- Email: [email protected]
Frequency of silent myocardial ischemia following coronary stenting
In conclusion, very early (prehospital) thrombolysis is associated with a threefold increase in abortion of myocardial infarction when compared with in-hospital treatment. Assessment of the number of aborted myocardial infarctions may well be a better criterion than mortality for the efficacy of early thrombolysis, especially when small patient cohorts are studied. Acknowledgment: We would like to thank the general practitioners, ambulance personnel, and cardiologists of both hospitals in Nijmegen for their help in making this study possible. Furthermore, they are very grateful to both the cardiologists and Astrid Dekker of the Hospital Rijnstate in Arnhem, for their generous help with examining the data of the inhospital-treated patients. 1. Hooghoudt TEH, Lamfers EJP, Uppelschoten A, Verheugt FWA. Study of
time intervals in myocardial ischemic syndromes (STIMIS). Cardiologie 1998; 5:23–30. 2. Theroux P. Coronary thrombolysis: prehospital use. Can J Cardiol 1993;6: 521–522.
3. The GUSTO Angiopgraphic Investigators. The effect of tissue plasminogen activator, streptokinase or both on coronary-artery patency, ventricular function, and survival after acute myocardial infarction. N Engl J Med 1993;329:1515– 1522. 4. Rawles J. Halving of mortality at 1 year by domiciliary thrombolysis in the Grampian Region Early Anistreplase Trial (GREAT). J Am Coll Cardiol 1994; 23:1–5. 5. Barbash GI, Roth A, Hod H, Miller HI, Modan M, Rath S. Improved survival but not left ventricular function with early and prehospital treatment with tissue plasminogen activator in acute myocardial infarction. Am J Cardiol 1990;66: 261–266. 6. Boersma E, Maas ACP, Dekkers JW, Simoons ML. Early thrombolytic treatment in acute myocardial infarction: reappraisal of the Golden Hour. Lancet 1996;348:771–775. 7. Reimer KA, Lowe JE, Rasmussen MM, Jennings RB. The wavefront phenomenon of ischemic cell death. I. Myocardial infarction size vs duration of coronary occlusion in dogs. Circulation 1977;56:786 –794. 8. Trent R, Adams J, Rawles J, on behalf of the GREAT Group. Electrocardiographic evidence of reperfusion occurring before hospital admission. Eur Heart J 1994;15:895– 897. 9. Milavetz J, Giebel DW, Christian TF, Schwartz RS, Holmes DR, Gibbons RJ. Time to treatment and salvage in myocardial infarction. J Am Coll Cardiol 1998;31:1246 –1251. 10. Grijseels EWM, Bouten MJM, Lenderink T, Deckers J, Hoes AW, Hartman JAM, Van der Does E, Simoons ML. Pre-hospital thrombolytic therapy with either alteplase or streptokinase. Eur Heart J 1995;16:1833–1838. 11. Khoury NE, Borzak S, Gokli A, Havstad SL, Smith ST, Jones M. Inadvertent thrombolytic administration in patients without myocardial infarction: clinical features and outcome. Ann Emerg Med 1996;28:289 –293.
Frequency of Silent Myocardial Ischemia Following Coronary Stenting Sekar Kathiresan, MD, Mark K. Jordan, MD, Giorgio Gimelli, MD, Julio Lopez-Cuellar, MD, Nassar Madhi, MD, and Ik-Kyung Jang, MD ilent myocardial ischemia, which occurs in up to 50% of patients who present with acute coronary S syndromes, has been shown to be associated with poor prognosis.1–5 Even after a percutaneous transluminal balloon angioplasty, ischemia was still detected in 22% of patients during the postprocedural period and half of them (11%) were silent.6 Coronary stenting has been shown to be superior to balloon angioplasty for immediate angiographic outcome and 6-month restenosis rate.7,8 It has also been shown that coronary stenting compared with balloon angioplasty almost completely corrects the underlying obstruction and restores coronary flow reserve.9 However, no data are available on the incidence of silent ischemia after coronary stenting. A computerized 12-lead electrocardiographic recording system was used to detect silent ischemia in patients who presented with an acute coronary syndrome and underwent successful coronary stenting. •••
Thirty patients who underwent successful 1-vessel coronary stenting after an acute coronary syndrome From the Department of Medicine and the Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. Dr. Jang’s address is: Cardiology Division, Bulfinch 105, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114. E-mail: [email protected]. Manuscript received March 5, 1999; revised manuscript received May 26, 1999, and accepted May 27.
