Am J Physiol Heart Circ Physiol 291: H351-H356, 2006.
First published January 20, 2006; doi:10.1152/ajpheart.00992.2005
0363-6135/06 $8.00
Variable ECG signs of ischemia during controlled occlusion of the left and right coronary artery in humans
Stefano F. De Marchi,
Pascal Meier,
Philipp Oswald, and
Christian Seiler
Department of Cardiology, University Hospital, Bern, Switzerland
Submitted 19 September 2005
; accepted in final form 17 January 2006
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ABSTRACT
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Infarct size (IS) increases with vascular occlusion time, area at risk for infarction, lack of collateral supply, absence of preconditioning, and myocardial demand for O2 supply. ECG S-T segment elevation is used as a measure of severity of ischemia and a surrogate for IS. This study in 50 patients with coronary artery disease undergoing a first 120-s balloon occlusion of a stenosis sought to determine whether S-T segment elevation, corrected for the above-mentioned variables, in the left coronary artery (LCA group, n = 36) is different from that in the right coronary artery (RCA group, n = 14) territory. After consideration of all known determinants of IS, particularly mass at risk and collateral supply, the LCA territory is more sensitive than the RCA region to a 2-min period of myocardial ischemia.
coronary disease; collateral circulation
ANNUAL MORTALITY RATE from all causes across Europe amounts to 11 per 1,000 inhabitants, with 5.4 per 1,000 (49%) due to cardiovascular disease and 2.4 per 1,000 (22%) due to ischemic heart disease (3). In patients suffering from coronary artery disease (CAD), the size of the myocardial infarction is the most important determinant of the outcome after such an event (22). Accordingly, the primary therapeutic strategy to reduce cardiovascular mortality is reduction of infarct size (IS). IS increases with coronary artery occlusion time, myocardial area at risk for infarction (AR), lack of collateral supply, absence of preconditioning, and myocardial demand for O2 (i.e., the product of contractility, heart rate, and ventricular wall stress) (16, 18).
As a surrogate for IS, clinical studies on the effect of various procedures on myocardial salvage have ubiquitously employed the magnitude of ECG changes during artificial coronary occlusion (2). In this context, the following unresolved clinical question has been raised (2): Does ischemia induced by balloon inflation in different coronary artery segments result in the same magnitude of ECG S-T segment shift? There has been evidence from experimental studies of 1) regional differences in infarct development and protection from within the left anterior descending coronary artery (LAD) territory (19) and 2) augmented coronary collateral conductance in small apical vs. large basal ARs (12). In humans, investigations on regional differences in myocardial ischemia have allowed little more than speculation that the territory of ischemia might be another determinant of IS. For example, during acute myocardial infarction, "tombstone" ECG S-T segment elevation is tightly associated with a large infarct in the LAD region, which could be explained by the large AR in this territory and/or site-specific myocardial vulnerability to ischemia (13). Quantitative collateral flow index (CFI) measurements in 450 patients with stable CAD have documented lower values in the LAD than in the left circumflex (LCX) and right coronary artery (RCA) regions (15).
The goal of the present study in 50 patients with chronic CAD was to test the hypothesis that intracoronary ECG S-T segment elevation corrected for the above-mentioned predictors of IS during a first 120-s balloon occlusion is different between left coronary artery (LCA) and RCA territory.
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METHODS
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Patients
Fifty patients (60 ± 10 yr old, 40 men and 10 women) with one- to three-vessel CAD and chronic, stable, exercise-induced angina pectoris were included in the study. All underwent percutaneous coronary intervention (PCI) of one stenotic lesion because of symptoms related to CAD. Patients were prospectively selected on the basis of the following criteria: 1) no previous Q wave infarction in the myocardial area undergoing PCI, 2) no baseline ECG S-T segment abnormalities, and 3) right dominance in the case of collateral measurement in the RCA. The present investigation was approved by the institutional ethics committee, and the patients gave informed consent to participate in the study.
