In a patient with atrial septal defect and incomplete right bundle-branch block atrial echo beats were observed after atrial premature beats, induced with a gradually decreasing delay during regular driving of the atrium. The time relations of these atrial echo beats could be accurately defined. Considerable prolongation of the atrioventricular (A-V) conduction of the premature atrial response was found to be a necessary condition for the occurrence of atrial reciprocation, which was restricted to small and very circumscript delay ranges. Three types of atrial echo responses could be discerned. The concept of a dual A-V conduction system was not sufflicient to explain the genesis of these three types. The assumption of a third pathway in the upper part of the A-V node was needed. Arguments in favor of a longitudinal dissociation of one of the two pathways postulated in the concept of dual A-V transmission were given.

The initiation and termination of tachycardias were studied in five patients with Wolff-Parkinson-White syndrome, type A. In all patients, electrical stimulation was performed from the right side of the heart. In three patients the effect of induced left-sided premature beats was studied as well. In contrast to patients with Wolff-Parkinson-White syndrome, type B, there was difficulty in initiation and termination of tachycardias with premature beats applied to the right atrium or ventricle. This could easily be accomplished with left-sided premature stimuli. In two patients the simultaneous recording of right and left atrial activation during a tachycardia, showing atrioventricular conduction by way of the A-V nodal-His pathway and ventriculoatrial conduction via the anomalous connection, revealed that left atrial activation occurred far in advance of right atrial activation. During regular driving of the right and the left atrium at identical rates the most pronounced pre-excitation pattern was seen after left atrial stimulation. Our results are in agreement with a circus movement or reciprocal mechanism by way of the A-V nodal-His pathway and the anomalous A-V connection as a causal mechanism for tachycardias in Wolff-Parkinson-White syndrome, type A. In contrast to the usual finding of atrioventricular conduction during the tachycardia via the A-V nodal—His pathway and ventriculoatrial conduction by way of the anomalous connection, one patient showed tachyeardias running in the opposite direction. A location of the anomalous pathway on the left side of the heart is supported by our findings.

We recorded direct-current extracellular electrograms simultaneously from 60 left ventricular epicardial sites in 38 alpha-chloralose-anesthetized dogs during repeated, 5 min coronary arterial occlusions. In each dog recordings made during control occlusions were compared with those made in occlusions after, or during, the following interventions on the sympathetic nervous system: left stellate ganglion stimulation, left stellectomy, right stellectomy, and clamping the abdominal aorta with intact sympathetic nerves to induce a rise of blood pressure equal to that present during left stellate stimulation. Heart rate was kept constant. Measurements included determination of TQ segment potentials and times of local activation. After 2 min of ischemia, the degree of TQ segment depression was increased by left stellate ganglion stimulation and was decreased by both left stellectomy and clamping the aorta. Also, the area showing negative TQ potentials, indicating decreased resting membrane potentials, was enlarged by both left stellate stimulation and right stellectomy and reduced by left stellectomy. No differences were found in the results of experiments in which the left anterior descending coronary artery was occluded and those in which the circumflex branch was occluded. Left stellate stimulation significantly improved conduction within the ischemic zone. No evidence was found to suggest that the arrhythmogenic effects of left stellate stimulation and of right stellectomy, confirmed in the present study, resulted from an increased likelihood for reentry in the subepicardium of the ischemic zone.