930
©1999 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 84 October 15, 1999
presentation at the Massachusetts General Hospital were enrolled. We excluded patients with baseline electrocardiographic changes that would preclude analysis of silent ischemia (left bundle branch block, ventricular pacing, and severe left ventricular hypertrophy with strain). After obtaining informed consent, a baseline electrocardiogram was recorded before the procedure. During the first inflation, a 12-lead electrocardiogram was recorded to use as a template. Shortly after the procedure, continuous electrocardiographic recording was initiated using a 12-lead portable programmable ST monitoring system (ELI 100/STM, Mortara Instruments, Milwaukee, Wisconsin). At the end of the monitoring, patients were interviewed by one of the investigators regarding anginal symptoms during the monitoring period. Ischemia was defined as either ST-segment deviation of at least 0.1 mV from the baseline involving 2 contiguous leads, 80 ms from the J point, and lasting for ⬎30 seconds or symmetric T-wave inversions of at least 0.3 mV. An interval of at least 2 minutes was required after the resolution of 1 episode for another episode to be counted as a discrete one. All patients were followed until the time of hospital discharge. Discrete variables were compared using Fisher’s exact test. A p value ⬍0.05 was considered significant. The clinical characteristics of the 30 patients are listed in Table I. Procedural success, as defined by 0002-9149/99/$–see front matter PII S0002-9149(99)00469-5
TABLE I Baseline Characteristics of Patients With and Without Silent Ischemia*
Mean age (yrs) Systemic hypertension Diabetes mellitus Hypercholesterolemia (low-density lipoprotein cholesterol ⬎130 mg/dl) Family history of CAD Cigarette smoker Previous myocardial infarction Presentation Unstable angina Non–Q-wave myocardial infarction ST elevation myocardial infarction No. of patients with procedure-related complications during coronary angioplasty and stenting No. of coronary arteries with ⱖ50% stenosis (no. of patients) 0 1 2 3 Medications during recording period Nitroglycerin intravenous or oral  blocker Aspirin Unfractionated heparin (intravenous) Ticlopidine Abciximab
Silent Ischemia (n ⫽ 10)
No Ischemia (n ⫽ 20)
64 6 1 3
57 12 6 14
5 1 2
10 6 5
4 2 4 3
14 2 4 9
0 7 2 1
0 8 11 1
8 7 9 2 9 1
19 19 19 3 19 7
Table II describes the target vessel, stent type, and frequency and duration of silent ischemic episodes in the 10 patients. The total number of ischemic episodes ranged from 1 to 7 (median 3). The duration of ischemic episodes ranged from 1 to 539 minutes (median 35). Clinical presentation of these 10 patients was ST elevation myocardial infarction in 4 patients, non-ST elevation myocardial infarction in 3, and unstable angina in 4. Mean peak creatine kinase in the silent ischemia group was 440 U/L and in the non–silent ischemia group 157 U/L. Four patients in the silent ischemia group and 5 in the non–silent ischemia group developed an elevated creatine kinase-MB relative index. The 4 patients in the silent ischemia group who developed a positive creatine kinase-MB fraction had ischemic episodes totaling 539, 163, 94, and 8 minutes. In the 10 patients with silent ischemia, mean heart rate at onset of the longest episode of ischemia was 82 beats/min, and it was 78 beats/min preceding the episode. The number of stents and the type of stent did not appear to be associated with a positive creatine kinase-MB fraction. Intravenous abciximab was administered to 1 of the 10 patients compared with 7 of the 20 in the non–silent ischemia group. There was no in-hospital mortality in the patients enrolled. •••
