Cocaine-Related Aortic Dissection in Perspective
2002; Lippincott Williams & Wilkins; Volume: 105; Issue: 13 Linguagem: Inglês
10.1161/01.cir.105.13.1529
ISSN1524-4539
AutoresKim A. Eagle, Eric M. Isselbacher, Roman W. DeSanctis,
Tópico(s)Cardiac Arrest and Resuscitation
ResumoHomeCirculationVol. 105, No. 13Cocaine-Related Aortic Dissection in Perspective Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBCocaine-Related Aortic Dissection in Perspective Kim A. Eagle, Eric M. Isselbacher, Roman W. DeSanctis and the International Registry for Aortic Dissection (IRAD) Investigators Kim A. EagleKim A. Eagle From Massachusetts General Hospital, Boston, Mass (E.M.I., R.W.D.), and the University of Michigan Medical Center, Ann Arbor, Mich (K.A.E.). , Eric M. IsselbacherEric M. Isselbacher From Massachusetts General Hospital, Boston, Mass (E.M.I., R.W.D.), and the University of Michigan Medical Center, Ann Arbor, Mich (K.A.E.). , Roman W. DeSanctisRoman W. DeSanctis From Massachusetts General Hospital, Boston, Mass (E.M.I., R.W.D.), and the University of Michigan Medical Center, Ann Arbor, Mich (K.A.E.). and the International Registry for Aortic Dissection (IRAD) Investigators From Massachusetts General Hospital, Boston, Mass (E.M.I., R.W.D.), and the University of Michigan Medical Center, Ann Arbor, Mich (K.A.E.). Originally published2 Apr 2002https://doi.org/10.1161/01.CIR.105.13.1529Circulation. 2002;105:1529–1530Cardiovascular complications of cocaine use have been ever more widely recognized and include the acceleration of atherosclerosis, coronary artery spasm, acute myocardial infarction, myocarditis, dilated cardiomyopathies, and cardiac arrhythmias. Less well known is the potentially lethal complication of aortic dissection. In the present issue of Circulation, Hsue and colleagues1 report on their 20-year experience with acute aortic dissection at an inner-city hospital. Remarkably, their findings indicate that 14 (37%) of 38 patients treated for acute dissection reported having used cocaine in the minutes or hours preceding their presentation. Cocaine, particularly crack cocaine, seemed to have played a significant role in precipitating aortic dissection among this cohort of young (age 41±8.8 years), predominantly black (11 of 14; 79%), and hypertensive (11 of 14; 79%) individuals. This study represents the largest cohort of cocaine-related dissection ever reported. Its findings provoke a number of questions for those of us who study or manage this rare but highly lethal condition.See p 1592How common is cocaine-related aortic dissection? Previous reports predominantly have been descriptions of a single patient2 or a summary of individual case reports.3 The presumption has been that cocaine is a very rare cause of a very rare condition. The report by Hsue et al1 would seem to challenge that logic, but the authors freely admit that the inner-city population served by their hospital likely is responsible for this. In fact, because they accumulated only 14 patients over 20 years at their hospital, a cocaine-related dissection was encountered less than once per year.The International Registry for Aortic Dissection (IRAD) represents a unique effort by 17 aortic centers around the world to characterize the current status of acute aortic dissection, including its predisposing conditions.4,5 We were able to work with IRAD’s coordinating center to characterize cocaine-related dissection as part of our response to the article by Hsue and colleagues.1The Table shows that among 921 cases of acute aortic dissection presenting to IRAD centers from 1996 through 2000 for whom knowledge of cocaine use was specifically coded as yes or no, only 5 (0.5%) were associated with cocaine. This would strongly suggest that cocaine is not likely to be responsible for >1% of aortic dissections and that for any single hospital, identification of more than a patient every few years with cocaine-related dissection would be unusual. Moreover, although hundreds of thousands of people abuse cocaine, clearly only a small minority develops aortic dissections. It may be that among cocaine users, it is the presence of pre-existent aortic disease that allows a cocaine-induced intimal injury to precipitate the aortic dissection process. In fact, 11 of 14 patients in the series by Hsue et al1 were hypertensive, and all were smokers—both of which are major risk factors for disease of the aortic media. Table 1107833. Prior Cocaine Use in IRADVariableNo History of Cocaine (n=916)Cocaine Before Dissection (n=5)PValues are number of patients (%) or mean±SD.Type A575 (62.8)1 (20)0.068Type B341 (37.2)4 (80)Age, years62.4±13.844.4±3.9<0.001Black race17 (2.0)4 (80) 50 000 cocaine users present to an emergency room with complaints of chest discomfort each year. Of these, an incredibly small percentage will have an aortic dissection. Far more common will be myocardial ischemia or infarction, myocarditis, cardiac arrhythmias, and other cocaine-related conditions. On the basis of the IRAD experience, the sudden onset of chest or back pain (especially when severe and sharp or stabbing) is suggestive of aortic dissection.4 Certainly, any time such pain is accompanied by other suggestive findings, such as a blood pressure differential or pulse deficits, the murmur of aortic insufficiency, syncope, or an abnormal aortic