Left ventricular ejection fraction was assessed by biplane cross sectional echocardiography in 65 patients with a first acute myocardial infarction on the first day. In 30 patients (group 1) measurements were repeated on the third day and in another 35 patients (group 2) at three months. Changes in ejection fraction of 0.05 or less were arbitrarily called insignificant. In group 1 only two patients showed a decrease of more than 0.1 between days 1 and 3, and both had an enzymatically confirmed infarct extension. The remaining patients had no complications. In group two 11 patients had decreases of more than 0.1 between day 1 and three months: three of them had an enzymatically confirmed reinfarction (perioperative in one) and four a possible reinfarction, and in two an angiographically confirmed left ventricular aneurysm developed. In two no complications occurred. The other complications that occurred were an enzymatically confirmed but small reinfarction, an angiographically confirmed but circumscript aneurysm, and an uncomplicated bypass operation in one patient each. These three patients had a small increase (between 0.05 and 0.1) in ejection fraction. Reproducibility of the method of measuring the ejection fraction was assessed concurrently in 20 outpatients with a previous myocardial infarction who were studied twice on the same day (with a 30 minute interval) by two different observers. The mean absolute difference in ejection fraction between the paired observations was 0.036 +/- 0.023 with a range of 0 to 0.07. Thus only changes in ejection fraction of more than 0.1 correlate with clinically recognised complications. Changes between 0.05 and 0.1 may be due to spontaneous variability or to the limited reproducibility of the method.

Ventricular tachycardias that are medically refractory can be treated surgically by resection of the area that generates the arrhythmia. The origin of a tachycardia can be determined during operation by recording endocardial electrograms. Tachycardias occurring spontaneously, or induced during the operative procedure, often last for only a few cycles and require the simultaneous recording of endocardial signals from numerous sites (mapping). The conventional technique of sequential mapping by using a roving probe cannot be applied in such cases. We, therefore, developed a flexible computerized system which enables us to record simultaneously from a multiple of 16 electrode terminals. The basic concept can accommodate 64 channels. A multielectrode array consisting of an inflatable balloon, uniformly covered with electrode terminals, is used to map the whole endocardial surface simultaneously. A rectangular grid covered with electrode terminals is used for refined resolution. Optically isolated amplifiers are used, providing ohmic isolation between the patient and the support electronics. After amplification and filtering, the endocardial signals are collected in groups of 16 and transferred to data acquisition units. Each unit contains a 16-channel multiplexing A/D converter and a 16K circular buffer. An LSI-11 based minicomputer controls the acquisition units and accounts for the transition of data to disk. Preselection of data is carried out during acquisition in order to reduce operation time. After acquisition, hard copies of the signals are made on a 16-channel chart recorder.

Left ventricular volume and ejection fraction were measured in 22 survivors of acute myocardial infarction by means of two-dimensional echocardiography and using a Simpson's rule algorithm. Ten of the 22 patients experienced complications. For the group as a whole, there were no significant trends in left ventricular volume and ejection fraction between the first and third days and the third month after infarction. In the subgroups with uncomplicated and complicated infarction, there were trends towards increasing and decreasing ejection fractions, respectively, which failed to attain statistical significance, however. The difference in ejection fraction between both subgroups had become significant at 3 months; 55.2 +/- 11.1% in uncomplicated v. 41.3 +/- 6.9% in complicated cases (P less than 0.01). Individual changes in ejection fraction falling outside the limits of reproducibility of the method as assessed previously were observed between day 1 and day 3 in only 2 patients with uncomplicated and in 2 patients with complicated infarction. Between day 1 and 3 months such changes occurred in 8 patients with uncomplicated infarction (upward in 5 and downward in 3), and in 8 patients with complicated infarcts (upward in 3 and downward in 5). We conclude that changes in ejection fraction as measured by two-dimensional echocardiography tend to correlate with complications.