Among 30 patients who presented with an acute coronary syndrome, the incidence of silent myocardial ischemia was 33%, even after successful stenting. This incidence is higher than that after balloon angio*There was no significant difference between the 2 groups for any of the characteristics listed. plasty. Krucoff et al6 reported that in 200 patients CAD ⫽ coronary artery disease. undergoing balloon angioplasty, 22% had episodes of transient myocardial ischemia and 50% of these patients (11%) had ST changes in the TABLE II Target Coronary Artery, Number and Type of Stent, Creatine Kinase-MB, and Frequency and Duration of Ischemic Episodes in 10 Patients absence of chest pain. No patient in With Silent Ischemia our study had angina. Silent myocardial ischemia likely Total Total Target No. Type No. of Duration of resulted from transient thrombus forPatient Coronary of of Creatine Ischemic Ischemia mation or coronary spasm from vaNo. Artery Stents Stent Kinase-MB Episodes (min) soactive substances released from 1 LAD 1 J&J ⫹ 1 8 the injured endothelium or activated 2 LAD 1 Multi-Link ⫹ 4 163 platelets. We found no increase in 3 LAD 1 Nir ⫺ 2 27 heart rate preceding the episodes of 4 LAD 2 J&J ⫺ 1 1 silent ischemia. This finding concurs 5 LAD 1 GRII ⫹ 7 62 with those of Patel et al2 and indi6 Lc 1 Multi-Link ⫺ 1 36 7 Lc 1 Nir ⫺ 5 94 cates that alteration in coronary flow 8 Lc 1 J&J ⫺ 1 35 rather than an increase in myocardial 9 Right 1 J&J ⫹ 6 539 demand led to ischemia. 10 Right 3 J&J ⫺ 1 9 The correlation between silent LAD ⫽ left anterior descending; Lc ⫽ left circumflex. ischemia and adverse clinical outcome has been demonstrated in patients with acute coronary synThrombolysis In Myocardial Infarction (TIMI) grade dromes.10 Gottlieb et al1 studied 70 patients with 3 flow without dissection or filling defect, was unstable angina and showed that silent ischemia ocachieved in all patients. During a median recording curred in 50% of the patients despite intensive medical time of 22 hours, 10 patients (33%) had transient therapy, and in a multivariate analysis, the presence of ischemia. All ischemic episodes in the 10 patients silent ischemia was the strongest predictor for adverse were asymptomatic. Although there was no significant cardiovascular outcome. In addition, a recent study of difference, those with silent ischemia tended to be patients with unstable angina showed that abciximab older, and had a higher incidence of ST elevation prevented silent ischemia and adverse clinical myocardial infarction and 1-vessel disease. events.11 BRIEF REPORTS
931
Our study was limited by the size and selected nature of the sample and thus, neither the significance of silent ischemia in relation to adverse clinical outcome nor the role of abciximab in the prevention of silent ischemia could be evaluated. To assess more confidently the frequency of silent ischemia after coronary stenting and to define the prognostic significance, larger studies are warranted. In conclusion, in 30 patients with an acute coronary syndrome who underwent 1-vessel coronary stenting, the incidence of silent myocardial ischemia was 33%. 1. Gottlieb SO, Weisfeldt ML, Ouyang P, Mellits ED, Gerstenblith G. Silent
ischemia as a marker for early unfavorable outcomes in patients with unstable angina. N Engl J Med 1986;314:1214 –1219. 2. Patel DJ, Knight CJ, Holdright DR, Mulcahy D, Clarke D, Wright C, Purcell H, Fox KM. Pathophysiology of transient myocardial ischemia in acute coronary syndromes. Circulation 1997;95:1185–1192. 3. Holdright D, Patel D, Cunningham D, Thomas R, Hubbard W, Hendry G, Sutton G, Fox K. Comparison of the effect of heparin and aspirin versus aspirin alone on transient myocardial ischemia and in-hospital prognosis in patients with unstable angina. J Am Coll Cardiol 1994;24:39 – 45. 4. Nademanee K, Intarachot V, Josephson M, Rieders D, Vaghaiwalla F, Singh
BN. Prognostic significance of silent myocardial ischemia in patients with unstable angina. J Am Coll Cardiol 1987;10:1–9. 5. Patel DJ, Knight CJ, Holdright DR, Mulcahy D, Clarke D, Wright C, Purcell H, Fox KM. Long-term prognosis in unstable angina: the importance of early risk stratification using continuous ST segment monitoring. Eur Heart J 1998;19: 240 –249. 6. Krucoff MW, Pope JE, Bottner RK, Adams IM, Wagner GS, Kent KM. Dedicated ST segment monitoring in the CCU after successful coronary angioplasty: incidence and prognosis of silent and symptomatic ischemia. In: Arnim Th, Maseri A, eds. Silent Ischemia: Current Concepts and Management. Darmstadt: Steinkopff Verlag, 1987:140 –146. 7. Fischman D, Leon M, Baim D, Schatz RA, Savage MP, Penn I, Detre K, Veltri L, Ricci D, Nobuyoshi M, et al. A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary disease. N Engl J Med 1994;331:496 –501. 