The study population was divided into two groups according to the coronary artery territory undergoing PCI: the LCA group (n = 36) and the RCA group (n = 14). The study was designed to account for the determinants of IS as follows: coronary balloon occlusion time was uniformly 120 s, CFI was obtained quantitatively, AR was quantified, only patients with a history of exercise-induced angina pectoris were recruited, the first of at least one coronary occlusion served as the study end point (thus accounting for ischemic preconditioning), ECG R-R interval at the end of the 120-s occlusion was measured, and the degree of anterior-to-inferior left ventricular (LV) wall curvature radius was estimated at end diastole.
Cardiac Catheterization and Coronary Angiography
For diagnostic purposes, patients underwent left heart catheterization from the right femoral artery approach. Biplane left ventriculography was followed by coronary angiography. Central venous pressure (CVP) was measured via the femoral vein. Offline measurements were as follows: Coronary artery stenoses were estimated quantitatively as percent diameter reduction, with the guiding catheter used for calibration. As a part of AR assessment (see below), a measure of the proximity of the stenotic lesion undergoing PCI was quantitatively determined as the ratio of the summed coronary artery branch lengths distal to the stenosis to the summed branch lengths of the respective coronary artery (LAD, LCX, and RCA) (21). As an estimate of regional ventricular wall stress, the end-diastolic LV cavity curvature radii of the anterior and inferior wall were measured (simultaneously obtained from the 60° right anterior oblique view of the ventriculography), and the anterior-to-inferior radius ratio was determined.
Coronary Collateral Assessment
In all patients, recruitable coronary collateral flow during vascular balloon occlusion relative to normal antegrade flow through the nonoccluded coronary artery (CFI, no unit) was determined using intracoronary pressure measurements. A 0.014-in. fiber-optic pressure-monitoring wire (RadiWire, Radi, Uppsala, Sweden) was set at zero, calibrated, advanced through the guiding catheter, and positioned distal to the stenosis to be dilated. CFI was determined by simultaneous measurements of mean aortic pressure (Pao, mmHg, via the angioplasty guiding catheter), distal coronary occlusive pressure (Poccl, mmHg), and CVP: CFI = (Poccl – CVP)/(Pao – CVP) (Fig. 1). Sensor-derived CFI measurements have been previously validated (20).
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Fig. 1. Determination of collateral flow index (CFI) in a patient of left coronary artery (LCA) group. Intracoronary ECG lead V1 recording is shown at top. Simultaneously obtained intracoronary ECG (via guide wire) and mean aortic pressure (Pao), distal coronary occlusive pressure (Poccl), and central venous pressure (CVP) before and at the start of coronary balloon occlusion are shown at left. After 30 and 120 s of vessel occlusion (middle and right), S-T segment on intracoronary ECG lead was elevated, indicating that coronary collaterals were insufficient to prevent myocardial ischemia (maximal S-T elevation = 1.2 mV). CFI is calculated as follows: [Poccl (mmHg, scale 0–150 mmHg) – CVP (mmHg, scale 0–30 mmHg)] ÷ [Pao (mmHg, scale 0–150 mmHg) – CVP]. CFI = 0.05.
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Intracoronary ECG
As the primary study end point, a unipolar intracoronary ECG was obtained in all patients from the angioplasty guide wire (Figs. 1 and 2), in addition to three surface leads in the RCA group (II, III, and aVF) and three surface leads in the LCA group (I, III, and aVL). A cross clamp was attached close to the end of the wire and connected to ECG lead V1; i.e., the active electrode of the intracoronary ECG corresponded anatomically to the distal LAD in the majority of cases in the LCA group (anteroapical wall of the LV) and to the distal RCA in the RCA group (inferoapical wall of the LV). The intracoronary ECG is widely accepted as a sensitive tool for detection of myocardial ischemia (8, 9).
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Fig. 2. Determination of CFI in a patient of the right coronary artery (RCA) group. Intracoronary ECG lead V1 recording is shown at top. Phasic Pao, Poccl, and CVP before balloon occlusion are shown at left. After 30 and 120 s of vessel occlusion (middle and right), S-T segment on intracoronary ECG lead was elevated, indicating that coronary collaterals were insufficient to prevent myocardial ischemia (maximal S-T elevation = 0.8 mV). CFI = 0.05.
