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The electrocardiogram has been shown in epidemiologic studies to be an independent predictor of survival. These studies have adjusted for selected covariates simultaneously. This article assesses the value of the electrocardiogram as a predictor of survival when introduced at progressive stages of the common clinical encounter. Data collected from 4,518 patients ages of 60 to 96 years with isolated systolic hypertension who were followed-up for up to 6 years as part of the Systolic Hypertension in the Elderly Project were analyzed. Survival curves and 3- and 5-year survival rates (Cox regression methods) of groups with normal and abnormal resting electrocardiograms were compared. Blocks of covariates representing demographic information, risk factors for cardiovascular disease, clinical history, and physical examination findings were added to the survival models sequentially to mimic the sequence of the common clinical encounter, and the independent significance of the electrocardiogram as a predictor of survival was assessed at each step. An abnormal electrocardiogram was associated with reduced survival when no adjustment for covariates is made. Survival was also significantly (P

This study was designed to determine the impact of noncritical (less than 70% narrowing of the luminal diameter) coronary stenoses on the long-term survival rate of patients with coronary artery disease. The survival rate of 3,342 patients with normal coronary arteries (Group 1A) was compared with that of 2,184 patients with only noncritical stenoses (Group IB). Similarly, the survival rate of 1,128 patients with one or more critical lesions (Group 2A) was compared with that of 5,944 cases with noncritical plus critical lesions (Group 2B). Patients with noncritical lesions had significantly lower 10-year survival rates (85.8%) than did those with normal coronary arteries (90.1%). However, the difference in survival rate was attributable to older age, male sex, and higher prevalence of cigarette smoking, diabetes mellitus, and hypertension in Group IB than in Group 1A; presence of noncritical stenoses was not a statistically significant independent determinant of survival. Long-term survival rates of the patients with one or more critical lesions (Group 2A) were equivalent to that of patients with critical stenoses plus one or more noncritical lesions (Group 2B). Therefore, 1) patients with only noncritical stenoses have more risk factors for coronary artery disease than do those with normal coronary arteries; 2) these patients have a reduced long-term survival rate that reflects these risk factors rather than the presence of noncritical lesions; and 3) in patients with critical lesions, the presence of additional non-critical stenoses does not affect the long-term survival rate.

The detection and assessment of cardiac chamber hypertrophy has long been an important objective of clinical electrocardiography. Its importance has increased in recent years with the recognition that hypertrophy can be reversed with therapy, and that by doing so, adverse clinical outcomes can be

The safety and efficacy of a 10- to 15-mg/h continuous infusion of intravenous diltiazem were evaluated in 47 patients with atrial fibrillation or flutter who first responded to 20 mg or 20 mg followed by one or more 25-mg bolus doses of open label intravenous diltiazem. Of the 47 patients, 44 responded to the bolus injection and were randomized under double-blind conditions to receive either a continuous infusion of intravenous diltiazem (10 to 15 mg/h) (23 patients) or placebo (21 patients) for up to 24 h.Seventeen (74%) of the 23 patients receiving diltiazem infusion and none of the 21 with placebo infusion maintained a therapeutic response for 24 h (p < 0.001). Over 24 h, patients receiving diltiazem infusion lost response significantly more slowly than did those receiving placebo infusion (p < 0.001). Nonresponders to the double-blind infusion were given an additional bolus injection of open label intravenous diltiazem and administered an open label 24-h intravenous diltiazem infusion. The overall proportion of patients maintaining a response to a 24-h infusion of intravenous diltiazem under double-blind or open label conditions combined was 83% (34 of 41).Efficacy of the 24-h infusion of intravenous diltiazem was similar in elderly versus young patients, those who did versus those who did not receive digoxin and those weighing

This study was undertaken to quantify basic cardiac electrical field properties using the Karhounen-Loeve (K-L) numerical expansion technique after experimental myocardial infarction. Transmural anterior myocardial infarction was produced in seven dogs by injection of liquid latex into the anterior descending artery; posterior myocardial infarction was produced in five dogs by injection of the circumflex artery. Body surface potentials from 84 electrodes were recorded during sinus rhythm prior to and 1 week after infarction. Electrical field properties during the QRS, ST, and QRST intervals were computed by the K-L method based upon areas calculated for each lead. The ratio of the sum of magnitude of the first three eigenvectors to the sum of all computed eigenvectors expressed as a percentage was used as a measure analogous to field dipolarity. Values before infarction were high during the QRS (97.1% +/- 2.0%, mean +/- 1SD), ST (96.0% +/- 5.1%), and QRST (97.7% +/- 2.7%) intervals, with no significant difference between the three periods. After infarction, the ratio during QRS decreased significantly, with lower values after posterior (61.9% +/- 11.7%) than after anterior (91.1% +/- 6.0%) infarction (p less than 0.001). Values during ST and QRST intervals were not significantly changed by infarction. Spatial patterns of the first eigenvector indicated that the derived QRS area electric field is directed away from the myocardial lesion for both anterior and posterior infarcts. Thus, experimental myocardial infarction produces significant changes in cardiac electrical field properties as measured by the K-L technique.

Previous studies have documented a reduced survival time in patients with an electrocardiographic (ECG) ST-T wave abnormality. This study was designed to determine the clinical, hemodynamic and angiographic correlates of this observation. Data from 9,731 patients undergoing cardiac catheterization from 1976 through 1986 were analyzed; 5,531 had severe (greater than 70%) obstruction of at least one major coronary artery, 1,706 had mild (10 to 69%) obstruction and 2,494 had no obstruction. Of the patients with severe obstruction, 2,536 were treated medically and 2,995 were treated by surgical revascularization. Patients with an ST-T abnormality had more clinical risk factors (including older age and greater prevalence of diabetes mellitus, hypertension and prior myocardial infarction) and greater left ventricular dysfunction (including higher end-diastolic pressure and ventricular volume, reduced ejection fraction and greater prevalence of contraction abnormality) than did those without this ECG pattern. Survival time was significantly (p less than 0.01) reduced in subsets of patients with an ST-T abnormality and with severe or mild coronary artery disease; in those without coronary disease, ST-T changes did not correlate with reduced survival. Stepwise regression analysis was applied to each group to determine the independent predictors of 5-year survival. In patients with severe disease or no disease, an ST-T abnormality was not chosen as an independent predictor of 5-year survival; in the group with mild disease, ST-T changes were an independent predictor of reduced survival. Thus, the independent impact of an ST-T abnormality on survival is dependent on the severity of underlying coronary artery disease.