8. Serruys P, De Jaegere P, Kiemeneji F, Macaya C, Rutsch W, Heyndrickx G, Emanuelsson H, Marco J, Legrand V, Materne P, et al. A comparison of balloon expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med 1994;331:489 – 495. 9. Kern MJ, Dupouy P, Drury JH, Aguirre FV, Aptecar E, Bach RG, Caracciolo EA, Donohue TJ, Dubois Rande JL, Geschwind HJ, Mechem CJ, Kane G, Teiger E, Wolford TL. Role of coronary artery lumen enlargement in improving coronary blood flow after balloon angioplasty and stenting: a combined intravascular ultrasound doppler flow and imaging study. J Am Coll Cardiol 1997;29:1520 – 1527. 10. Stern S, Gavish A, Zin D, Tzivoni. Clinical outcome of silent myocardial ischemia. Am J Cardiol 1988;61:16F–18F. 11. Klooteijk P, Meij S, Melkert R, Lenderink T, Simoons ML. Reduction of recurrent ischemia with abciximab during continuous ECG-ischemia monitoring in patients with unstable angina refractory to standard treatment (CAPTURE). Circulation 1998;98:1358 –1364.
Prevalence of Coronary Artery Disease, Ischemic Stroke, Peripheral Arterial Disease, and Coronary Revascularization in Older African-Americans, Asians, Hispanics, Whites, Men, and Women Jose Ness,
MD,
and Wilbert S. Aronow,
lder African-Americans, Hispanics, and whites in a long-term health care facility had a similar O prevalence of coronary artery disease (CAD). Older 1
African-Americans had a higher prevalence of atherothrombotic brain infarction than older whites and Hispanics in this study.1 Older African-Americans also had a higher prevalence of peripheral arterial disease (PAD) than older whites.1 We present data from a retrospective analysis of medical records investigating the prevalence of CAD, ischemic stroke, and PAD in older African-Americans, Asians, Hispanics, and whites living in the community and who were examined in an academic geriatrics practice and the prevalence of coronary revascularization in these older African-Americans, Asians, Hispanics, whites, men, and women with CAD. •••
JN, a Fellow in Geriatrics and Adult Development, performed a retrospective analysis of medical records from all patients examined from April 1998 to December 1998, at the Phyllis and Lee Coffey Geriatrics From the Department of Geriatrics and Adult Development, Mount Sinai School of Medicine, New York, New York. Dr. Aronow’s address is: Hebrew Hospital Home, 801 Co-op City Blvd., Bronx, New York 10475. Manuscript received April 9, 1999; revised manuscript received and accepted May 20, 1999.
932
©1999 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 84 October 15, 1999
MD
Practice, a primary care outpatient geriatrics practice of the Department of Geriatrics and Adult Development at Mount Sinai Medical Center, according to a protocol designed by WSA. All electrocardiograms were reviewed with WSA for the diagnosis of Q-wave myocardial infarction. CAD was diagnosed if the patient had coronary revascularization by coronary artery bypass graft surgery or by percutaneous transluminal coronary angioplasty (n ⫽ 104), coronary angiographic evidence of significant CAD without revascularization (n ⫽ 2), a documented clinical history of myocardial infarction or electrocardiographic evidence of Q-wave myocardial infarction (n ⫽ 465), or typical angina pectoris with myocardial ischemia documented by stress testing without prior myocardial infarction (n ⫽ 41). The medical records were also reviewed by JN for clinical evidence of ischemic stroke and PAD. Patients with carotid arterial disease were classified as having PAD. Of the 1,802 patients included in this study, 58% were white, 23% were African-Americans, 18% were Hispanics, and 2% were Asians. All patients in this study lived in the community. The 24 physicians in the primary care geriatrics practice were the primary care physicians for the patients in this study. However, consultants also saw these patients. For analyses comparing the groups, an analysis of variance was used for 0002-9149/99/$–see front matter PII S0002-9149(99)00470-1
time intervals in myocardial ischemic syndromes (STIMIS). Cardiologie 1998; 5:23–30. 2. Theroux P. Coronary thrombolysis: prehospital use. Can J Cardiol 1993;6: 521–522.