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Study Protocol
After diagnostic coronary angiography, 
10 min were allowed for dissipation of the effect of the contrast medium on coronary vasomotion. Before PCI, 5,000 units of heparin were given. Two puffs of oral nitroglycerin spray were applied shortly before coronary pressure measurements. The pressure guide wire was positioned distal to the stenosis to be dilated. During the entire protocol, i.e., before angioplasty balloon insertion, the intracoronary ECG obtained from the pressure guide wire and the surface lead ECG were recorded. Simultaneous recording of Pao via the 6-Fr guiding catheter, Poccl, CVP, and the ECG was started before and continued throughout the 120-s balloon occlusion. Coronary occlusions were performed using angioplasty balloons appropriately sized for the stenotic lesion to be dilated. For data analysis, the recordings before and during the first balloon occlusion were used.
Data Analysis
Intraindividual analysis.
Intracoronary ECG S-T segment elevation (mV) before and every 10 s during coronary occlusion was measured in absolute terms and relative to the respective R wave amplitude. Relative S-T segment elevation was determined as one of two ways to account for AR; the other method is the angiographic proximity index of the stenosis location. The intraindividual change of these variables during the entire occlusion was analyzed (Fig. 3).
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Fig. 3. Intraindividual ECG S-T segment changes before and during 120 s of coronary balloon occlusion recorded via angioplasty guide wire positioned distal to occluded vascular site. Left: absolute S-T segment elevation measured in LCA (gray circles) and RCA (black circles) groups. Right: S-T segment elevation relative to respective R wave amplitude recorded in LCA (gray circles) and RCA (black circles) groups.
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Interindividual analysis.
Absolute and relative intracoronary ECG S-T segment elevation obtained at 120 s of coronary occlusion for a given CFI was compared between individuals of the LCA and RCA groups (Fig. 4). ECG R-R intervals were measured and averaged over the five last cardiac cycles before coronary balloon deflation.
Statistical Analysis
Between-group comparisons of continuous demographic, hemodynamic, angiographic, ECG, and collateral flow data were performed by a two-sided unpaired Student's t-test. A 
2 test (2 x 2 table) was used for comparison of categorical variables among the study groups. A two-way ANOVA for repeated measures was used for intraindividual changes of ECG S-T segment elevation before and during occlusion. Possible correlations between different time points were taken into account by adjustment of the significance level according to Bonferroni's correction (P < 0.01). Linear regression analysis with Bonferroni's correction for significance determination was used for the interindividual relation between ECG S-T segment elevation and CFI at 120 s of occlusion. Multiple regression analysis was performed with ECG-relative S-T segment elevation as the dependent variable and CFI, group association, R-R interval at the end of occlusion, and anterior-to-inferior ventricular curvature radius ratio as independent variables. Values are means ± SD, unless otherwise indicated.
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RESULTS
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Patient Characteristics and Clinical Data at Baseline
There were no statistically significant differences between the two groups regarding age, gender, body mass index, angina pectoris class and duration, and frequency of cardiovascular risk factors and use of cardiovascular drugs (Table 1).
Coronary Angiographic Data
The number of diseased coronary arteries was similar in both groups (Table 2). In accordance with the definition of the study groups, the vessels undergoing PCI, as well as CFI and intracoronary ECG measurements, were different between the LCA and RCA group. The vascular location where PCI was performed was similar between the groups. Quantitatively, the stenosis location in each of the three main coronary arteries (LAD, LCX, and RCA) was 68 and 63% proximal in the LCA and RCA groups, respectively, where 100% proximity indicates ostial stenosis location (Table 2). Percent diameter stenosis was not statistically different between the groups.