The ability of the Karhunen-Loeve (K-L) numerical expansion technique to detect the presence of myocardial infarction is assessed by combining pools of QRS area data collected from 12 canines. First, potentials during normal sinus rhythm are recorded from 84 body surface electrodes. This set of potentials serves as control (CTL) data. Next, the dogs are divided into two groups for gathering data from both anterior and posterior infarcts in the left ventricle. One group consists of seven dogs all with anterior infarcts and a second group of five dogs all with posterior infarcts. One week after the infarcts are induced, potentials are again recorded during sinus rhythm. These potentials serve as anterior infraction (AI) and posterior infarction (PI) data sets. From the potential data, the QRS area for each lead is calculated for all three experimental populations. The CTL, AI, and PI QRS area data are grouped together in different combinations to study the effects of data pooling in identifying myocardial infarction with the K-L numerical expansion technique. The results indicate that the calculation of percent dipolarity of the QRS waveforms depends on the combination of data present in a given data pool. >

The relationship among postmenopausal estrogen use, coronary stenosis, and survival was examined retrospectively in 2268 women undergoing coronary angiography. The patients were selected for study if their age was 55 years or older at the time of angiography or if they had previously undergone bilateral oophorectomy. Postmenopausal estrogen use in 1178 patients with coronary artery disease (greater than 70% stenosis) and 644 patients with mild to moderate coronary artery disease (5% to 69% stenosis) was compared with 446 control subjects (0% stenosis) using life-table analysis. Over 10 years of follow-up, there was no significant difference in survival among patients initially free of coronary lesions on arteriography who had either never used (377) or ever used (69) estrogens. Among patients with mild to moderate coronary stenosis, 10-year survival of those who had never used estrogens was 85.0% and it was 95.6% among 99 "ever users." Survival was 60.0% among those with more than 70% coronary stenosis who had never used estrogen and it was 97.0% among 70 ever users. The "never users" group were older (65 vs 59 years), had a lower proportion of cigarette smokers (40% vs 57.1%), a higher proportion of subjects with diabetes (21.7% vs 12.9%) and hyperlipidemia (58% vs 44%), and approximately equal numbers of hypertensives (56.0% vs 54.3%). Cox's proportional hazards model was used to estimate survival as a function of multiple covariables. Estrogen use was found to have a significant, independent effect on survival in women. We conclude that estrogen replacement after menopause prolongs survival when coronary artery disease is present, but it has less effect in the absence of coronary artery disease.

Previous studies have demonstrated that regionalization of resources for cardiac catheterization, percutaneous coronary artery angioplasty (PTCA), and coronary artery bypass graft surgery (CABG) reduces the rate of procedure use. It was hypothesized that the impact of regionalization would be greater for the elderly and for African-Americans than for other populations. Discharge medical records of 30,901 patients admitted to a Veterans Affairs (VA) medical center between October 1, 1993, and September 30, 1994, with a diagnosis of coronary artery disease were analyzed. The presence of a cardiac catheterization laboratory in the patients’ local VA facility significantly increased the likelihood of undergoing catheterization, PTCA, and CABG, as determined by odds ratios and associated confidence limits estimated by logistic regression techniques. The presence of a cardiac surgical facility also significantly increased the likelihood of having the procedures. The odds ratios estimating the effects of resource availability were significantly greater for the subgroup of patients aged ≥70 years than for the younger subgroup for catheterization, PTCA, and CABG and for African-Americans than for white patients for PTCA and CABG. Thus, within the VA health care system, regionalization of cardiac procedures has a significant impact on utilization rates of tertiary cardiac procedures. These differences are significantly greater for the elderly and for African-Americans than for the general population.

Myocardial ischemia caused by inadequate coronary blood flow produces abnormalities of the S-T segment and T wave as well as alterations in the QRS complex. In this chapter, we shall explore the mechanisms as well as the patterns of these changes that occur in the absence of acute myocardial infarction. Specific attention will be given to the electrocardiographic abnormalities produced by exercise stress testing.

In the previous chapter, we described the effects of acute myocardial infarction on ventricular repolarization forces. We will now proceed to detail the electrophysiologic consequences of injury and infarction on ventricular activation. After developing the physiologic bases for changes in the QRS complex, resulting abnormalities in the body surface potential distribution will be described, and data documenting the diagnostic utility of electrocardiographic mapping will be presented.

The initial portions of the electrocardiographic waveform — the P wave and the P-R segment — reflect depolarization and repolarization of the atria. Sequences of activation and recovery defined by direct myocardial recordings provide a sound basis for interpreting normal body surface potential patterns. In this chapter, as in subsequent chapters of part III, we shall begin by describing the results of direct cardiac recordings. We will then emphasize the relation between these data and body surface potential distributions.

The objective of this study was to quantify the features of intracavitary potential recordings before and after experimental myocardial infarction. Potentials were recorded within the left ventricular cavity in 10 dogs using a cylindrical [45mm × 10mm] probe with 40 evenly spaced unipolar recording electrodes on its surface, before and after acute occlusion of the left anterior descending coronary artery. Analysis of control and post-infarct waveforms was based on QRS and ST-T area, and maximum negative potential and maximum negative dV/dt during the QRS complex. Infarction resulted in significant [p

ST-segment depression is the characteristic electrocardiographic response to myocardial ischemia. A hypothesis is presented defining the structural and functional requirements for ischemic blood flow and ST-T wave potential gradients for ST-segment depression to occur. Both flow and potential gradients may be either transmural or transventricular. ST-segment depression results only when both are concordant (e.g., both transmural); however, ischemic ST-segment depression does not follow when flow and potential gradients are discordant (e.g., one transmural and one transventricular).