3. The GUSTO Angiopgraphic Investigators. The effect of tissue plasminogen activator, streptokinase or both on coronary-artery patency, ventricular function, and survival after acute myocardial infarction. N Engl J Med 1993;329:1515– 1522. 4. Rawles J. Halving of mortality at 1 year by domiciliary thrombolysis in the Grampian Region Early Anistreplase Trial (GREAT). J Am Coll Cardiol 1994; 23:1–5. 5. Barbash GI, Roth A, Hod H, Miller HI, Modan M, Rath S. Improved survival but not left ventricular function with early and prehospital treatment with tissue plasminogen activator in acute myocardial infarction. Am J Cardiol 1990;66: 261–266. 6. Boersma E, Maas ACP, Dekkers JW, Simoons ML. Early thrombolytic treatment in acute myocardial infarction: reappraisal of the Golden Hour. Lancet 1996;348:771–775. 7. Reimer KA, Lowe JE, Rasmussen MM, Jennings RB. The wavefront phenomenon of ischemic cell death. I. Myocardial infarction size vs duration of coronary occlusion in dogs. Circulation 1977;56:786 –794. 8. Trent R, Adams J, Rawles J, on behalf of the GREAT Group. Electrocardiographic evidence of reperfusion occurring before hospital admission. Eur Heart J 1994;15:895– 897. 9. Milavetz J, Giebel DW, Christian TF, Schwartz RS, Holmes DR, Gibbons RJ. Time to treatment and salvage in myocardial infarction. J Am Coll Cardiol 1998;31:1246 –1251. 10. Grijseels EWM, Bouten MJM, Lenderink T, Deckers J, Hoes AW, Hartman JAM, Van der Does E, Simoons ML. Pre-hospital thrombolytic therapy with either alteplase or streptokinase. Eur Heart J 1995;16:1833–1838. 11. Khoury NE, Borzak S, Gokli A, Havstad SL, Smith ST, Jones M. Inadvertent thrombolytic administration in patients without myocardial infarction: clinical features and outcome. Ann Emerg Med 1996;28:289 –293.
Frequency of Silent Myocardial Ischemia Following Coronary Stenting Sekar Kathiresan, MD, Mark K. Jordan, MD, Giorgio Gimelli, MD, Julio Lopez-Cuellar, MD, Nassar Madhi, MD, and Ik-Kyung Jang, MD ilent myocardial ischemia, which occurs in up to 50% of patients who present with acute coronary S syndromes, has been shown to be associated with poor prognosis.1–5 Even after a percutaneous transluminal balloon angioplasty, ischemia was still detected in 22% of patients during the postprocedural period and half of them (11%) were silent.6 Coronary stenting has been shown to be superior to balloon angioplasty for immediate angiographic outcome and 6-month restenosis rate.7,8 It has also been shown that coronary stenting compared with balloon angioplasty almost completely corrects the underlying obstruction and restores coronary flow reserve.9 However, no data are available on the incidence of silent ischemia after coronary stenting. A computerized 12-lead electrocardiographic recording system was used to detect silent ischemia in patients who presented with an acute coronary syndrome and underwent successful coronary stenting. •••
Thirty patients who underwent successful 1-vessel coronary stenting after an acute coronary syndrome From the Department of Medicine and the Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. Dr. Jang’s address is: Cardiology Division, Bulfinch 105, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114. E-mail: [email protected]. Manuscript received March 5, 1999; revised manuscript received May 26, 1999, and accepted May 27.
