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Usefulness of silent subendocardial ischemia detected by ST-segment depression in postmyocardial infarction patients as a predictor of ventricular arrhythmias
ST-Segment Depression in Postmyocardial Predictor of Ventricular Arrhythmias
Patients as a
Infarction
Ana Maria Camacho, MD, Josep Guindo, MD, and Antonio Bay&-de-Luna, MD here is conclusiveexperimental and clinical evidence that severe,transmural and persistentacute ischemia T (silent or symptomatic), the maximum exponentof which
of technetium-99m; each cardiac cycle comprised 21 frames of 740,000 counts each). During Holter electrocardiography, episodes of evident silent myocardial is myocardial infarction, can trigger malignant ventricu- ischemia were defined as those producing ST-segment lar arrhythmias and suddencardiac death.’ Furthermore, depression I1 mm, lasting >l minute, and with an intera relation betweensevereacute transmural but transient val of 1 minute between episodes. For each episode, we ischemia appearing during Prinzmetal’s angina* or dur- also studied periods of 5 minutes before and after STing percutaneoustransluminal angioplasty3and ventricu- segment depression, and considered these to be periods lar arrhythmias is well known, although such arrhyth- of probable silent ischemia. We wanted to determine mias are rarely malignant. However, the relation between whether the incidence of ventricular arrhythmias during ventricular arrhythmias and subendocardialischemia (si- these periods is greater than that during control periods lent or symptomatic) has only beenpartially studied, and (without ischemia). Global silent ischemia was defined results are contradictory.4-7 as the sum of evident and probable silent ischemia. To determine whether there is a clear relation beOf the 70 postmyocardial patients studied, 21 pretween episodes of silent myocardial ischemia detected by sented with silent myocardial ischemia by Holter elecHolter electrocardiography and ventricular arrhythtrocardiography (30%). In all, we recorded 113 episodes mias, we prospectively studied 70 consecutive postmyoof ST-segment depression 110 (97.3%) were silent, and cardial infarction patients (65 men and 5 women, aged only 3 (2.7%) (all occurring in 1 patient) were symptom<7.5 years, mean 54 f IO). The infarction involved the atic. During 643 hours and 54 minutes of Holter monianterior wall in 28 cases (40%), inferior wall in 38 (54%) toring, we recorded 601 hours and 20 minutes without and was non-Q-wave in 4 (6%). No patient had other ischemia, 24 hours and 18 minutes of evident silent ischassociated heart disease. No patient was an insulin-deemia, and 18 hours and 10 minutes of probable silent pendent diabetic, nor did any have arterial hypertension ischemia (42 hours and 28 minutes of global silent ischemia) . or other disease-producing alterations in the STsegment on baseline electrocardiogram. The duration of 110 episodes of silent myocardial Ten to 20 days after the acute phase of myocardial ischemia ranged between 1 and 51 minutes (mean 11.9 f infarction, all patients in the study underwent Holter 9.4). ST-segment depression ranged from 1 to 2.5 mm electrocardiography (24 to 48 hours of recording) (Ni(mean 1.2 f 2.4). Ventricular premature complexes aphon-Kohden 3-channel model, DMC-3OOOK, Tokyo, Ja- peared in 19 of the 110 events (17.2%). TableZshows the pan), exercise testing (modified Bruce protocol) and iso- incidence of ventricular arrhythmias during periods of topic ventriculography (Gammacamera GE-Maxi con- evident, probable and global ischemia, and without ischnected in line with a digital Gamma-II; images were emia. There were no signij?cant differences between obtained after in vivo red blood cell labeling with 20 mCi groups. Furthermore, we found no statistically significant differences between episodes with and without ventricular arrhythmias regarding duration of events, heart From the Department of Cardiology and Cardiac Surgery, Hospital de rate and ST-segment depression. Although ventricular la Santa Creu i Sant Pau, Universidad Aut6noma de Barcelona,Avda. premature complexes were more frequent in patients San Antonio Maria Claret, 167, Barcelona 08025, Spain. This work with (309 f 776124 hours) than in those without (116 f was supported in part by FISS Grant 900518 from the “Fond0 de Investigacibn de la Seguridad Social,” Madrid, Spain. Manuscript re- 313124 hours) silent myocardial ischemia, differences ceived September 18, 1991;revised manuscript received and accepted were not statistically significant. The percentage of paJanuary 3, 1992. tients with frequent ventricular premature complexes
TABLE I Relation Holter Monitoring
Between
Silent lschemia Absent Present Probable Global
Silent Myocardial
lschemia
and Ventricular
Time 601 24 18 42
hours, hours, hours, hours,
20 18 10 28
VPC minutes minutes minutes minutes
6,400 176 339 515
= = = =
10.64 7.33 18.80 12.20
Arrhythmias
in
Couplets and Runs x hour x hour x hour x hour
48 2 2 4
= = = =
0.07 0.08 0.11 0.10
x x x x
hour hour hour hour
VPC = ventricular premature complexes.