Clinical, hemodynamic and coronary angiographic data from 9,801 patients were evaluated to determine the correlates of ST-segment depression, with or without T-wave inversion, on the resting routine electrocardiogram. The relative risk (RR) of having a measured clinical or angiographic variable was computed whether or not ST-T-wave abnormalities were observed. ST-segment depression was seen significantly more often in subjects greater than 55 years of age (RR = 1.4) who were women (RR = 1.3) or nonwhite (RR = 1.5), were hypertensive (RR = 1.8), had diabetes mellitus (RR = 1.6) or who smoked cigarettes (RR = 1.5). Angiographic findings related to presence of ST-T-wave abnormalities included severe coronary obstruction (less than 70%), higher number of diseased vessels, and the presence of obstruction in the left anterior descending coronary artery. In a multivariate model, the most significant correlates of ST-T-wave abnormalities were presence of left ventricular contraction abnormality, followed by age, gender, presence of left anterior descending coronary artery disease, elevated end-systolic volume index, and a diagnosis of hypertension. Thus, electrocardiographic ST-T abnormalities has specific and significant clinical and pathophysiologic correlates.

The effect of age at the time of coronary artery bypass graft surgery on postoperative survival was studied in 2,507 patients with significant coronary artery disease. Patients were subdivided into five groups based on age at the time of surgery: 20 to 39, 40 to 49, 50 to 59, 60 to 69 and greater than or equal to 70 years. The observed death rate was compared with that expected for subjects from the general U.S. population matched for age, gender, race and calendar year. For patients less than or equal to 59 years of age, the ratio of observed to expected death rates was significantly greater than unity (observed/expected = 4.9 for ages 20 to 39, 1.9 for ages 40 to 49 and 1.3 for ages 50 to 59 years, p less than 0.01). The prevalence of risk factors, including diabetes mellitus, hypertension, hypercholesterolemia and cigarette smoking, was evaluated in the different age subgroups. When patients were subdivided on the basis of history of cigarette smoking, the decreased relative survival rate of younger (less than 60 years old) patients existed only in those who smoked (observed/expected = 6.0 for ages 20 to 39, 2.2 for ages 40 to 49 and 1.4 for ages 50 to 59 years). In nonsmokers, observed/expected ratios for every age group were not significantly different from unity. Thus, the reduced relative survival rate of younger patients after coronary artery bypass graft surgery may be attributed to the interactive harmful effects of cigarette smoking.

The relationship among postmenopausal estrogen use, coronary stenosis, and survival was examined retrospectively in 2268 women undergoing coronary angiography. The patients were selected for study if their age was 55 years or older at the time of angiography or if they had previously undergone bilateral oophorectomy. Postmenopausal estrogen use in 1178 patients with coronary artery disease (greater than 70% stenosis) and 644 patients with mild to moderate coronary artery disease (5% to 69% stenosis) was compared with 446 control subjects (0% stenosis) using life-table analysis. Over 10 years of follow-up, there was no significant difference in survival among patients initially free of coronary lesions on arteriography who had either never used (377) or ever used (69) estrogens. Among patients with mild to moderate coronary stenosis, 10-year survival of those who had never used estrogens was 85.0% and it was 95.6% among 99 "ever users." Survival was 60.0% among those with more than 70% coronary stenosis who had never used estrogen and it was 97.0% among 70 ever users. The "never users" group were older (65 vs 59 years), had a lower proportion of cigarette smokers (40% vs 57.1%), a higher proportion of subjects with diabetes (21.7% vs 12.9%) and hyperlipidemia (58% vs 44%), and approximately equal numbers of hypertensives (56.0% vs 54.3%). Cox's proportional hazards model was used to estimate survival as a function of multiple covariables. Estrogen use was found to have a significant, independent effect on survival in women. We conclude that estrogen replacement after menopause prolongs survival when coronary artery disease is present, but it has less effect in the absence of coronary artery disease.

The electrocardiographic effects of tachycardia in normal dogs and in dogs with progressive coronary stenosis were studied. In five animals, left atrial electrodes were surgically implanted and body surface isopotential patterns were recorded from 84 torso electrodes; pacing at rates of up to 250 beats/min increased recorded voltages registered during the ST segment but did not alter the spatial distribution of these potentials. In 10 dogs, an ameroid constrictor was also implanted about the left circumflex coronary artery. One week after surgery, pacing to rates of 250 beats/min had no effect on ST segment isopotential patterns. However, 2 and 3 weeks postoperatively, when significant coronary constriction was anticipated, pacing-induced ST segment depression was recorded along the inferior anterior and posterior chest surfaces. Abnormal negative voltages were more intense at 3 than at 2 weeks, but the distribution of these abnormalities was unchanged. This pattern was consistent with the location of ischemic myocardium. Calculation of early (10 to 40 ms) ST segment slopes demonstrated that downsloping forms were recorded over most of the area with abnormal ST segment voltages, but that horizontal or upsloping depression occurred at the margins of the abnormal zones. The findings suggest that this canine model may be a useful analog to clinical exercise stress testing to aid in evaluating the significance of clinical electrocardiographic patterns.