930
©1999 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 84 October 15, 1999
presentation at the Massachusetts General Hospital were enrolled. We excluded patients with baseline electrocardiographic changes that would preclude analysis of silent ischemia (left bundle branch block, ventricular pacing, and severe left ventricular hypertrophy with strain). After obtaining informed consent, a baseline electrocardiogram was recorded before the procedure. During the first inflation, a 12-lead electrocardiogram was recorded to use as a template. Shortly after the procedure, continuous electrocardiographic recording was initiated using a 12-lead portable programmable ST monitoring system (ELI 100/STM, Mortara Instruments, Milwaukee, Wisconsin). At the end of the monitoring, patients were interviewed by one of the investigators regarding anginal symptoms during the monitoring period. Ischemia was defined as either ST-segment deviation of at least 0.1 mV from the baseline involving 2 contiguous leads, 80 ms from the J point, and lasting for ⬎30 seconds or symmetric T-wave inversions of at least 0.3 mV. An interval of at least 2 minutes was required after the resolution of 1 episode for another episode to be counted as a discrete one. All patients were followed until the time of hospital discharge. Discrete variables were compared using Fisher’s exact test. A p value ⬍0.05 was considered significant. The clinical characteristics of the 30 patients are listed in Table I. Procedural success, as defined by 0002-9149/99/$–see front matter PII S0002-9149(99)00469-5
TABLE I Baseline Characteristics of Patients With and Without Silent Ischemia*
Mean age (yrs) Systemic hypertension Diabetes mellitus Hypercholesterolemia (low-density lipoprotein cholesterol ⬎130 mg/dl) Family history of CAD Cigarette smoker Previous myocardial infarction Presentation Unstable angina Non–Q-wave myocardial infarction ST elevation myocardial infarction No. of patients with procedure-related complications during coronary angioplasty and stenting No. of coronary arteries with ⱖ50% stenosis (no. of patients) 0 1 2 3 Medications during recording period Nitroglycerin intravenous or oral  blocker Aspirin Unfractionated heparin (intravenous) Ticlopidine Abciximab
Silent Ischemia (n ⫽ 10)
No Ischemia (n ⫽ 20)
64 6 1 3
57 12 6 14
5 1 2
10 6 5
4 2 4 3
14 2 4 9
0 7 2 1
0 8 11 1
8 7 9 2 9 1
19 19 19 3 19 7
Table II describes the target vessel, stent type, and frequency and duration of silent ischemic episodes in the 10 patients. The total number of ischemic episodes ranged from 1 to 7 (median 3). The duration of ischemic episodes ranged from 1 to 539 minutes (median 35). Clinical presentation of these 10 patients was ST elevation myocardial infarction in 4 patients, non-ST elevation myocardial infarction in 3, and unstable angina in 4. Mean peak creatine kinase in the silent ischemia group was 440 U/L and in the non–silent ischemia group 157 U/L. Four patients in the silent ischemia group and 5 in the non–silent ischemia group developed an elevated creatine kinase-MB relative index. The 4 patients in the silent ischemia group who developed a positive creatine kinase-MB fraction had ischemic episodes totaling 539, 163, 94, and 8 minutes. In the 10 patients with silent ischemia, mean heart rate at onset of the longest episode of ischemia was 82 beats/min, and it was 78 beats/min preceding the episode. The number of stents and the type of stent did not appear to be associated with a positive creatine kinase-MB fraction. Intravenous abciximab was administered to 1 of the 10 patients compared with 7 of the 20 in the non–silent ischemia group. There was no in-hospital mortality in the patients enrolled. •••
