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Understanding the dynamic electrocardiographic changes that occur during ischemia
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Journal of Electrocardiology 41 (2008) 431 – 432 www.jecgonline.com
Editorial
Understanding the dynamic electrocardiographic changes that occur during ischemia The main concepts and terminology that have been used to describe and explain the changes seen on the surface 12-lead electrocardiogram (ECG) were conceived many years ago. At those times, we lacked understanding of the pathophysiology of ischemia, and we did not have sophisticated imaging tools to test these hypotheses. In this respect, electrocardiography has had many similarities with alchemistry, as intelligent and knowledgeable scholars contemplated and generated hypotheses and concepts that were hard to prove or disprove. In the traditional electrocardiographic nomenclature, changes in the T waves reflect ischemia. ST elevation reflects “injury,” whereas ST depression reflects ischemia. Changes in the QRS, especially in its initial portion, were considered to reflect irreversible damage or infarction. However, acute ischemia may induce simultaneous changes in all segments, including the P wave, PR segment, QRS, ST segment, T wave, and U wave. These acute changes may further evolve or disappear, depending on the severity and duration of ischemia and the nature of reperfusion. The magnitude and direction of these changes depend on the size and location of the myocardium supplied by the occluded coronary artery. Moreover, the magnitude of these changes is dependent on the “severity” of ischemia, which is affected by the presence of residual myocardial perfusion via collateral vessels or incomplete (or intermittent) occlusion of the culprit artery and metabolic factor such as ischemic or pharmacologic preconditioning. In addition, presence of concomitant stenoses in other arteries or scars in remote zones of the heart may affect the magnitude and direction of these dynamic electrocardiographic changes. To analyze these multiple changes, investigators have tried to concentrate on one or more variables (such as the QRS, ST segments, or T waves) while ignoring others. On the other hand, some investigators have used “patterns” or “scores” that include simultaneous changes in several segments of the ECG complexes.1,2 Another approach to simplify the analyses is to concentrate on a specific subgroup of patients (single vessel disease without prior myocardial infarction, left anterior descending disease, etc). With this approach, the findings are limited to this particular subgroup and may not apply to the general population. For example, criteria to differentiate right coronary artery occlusion from left circumflex artery occlusion that were studied in patients with first ST-elevation myocardial infarction who had a 0022-0736/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2008.02.024
single artery lesion may not apply to the general population presenting with ST-segment elevation in the inferior leads. In the present issue of the journal, Sinno et al3 explored the mechanisms of changes in the R wave amplitude during acute ischemia. The investigators studied 50 patients with single-vessel coronary artery disease undergoing percutaneous coronary interventions. A total of 20 patients had a left anterior descending artery lesion, 14 left circumflex artery lesion, and 16 right coronary artery lesion. The investigators have initially chosen to analyze the magnitude of R wave amplitude changes in each lead for the group as a whole and found that the increase in mean R wave amplitude reached statistical significance in limb leads I, II, aVL and leads V2V6. The increase in mean R wave amplitude was higher in leads V3-V6 when compared with the other precordial or limb leads. In a secondary analysis, they found that the mean R wave amplitude increased more in the inferior leads in patients who had occlusion of the right coronary artery and in leads I, aVL, V5, and V6 when the left circumflex artery was occluded. Thus, it is plausible that the changes in R wave amplitude match the changes in ST amplitude; however, the investigators do not report on the ST changes. This type of analysis clearly demonstrates the difficulties in analyzing these diverse changes as a group. It is plausible that the magnitude and direction of the changes in R wave amplitude are completely different for proximal right coronary artery occlusion and right posterior descending occlusion. If indeed the changes in R wave amplitude resemble changes in the ST segment, lumping all left circumflex artery occlusion together may be wrong. For example, occlusion of a proximal nondominant left circumflex artery before the first marginal branch causes ST elevation in leads I and aVL with ST depression in lead V2, whereas distal occlusion of a dominant left circumflex artery may cause ST elevation in the inferior leads with reciprocal ST depression in leads I and aVL. To account for all possible subgroups, a much larger cohort of patients is needed. Using similar methods for exploring the significance of ST elevation in the various leads during acute ischemia, one may conclude that statistically significant ST elevation does not occur in lead aVL because patients with right coronary artery occlusion or distal left circumflex artery occlusion may have ST depression in aVL, whereas those with proximal left anterior descending artery or proximal left circumflex artery