To determine if the peak-systolic pressure/end-systolic volume ratio [PSP/ESV], a load-insensitive index of left ventricular function, predicted perioperative mortality and long-term survival after coronary artery bypass surgery or medical treatment, 4,829 patients with coronary artery disease were studied retrospectively. Cardiac volumes, ejection fraction, and PSP/ESV ratio were computed using standard methods, and follow-up was performed using annual questionnaires. PSP/ESV ratio values were not significantly different (p = .09) between those who died during hospitalization (n = 101) after coronary surgery and those who were discharged. Long-term follow-up in surgically treated patients demonstrated a 97% 3-year and 93% 5-year survival for those with PSP/ESV over 2.292. These were significantly greater (p = .0026) in value in patients with PSP/ESV less than 1.237 (3-year and 5-year survival of 92 and 79.2%, respectively). In the medical group, survival rate for those with PSP/ESV over 2.292 at 5 years was 89.3%, while for those with PSP/ESV less than 1.237 it was 52.5% (p less than .001). Multivariate analysis, however, showed ejection fraction to be a more significant predictor of survival in both the groups compared with PSP/ESV ratio. Thus, PSP/ESV ratio does predict long-term survival in coronary disease patients treated either surgically or medically. Ejection fraction was nevertheless a more powerful predictor of outcome.

This study in dogs was designed to determine the effects of residual stenosis on infarct size and on the transmural distribution of coronary flow in the central and peripheral ischemic perfusion bed. A plastic shunt containing a Doppler flow probe was inserted between the left anterior descending coronary artery and the subclavian artery. The dogs were divided into two groups. Group 1 (N = 7) underwent total shunt occlusion for 2 hours followed by reperfusion at 50% of control flow for 2 hours. Group 2 (N = 8) underwent 2 hours of total occlusion followed by 2 hours of total reperfusion. Regional blood flow was measured by radiolabeled microspheres, and infarct areas were quantitated with triphenyl tetrazolium chloride staining. Infarct sizes expressed as a percentage of the left ventricle or as a percentage of perfusion territory were significantly (p less than 0.05) smaller in animals with total reperfusion (group 2) than in dogs with partial reperfusion (group 1). Endocardial flows in the central infarct zone were significantly higher in dogs with total reperfusion than was observed with partial reperfusion; epicardial flows were not significantly different. In the peripheral region both endocardial flows and epicardial flows with total reperfusion were significantly higher than with partial reperfusion. These studies suggest that residual stenosis after thrombolysis may increase infarct size and reduce endocardial flow in the central infarct zone and transmural flow in the peripheral zone.

Electrocardiographic R and S wave changes occur after transmural myocardial infarction. It was the purpose of this study to define the spatial characteristics of these changes and their pathologic determinants after nontransmural as well as transmural necrosis. Twenty-six dogs were studied after occlusion of the left circumflex coronary artery for 60 to 240 minutes, followed by re-perfusion. Electrocardiographic potentials were recorded before and 1 week after infarction using an 84 electrode array to compute maximal and root-mean-square R and S wave voltages. Infarct size was quantitated by computer-aided evaluation of heart slices stained by tri-phenyltetrazolium chloride. R and S wave amplitudes after infarction varied widely from one torso site to another in a pattern generally consistent with the inferoposterior location of the in-farcted zones. Although changes in peak R and S wave potentials did not significantly correlate with infarct size, differences in pre- and postocclusion root-mean-square R and S wave amplitudes did, with correlation coefficients of −0.79 and −0.63, respectively. Root-mean-square values increased for small lesions and decreased for larger ones. These data indicate that nontransmural as well as transmural infarction can produce R and S wave changes that are dependent on overall lesion size and the specific lead studied. Such changes may represent useful methods to quantitate lesion size.

Clinical and experimental data have documented the ability of nontransmural myocardial infarction to produce abnormal Q waves on both the epicardial and body surfaces. We undertook this study to define the anatomic determinants of such Q wave development. Thirty dogs were studied before and after occlusion-reperfusion (26 dogs) or latex embolization (four dogs) of the left circumflex coronary artery. Occlusion was maintained for 60 to 240 min before reperfusion to produce nontransmural lesions of various sizes. Electrocardiographic data were registered from 84 torso electrodes by body surface mapping techniques before and 1 week after infarction. Infarct size was quantitated by computer analysis of heart slices stained with triphenyl tetrazolium chloride. Six dogs did not develop infarction. Of the remaining 24, 10 did and 14 did not develop significant changes in body surface Q wave duration and width. The incidence of Q wave changes was not different in dogs with nontransmural and those with transmural lesions. Infarct size (expressed as a percentage of the left ventricle infarcted), the percentage of endocardium subjacent to infarction, the average depth of necrosis, the percent of the four outer fifths of the ventricular wall infarcted, and the duration of occlusion were significantly (p less than .05) greater in dogs with than in those without Q wave changes. Logistic regression modeling demonstrated that only two anatomic parameters--percentage of left ventricle infarcted and average lesion depth--significantly and independently predicted Q wave development. A model including only these two variables accurately classified all 24 cases.(ABSTRACT TRUNCATED AT 250 WORDS)

It has been demonstrated that temporary occlusion of major epicardial arteries of the dogs produces a nontransmural myocardial infarction (MI) whose size is reduced by early reperfusion. This study was undertaken to determine the location and extent of MI following acute occlusion and reperfusion of the septal artery (SA). The SA was occluded for four hours in group I (7 dogs). Occlusion time for group II (6 dogs) was 2 hours and for group III (6 dogs) was 1 hour, followed by 2 and 3 hours of reperfusion, respectively. The hearts were then removed and cut into transverse slices from base to apex. The triphenyl tetrazolium chloride technique identified the areas of infarction, which were quantitated with a microcomputer-based graphics system. To determine the extent of necrosis across the interventricular septum (IVS), the IVS was divided into 5 transverse segments of equal depth and the amount of MI was determined for each. In group I, MI involved 3.42 +/- 0.9% (mean +/- SEM) of the left ventricle (LV) and 13.49 +/- 3.4% of the IVS. In group II, 6.11 +/- 1.3% of the LV and 25.00 +/- 5.5% of the IVS were infarcted. In group III, 5.63 +/- 1.3% of the LV and 31.9 +/- 14.3% of the septum were infarcted. MI was larger on the left side of the IVS than on the right in all groups, and the extent of MI did not differ significantly between the three groups. This study showed that early reperfusion of the SA did not reduce MI as reported for other coronary beds.