BRIEF REPORTS
1243
(L 1O/hour) or complex ventricular arrhythmias (pairs or salvos) was similar in both groups. Twenty-eight patients presented with ST-segment depression II mm during exercise testing. Mean STsegmentdepressionwas 1.8 mm (range 1 to 3.5 mm). In 1I patients, ST deviation was accompaniedby angina. Ventricular arrhythmias were present in 13 patients (I 9%); 7 of 42 (17%) without ST-segment depression,2 of 11 (18?&) with angina and ST-segment depression, and 4 of 17 (24%) with ST-segment depressionwithout angina (p = not significant). The mean ejectionfraction for all patients was 43%, and no differences were observedbetweenthosewith and without ischemia,or those with silent and symptomatic ischemia. There are contradictory results regarding the association of silent ischemia and ventricular arrhythmias in patients with stable coronary artery disease.Although a relation betweenthe 2 was reported in studiesby Stern et al4 and Carboni et aL5 studies by Hausmann et al6 and Graboys et al7appearto indicate the contrary. In patients with malignant ventricular arrhythmias, Gomes et al* and Bayb de Luna et al9 were not able to demonstrate that silent ischemia had an important role in triggering such arrhythmias. However, ST-segmentalterations suggestive of myocardial ischemia have been found in approximately onethird of patients who died suddenlywhile undergoing Holter monitoring.9J0Our study differs from those published to date in that all our patients had a recent myocardial infarction with a moderatelydepressed ventricular function (mean ejection fraction 43%). We conclude that in this selectedgroup of postmyo cardial infarction patients with moderateleft ventricular dysfunction, silent subendocardial ischemia (defined as ST-segment depressionbetween 1 and 2.5 mm) is not accompaniedby an increasein ventricular arrhythmias. However, the high-density ventricular arrhythmias dur-
1244
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
69
ing nonischemic periods suggestthat postinfarction patients have a global mechanism for arrhythmias, which may mask the relation of silent ischemia to arrhythmias. It remains unclear whether more severesubendocardial ischemia is associatedwith ventricular arrhythmias. As with Prinzmetal angina,2 in which a clear association between the degreeof ST elevation and ventricular arrhythmias has beendemonstrated,a correlation between the degreeof ST depressionand the incidenceof ventricular arrhythmias may be possiblein subendocardialischemia. Further studiesshould be performed to investigate this possibility.
1. Kannel W, Cupples L, D’Agostino R. Sudden death risk in overt coronary heart disease: the Framingham Study. Am Hearf J 1987;113:799-804. 2. Bay& de Luna A, Carreras F, Cladellas M, Oca F, Sages F, Garcia Moll M. Holter ECG study of the electrocardiographic phenomena in Prinzmetal angina attacks with emphasis on the study of ventricular arrhythmias. J Electrocardiol 1985;18:267-276. 3. Meinertz T, Zehender M, Hohnloser S, Just H. Prevalence of ventricular arrhvthmias during silent mvocardial &hernia. Cardiwasc Reu & Reo 1988: (suppl):34-38. 4. Stem S, Banai S, Keren A, Tzivoni D. Ventricular ectopic activity during ischemia episodes in ambulatory patients. Am J Cardiol 1990;65:412-416. 5. Carboni GP, Lahiri A, Cashman PMM, Raftery EB. Mechanisms of arrhythmias accompanying ST-segment depression on ambulatory monitoring in stable angina pwtoris. Am J Cardiol 1987;60:124t-1253. 6. Hausmann D, Nikutta P, Trappe HJ, Daniel WG, Wenzlaff P, Lichtlen PR. Incidence of ventricular arrhythmias during transient myocardial ischemia in patients with stable coronary artery disease. J Am Coil Cardiol 1990;16:49-54. 7. Graboys TB, Stein Im, Cueni L, Lampert S, Low B. Is the presence of silent ischemia associated with the provocation of ventricular arrhythmias? (at&r) Circulation 1987;76:IV-365. (1. Games JA, Alexopodlos D, Winters SL, Deshmukb P, Fuster V, Suh K. The role of silent &hernia, the arrhythmic substrate and the short-long sequence in the genesis of sudden cardiac death. J Am Coil Cardiol 1989;14:1618-1625. 9. Bayb de Luna A, Coumel P, Leclercq JF. Ambulatory sudden cardiac death: mechanisms of production of fatal arrhythmia on the basis of data from 157 cases. Am Heart J 1989;117:151-157. 10. Pepine CJ, Gottlieb SO, Morganroth J. Ambulatory ischemia and sudden death: an analysis of 35 cases of death during ambulatory minitoring (abstr). J Am CON Cardiol 1991;17:63A.
