Transient coronary occlusion with mental stress

Volume 132, Number 6 American Heart Journal

Papademetriou et al.

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Transient coronary occlusion with mental stress Vasilios Papademetriou, MD, a J o h n S. Gottdiener, MD, b Willem J. Kop, PhD, c Robert H. Howell, MS, c and David S. Krantz, P h D W a s h i n g t o n , D.C., a n d Bethesda, M d .

From the aCardiologySection, Veterans Affairs Medical Center, and the bCardiologyDivision,GeorgetownUniversityMedicalCenter, Washington, D.C., and the ~Department of Medical and ClinicalPsychology,Uniformed Services University of the Health Sciences, Bethesda, Maryland. Supported in part by NIH grant HL47337. The opinions and assertions expressed herein are those of the authors and are not to be construed as reflectingthe views of the USUttS or the U.S. Department of Defense. Reprint requests: Vasilios Papademetriou, MD, Cardiovascular Research Clinic (151-E), Veterans Affairs Medical Center, 50 Irving St. NW, Washington, DC 20422. Am Heart J 1996;132:1299-1301.

Nonexertional stress, including m e n t a l stress, m a y induce myocardial ischemia in patients with obstructive coronary a r t e r y disease. 15 Previous studies have shown t h a t mental stress is associated with increased oxygen demand 3 and coronary vasoconstriction. 2, 4 However, total occlusion of coronary arteries during m e n t a l stress has not been described. We report a t r a n s i e n t total occlusion of the left anterior descending artery in a patient experiencing mental stress during clinically indicated cardiac catheterization. The p at i en t is a participant of the IRB approved Triggers of Myocardial Ischemia Study (TOMIS) protocol and gave informed consent before catheterization. The p at i en t was a 55-year-old white m a n with a history of inferior wall myocardial infarction (MI) in 1989 and exertional angina, shortness of breath, and dizziness since t h a t time. The patient also described occasional episodes of nocturnal angina accompanied by n a u s e a and diaphoresis. A workup revealed a positive exercise test result with 2.2 m m ST-segment depression in leads V4 and V5 (maximal h e a r t rate of 149 beats/min and systolic blood pressure of 170 m m Hg) and normal left ventricular function. Exercise t h a l l i u m scintigraphy test results were Consistent with anterolateral myocardial ischemia. His past medical history was significant for hypertension, hypercholesterolemia, 50 pack-years of smoking, and a positive family history for coronary a r t e r y disease. The medical r e gi me n included t r a n s d e r m a l nitroglycerine, amlodipine, Tenormin (atenolol), aspirin, gemfibrozil, and indapamide. The first three agents were tapered and discontinued 24 hours before the study. Physical ex am i n at i o n revealed a blood pressure of 124/72 m m Hg, pulse of 52 beats/min, and a grade 2/6 systolic ejection m u r m u r . The electrocardiog r a m was significant for nonspecific ST changes. Cardiac catheterization was performed by standard techniques. Before angiography and m e n t a l stress, 3,000 units ofhep-

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Fig. 1. LAD coronary artery. Initial angiography (left panel), total occlusion of LAD after mental stress (middle panel), and revascularization (right panel). arin were administered intravenously. At cardiac catheterization, left ventricular global and regional function were normal. The right coronary artery had minimal luminal irregularities. The left anterior descending (LAD) branch (Fig. 1) had two significant obstructive lesions: a proximal lesion of 70% and a mid-lesion of approximately 90%. The left circumflex artery had an approximately 60% obstructive lesion. Mental stress was performed according to research protocol. 5 After baseline evaluation, the patient was vigorously prompted by the examiner to rapidly and accurately subtract serial 76 from a four-digit number while an audiotape played the sound of constant ticking of a metronome at high volume. With mental stress, systolic blood pressure increased from 110/68 mm Hg to 138/76 mm Hg, and heart rate increased from 74 beats/min to 81 beats/ rain. At completion of mental stress (2 minutes), the patient complained of substernal chest pain radiating to the left shoulder and arm. The electrocardiogram (ECG) showed 4 mm ST-segment depression in the inferior leads; precordial leads were not monitored. Repeat angiogram of the left coronary artery showed total occlusion of the proximal LAD (Fig. 1, middle panel). Nitroglycerin was infused at 200 pg aliquots intracoronary three times at 2-minute intervals without resolution of the chest pain; sublingual nifedipine (10 mg) was administered, and a fourth dose of intracoronary nitroglycerine was infused. While preparations were being made for percutaneous coronary angioplasty, the patient reported easing of the pain. On repeat angiography (Fig. 1, right panel), the LAD was patent and similar in appearance to baseline. Chest pain and ECG abnormalities resolved. No evidence of myocardial necrosis was present on sequential ECGs and cardiac enzymes. Coronary artery bypass grafting was performed 3 days later and the patient was discharged without further complications. Quantitative coronary angiography of the circumflex artery lesion revealed a minor reduction with mental stress in minimal luminal diameter (1.15 to 1.10). A similar nonsignificant change was observed in a nondiseased obtuse marginal segment (1.85 to 1.78 mm).