We determined the electrocardiographic response to pacing-induced tachycardia in 45 dogs. Pacing was performed using left atrial, left atrial-right ventricular sequential or left atrial-left ventricular sequential modes at rates of 90 to 250 beats·min−1. Body surface isopotential maps in 15 dogs with normal coronary circulations defined the normal response to rate; surface potential extrema during the S-T segment increased in strength with increasing rate but spatial features remained constant. In the other 30 dogs, an ameroid constrictor was placed around the left circumflex coronary artery. Two weeks after implantation, atrial pacing to rates of 190 beats·min−1 or greater resulted in flat. S-T segment depression, with new and abnormal negative voltages registered over the inferior and left posterior torso. However, with either form of ventricular pacing, tachycardia with coronary obstruction did not alter the S-T segment response seen in control animals, in either intensity or spatial parameters. We interpret these findings to suggest that: 1) in normal dogs, tachycardia produced a common electrocardiographic effect regardless of activation pattern; and 2) tachycardia in the presence of coronary constriction results in subendocardial myocardial ischaemia that, with atrial pacing, reverses the normal transmural S-T segment potential gradient and causes body surface S-T segment depression, but 3) with primary ventricular stimulation, the subendocardial ischaemia does not alter the transventricular repolarisation gradients sufficiently to generate body surface S-T segment shifts.

Electrocardiographic (ECG) effects of experimental, isolated right ventricular infarction were studied in 10 dogs during sinus rhythm as well as during ectopic right and left ventricular pacing. Infarction was produced by injecting latex into the right coronary artery and ECG consequences were examined by body surface isopotential mapping methods using an 84 electrode torso array. During sinus rhythm, subtraction of preinfarction from postinfarction maps demonstrated that right ventricular necrosis produced abnormal negative potentials over the right hemithorax during the early, middle and late portions of the QRS complex. These patterns corresponded to loss of R waves and deepening of preexistent or development of new Q and S waves in waveforms from this region. Patterns during ectopic ventricular stimulation were compared with mean maps derived from 13 control dogs. Both left and right ventricular pacing after right ventricular infarction resulted in a right-sided abnormal minimum, similar in location to that observed during sinus rhythm, throughout the QRS complex. Thus, 1) right ventricular necrosis does produce QRS complex changes over the right torso that are analogous to those produced by left ventricular infarction, and 2) the dominant pattern of an abnormal right-sided minimum was present regardless of the ventricular activation pattern. This latter finding suggests that the region of right ventricular necrosis provided a supplementary path for current to reenter the heart regardless of the current source, so that an overlying electrode would record negative voltage with all activation patterns.

The ability of parameters derived from standard, scalar ECG leads to predict abnormal body surface isopotential distributions was tested in 25 dogs. Atrial pacing to rates of 170 beats per minute or greater, two weeks after implantation of an ameroid constrictor on the left circumflex coronary artery, resulted in abnormal isopotential patterns due to subendocardial ischemia. A total of 96 scalar ECG variables (potential and slope measurements at 20, 40, 60 and 80 msec into the ST-segment in each of 12 leads) were computed. Ability of each variable and potential-slope pairs to distinguish normal from ischemic map forms was tested using discriminant function analysis and simple classification procedures. Results demonstrated that accuracy of prediction was lead-dependent, and time-dependent, with different sensitivities, specificities and boundary values in different leads and at different instants during the ST-segment. These new concepts may have direct relevance to the selection of clinical exercise ECG diagnostic criteria.

The QT interval is a clinically important electrocardiographic measurement. This study attempted to determine 1) whether this interval was spatially distributed in a physiologically meaningful way on the torso of normal subjects, and 2) if these spatial patterns were altered in patients with acute myocardial infarction. To do so, 30 patients were studied within 72 hours of the onset of acute myocardial infarction (15 with an anterior and 15 with a posterior lesion) along with 50 normal control subjects. Electrocardiographic signals were registered from 150 torso electrodes; the QT interval in each lead was determined by a combined automated-manual method, and the durations displayed as "isointerval maps." In the normal subjects, the difference between the longest and shortest interval in each case was 59.4 +/- 12.9 ms. Long QT intervals were spatially located over the left lateral torso and short QT intervals were found over the right inferior chest. Acute infarction modified this distribution in relation to lesion location; the longest QT intervals were centrally positioned in anterior infarction and caudally located in inferior infarction. Thus, QT intervals in normal and abnormal states have distinctive spatial distributions that are consistent with known regional myocardial electrophysiology.

Collateral flow to the interventricular septum in the dog was measured after septal artery ligation (N = 8) and compared to that in the left ventricular free wall after occlusion of the left anterior descending coronary artery (N = 10) in other animals. Flow was quantitated by radiolabelled microsphere injection before, and 90 s, 2 h and 4 h after occlusion. Perfusion territory size was measured after colored dye infusion; the septal artery bed occupied 21.74 +/- 5.44% of the left ventricle and was significantly smaller than the anterior descending artery zone (40.72 +/- 7.56%). Regional blood flow prior to occlusion was equal in both beds and symmetric across the ventricular wall; endocardial/epicardial and left/right ratios in the anterior descending and septal artery beds were 0.97 +/- 0.14 and 1.14 +/- 0.17, respectively. 90 s after occlusion, left and right septal and endocardial and epicardial anterior descending flows were significantly (p less than 0.05) reduced. Right septal flows exceeded left sided flows to produce a transseptal gradient. However, right septal flow was significantly greater than epicardial anterior bed values, and free wall endocardial/epicardial was significantly lower than septal left/right ratios. By 2 h after occlusion, left and right septal flows were no longer significantly different from preocclusion values, whereas anterior descending flows remained significantly below control for the full 4-h period. Thus, significant differences between the two beds exist, with greater acute collateral flows and more rapid correction of flow deficits in the septum than in the free wall.

