The comparative predictive accuracy of spectral turbulence analysis and time-domain analysis for sustained monomorphic ventricular tachycardia in postinfarction patients with conduction defects.

Signal-averaged electrocardiograms obtained in 86 postinfarction patients with right bundle branch block (RBBB), left bundle branch block (LBBB), or intraventricular conduction defect (IVCD), underwent time-domain analysis (TDA) and spectral turbulence analysis (STA) to determine which approach provided the more effective marker for patients with sustained monomorphic ventricular tachycardia. TDA parameter included the root mean square value of the last 40 ms of the vectormagnitude complex and the duration of the low amplitude signal below 40 microV. STA utilized a summation lead (X + Y + Z) and quantitated four parameters: interslice correlation mean, interslice correlation standard deviation, low slice correlation ratio, and spectral entropy. High-pass filters of 40 Hz and 25 Hz were used to study the total patient population with noise levels > or = microV and a subset of 67 patients with noise levels < or = 0.5 microV. The techniques compared their effectiveness as measured by their positive predictive values (PPV), negative predictive values (NPV), sensitivity (Sn), and specificity (Sp). In RBBB, STA was uniformly a more powerful tool utilizing either filter at both noise levels. In LBBB, STA was consistently more powerful at both noise levels at 40 Hz and, generally, more powerful at 25 Hz with isolated exceptions. In conduction defects in which QRS was > 100 ms but < 120 ms, TDA was equal to or more effective than STA, with the exception of PPV and Sp at 40 Hz at 1-microV noise level and the Sp at 0.5 microV. The addition of ejection fraction data to STA score resulted in further overall improvement in performance, but above conclusions were unchanged.

Assessment of late potentials in patients with essential hypertension by the signal-averaged electrocardiogram with five year follow-up.

Both the Framingham and Manitoba Heart Studies have identified electrocardiographic left ventricular (LV) hypertrophy (LVH) as a risk factor for sudden cardiac death. Low amplitude ventricular late potentials in the terminal part of ventricular activation have been associated with sustained ventricular tachycardia and have identified those at risk for sudden cardiac death. Therefore, we prospectively examined 23 essential hypertensives without known symptomatic coronary heart disease by two-dimensional echocardiography and signal averaged electrocardiograms (SAECGs) for the detection of ventricular late potentials. The SAECG vector-magnitude complex measurements included the total duration of the complex (QRSd), the voltage in the last 40 ms (V40), and the duration of low amplitude signals < 40 microV in the terminal portion of the complex (LASd). Echocardiographic parameter means were: LV diastolic diameter = 46.0 +/- 4.5 mm, combined septal and posterior wall thickness = 23.3 +/- 4.2 mm, LV mass (Woythaler method) = 235.1 +/- 69.1 g, LV mass (Penn method) = 199.5 +/- 55.3 g and ejection fraction = 63.9 +/- 6.2%. SAECG measurement means were QRSd = 88.2 +/- 9.9 ms, V40 = 63.1 +/- 34.7 microV RMS, and LASd = 23.5 +/- 10.0 ms. No echocardiographic parameter correlated with SAECG duration; however, age correlated with QRSd (r = 0.48, P = 0.02). Posterior wall thickness (r = -0.43, P = 0.04), LV mass index (r = -0.44, P = 0.03) and LV mass/height (r = -0.49, P = 0.02) inversely correlated with LASd.(ABSTRACT TRUNCATED AT 250 WORDS)

Relation of peri-infarction block to ventricular late potentials in patients with inferior wall myocardial infarction.

This study explores the relation of the presence of peri-infarction block to ventricular late potentials in patients with inferior wall myocardial infarction (MI). The hypothesis was that both the gross peri-infarction block pattern and subtle low-level ventricular late potentials are expressions of conduction abnormality associated with infarction. The consequent question arose whether peri-infarction block may have the same association with sustained ventricular arrhythmias that has been demonstrated in postinfarction patients with ventricular late potentials. Seventy patients with documented Q-wave MI were divided into those with (23) and those without (47) peri-infarction block. Signal-averaged electrocardiograms were obtained. Analysis of the vectormagnitude complex revealed that the total duration of that complex and the duration of terminal potential under 40 microV in the peri-infarction group exceeded that in the group without peri-infarction block (p less than 0.0001). The voltage in the last 40 ms of the vectormagnitude complex was also significantly less in the peri-infarction group (p less than 0.0005). There were 13 instances of sustained ventricular tachycardia, ventricular fibrillation or sudden death occurring subsequent to infarction not associated with the acute ischemic event, 11 of which occurred in the peri-infarction group. The significantly higher incidence of late potentials along with the significantly higher incidence of sustained ventricular arrhythmias in the peri-infarction block on the surface electrocardiogram may provide another marker for identifying persons at increased risk for these arrhythmias subsequent to MI.