Hemodynamic, Ventriculographic, CFI, and ECG Data
Heart rate, LV ejection fraction, and blood pressure before coronary occlusion were similar between the groups (Table 3). In the LCA and RCA groups, anterior LV wall curvature was 9–15% larger than inferior wall curvature. Individually, anterior LV wall curvature radius was significantly larger than the respective inferior radius (P = 0.004 by paired t-test). Pressure parameters for the calculation of CFI, as well as CFI obtained at 120 s of coronary occlusion, were not significantly different between the groups (Table 3). Absolute values of intracoronary ECG S-T segment elevation, as well as values corrected for R wave amplitude, were higher in the LCA than in the RCA group (Fig. 3, Table 3). The average maximal R wave amplitude remained flat after 30–40 s of coronary occlusion in both groups. In all study patients, at least one of the three peripheral ECG leads showed similar S-T segment changes during coronary occlusion, concordant or discordant to those obtained via the intracoronary ECG lead. The R-R interval near the end of the 120-s occlusion was significantly shorter in the LCA than in the RCA group (Table 3). There was a significant inverse relation between CFI and intracoronary ECG S-T segment elevation (Fig. 4). However, for absolute and relative intracoronary ECG S-T segment elevation, this relation was less steep for the LCA group than for the RCA group (Fig. 4). By multiple regression analysis, the following variables were independent predictors of intracoronary ECG S-T segment elevation corrected for R wave amplitude: CFI (P = 0.0002), LCA or RCA group association (P = 0.002), and R-R interval at 120 s of occlusion (P = 0.02). Anterior-to-inferior LV wall curvature radius (P = 0.12) was not an independent predictor.
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DISCUSSION
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The novel result of this study in patients with chronic stable angina pectoris is that, after all known determinants of infarct size are taken into account, susceptibility to ischemia is greater in the LCA than in the RCA region.
Variably Vulnerable Myocardial Areas
Artificial reasons.
Before false causes for regional differences in myocardial ischemic tolerance are examined, the following issues concerning the reliability of the ECG as a gauge for ischemia must be considered: 1) Does ECG S-T segment elevation reflect potential IS? More than 30 years ago, Maroko and co-workers (14) proposed a direct relation between the degree of S-T segment elevation and the magnitude of ischemic injury in a given heart. Experimental studies in rabbits have documented that a reduction of normalized ECG S-T segment elevation by ischemic preconditioning from 1 to 0.625 is associated with a decrease in IS from 38 to 8% of the ischemic AR (1, 6). 2) Is the ECG electrode location representative for the myocardial area of interest? Friedman et al. (9) demonstrated that myocardial ischemia during percutaneous transluminal coronary angioplasty can be detected with greater sensitivity by intracoronary ECG than by surface ECG (9). 3) Is the time of coronary occlusion sufficient to fully manifest ischemia? It has been indicated in human studies on ischemic preconditioning that vascular occlusion for 90–120 s is effective in decreasing S-T segment deviation during subsequent bouts of ischemia (2).
In this context, recent clinical evidence that "tombstoning" ECG pattern was more strongly associated with acute anterior than inferior infarction could be interpreted as supportive of our study results (13). However, it is probably the more extensive myocardial territory (i.e., AR) being supplied by the LAD than the particular anterior site that explains the huge S-T segment elevations. The findings of the present study support but also amend this notion by showing that, after normalization of S-T segment elevation for the respective R amplitude, the variable S-T segment shift is much smaller but does not disappear (Fig. 3). Thus variable ECG signs of myocardial ischemia in the LCA and RCA regions are partly artificial with regard to the site of ischemia. This may also serve to illustrate that direct measurement of or correction for all the determinants of S-T segment elevation or IS, as in the present study, is mandatory for interpretation of the contribution of each variable to the manifest sign of ischemia. Because the relevance of coronary occlusion time to ischemic injury is unequivocal, we accounted for it by keeping it constant at 120 s. As indicated, correction for AR was accomplished by normalization of S-T segment elevation for R amplitude. In addition, the proximity of the stenosis undergoing PCI was quantitatively determined, and by documenting similarity among the groups in this AR parameter, an influence of AR on the study results was excluded. Because variable collateral supply to an occluded coronary vascular region has a very powerful influence on ECG signs of ischemia (5), CFI was directly measured in the present study. Therefore, an uncertain effect of collateral flow on the study findings can be excluded.
Natural reasons.