Previously reported clinical studies have suggested an important diagnostic role for exercise-induced QRS changes. To explore the spatial features of such alterations, anterior thoracic isopotential distributions were examined at rest and at 85 percent of maximal heart rate in 30 normal male volunteers. Results demonstrated that exercise caused a reduction in positive forces and an augmentation of negative voltages at most anterior thoracic sites. However, the locations of map extreme were not significantly altered. Difference maps, computed by subtracting time-aligned distributions at rest and during exercise, suggested that exercise generated an electrical field characterized by a central anterior minimum bordered superiorly by positive potentials. The minimum reached a peak magnitude in the middle portion of the QRS pattern, then declined in intensity. Although difference patterns during inscription of the QRS complex were similar to those computed during the P-R and S-T segments, time-intensity curves were discontinuous with marked and abrupt early increases and late decreases in strength in the QRS complex. These results suggest that two commonly considered mechanisms (effects of changes in intracavitary blood mass and of atrial repolarization) cannot be solely responsible for the observed effects.

Most attempts to quantitate myocardial function rely on morphologic features of complex pressure waveforms to reflect the functional properties of the ventricular myocardium. Relationships between waveform components and the function of the organ generating them were examined in 38 rhesus monkeys by harmonic analysis of left ventricular pressure waveforms. In the basal state, harmonic content was closely correlated (r=0.98) with hemodynamic state, as quantitated by heart rate, systolic and diastolic pressures, left ventricular end-diastolic pressure and maximum contractile element velocity. Hemodynamic indices were expressed as significant linear functions of harmonic terms (r=0.71--0.83), in patterns consistent with the principle of superposition. In 20 animals, infusions of dextran, methoxamine, propranolol or ouabain were used to further assess this relationship. Results demonstrated (1) significant correlation between changes in hemodynamic and harmonic parameter (4= 0.99), (2) correlations between each harmonic term and the set of hemodynamic indices such that specific terms varied directly with contractility but not with loading, whereas others correlated significantly only with loading, and (3) that the patterns in these correlations were of such specificity as to permit construction of significant discriminant functions (p less than 0.0001) that accurately characterized the pharmacologically induced hemodynamic change in 85% (56/67) of trials.

Cigarette smoking is a risk factor for development of coronary atherosclerosis. We examined the relationship between smoking and the anatomic location of coronary artery stenosis in 8,705 patients undergoing cardiac catheterization for suspected coronary artery disease (CAD). The smoking history of patients with CAD (greater than or equal to 70 percent stenosis) was compared with that of control subjects (0 percent stenosis) for each of nine anatomic locations (proximal, middle, and distal segments of right [RCA], anterior descending [LAD], and circumflex arteries [LCX]), using a case-control method. The odds ratio (OR) estimate of relative risk of CAD for smokers relative to nonsmokers was 2.8, with a 95 percent confidence interval (CI) of 2.5 to 3.1. Relative risk was greater for RCA stenosis (OR = 5.8; CI = 4.6-7.2) than for LCX (OR = 3.5; CI = 2.7-4.5) or LAD (OR = 2.1; CI = 1.8-2.4) lesions when comparing smokers with nonsmokers. After control for age, gender, history of diabetes mellitus, and serum cholesterol level, the adjusted relative risk for an RCA lesion (Mantel-Haenszel odds ratio [MOR] = 4.9) was significantly elevated (p less than 0.05) compared with the LAD (MOR = 1.9) but not with the LCX (MOR = 3.1). The relative risks of CAD were the same (p greater than 0.05) for the proximal, middle, and distal coronary segments. Thus, smoking increased the risk of all coronary lesions but did so more for the RCA than for other vessels, suggesting a spatial pattern to the increased risk produced by smoking.

The ratio of peak systolic pressure to end-systolic volume (PSP/ESV) is a measure of contractility that is relatively independent of loading conditions. To define the relation of this index to the natural history of chronic mitral insufficiency, follow-up studies were performed in 76 patients. All had isolated mitral insufficiency and were followed up for an average of 48 months. None underwent surgery. Cardiac volumes, ejection fraction and PSP/ESV ratio were calculated and Cox multiple regression analyses were performed to determine the relation of functional status, ejection fraction and PSP/ESV ratio to morbidity and mortality. Twenty-three patients died during follow-up; in 70% of those who died, the PSP/ESV ratio was reduced below the 20th percentile. However, as an independent predictor of mortality, this ratio was less sensitive (p greater than 0.05) than ejection fraction (p less than 0.01). Similarly, functional status change was predicted more accurately by ejection fraction (p less than 0.01) than by the PSP/ESV ratio (p greater than 0.05). Thus, although a decreased PSP/ESV ratio was associated with a higher mortality rate, other clinical and laboratory variables were superior to this index for determining morbidity and mortality in patients with isolated mitral insufficiency.

Prior studies have shown that tachycardia results in ST segment depression in dogs with chronic, gradual coronary occlusion. This response was compared with that produced by acute, total occlusion of the left anterior descending artery. Ten dogs served as controls; in another 10 dogs, an ameroid constrictor was implanted about the left anterior descending artery. This artery was acutely ligated in a third set of 10 animals, and in a final set of 10, the distal left anterior descending coronary vasculature was embolized by latex injection. Tachycardia was produced by atrial pacing from rates of 90 to 250 beats/min using implanted atrial electrodes. Electrocardiographic signals registered from 84 torso electrodes were used to construct body surface isopotential maps during the ST segment. In normal dogs, pacing increased repolarization potentials without shifts in spatial features. New and abnormal anterior negativity, correlating with significant ST depression, appeared at rates of 170 beats/min or faster in dogs with ameroid constriction. However, in both groups with acute occlusion that produced transmural myocardial infarction, tachycardia resulted in increases in anterior ST elevation and reciprocal ST depression. Specific findings demonstrated the lead dependency of the response to tachycardia and the greater than normal increase in potential magnitudes after infarction than in control cases. The similarity of the response with acute occlusion and with embolization suggested that the response to tachycardia after infarction was not dependent on coronary collateral function but may represent a direct electrophysiologic effect of rate. Thus, these acute occlusion models simulate exerciseinduced ST segment elevation as it may be seen clinically.