This case demonstrates the potentially catastrophic effects of mental stress in patients with coronary artery disease. Despite modest increases in blood pressure and heart rate, mental stress was followed by complete occlusion of the proximal segment of the LAD and evidence of marked ischemia on the electrocardiogram. The observed coronary occlusion is most likely the result of intense coronary vasoconstriction. Moderate decreases in luminal diameter after mental stress have been reported in previous studies, with an average reduction of 24% in diseased segments. 4 Furthermore, a close relation between mental stress and acetylcholine-induced coronary constriction has also been observed, indicating that mental stress-induced coronary constriction is caused by coronary endothelial dysfunction. Our observation that mental stress triggered complete occlusion parallels the observation that acetylcholine may have occlusive effects in lesions >50%. 6 Activations of the sympathetic nervous system and increased levels of catecholamines have been demonstrated to result in a constrictive response in the smooth muscle cells. However, in normal coronary arteries, the intact endothelium modulates these constrictor effects through the release of endothelium-derived relaxing factor, 7 Studies in isolated vascular rings have shown that removal of the endothelium results in a marked increase in constrictor response with catecholamines. 7 Furthermore, the constrictor response to phenylephrine is exaggerated in coronary segments with endothelial dysfunction in patients with stable coronary disease, which suggests a-sympathetic involvement. 6 The extent of endothelial dysfunction is related to severity of the coronary lesion, 4, 6 which may explain why, in this case, the overall more severely diseased left anterior descending artery occluded and the circumflex did not. We also considered the possibility of an occlusive thrombus in this case 9,10 but regard this as unlikely because no residual structural alteration of the affected coronary lesion was apparent. Ischemia elicited by mental stress is known to occur at essentially lower heart rates than exercise-induced ischemia. 1 This finding indicates that ischemia with mental

Volume 132, Number 6 American Heart Journal

cause stress m a y be related to decreased coronary supply a t a relatively low cardiac demand. Studies d e m o n s t r a t i n g coronary constrictive effects of m e n t a l stress support this hypothesis. 4 Mental stress-induced ischemia is observed i n approximately 50% of patients with stable coronary disease a n d is related to a n increased likelihood of ambulatory ischemia d u r i n g sedentary activities. 5 F u t u r e investigations need to address the relative contribution of neuroendocrine versus direct autonomic nervous system effects on coronary constriction with m e n t a l stress. This report demonstrates t h a t in some individuals m e n t a l stress can produce total coronary occlusion, which could lead to major clinical consequences such as myocardial infarction or sudden cardiac death. REFERENCES

1. RozanskiA, BaireyCN, Krantz DS, et al. Mentalstress and the induction of silent myocardialischemiain patients with coronaryartery disease. N Engl J Med 1988;318:1005-12. 2. DeanfieldJE, SheaM,KensettM. Silentischemiadue to mentalstress. Lancet 1984;2:1001-5. 3. BaireyCN, Krantz DS, RozanskiA. Mental stress as an acute trigger ofischemicleftventricu]ardysfunctionand bloodpressure elevationin coronary artery disease. Am J Cardiol 1990;66:28-31G. 4. YeungAC,VekshteinVI, KrantzDS, RyanTJ, GanzP, SelwynAP. The effect ofatherosclerosison the vasomotorresponse ofcoronaryarteries to mental stress. N Engl J Med 1991;325(22):1551-6. 5. GottdienerJS, Krantz D, HowellR, Hecht G, KleinJ. FalconerJJ, et al. Inductionof silent myocardialischemiawith mental stress testing: relationto the triggers ofischemiaduring dailylifeactivitiesand to ischemic functionalseverity.J Am Coll Cardiol 1994;24:1645-51. 6. LudmerPL, SelwynAP, ShookTL, WayneRR, MudgeGH, Alexander RW, et al. Paradoxical vasoconstrictioninduced by acetylcholinein atherosclerotic coronaryarteries. N Engl J Med 1986;315:1046-51. 7. MeredithIT, YeungAC, WeidingerFF, AndersonTJ, Uehata A, Ryan TJ, et al. Role of impaired endothelium-dependentvasodilationin ischemic manifestationsof coronary artery disease. Circulation1993; 87(suppl):V56-66. 8. Vita JA, Furchgott CB, YeungAC, VekshteinVI, Fantasia GM, Fish RD, et al. Patients with evidenceof coronaryendothelialdysfunction as assessed by acetylcholineinfusiondemonstratemarked increasein sensitivityto constrictoreffects of catecholamines. 1992;85:1390-7. 9. Patterson SM, Krantz DS, Hecht GM, Vargot SL, GoldsteinDS, Gottdiener JS. Prothromboticeffects of mental and cold pressor stress: changes in platelet fimction,bloodviscosityand plasma volume.Psychosom Med 1995;57:592-9. 1.0. Jern C, Erikson E, Tengborn L, Risberg B, Wadenvik H, Je1~ S. Changes of plasma coagulationand fibrinolysisin response to mental stress. Thromb Haemostas 1989;62:767-71.