MAY 1, 1992
Patients as a
Infarction
Ana Maria Camacho, MD, Josep Guindo, MD, and Antonio Bay&-de-Luna, MD here is conclusiveexperimental and clinical evidence that severe,transmural and persistentacute ischemia T (silent or symptomatic), the maximum exponentof which
of technetium-99m; each cardiac cycle comprised 21 frames of 740,000 counts each). During Holter electrocardiography, episodes of evident silent myocardial is myocardial infarction, can trigger malignant ventricu- ischemia were defined as those producing ST-segment lar arrhythmias and suddencardiac death.’ Furthermore, depression I1 mm, lasting >l minute, and with an intera relation betweensevereacute transmural but transient val of 1 minute between episodes. For each episode, we ischemia appearing during Prinzmetal’s angina* or dur- also studied periods of 5 minutes before and after STing percutaneoustransluminal angioplasty3and ventricu- segment depression, and considered these to be periods lar arrhythmias is well known, although such arrhyth- of probable silent ischemia. We wanted to determine mias are rarely malignant. However, the relation between whether the incidence of ventricular arrhythmias during ventricular arrhythmias and subendocardialischemia (si- these periods is greater than that during control periods lent or symptomatic) has only beenpartially studied, and (without ischemia). Global silent ischemia was defined results are contradictory.4-7 as the sum of evident and probable silent ischemia. To determine whether there is a clear relation beOf the 70 postmyocardial patients studied, 21 pretween episodes of silent myocardial ischemia detected by sented with silent myocardial ischemia by Holter elecHolter electrocardiography and ventricular arrhythtrocardiography (30%). In all, we recorded 113 episodes mias, we prospectively studied 70 consecutive postmyoof ST-segment depression 110 (97.3%) were silent, and cardial infarction patients (65 men and 5 women, aged only 3 (2.7%) (all occurring in 1 patient) were symptom<7.5 years, mean 54 f IO). The infarction involved the atic. During 643 hours and 54 minutes of Holter monianterior wall in 28 cases (40%), inferior wall in 38 (54%) toring, we recorded 601 hours and 20 minutes without and was non-Q-wave in 4 (6%). No patient had other ischemia, 24 hours and 18 minutes of evident silent ischassociated heart disease. No patient was an insulin-deemia, and 18 hours and 10 minutes of probable silent pendent diabetic, nor did any have arterial hypertension ischemia (42 hours and 28 minutes of global silent ischemia) . or other disease-producing alterations in the STsegment on baseline electrocardiogram. The duration of 110 episodes of silent myocardial Ten to 20 days after the acute phase of myocardial ischemia ranged between 1 and 51 minutes (mean 11.9 f infarction, all patients in the study underwent Holter 9.4). ST-segment depression ranged from 1 to 2.5 mm electrocardiography (24 to 48 hours of recording) (Ni(mean 1.2 f 2.4). Ventricular premature complexes aphon-Kohden 3-channel model, DMC-3OOOK, Tokyo, Ja- peared in 19 of the 110 events (17.2%). TableZshows the pan), exercise testing (modified Bruce protocol) and iso- incidence of ventricular arrhythmias during periods of topic ventriculography (Gammacamera GE-Maxi con- evident, probable and global ischemia, and without ischnected in line with a digital Gamma-II; images were emia. There were no signij?cant differences between obtained after in vivo red blood cell labeling with 20 mCi groups. Furthermore, we found no statistically significant differences between episodes with and without ventricular arrhythmias regarding duration of events, heart From the Department of Cardiology and Cardiac Surgery, Hospital de rate and ST-segment depression. Although ventricular la Santa Creu i Sant Pau, Universidad Aut6noma de Barcelona,Avda. premature complexes were more frequent in patients San Antonio Maria Claret, 167, Barcelona 08025, Spain. This work with (309 f 776124 hours) than in those without (116 f was supported in part by FISS Grant 900518 from the “Fond0 de Investigacibn de la Seguridad Social,” Madrid, Spain. Manuscript re- 313124 hours) silent myocardial ischemia, differences ceived September 18, 1991;revised manuscript received and accepted were not statistically significant. The percentage of paJanuary 3, 1992. tients with frequent ventricular premature complexes
TABLE I Relation Holter Monitoring
Between
Silent lschemia Absent Present Probable Global
Silent Myocardial
lschemia
and Ventricular
Time 601 24 18 42
hours, hours, hours, hours,
20 18 10 28
VPC minutes minutes minutes minutes
6,400 176 339 515
= = = =
10.64 7.33 18.80 12.20
Arrhythmias
in
Couplets and Runs x hour x hour x hour x hour
48 2 2 4
= = = =
0.07 0.08 0.11 0.10
x x x x
hour hour hour hour
VPC = ventricular premature complexes.