S-T segment elevation is commonly observed in the electrocardiogram of normal persons. To study the possible origins of such patterns, 45 normal volunteers were examined. Electrocardiographic potentials were registered from 150 torso electrodes and processed to construct isopotential maps at 2 ms intervals throughout the QRS-T interval. The maximal potentials recorded from any of the 150 electrodes were 198 +/- 76.4 and 272.1 +/- 84.2 microV at instants 40 and 80 ms into the S-T segment, respectively. Maximal voltages recorded by the six standard precordial V leads at these respective time points were 109.7 +/- 57.0 and 163.6 +/- 66.9 microV. Torso maximal potentials were significantly stronger than were those sensed by V leads; the two were significantly correlated but predictability was limited. The duration of overlap between the onset of ventricular recovery and the end of the excitation was determined from isopotential maps and ranged rom 4 to 16 ms. There was no significant correlation (p greater than 0.05) between these values and either torso or V lead potentials at either 40 or 80 ms into S-T segment. These data suggest that (1) standard precordial leads do not accurately predict maximal torso potentials during the S-T segment, and (2) the degree of overlap between repolarization and depolarization is not a major determinant of precordial voltage. Hence, the rationale for use of the term "early repolarization" to describe this clinical condition is not substantiated.

Junctional depression is often observed during physical exercise in overtly normal subjects. To explore its pathogenesis, 15 normal volunteers were studied during supine, bicycle ergometer, submaximal stress tests. Electrocardiograms were simultaneously recorded from 42 electrodes on the left anterior precordium at two minute intervals at rest and during exercise. Data were used to construct isopotential maps throughout the P-QRS-T intervals. At rest, maps throughout the ST segment were dominated by a single maximum along the upper left sternal border. During exercise, all subjects developed junctional depression that was maximal along the lower left sternal border. Exercise maps during the early to mid-ST segment showed an intense minimum along the lower left sternal border that was continuous with terminal QRS forces in both intensity and location. Later in ST, this minimum decreased in strength and was replaced by a maximum located in the same area as that observed at rest. These observations suggest that junctional depression is the result of competition between two effects, one being normal repolarization which is obscured in the early ST segment by the second, possibly representing delayed terminal depolarization forces.

Dipole ranging is a method to determine the location, strength and orientation of the heart vector from body surface measurements. This technique was applied to electrocardiographic data recorded from forty-five normal subjects and from twenty patients suffering an acute myocardial infarction. Moments and locations during the QRST interval were determined by the potential integration formulae of Gabor and Nelson. Results in the normal population showed stability of both variables during cardiac recovery. In subjects with acute infarction, dipole loci were stable during much of the ST-segments of loci compatible with the anatomic positions of the lesions. Thus, dipole ranging methods can provide physiologically relevant information when applied to human electrocardiographic problems.

Benazepril hydrochloride is a nonsulfhydryl, long-acting angiotensin-converting enzyme inhibitor that is orally effective. This study was designed to determine the acute hemodynamic effects of this agent in patients with chronic congestive heart failure. Twenty-six patients with New York Heart Association class III or IV congestive heart failure and left ventricular ejection fractions less than 35%, cardiac indexes less than 2.1 L/min/m2, and pulmonary artery wedge pressures greater than 12 mm Hg were given 2 or 5 mg benazepril hydrochloride. All does produced significant (p less than 0.05) increases in cardiac output (26.7% to 31.6% above control) and heart rate (5.4% to 11.2% above control) and decreases in systemic (27.1% to 32.0% below control) and pulmonary (34.8% to 55.5% below control) vascular resistances, mean pulmonary (25.3% to 30.3% below control) and systemic (13.4% to 18.5% below control) arterial pressures, and pulmonary artery wedge pressure (46.9% to 51.1% below control). Twenty-four hours after an initial dose, systemic vascular resistance and pulmonary artery wedge pressures remained below control levels. Angiotensin-converting enzyme activity fell by 67.8% +/- 6.4%, with a 15.8% +/- 7.6% decline in aldosterone levels. Thus benazepril hydrochloride is an effective angiotensin-converting enzyme inhibitor that produces hemodynamic effects that persist for 24 hours after a single oral dose.

Electrophysiologic studies were performed in a 76 year old patient for evaluation of sinus bradycardia. Atrial extrastimuli were induced during sinus rhythm at progressively decreasing coupling (A 1 -A 2 ) Intervals. At an A 1 -A 2 interval of 420 msec, right bundle branch block developed, and at 370 msec conduction failed below the His bundle. When the interval was reduced to 320 msec, conduction resumed with a normal QRS pattern with an abrupt increase in A-H intervals from 165 to 305 msec. These findings are interpreted as type I or atrioventricular (A-V) nodal gap conduction physiologically related to conversion from a rapid to a slow A-V nodal conduction mode.