Simultaneous measurement of CFI has allowed a view of site-specific ischemic vulnerability that is different from temporal S-T segment elevation during occlusion (Fig. 3). The influence of collateral supply on the S-T segment elevation at 120 s of occlusion is less pronounced in the LCA than in the RCA region (Fig. 4); i.e., ischemia in the LCA area is diminished less by a given collateral flow, and, therefore, the LCA territory is genuinely more vulnerable to ischemia than the RCA region. How can that be interpreted on the basis of evidence from the literature and the results of the present study? Site-specific myocardial perfusion variability is well known, even from human studies (4, 23). Absolute blood supply during vessel patency has been consistently found to be higher in the anterior than in the inferior territory: 0.88 and 0.76 ml·min–1·g–1, respectively (23). Ghaleh and co-workers (10) found in baboons that regional heterogeneity of myocardial perfusion foretells salvage during reperfusion; i.e., infarcted tissue regions demonstrated higher preocclusion blood flow than salvaged myocardial areas. Higher vulnerability to ischemia of territories with augmented myocardial perfusion has been explained by the local level of flow-metabolism matching; i.e., high-flow sample sites exhibit a higher oxidative metabolism than low-flow sample sites (7). In addition, regional differences of myocardial ischemic tolerance have been elucidated by variable myocardial perfusion distances (19). That particular aspect was not investigated in the present study; however, in a recent study from our laboratory, no difference in contrast-echo-derived relative myocardial blood volume could be found between the anterior and inferior wall (0.164 and 0.160, respectively) or between those sites and the septal wall (0.110) (23).
Among the study groups, a number of other factors that have been described to modulate regional perfusion and directly influence myocardial tolerance to ischemia could potentially be mismatched: gender, cardiovascular drugs (e.g., 
-blockers), presence of myocardial preconditioning, LV wall stress, and site-variable neural reaction to ischemia (4, 17). No statistical group differences were observed in gender frequency or use of cardiovascular drugs. The study was designed to control for the influence of ischemic preconditioning by including only patients with exercise-induced angina pectoris and by analyzing the first of possibly several coronary occlusions during PCI. Measurement of one of the factors determining LV wall stress, curvature radius of the wall, revealed it to be 
10% higher anteriorly than inferiorly, which is in agreement with data on finite-element analysis of local LV wall stress (11). However, this variable did not independently influence site-specific signs of myocardial ischemia. It is a limitation of the present study that anterior and inferior LV wall thicknesses were not directly obtained but were assumed to be equal and, thus, not to influence LV wall stress. Also, the third determinant of wall stress, LV pressure, was not measured during coronary occlusion; thus, uneven influence among the groups of this variable during diastole on the study findings cannot be excluded. Furthermore, we could not account for a potential influence on myocardial O2 supply of the thebesian venous system, which is more pronounced in the right ventricle than in the LV. Finally, there is evidence from the present study that the parasympathetic response to ischemia is site specific and more pronounced during inferior than anterior ischemia, which explains, in part, the variable ECG response to coronary occlusion.
Study Limitations
In addition to the above-described limitations of not measuring LV filling pressure and LV wall thicknesses during coronary occlusion, we may have overcorrected for AR by normalizing S-T segment elevation for the respective R wave amplitude, in addition to determining the angiographic stenosis proximity index. However, with regard to the study hypothesis, such an overcorrection would be a conservative measure; i.e., detected differences in ischemia between the LCA and the RCA would be more important with than without the correction.
On the basis of the results presented in Fig. 3, it could be speculated that the site-specific S-T segment elevation curves may have separated even further if coronary occlusion had been prolonged over 120 s. For ethical reasons, such a procedure has not been performed.
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GRANTS
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This work was supported by Swiss National Science Foundation Grant 3200BO-100065/1.
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FOOTNOTES
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Address for reprint requests and other correspondence: C. Seiler, Dept. of Cardiology, Univ. Hospital, CH-3010 Bern, Switzerland (e-mail: christian.seiler{at}insel.ch)
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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Copyright © 2006 by the American Physiological Society.
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ABSTRACT
METHODS
LCA (r = 0.5, P = 0.003), CFI = 0.40 – 2.2ST