432
Editorial / Journal of Electrocardiology 41 (2008) 431–432
occlusion may have ST elevation in this lead. Using simple averages for the ST segment for the whole group would have missed the above-mentioned findings. If indeed changes in the R wave amplitude match changes in the ST segment, is ST segment depression associated with decrease in R wave amplitude? On the other hand, can it be that in some cases the changes in the R wave amplitude and the ST segment will not match? For example, I have described that in the rabbit, ST-segment elevation can be seen in the early stages of both coronary artery occlusion and reperfusion.4 ST-segment elevation during reperfusion could be distinguished from the ischemic episodes by the prompt decline in the R wave amplitude in the former compared with no change or increase in the latter.4 Interestingly, the authors found that left anterior descending artery occlusion did not induce increase in R wave amplitude in leads traditionally considered showing ST elevation during its occlusion (V1-V4). Although statistics are not provided, right coronary artery occlusion caused a greater increase in R wave amplitude in lead V1 than left anterior descending or left circumflex artery occlusion. In contrast, left circumflex artery occlusion caused a greater increase in R wave amplitude in lead V2 than either left anterior descending or right coronary artery occlusion. The increase in R wave amplitude in lead V3 was the smallest in the left anterior descending artery group. These findings are disconcordant to our current understanding and may be the result of the small number of patients in each group and the heterogeneity within each group (proximal vs distal occlusion, number and size of side branches and the dominancy of the other coronary arteries). Alternatively, can it be that these changes occur during the terminal part of the QRS, thus seen only in leads with qR configuration? In leads with rS configuration (usually V1-V3), the R wave occurs in the initial part of the QRS. Can it be that similar changes in these leads are manifested as shortening of the S wave? Four patients underwent intracoronary ECG during procedure (1 patient with left circumflex, 1 with right coronary artery, and 2 with left anterior descending lesion). R wave amplitude increased during balloon occlusion in 3 patients. It is not stated who were the patients with the increase (left vs right coronary artery occlusion?). In Table 4,
the investigators are summarizing the changes in the surface ECG and the intracoronary ECG. Again, it is difficult to draw conclusions from this table because the 4 patients had lesions in different arteries. The investigators conclude that as the magnitude of R wave increased also in the intracoronary ECG, the explanation for the observed changes in the R wave amplitude is evasion of canceling vectors due to regional changes in conductance. The clinical implications of the changes in the R wave amplitude should be further investigated. Are these changes more sensitive or specific for ischemia than changes in the ST segment and T waves for monitoring ischemia? Are these changes having additional prognostic or therapeutic implications? Do the combination of R wave and ST monitoring have an advantage over the traditional ST monitoring? Are the changes in the R wave amplitude specific for ischemia? For example, changes in body positioning may change R wave amplitude. A good example is T wave amplitude. Although it is clear that acute ischemia may cause either ST depression with T wave inversion or increase in the amplitude of the T wave (tall peaked T waves), the large variations in T wave amplitude in normal subjects limits the use of T wave for detecting ischemia. Yochai Birnbaum, MD The Division of Cardiology University of Texas Medical Branch Galveston, TX, USA References 1. Barbagelata A, Di Carli MF, Califf RM, et al. Electrocardiographic infarct size assessment after thrombolysis: insights from the Acute Myocardial Infarction STudy ADenosine (AMISTAD) trial. Am Heart J 2005;150:659. 2. Birnbaum Y, Ware DL. Electrocardiogram of acute ST-elevation myocardial infarction: the significance of the various “scores”. J Electrocardiol 2005; 38:113. 3. Sinno MCN, Kowalski M, Kenigsberg DN, Krishnan SC, Khanal S. Rwave amplitude changes measured by electrocardiography during early transmural ischemia. J Electrocardiol 2008;41:425. 4. Birnbaum Y, Hale SL, Kloner RA. Changes in R wave amplitude: ECG differentiation between episodes of reocclusion and reperfusion associated with ST-segment elevation. J Electrocardiol 1997;30:211.