To determine the incidence, natural history, and relation to anticoagulant therapy of left ventricular thrombus (LVT) following acute myocardial infarction (MI), we performed two-dimensional echocardiography in 96 consecutive patients with isolated MI during the acute episode and after four and 12 months. Only patients with anterior MI received oral anticoagulant therapy on admission and throughout the study period. The LVT was identified in 21/65 patients with anterior and in 1/31 patients with inferior MI. The large majority of LVT cases were seen for the first time during the acute phase of MI. LVT was associated with a significantly higher peak value of CK-MB (118 +/- 24 vs 76 +/- 35, p less than 0.001) and Killip class (2.5 +/- 0.8 vs. 1.5 +/- 0.7, p less than 0.002). Patients with anterior MI and LVT more frequently had segmental dyskinesia during acute MI than patients without LVT (86 percent vs 18 percent, p less than 0.001). In four patients LVT resolved during the study period. Discontinuation of anticoagulant therapy in four patients with an aneurysm led to LVT formation in three. Two patients suffered a clinically recognized embolic event; one never had LVT demonstrated by echocardiography. Thus, LVT usually develops in the early days following large anterior MI, complicated by pump failure and segmental dyskinesia, even when patients receive oral anticoagulant therapy. Surprisingly, the incidence of embolic events was low (1/22) in our LVT patients.

Left ventricular volume and ejection fraction were measured by 2-dimensional echocardiography from 2 orthogonal apical long axis views in 90 patients admitted with acute transmural myocardial infarction. Results were correlated with worst Killip class during hospital stay, enzymatic infarct size (peak CK-MB) and mortality. We used two algorithms, a biplane area-length algorithm and a modification of Simpson's rule. Both algorithms yielded essentially the same results: there were statistically significant trends towards higher end-diastolic and end-systolic volumes and lower ejection fraction with higher Killip -class. Ejection fraction was lower (P less than 0.01) in the 6 patients dying from cardiogenic shock (28.0 +/- 7.8% v. 46.6 +/- 10.1% in survivors with the area--length algorithm; 28.1 +/- 6.2% v. 48.1 +/- 10.2% with modified Simpson's rule). In 5 patients dying from other causes ejection fraction was 46.0 +/- 14.9% with the area-length method or 46.2 +/- 14.5% with Simpson's rule (not different from survivors). Correlation with peak CK-MB was only modest, though statistically significant: the regression equation was: y = -0. 39x + 54 (r = -0.35; P less than 0.01) with the area-length method; and y = -0. 41x + 55 (r = -0.37; P less than 0.01) with Simpson's rule. Left ventricular ejection fraction measured at the bedside in patients with acute myocardial infarction, can provide useful clinical information. Patients likely to develop shock can be identified shortly after admission.

In a prospective serial study of 96 patients with acute myocardial infarction, two dimensional echocardiography identified left ventricular thrombus in 18 patients. The majority of thrombi (15) developed within the first 4 days after admission. In three patients thrombi were identified for the first time 4 months after the acute episode. All 18 patients had received therapeutic anticoagulants on admission and had large anterior wall infarctions complicated by severe pump failure and motion abnormalities echocardiographically. None of the patients had systemic embolisation during the study period. Thus, left ventricular thrombus is a not uncommon though silent complication of acute anterior wall infarction even when patients receive therapeutic anticoagulants.

Two-dimensional echocardiography (2DE) was performed during 30-degree left lateral decubitus bicycle exercise in 52 patients who undewent cardiac catheterization for suspected coronary artery disease (CAD). Adequate echocardiograms were obtained in 39 patients (75%). Thirty-five of these patients underwent radionuclide angiography (RNA) with the same exercise protocol as for echocardiography. Exercise-induced or increased initial asynergy was considered to be a positive test by both 2DE and RNA. Echocardiographic, scintigraphic, and coronary anglographic date were compared to each other. Significant CAD (greater than 50% luminal obstruction) was present in 26 patients (66%). One of 15 patients with exercise-induced asynergy by 2DE had no CAD. Six 2DE and two RNA studies during exercise were falsely negative, sensitivity 76% versus 91%. Inclusion of RNA ejection fraction data would increase the sensitivity but decrease the specificity of RNA. Exercise-induced septal asynergy was far more frequently present by 2DE than by RNA (11 versus 6) in the 17 patients who had exercise-induced anterior asynergy by both methods. We conclude that it was possible to perform exercise 2DE in 75% ofour patients. Exercise-induced asynergy on 2DE was specific (92%) for CAD. The sensitivity of 2DE in detecting CAD was less than that of RNA.