (+/- SEM) was 0.653 +/- 0.011 in 230 patients receiving thrombolytic therapy; this value was significantly (p less than 0.001) higher than that observed in 218 patients receiving conventional therapy (0.504 +/- 0.012). In the thrombolysis group Q24/Q72 was independent of infarct size, whereas in the control group Q24/Q72 was negatively correlated with infarct size (r = -0.26; p less than 0.001). Plotted against the sum of ST segment elevations at admission (sigma ST) mean Q24 values were similar in both treatment groups, but mean Q48 and especially Q72 values were larger in the control group than in the thrombolysis group. We conclude that: (1) in reperfused infarctions the time course for development of infarct is accelerated in comparison to unreperfused infarcts; (2) this accelerated process of necrosis lasts about 40 to 50 hours, a duration that is hardly influenced by infarct size; and (3) the reperfusion-induced acceleration of enzyme release resembles the reoxygenation-induced enzyme release from anoxic hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

The treatment of acute myocardial infarction (AMI) has changed dramatically with the introduction of thrombolytic therapy, immediate angioplasty and emergency coronary artery bypass surgery. Several studies1e3 have shown that the success rate of these procedures depends on the time interval between the onset of complaints and the achievement of reperfusion. In patients admitted with an inferior wall AMI, the coronary artery causing the AM1 can be the right or the left circumflex artery. Our previous investigations, as well as those of others,4-6 have shown that the recording of lead V4R in the acute phase of an inferior wall AM1 can distinguish those patients with a proximal occlusion of the right coronary artery from those with an occlusion of the distal right or left circumflex artery, the first group of patients showing ST-T-segment elevation I1 mm in lead V4R. However, it is not possible to differentiate between occlusion of a distal right coronary artery and a circumflex artery using this criterion. In these patients (possible candidates for intracoronary thrombolytic therapy), coronary arteriography might start with the “wrong” coronary artery leading to a delay in reperfusion. Retrospectively, we have analyzed the configuration of the ST-T segment in lead V4R to determine if changes in the ST-T segment can help predict the site of coronary occlusion in inferior wall AMI.

The decision of when and how to treat ventricular tachycardia is primarily determined by the type and severity of concomitant heart disease. After the ventricular origin of the tachycardia is established, extensive investigation into this problem is mandatory. Long-term medical treatment in patients with ventricular tachycardia in the setting of coronary artery disease is unsatisfactory. Although drug selection with the use of programmed cardiac stimulation seems logical and promising, the long-term value of this method remains to be demonstrated. The extensive myocardial damage present in most patients with coronary artery disease and ventricular tachycardia makes it unlikely that drug therapy will be the ultimate answer. These considerations justify careful evaluation of the long-term efficacy of surgical therapy of symptomatic ventricular tachycardia, especially in patients with arrhythmia in the subacute or chronic phase of myocardial infarction.

Of 110 patients without organic heart disease undergoing electrophysiological evaluation, 72 patients (65%) manifested some form of repetitive ventricular response to ventricular stimulation. In 58 (53%) bundle branch re-entry was induced and in 19 patients (17%) intraventricular re-entry. In five patients (4%) both types of repetitive responses were initiated. The indication for study was documented as ventricular tachycardia or fibrillation in 13% of the patients, supraventricular tachycardia in 51% and Wolff-Parkinson-White syndrome, syncope or conduction disturbances in the remaining patients. The incidence of clinical and inducible ventricular tachycardia or fibrillation was 8 and 2% respectively, in the group of patients manifesting only bundle branch re-entry, 37 and 32% in patients with intraventricular re-entry and 8 and 11% in patients without repetitive ventricular responses during ventricular stimulation. The predictive value of intraventricular re-entry as an indicator of severe ventricular arrhythmias was 36%. We conclude that in our population of patients without organic heart disease, bundle branch re-entry is a frequent finding and is not related to ventricular arrhythmias, that intraventricular re-entry is less frequent and although it is associated with a higher incidence of ventricular tachycardia or fibrillation, it is a poor predictor of these arrhythmias in this study population.

One hundred eighty of 1260 patients consecutively admitted to the hospital because of unstable angina pectoris had the typical ST-T segment changes suggestive of a critical stenosis in the proximal LAD. In 108 patients the ECG abnormalities were present at the time of admission. In the remaining 72 patients they developed shortly thereafter. The difference between these two groups was a longer duration of anginal complaints in the former (mean 2.3 days). Results of coronary angiography, performed a mean of 4.6 days after the last attack of chest pain, showed 50% or more narrowing in the proximal LAD in all patients. Thirty-three patients had complete occlusion of the LAD and 75 had collateral circulation to the LAD. Results of left ventricular angiography showed abnormal systolic left ventricular wall motion in 137 patients and normal systolic motion in the remaining 43 patients. The difference between these two groups was a shorter mean time interval between the last attack of chest pain and angiography in the former group (p less than 0.001). Twenty-four patients had only abnormal diastolic wall motion. Twenty-one patients had a small increase in the creatine kinase level at the time of admission. Fifteen patients (nine before and six during early revascularization) had an anterior wall myocardial infarction in the hospital; these patients had a patent but severely narrowed LAD and a low incidence of collateral circulation to the LAD.(ABSTRACT TRUNCATED AT 250 WORDS)

The mechanisms of cardiac arrhythmias are extremely difficult to evaluate in the intact human heart. This can only be accomplished under exceptional circumstances such as in the Wolff-Parkinson-White syndrome. Here an anatomically determined pathway can be identified in which propagation of an impulse leads to the typical circus movement tachycardia of the syndrome. Intracellular potentials cannot be obtained in the intact human heart at the present time, making discussions on the possible role of the slow response in the genesis of clinically occurring ventricular arrhythmias purely speculative. We want to stress therefore that we cannot draw any practical conclusions about consequences of the slow response concept in relation to the treatment of ventricular arrhythmias in man. In discussing the possible role of the slow response as mechanism of clinically occurring ventricular arrhythmias we have to rely heavily upon the notion that this mechanism can be blocked by verapamil [1].

The incidence of intracoronary thrombus and the effects of thrombolytic therapy were studied in 41 patients with unstable angina. All patients underwent coronary angiography 2 to 69 h (mean 19) after their last attack of chest pain. Immediately after angiography, 21 patients received intracoronary streptokinase (250,000 IU in 45 min) and were retrospectively analyzed. Twenty patients received intravenous recombinant tissue-type plasminogen activator (rt-PA) (100 mg in 3 h) and were involved in a prospective study. Eleven of the 21 patients from the streptokinase group and 11 of the 20 patients from the rt-PA group showed a decrease in the severity of the coronary stenosis on repeat angiography 1 day later. A decrease in coronary obstruction was primarily observed in 10 of 13 patient; with a complete stenosis and in 6 of 9 patients with a subtotal stenosis and markedly diminished coronary flow. Improvement in coronary anatomy was not determined by the clinical characteristics of the patients. Twenty-eight of the 41 patients had angiographic evidence of intracoronary thrombus formation before and 16 had such evidence after thrombolytic treatment. Nine patients developed a small increase in serum cardiac enzymes before or during treatment. Ischemic symptoms and the incidence of surgical or angioplastic intervention were not different in patients with or without a reduction in coronary artery stenosis after fibrinolytic therapy. These observations suggest a high incidence of coronary thrombosis in patients with unstable angina. The data do not permit assessment of the clinical therapeutic efficacy of thrombolylic therapy. Better risk stratification and placebo-controlled prospective studies are required to obtain information on the risk/benefit ratio of such therapy in unstable angina.