Ventricular late potentials in normal subjects.

Low-amplitude late potentials detected in the terminal part of ventricular activation have been evaluated as a possible means of identifying patients prone to sustained ventricular tachyarrhythmias. These signals are usually absent in those without such arrhythmias and in normal subjects. 67 healthy subjects, with no suggestion of cardiac disease from examination or electrocardiograms, were studied in an effort to report the incidence of late potentials in normal subjects. Three subjects met the criteria for abnormal late potentials (4%); the vectormagnitude complexes of these subjects were indistinguishable from those seen in patients with spontaneous sustained ventricular tachycardia after myocardial infarction. Measured indices from our subjects were compared with those of normal subjects studied by other investigators utilizing similar analytic techniques and similar software and equipment. Explanations are considered for the occurrence of false-positives. It is concluded that the incidence of late potentials in normal subjects is very low and thought to represent some type of false-positive expression related either to the recording or analytic technique. However, in certain instances, the occurrence of late potentials in a seemingly normal person may be a predictor of underlying structural pathology.

A model for thermal gradients during renal vascular anastomoses.

Quantitative knowledge of warm ischemic intervals is of special importance in organ transplantation. Warm ischemia as a function of time is deleterious to tissue survival. In a laboratory model of a preserved transplantable organ, we determined thermal gradients in pig kidneys similar in size to human kidneys. Sixteen nonviable porcine kidneys cooled to 0 degrees C were placed in an artificial "iliac fossa." The posterior renal wall was in contact with the normothermic fossa. The anterior renal wall was exposed to the ambient temperature of the "operating room." The temperature of both walls was monitored for a minimum of 2 hr. Temperature changes relative to time and kidney weight were studied. The temperature of the posterior wall rises above 20 degrees C within 5 to 10 min; the anterior wall attains this temperature within 30 to 40 min. The thermal gradient between the two walls is significantly greater for larger kidneys (200 g) than for smaller kidneys (100 g). Implications for biochemical pathology are discussed.

Effect of canine cardiac nerves on heart rate, rhythm, and pacemaker location.

In open-chest dogs, right- and left-sided cardiac nerves were stimulated to determine their effect on heart rate, rhythm, and pacemaker location. The majority of the nerves produced chronotropic changes; 72% of the induced rhythms originated from within the atrial pacemaker complex. Ten percent of the stimulations produced an atrio-ventricular (AV) nodal rhythm; most of the time this was induced by the left posterior and anterior ansae and ventrolateral nerves. The dominance of a lateral right atrial pacemaker was observed in 8% of the stimulations; the dorsal cardiac and innominate nerves induced this rhythm the majority of the time. The general trend was for a cranial shift in the location of the pacemaker within the pacemaker complex with sympathetic stimulation and a caudal shift with parasympathetic stimulation. Exceptions to the pattern may be explained by the preferential effect of the nerves on the pacemakers in the right atrium. The study demonstrates, in the canine model, that in addition to the sinus and AV nodes, there is a system of pacemakers controlled by the cardiac nerves.

Activation sequence and potential distribution maps demonstrating multicentric atrial impulse origin in dogs.

We examined the onset of atrial epicardial excitation by recording unipolar potentials from 360 electrodes arranged in templates affixed to the superior vena cava and right atrium in dogs. Both activation sequence and potential distribution maps were obtained for the period of impulse origin beginning before the surface P wave and continuing through the first 15-20 msec of atrial depolarization. The activation maps demonstrated impulse origin from multiple widely separated sites, resulting in two to three individual wavefronts that merged to form a single widely disseminated wavefront spread over a 50 X 20 mm area by 10-15 msec. Atrial potential maps obtained for the same time periods revealed multiple sites of primary negativity corresponding to the points of impulse origin in the activation maps. The potential distributions and evolution of these maps also indicated the presence of multiple wavefronts originating from widely separated locations, and suggested an extensively dispersed source of impulse origin. One of these sites at the superior cavo-appendicular junction corresponded to the rostral portion of the sinus node and the site of classical unifocal origin. Additional sites of impulse origin and primary negativity distant to the sinus node were noted either concurrently in the same map or in other maps associated with different patterns of impulse initiation. Classical physiological and pharmacological interventions were used to alter adrenergic and cholinergic input to the atrium, and resulted in coincident changes of both the patterns of impulse origin and heart rate. In addition, we examined spontaneous changes in the patterns of impulse initiation which accompanied beat-to-beat changes in cycle length (sinus arrhythmia). There was close agreement between activation and potential maps over the entire steady state and dynamic range of impulse origin. The data can be explained by the concept of a widely distributed system of functionally differentiated but coordinated atrial pacemakers.