Among 30 patients who presented with an acute coronary syndrome, the incidence of silent myocardial ischemia was 33%, even after successful stenting. This incidence is higher than that after balloon angio*There was no significant difference between the 2 groups for any of the characteristics listed. plasty. Krucoff et al6 reported that in 200 patients CAD ⫽ coronary artery disease. undergoing balloon angioplasty, 22% had episodes of transient myocardial ischemia and 50% of these patients (11%) had ST changes in the TABLE II Target Coronary Artery, Number and Type of Stent, Creatine Kinase-MB, and Frequency and Duration of Ischemic Episodes in 10 Patients absence of chest pain. No patient in With Silent Ischemia our study had angina. Silent myocardial ischemia likely Total Total Target No. Type No. of Duration of resulted from transient thrombus forPatient Coronary of of Creatine Ischemic Ischemia mation or coronary spasm from vaNo. Artery Stents Stent Kinase-MB Episodes (min) soactive substances released from 1 LAD 1 J&J ⫹ 1 8 the injured endothelium or activated 2 LAD 1 Multi-Link ⫹ 4 163 platelets. We found no increase in 3 LAD 1 Nir ⫺ 2 27 heart rate preceding the episodes of 4 LAD 2 J&J ⫺ 1 1 silent ischemia. This finding concurs 5 LAD 1 GRII ⫹ 7 62 with those of Patel et al2 and indi6 Lc 1 Multi-Link ⫺ 1 36 7 Lc 1 Nir ⫺ 5 94 cates that alteration in coronary flow 8 Lc 1 J&J ⫺ 1 35 rather than an increase in myocardial 9 Right 1 J&J ⫹ 6 539 demand led to ischemia. 10 Right 3 J&J ⫺ 1 9 The correlation between silent LAD ⫽ left anterior descending; Lc ⫽ left circumflex. ischemia and adverse clinical outcome has been demonstrated in patients with acute coronary synThrombolysis In Myocardial Infarction (TIMI) grade dromes.10 Gottlieb et al1 studied 70 patients with 3 flow without dissection or filling defect, was unstable angina and showed that silent ischemia ocachieved in all patients. During a median recording curred in 50% of the patients despite intensive medical time of 22 hours, 10 patients (33%) had transient therapy, and in a multivariate analysis, the presence of ischemia. All ischemic episodes in the 10 patients silent ischemia was the strongest predictor for adverse were asymptomatic. Although there was no significant cardiovascular outcome. In addition, a recent study of difference, those with silent ischemia tended to be patients with unstable angina showed that abciximab older, and had a higher incidence of ST elevation prevented silent ischemia and adverse clinical myocardial infarction and 1-vessel disease. events.11 BRIEF REPORTS
931
Our study was limited by the size and selected nature of the sample and thus, neither the significance of silent ischemia in relation to adverse clinical outcome nor the role of abciximab in the prevention of silent ischemia could be evaluated. To assess more confidently the frequency of silent ischemia after coronary stenting and to define the prognostic significance, larger studies are warranted. In conclusion, in 30 patients with an acute coronary syndrome who underwent 1-vessel coronary stenting, the incidence of silent myocardial ischemia was 33%. 1. Gottlieb SO, Weisfeldt ML, Ouyang P, Mellits ED, Gerstenblith G. Silent
ischemia as a marker for early unfavorable outcomes in patients with unstable angina. N Engl J Med 1986;314:1214 –1219. 2. Patel DJ, Knight CJ, Holdright DR, Mulcahy D, Clarke D, Wright C, Purcell H, Fox KM. Pathophysiology of transient myocardial ischemia in acute coronary syndromes. Circulation 1997;95:1185–1192. 3. Holdright D, Patel D, Cunningham D, Thomas R, Hubbard W, Hendry G, Sutton G, Fox K. Comparison of the effect of heparin and aspirin versus aspirin alone on transient myocardial ischemia and in-hospital prognosis in patients with unstable angina. J Am Coll Cardiol 1994;24:39 – 45. 4. Nademanee K, Intarachot V, Josephson M, Rieders D, Vaghaiwalla F, Singh
BN. Prognostic significance of silent myocardial ischemia in patients with unstable angina. J Am Coll Cardiol 1987;10:1–9. 5. Patel DJ, Knight CJ, Holdright DR, Mulcahy D, Clarke D, Wright C, Purcell H, Fox KM. Long-term prognosis in unstable angina: the importance of early risk stratification using continuous ST segment monitoring. Eur Heart J 1998;19: 240 –249. 6. Krucoff MW, Pope JE, Bottner RK, Adams IM, Wagner GS, Kent KM. Dedicated ST segment monitoring in the CCU after successful coronary angioplasty: incidence and prognosis of silent and symptomatic ischemia. In: Arnim Th, Maseri A, eds. Silent Ischemia: Current Concepts and Management. Darmstadt: Steinkopff Verlag, 1987:140 –146. 