Journal of Electrocardiology 41 (2008) 431 – 432 www.jecgonline.com
Editorial
Understanding the dynamic electrocardiographic changes that occur during ischemia The main concepts and terminology that have been used to describe and explain the changes seen on the surface 12-lead electrocardiogram (ECG) were conceived many years ago. At those times, we lacked understanding of the pathophysiology of ischemia, and we did not have sophisticated imaging tools to test these hypotheses. In this respect, electrocardiography has had many similarities with alchemistry, as intelligent and knowledgeable scholars contemplated and generated hypotheses and concepts that were hard to prove or disprove. In the traditional electrocardiographic nomenclature, changes in the T waves reflect ischemia. ST elevation reflects “injury,” whereas ST depression reflects ischemia. Changes in the QRS, especially in its initial portion, were considered to reflect irreversible damage or infarction. However, acute ischemia may induce simultaneous changes in all segments, including the P wave, PR segment, QRS, ST segment, T wave, and U wave. These acute changes may further evolve or disappear, depending on the severity and duration of ischemia and the nature of reperfusion. The magnitude and direction of these changes depend on the size and location of the myocardium supplied by the occluded coronary artery. Moreover, the magnitude of these changes is dependent on the “severity” of ischemia, which is affected by the presence of residual myocardial perfusion via collateral vessels or incomplete (or intermittent) occlusion of the culprit artery and metabolic factor such as ischemic or pharmacologic preconditioning. In addition, presence of concomitant stenoses in other arteries or scars in remote zones of the heart may affect the magnitude and direction of these dynamic electrocardiographic changes. To analyze these multiple changes, investigators have tried to concentrate on one or more variables (such as the QRS, ST segments, or T waves) while ignoring others. On the other hand, some investigators have used “patterns” or “scores” that include simultaneous changes in several segments of the ECG complexes.1,2 Another approach to simplify the analyses is to concentrate on a specific subgroup of patients (single vessel disease without prior myocardial infarction, left anterior descending disease, etc). With this approach, the findings are limited to this particular subgroup and may not apply to the general population. For example, criteria to differentiate right coronary artery occlusion from left circumflex artery occlusion that were studied in patients with first ST-elevation myocardial infarction who had a 0022-0736/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2008.02.024
single artery lesion may not apply to the general population presenting with ST-segment elevation in the inferior leads. In the present issue of the journal, Sinno et al3 explored the mechanisms of changes in the R wave amplitude during acute ischemia. The investigators studied 50 patients with single-vessel coronary artery disease undergoing percutaneous coronary interventions. A total of 20 patients had a left anterior descending artery lesion, 14 left circumflex artery lesion, and 16 right coronary artery lesion. The investigators have initially chosen to analyze the magnitude of R wave amplitude changes in each lead for the group as a whole and found that the increase in mean R wave amplitude reached statistical significance in limb leads I, II, aVL and leads V2V6. The increase in mean R wave amplitude was higher in leads V3-V6 when compared with the other precordial or limb leads. In a secondary analysis, they found that the mean R wave amplitude increased more in the inferior leads in patients who had occlusion of the right coronary artery and in leads I, aVL, V5, and V6 when the left circumflex artery was occluded. Thus, it is plausible that the changes in R wave amplitude match the changes in ST amplitude; however, the investigators do not report on the ST changes. This type of analysis clearly demonstrates the difficulties in analyzing these diverse changes as a group. It is plausible that the magnitude and direction of the changes in R wave amplitude are completely different for proximal right coronary artery occlusion and right posterior descending occlusion. If indeed the changes in R wave amplitude resemble changes in the ST segment, lumping all left circumflex artery occlusion together may be wrong. For example, occlusion of a proximal nondominant left circumflex artery before the first marginal branch causes ST elevation in leads I and aVL with ST depression in lead V2, whereas distal occlusion of a dominant left circumflex artery may cause ST elevation in the inferior leads with reciprocal ST depression in leads I and aVL. To account for all possible subgroups, a much larger cohort of patients is needed. Using similar methods for exploring the significance of ST elevation in the various leads during acute ischemia, one may conclude that statistically significant ST elevation does not occur in lead aVL because patients with right coronary artery occlusion or distal left circumflex artery occlusion may have ST depression in aVL, whereas those with proximal left anterior descending artery or proximal left circumflex artery