Quantitative relation between sites of atrial impulse origin and cycle length.

Having previously described the multicentric origin of the atrial impulse from sites widely distributed over the right atrium as well as an intrinsic link between these sites of origin and cycle length (CL), we undertook a quantitative study of this relationship. In 132 dogs anesthetized with pentobarbital sodium or fentanyl citrate, we recorded atrial activation sequence maps from 360 closely positioned electrodes and determined locations of impulse origin at heart rates between 80 and 240 (CL between 750 and 250). We used cardiac nerve stimulation and agonist-antagonist infusion to produce changes in CL and impulse origin. Results demonstrate a significant correlation between site of impulse origin and CL. These sites, associated with both the sinus node (SN) and extranodal sites, function predictably and consistently controlling impulse initiation at heart rates above and below rates at which the SN predominates. This relationship can be used to specify an anatomic-functional model of atrial pacemaker hierarchy and to quantitate the response of different atrial regions to specific pharmacological and physiological interventions.

Widespread distribution and rate differentiation of the atrial pacemaker complex.

In a study to examine the basis of rate-related changes in the electrocardiographic P wave we found a multicentric rather than unifocal origin of the atrial depolarization wave in dogs. Three to five pacemakers, or origin points, were distributed over a 30- to 40-mm area compared to the 11-mm size of the sinus node. Two or three of the sites could excite simultaneously, or one specific site would dominate excitation. Each separate origin point dominated excitation within a specific range of heart rates, and on reaching either the upper or lower limits of this range, a new focus abruptly dominated and initiated the atrial wave front. We have obtained evidence to suggest that these findings may be explained by a widely distributed atrial pacemaker complex. The spatial distribution of this system exceeded the dimensions of the canine sinus node by a factor of three to four times. The pacemaker centers, although distributed, were consistently located at specific positions along the superior vena caval-right atrial junction. Also, each separate pacemaker site appeared functionally differentiated to generate a specific range of heart rates. We propose that in addition to the sinus node there are other specialized atrial pacemaker centers, and that this specialization, including the differentiated response and coordination, is conferred by focal receptor characteristics and their inputs.

Multicentric origin of the atrial depolarization wave: the pacemaker complex. Relation to dynamics of atrial conduction, P-wave changes and heart rate control.

In studies to ascertain the basis of dynamic changes in the P wave, bipolar epicardial potentials were recorded from multiple atrial electrodes in dogs. One hundred to 120 activation times were displayed by a digital computer and used to construct atrial isotemporal activation sequence maps. Changes in heart rate or beat-to-beat cycle length were induced by vagal stimulation or infusion of autonomic mediating drugs. Changes in cycle length were associated with dynamic changes in the atrial activation sequence and surface P-wave. A conspicuous finding was that epicardial atrial depolarization began at three widely separated locations. These three points were consistently present in all animals and were generally located at the 12, 3, and 6 o'clock positions of the superior vena cava-right atrial junction. The dynamic changes in P waves and atrial activation sequence which accompanied the changes in cycle length were due to sudden shifts in the point of earliest activity between the three early sites. Asymmetric atrial depolarization with more rapid conduction along the crista terminalis, superior interatrial band, and pectinate muscles was present in all dogs. Although the anisotropic atrial geometry played an important role in the asymmetric conduction, the widely distributed onset of activity contributed significantly to the uneven spread. The multiple points of origin of the atrial wavefront might be explained by either a trifocal, distributed pacemaker or the epicardial exits of three specialized pathways conducting an impulse emanating from a single focus. These data explain the dynamic variation in P-wave morphology in normal hearts and also imply a relationship between the altered origin of atrial depolarization, atypical P waves, brady- or tachyarrhythmias, and heart rate control.