Patients with acute inferior myocardial infarction commonly have ST segment depression in the anterior precordial leads. This may reflect either reciprocal changes from the inferior ST elevation or primary ST depression from additional anterior subendocardial ischemia. From a biophysical perspective reciprocal changes should be uniformly anticipated from basic dipole theory. Detection will vary with the size, location, orientation, and electrical intensity of the lesion and with the ECG lead system deployed to register the anterior changes. Alternatively, acute occlusion of the right coronary artery may produce ischemia in the anterior left ventricular wall supplied by a stenotic anterior descending coronary artery. Anterior ischemia may result from the abnormal hemodynamics or the reduced collateral flow produced by acute right coronary artery occlusion. Thus both mechanisms are based on sound physiologic principles. A review of the clinical literature suggests that such patients represent a heterogeneous group. In some instances coexistent anterior ischemia is present, whereas in others the anterior ST depression is the passive reflection of inferior ST elevation augmented in many cases by a large infarct size or more extensive posterobasal or septal involvement.

Ventricular bigeminy may be either overt or concealed. In this study, we attempted to determine the frequency with which the overt form converted to the concealed variety. Ambulatory electrocardiographic recordings from 25 patients with greater than 40 episodes of monomorphic ventricular bigeminy were examined. A statistically significant (P less than 0.01, binomial distribution) predominance of odd or even number of sinus beats between the end of a bigeminal episode and the next ventricular premature beat was considered to be evidence for conversion of overt to concealed bigeminy. In 14 of the 25 cases, the number of episodes of bigeminy followed by odd numbers of sinus beats was beyond these statistical bounds. In 74 episodes in 9 patients, progressive prolongation of the coupling interval during bigeminy occurred before termination. These data demonstrate the high prevalence of concealment as a mode of termination of bigeminy. In a small number of episodes, this occurs in a pattern suggestive of progressive delay of conduction in or around an arrhythmogenic locus.

The presence of ventricular tachycardia (VT) is commonly considered to represent a risk factor for sudden cardiac death as well as an indication for antiarrhythmic drug therapy. Although spontaneous VT is generally diagnosed by the presence of three or more consecutive ectopic beats, proposed criteria for induced VT require six or more complexes at rates exceeding 90 or 100 beats/min. To determine the clinical implications of a similar change in the diagnostic criteria for spontaneous VT, the authors examined 324 consecutive 24-hour ambulatory electrocardiograms. Of these, 111 (34.3%) had episodes of three or more ventricular premature beats. If six or more beats were required, only 34 (30.6%) would have been diagnosed as having VT. Requiring a minimum rate of 90 or 100 beats/min had less consequence, eliminating only 10 (9.0%) and 12 (10.8%) patients, respectively. Patients with only three to five beat runs had significantly fewer isolated premature beats (4,462.8 +/- 588.4 vs 7,158.1 +/- 1,688.1) and ventricular couplets (186.2 +/- 39.2 vs 294.3 +/- 74.4) per day, and slower average rates (142.1 +/- 4.6 vs 171.8 +/- 6.7 beats/min) during ventricular tachycardia than did those with runs of six or more beats. Thus, altering the definition of spontaneous VT has marked effects on the prevalence of this arrhythmia. Those patients excluded did, however, have a lower prevalence of associated electrocardiographic risk factors.

The relation between the severity of diabetes mellitus (DM) and the risk of significant coronary artery lesions were studied in 7,655 patients undergoing coronary arteriography for suspected coronary artery disease (CAD) between 1972 and 1982. The principal treatment regimen for DM was used to estimate the severity of DM. DM treated with insulin was defined as the most severe (n = 244), followed by DM treated with oral agents (n = 344) and with diet only (n = 380); 6,687 patients did not have DM. Severity of DM in patients with CAD (70% or greater diameter stenosis) was compared with that in control subjects without CAD (0% stenosis) for each of 9 anatomic locations (proximal, middle and distal portions of right, anterior descending and circumflex coronary arteries) using a retrospective case-control approach. The risk of CAD was highest in patients with DM treated with insulin (odds ratio estimate of the relative risk [OR = 3.0]), followed by patients with DM treated with oral agents (OR = 1.8) and lastly in those treated with diet alone (OR = 1.4). Severity of DM was a significant (p less than 0.05) independent predictor of CAD in a multivariate logistic regression model, whereas age at onset and duration of DM were not. The relative risk of CAD was the same (p greater than 0.05) for each of the 9 coronary segments. The data suggest that the risk of CAD increases with the severity of DM, which was a stronger predictor of CAD than duration of DM.(ABSTRACT TRUNCATED AT 250 WORDS)

The case of a 67-year-old man with combined ischemic and valvular heart disease is presented. Electrocardiographic abnormalities included left anterior fascicular block with a variable duration of the QRS complex. The width of the QRS complex was dependent on the length of the cycle, being broader with short than with long preceding R-R intervals. This is interpreted as a tachycardia-dependent focal block coexisting with a fixed delay in fascicular conduction.

Summary The effects of tachycardia on the QRS complex in the absence and in the presence of coronary arterial constriction are of possible clinical significance. To study the spatial and temporal distributions of these effects, a canine model simulating progressive coronary occlusion was studied. Tachycardia was induced by atrial pacing, coronary narrowing was produced by implantation of an ameroid constrictor about the left circumflex coronary artery and electrocardiographic effects were studied by isopotential mapping techniques at rates of, up to 250 beats per minute, one to three weeks after constrictor implant. In five dogs. pacing without coronary constriction demonstrated the spatial and temporal dependence of QRS changes; tachycardia-induced, changes varied from one torso site to another at any instant, and from one moment to another at any one torso location. Patterns in ten dogs with constrictors were dependent upon time after ameroid placement. Resting QRS and S-T segment distributions remained unchanged. One week after surgery, QRS and S-T segment patterns during pacing were as in controls. Two weeks after surgery, QRS patterns were as in controls but flat S-T segment depression resulted at high rates. After three weeks, QRS patterns during pacing were abnormal and S-T segment depression was observed. At each of the later times, the QRS response was similiar at rates which did and which did not cause S-T depression. Thus, the effects of tachycardia on excitation and recovery forces in the presence of restricted coronary flow are independent of one another. This suggests that the two responses to ischemia may be due to different basic mechanisms and, hence, that their detection may reflect different myocardial abnormalities.