contour on chest x-ray, one should suspect aortic dissection and order an appropriate imaging study. Unfortunately, the ECG may be unhelpful, inasmuch as it may suggest myocardial ischemia regardless of whether or not an acute dissection is present.4How should one treat cocaine-related aortic dissection? Given the rarity of this condition, the nuances of managing this particular type of aortic dissection are largely unknown. Treatment of dissection in general requires rapid identification of the extent and location of involvement and generally urgent aortic repair for acute dissection involving the ascending aorta. All patients require aggressive medical treatment, which is directed in particular at reducing aortic sheer forces and transaortic pressure with hopes of reducing the risk of dissection extension, aortic expansion, or rupture. This normally is accomplished with a combination of aggressive β blockade and the addition of an intravenous vasodilator, such as nitroprusside, in order to achieve a heart rate <60 beats per minute and a blood pressure <120/80 mm Hg. The patient with cocaine-related chest pain is particularly challenging when myocardial ischemia is either suspected or definitely present. It has been argued that use of a β-blocker without simultaneous α blockade in such a patient can promote worsening of myocardial ischemia due to arterial vasoconstriction caused by relatively unopposed α-adrenergic stimulation. For this reason, one should consider the use of labetolol, which has both α- and β-blocking properties, first intravenously for short-term and then orally for long-term use. Another therapeutic option is the use intravenous nitroglycerin or verapamil because they reverse both the vasoconstriction and hypertension caused by acute cocaine exposure.10 Combination therapy thus might include labetolol with a dihydropyridine calcium channel–blocker or verapamil with nitroglycerin, with additional agents directed at systemic hypertension (nitroprusside) if necessary. In terms of long-term management of such a patient, the most important element must be a full-scale effort to eliminate cocaine use in the future.2 Aggressive control of blood pressure and heart rate is a given, as is careful surveillance of the aorta. This is performed serially with noninvasive imaging to watch for aneurysm formation or extension.11The article by Hsue and colleagues1 is an important contribution. It firmly connects cocaine use and aortic dissection, taking us from case reports to a cohort that exhibited certain features that should be committed to memory. Aortic dissection remains a rare but highly lethal condition. Cocaine is a rare cause of aortic dissection, but it does occur and we must maintain a high index of suspicion for it when we encounter cocaine users presenting to our emergency departments. In addition, further insights into the interactive effects of hypertension, smoking, and cocaine on the aorta may shed light not only on the mechanism of dissection among cocaine users, but also on acute and chronic underpinnings of aortic dissection in general.The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.FootnotesCorrespondence to Kim A. Eagle, MD, Division of Cardiology, TC 3910, University of Michigan Medical Center, 1500 E Medical Center Dr, Ann Arbor, MI 48109-0374. E-mail [email protected] References 1 Hsue PY, Salinas C, Bolger AF, et al. Acute aortic dissection induced by crack cocaine. Circulation. 2002; 105: 1592–1595.LinkGoogle Scholar2 Nallamothu BK, Saint S, Kolias TJ, et al. Of nicks and time. N Engl J Med. 2001; 345: 359–363.CrossrefMedlineGoogle Scholar3 Rushid J, Eisenberg MJ, Topol EJ. Cocaine-induced aortic dissection. Am Heart J. 1996; 132: 1301–1304.CrossrefMedlineGoogle Scholar4 Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000; 283: 897–903.CrossrefMedlineGoogle Scholar5 Mehta RH, Suzuki T, Hagan PG, et al, on behalf of the International Registry of Acute Aortic Dissection (IRAD) Investigators. Predicting death in patients with acute Type A aortic dissection. Circulation. 2002; 105: 200–206.CrossrefMedlineGoogle Scholar6 Kloner RA, Hale S, Alker K, et al. The effects of acute and chronic cocaine use on the heart. Circulation. 1992; 85: 407–419.CrossrefMedlineGoogle Scholar7 Kolodgie FD, Virmani R, Cornhill JF, et al. Increase in atherosclerosis and adventitial mast cells in cocaine abusers: an alternative mechanism of cocaine-associated coronary vasospasm and thrombosis. J Am Coll Cardiol. 1991; 17: 1553–1560.CrossrefMedlineGoogle Scholar8 Kolodgie FD, Wilson PS, Mergner WJ, et al. Cocaine-induced increase in the permeability function of human vascular endothelial cell monolayers. Exp Mol Pathol. 1999; 66: 109–122.CrossrefMedlineGoogle Scholar9 Gan X, Zhang L, Berger O, et al. Cocaine enhances brain endothelial adhesion molecules and leukocyte migration. Clin Immunol. 1999; 91: 68–76.CrossrefMedlineGoogle Scholar10 Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med. 2001; 345: 351–358.CrossrefMedlineGoogle Scholar11 Erbel R, Alfonso F, Boileau C, et al. Diagnosis and management of aortic dissection: recommendations of the Task Force on Aortic Dissection, European Society of Cardiology. Eur Heart J. 2001; 22: 1642–1681.CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. 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