BRIEF REPORTS
1243
(L 1O/hour) or complex ventricular arrhythmias (pairs or salvos) was similar in both groups. Twenty-eight patients presented with ST-segment depression II mm during exercise testing. Mean STsegmentdepressionwas 1.8 mm (range 1 to 3.5 mm). In 1I patients, ST deviation was accompaniedby angina. Ventricular arrhythmias were present in 13 patients (I 9%); 7 of 42 (17%) without ST-segment depression,2 of 11 (18?&) with angina and ST-segment depression, and 4 of 17 (24%) with ST-segment depressionwithout angina (p = not significant). The mean ejectionfraction for all patients was 43%, and no differences were observedbetweenthosewith and without ischemia,or those with silent and symptomatic ischemia. There are contradictory results regarding the association of silent ischemia and ventricular arrhythmias in patients with stable coronary artery disease.Although a relation betweenthe 2 was reported in studiesby Stern et al4 and Carboni et aL5 studies by Hausmann et al6 and Graboys et al7appearto indicate the contrary. In patients with malignant ventricular arrhythmias, Gomes et al* and Bayb de Luna et al9 were not able to demonstrate that silent ischemia had an important role in triggering such arrhythmias. However, ST-segmentalterations suggestive of myocardial ischemia have been found in approximately onethird of patients who died suddenlywhile undergoing Holter monitoring.9J0Our study differs from those published to date in that all our patients had a recent myocardial infarction with a moderatelydepressed ventricular function (mean ejection fraction 43%). We conclude that in this selectedgroup of postmyo cardial infarction patients with moderateleft ventricular dysfunction, silent subendocardial ischemia (defined as ST-segment depressionbetween 1 and 2.5 mm) is not accompaniedby an increasein ventricular arrhythmias. However, the high-density ventricular arrhythmias dur-
1244
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
69
ing nonischemic periods suggestthat postinfarction patients have a global mechanism for arrhythmias, which may mask the relation of silent ischemia to arrhythmias. It remains unclear whether more severesubendocardial ischemia is associatedwith ventricular arrhythmias. As with Prinzmetal angina,2 in which a clear association between the degreeof ST elevation and ventricular arrhythmias has beendemonstrated,a correlation between the degreeof ST depressionand the incidenceof ventricular arrhythmias may be possiblein subendocardialischemia. Further studiesshould be performed to investigate this possibility.
1. Kannel W, Cupples L, D’Agostino R. Sudden death risk in overt coronary heart disease: the Framingham Study. Am Hearf J 1987;113:799-804. 2. Bay& de Luna A, Carreras F, Cladellas M, Oca F, Sages F, Garcia Moll M. Holter ECG study of the electrocardiographic phenomena in Prinzmetal angina attacks with emphasis on the study of ventricular arrhythmias. J Electrocardiol 1985;18:267-276. 3. Meinertz T, Zehender M, Hohnloser S, Just H. Prevalence of ventricular arrhvthmias during silent mvocardial &hernia. Cardiwasc Reu & Reo 1988: (suppl):34-38. 4. Stem S, Banai S, Keren A, Tzivoni D. Ventricular ectopic activity during ischemia episodes in ambulatory patients. Am J Cardiol 1990;65:412-416. 5. Carboni GP, Lahiri A, Cashman PMM, Raftery EB. Mechanisms of arrhythmias accompanying ST-segment depression on ambulatory monitoring in stable angina pwtoris. Am J Cardiol 1987;60:124t-1253. 6. Hausmann D, Nikutta P, Trappe HJ, Daniel WG, Wenzlaff P, Lichtlen PR. Incidence of ventricular arrhythmias during transient myocardial ischemia in patients with stable coronary artery disease. J Am Coil Cardiol 1990;16:49-54. 7. Graboys TB, Stein Im, Cueni L, Lampert S, Low B. Is the presence of silent ischemia associated with the provocation of ventricular arrhythmias? (at&r) Circulation 1987;76:IV-365. (1. Games JA, Alexopodlos D, Winters SL, Deshmukb P, Fuster V, Suh K. The role of silent &hernia, the arrhythmic substrate and the short-long sequence in the genesis of sudden cardiac death. J Am Coil Cardiol 1989;14:1618-1625. 9. Bayb de Luna A, Coumel P, Leclercq JF. Ambulatory sudden cardiac death: mechanisms of production of fatal arrhythmia on the basis of data from 157 cases. Am Heart J 1989;117:151-157. 10. Pepine CJ, Gottlieb SO, Morganroth J. Ambulatory ischemia and sudden death: an analysis of 35 cases of death during ambulatory minitoring (abstr). J Am CON Cardiol 1991;17:63A.
MAY 1, 1992