432
Editorial / Journal of Electrocardiology 41 (2008) 431–432
occlusion may have ST elevation in this lead. Using simple averages for the ST segment for the whole group would have missed the above-mentioned findings. If indeed changes in the R wave amplitude match changes in the ST segment, is ST segment depression associated with decrease in R wave amplitude? On the other hand, can it be that in some cases the changes in the R wave amplitude and the ST segment will not match? For example, I have described that in the rabbit, ST-segment elevation can be seen in the early stages of both coronary artery occlusion and reperfusion.4 ST-segment elevation during reperfusion could be distinguished from the ischemic episodes by the prompt decline in the R wave amplitude in the former compared with no change or increase in the latter.4 Interestingly, the authors found that left anterior descending artery occlusion did not induce increase in R wave amplitude in leads traditionally considered showing ST elevation during its occlusion (V1-V4). Although statistics are not provided, right coronary artery occlusion caused a greater increase in R wave amplitude in lead V1 than left anterior descending or left circumflex artery occlusion. In contrast, left circumflex artery occlusion caused a greater increase in R wave amplitude in lead V2 than either left anterior descending or right coronary artery occlusion. The increase in R wave amplitude in lead V3 was the smallest in the left anterior descending artery group. These findings are disconcordant to our current understanding and may be the result of the small number of patients in each group and the heterogeneity within each group (proximal vs distal occlusion, number and size of side branches and the dominancy of the other coronary arteries). Alternatively, can it be that these changes occur during the terminal part of the QRS, thus seen only in leads with qR configuration? In leads with rS configuration (usually V1-V3), the R wave occurs in the initial part of the QRS. Can it be that similar changes in these leads are manifested as shortening of the S wave? Four patients underwent intracoronary ECG during procedure (1 patient with left circumflex, 1 with right coronary artery, and 2 with left anterior descending lesion). R wave amplitude increased during balloon occlusion in 3 patients. It is not stated who were the patients with the increase (left vs right coronary artery occlusion?). In Table 4,
the investigators are summarizing the changes in the surface ECG and the intracoronary ECG. Again, it is difficult to draw conclusions from this table because the 4 patients had lesions in different arteries. The investigators conclude that as the magnitude of R wave increased also in the intracoronary ECG, the explanation for the observed changes in the R wave amplitude is evasion of canceling vectors due to regional changes in conductance. The clinical implications of the changes in the R wave amplitude should be further investigated. Are these changes more sensitive or specific for ischemia than changes in the ST segment and T waves for monitoring ischemia? Are these changes having additional prognostic or therapeutic implications? Do the combination of R wave and ST monitoring have an advantage over the traditional ST monitoring? Are the changes in the R wave amplitude specific for ischemia? For example, changes in body positioning may change R wave amplitude. A good example is T wave amplitude. Although it is clear that acute ischemia may cause either ST depression with T wave inversion or increase in the amplitude of the T wave (tall peaked T waves), the large variations in T wave amplitude in normal subjects limits the use of T wave for detecting ischemia. Yochai Birnbaum, MD The Division of Cardiology University of Texas Medical Branch Galveston, TX, USA References 1. Barbagelata A, Di Carli MF, Califf RM, et al. Electrocardiographic infarct size assessment after thrombolysis: insights from the Acute Myocardial Infarction STudy ADenosine (AMISTAD) trial. Am Heart J 2005;150:659. 2. Birnbaum Y, Ware DL. Electrocardiogram of acute ST-elevation myocardial infarction: the significance of the various “scores”. J Electrocardiol 2005; 38:113. 3. Sinno MCN, Kowalski M, Kenigsberg DN, Krishnan SC, Khanal S. Rwave amplitude changes measured by electrocardiography during early transmural ischemia. J Electrocardiol 2008;41:425. 4. Birnbaum Y, Hale SL, Kloner RA. Changes in R wave amplitude: ECG differentiation between episodes of reocclusion and reperfusion associated with ST-segment elevation. J Electrocardiol 1997;30:211.