7. Fischman D, Leon M, Baim D, Schatz RA, Savage MP, Penn I, Detre K, Veltri L, Ricci D, Nobuyoshi M, et al. A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary disease. N Engl J Med 1994;331:496 –501. 8. Serruys P, De Jaegere P, Kiemeneji F, Macaya C, Rutsch W, Heyndrickx G, Emanuelsson H, Marco J, Legrand V, Materne P, et al. A comparison of balloon expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med 1994;331:489 – 495. 9. Kern MJ, Dupouy P, Drury JH, Aguirre FV, Aptecar E, Bach RG, Caracciolo EA, Donohue TJ, Dubois Rande JL, Geschwind HJ, Mechem CJ, Kane G, Teiger E, Wolford TL. Role of coronary artery lumen enlargement in improving coronary blood flow after balloon angioplasty and stenting: a combined intravascular ultrasound doppler flow and imaging study. J Am Coll Cardiol 1997;29:1520 – 1527. 10. Stern S, Gavish A, Zin D, Tzivoni. Clinical outcome of silent myocardial ischemia. Am J Cardiol 1988;61:16F–18F. 11. Klooteijk P, Meij S, Melkert R, Lenderink T, Simoons ML. Reduction of recurrent ischemia with abciximab during continuous ECG-ischemia monitoring in patients with unstable angina refractory to standard treatment (CAPTURE). Circulation 1998;98:1358 –1364.
Prevalence of Coronary Artery Disease, Ischemic Stroke, Peripheral Arterial Disease, and Coronary Revascularization in Older African-Americans, Asians, Hispanics, Whites, Men, and Women Jose Ness,
MD,
and Wilbert S. Aronow,
lder African-Americans, Hispanics, and whites in a long-term health care facility had a similar O prevalence of coronary artery disease (CAD). Older 1
African-Americans had a higher prevalence of atherothrombotic brain infarction than older whites and Hispanics in this study.1 Older African-Americans also had a higher prevalence of peripheral arterial disease (PAD) than older whites.1 We present data from a retrospective analysis of medical records investigating the prevalence of CAD, ischemic stroke, and PAD in older African-Americans, Asians, Hispanics, and whites living in the community and who were examined in an academic geriatrics practice and the prevalence of coronary revascularization in these older African-Americans, Asians, Hispanics, whites, men, and women with CAD. •••
JN, a Fellow in Geriatrics and Adult Development, performed a retrospective analysis of medical records from all patients examined from April 1998 to December 1998, at the Phyllis and Lee Coffey Geriatrics From the Department of Geriatrics and Adult Development, Mount Sinai School of Medicine, New York, New York. Dr. Aronow’s address is: Hebrew Hospital Home, 801 Co-op City Blvd., Bronx, New York 10475. Manuscript received April 9, 1999; revised manuscript received and accepted May 20, 1999.
932
©1999 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 84 October 15, 1999
MD
Practice, a primary care outpatient geriatrics practice of the Department of Geriatrics and Adult Development at Mount Sinai Medical Center, according to a protocol designed by WSA. All electrocardiograms were reviewed with WSA for the diagnosis of Q-wave myocardial infarction. CAD was diagnosed if the patient had coronary revascularization by coronary artery bypass graft surgery or by percutaneous transluminal coronary angioplasty (n ⫽ 104), coronary angiographic evidence of significant CAD without revascularization (n ⫽ 2), a documented clinical history of myocardial infarction or electrocardiographic evidence of Q-wave myocardial infarction (n ⫽ 465), or typical angina pectoris with myocardial ischemia documented by stress testing without prior myocardial infarction (n ⫽ 41). The medical records were also reviewed by JN for clinical evidence of ischemic stroke and PAD. Patients with carotid arterial disease were classified as having PAD. Of the 1,802 patients included in this study, 58% were white, 23% were African-Americans, 18% were Hispanics, and 2% were Asians. All patients in this study lived in the community. The 24 physicians in the primary care geriatrics practice were the primary care physicians for the patients in this study. However, consultants also saw these patients. For analyses comparing the groups, an analysis of variance was used for 0002-9149/99/$–see front matter PII S0002-9149(99)00470-1