Cocaine-induced aortic dissection J o h n Rashid, MD, M a r k J. Eisenberg, MD, MPH, and Eric J. Topoi, MD Cleveland, Ohio Cocaine is k n o w n to a n u m b e r of cardiovascular complications, including myocardial infarction and ischemia, cardiac dysrhythmias, a n d stroke. Aortic dissection is another infrequently described yet life-threatening complication of From the Department of Cardiolog:fof the ClevelandClinicFoundation, l~.eprintrequests: Eric J. Topol,MD, Departmentof Cardiology,Cleveland ClinicFoundation/DeskF25, 9500 EuclidAve., Cleveland,OH 44195. Am Heart J 1996;132:1301-4. Copyright © 1996 by Mosby-YearBook, Inc. 0002-8703/96/$5.00 + 0 4/4/75318

Rashid, Eisenberg, and Topol 1301 cocaine abuse. I n this article, we report the case of a 42-year-old m a n who developed a n aortic dissection shortly after smoking "crack" cocaine. We also review the 11 previously reported cases of cocaine-induced aortic dissection. A 42-year-old black m a n with a history of essential hypertension a n d crack cocaine use came to a local hospital complaining of upper back a n d left leg pain. The patient had been smoking crack cocaine three to four times per week during the year before admission. On the day of admission, the patient noted the onset of palpitations approximately 40 m i n u t e s after smoking crack; he then suffered a syncopal episode. This episode was witnessed by the patient's wife, who immediately initiated cardiopulm o n a r y resuscitation. By the time the paramedics arrived, the p a t i e n t had regained consciousness and complained of back and left leg pain. At admission, the patient was found to have a n ischemic left leg, a n d he was sent for emergent revascularization. At surgery, a dissection of the left iliac artery was noted. A n abdominal and chest computed tomographic scan was t h e n performed a n d revealed a DeBakey type I aortic dissection. A transthoracic echocardiogram demonstrated severe aortic insufficiency, a pericardial effusion, a n d a markedly dilated ascending aortic root with a n i n t i m a l flap. The patient was transferred to the Cleveland Clinic Foundation. A transesophageal echocardiogram was performed t h a t revealed concentric left ventricular hypertrophy, normal left ventricular function, 4+ aortic insufficiency, a moderate pericardial effusion, and a n ascending aortic dissection originating j u s t anterior to the ostium of the right coronary artery a n d extending into the descending aorta. While being prepared for surgery, the patient became hypotensive and was immediately placed on bypass circulation. During surgery, a r u p t u r e at the anterior surface of the proximal ascending aorta was noted. A Bentall procedure was performed. A #25 St. Jude valve with a Dacron conduit was placed with distal insertion j u s t proximal to the inominate artery a n d reimplantation of the coronary arteries. The p a t i e n t had persistent fevers after surgery and was discharged to a n u r s i n g home 22 days after the operation. At the n u r s i n g home, he had a n additional 4 weeks of intravenous antibiotics. The pat i e n t was noted to be alive and well 4 months after surgery. Our case of cocaine-induced acute aortic dissection is similar in m a n y ways to the 11 previously reported cases (Table 1). 1"12Ten of the 12 patients were men. All the patients were younger t h a n 60 years of age, and most were younger t h a n 50. I n all cases, the subjects were long-term cocaine users whose aortic dissections occurred shortly after recent cocaine use. Patients were seen from m i n u t e s to hours after cocaine use. These findings are consistent with a n i m a l studies that show the peak onset of action from intravenous (IV) and i n h a l a t i o n (smoking) routes is one half to 2 minutes, whereas the peak effect by insuffiation (intranasal) is within 30 minutes, la The duration of effect b y the IV or i n h a l a t i o n route is 15 to 30 m i n u t e s a n d 1 hour by insuffiation use; the IV or i n h a l a t i o n plasma half-life is 60 m i n u t e s compared with 2 to 3 hours by the insuffiation route. 13 Eight of the 11 previously reported patients had a history of either u n t r e a t e d or poorly treated hypertension. The two youngest patients did not have a history ofhyper-