Cocaine-Induced Postpartum Coronary Artery Dissection: A Case Report and 80-Year Review of Literature

ABSTRACT:The incidence of cocaine-induced myocardial infarction (MI) in pregnancy is unknown. During the peripartum period, cocaine-abusing women are highly susceptible to MI caused by the effect of cocaine on a heart that is already stressed by hemodynamic changes of pregnancy. MI is an infrequent event during pregnancy and the peripartum period, with an estimated rate of 1 in 16,000 patients. Spontaneous coronary artery dissection (SCAD) can account for up to 27% of pregnancy-related MIs. We describe a case of MI diagnosed by increased troponin I levels in a postpartum patient with recent crack cocaine use in the setting of SCAD that required percutaneous coronary intervention of the left anterior descending  and diagonal arteries. We also provide a comprehensive review of published literature related to this clinical entity. 

J INVASIVE CARDIOL 2013;25(8):E163-E166

Key words: cocaine-induced MI

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Cocaine abuse is common among parturients, with a reported incidence of 11.8%-20%.^1,2 Studies have shown that myocardial infarction (MI) complicates approximately 1 in 16,000 deliveries.^3,4 Though rare, there has been a gradual rise in the incidence of pregnancy-related MI, attributed to factors such as increasing age at childbearing, tobacco and cocaine abuse.⁵ The incidence of cocaine-induced MI in pregnancy is unknown. Spontaneous coronary artery dissection (SCAD), which is infrequent in the general population, can account for up to 27% of pregnancy-related MIs, particularly during the postpartum period.^6,7 To our knowledge, there is no prior reported case of postpartum SCAD in the setting of cocaine use.  Here we report a case of MI diagnosed by increased troponin I levels in a postpartum patient with recent crack cocaine use in the setting of SCAD that required percutaneous coronary intervention of the left anterior descending (LAD) and diagonal arteries. The discussion provides a comprehensive review of literature, including the epidemiology, pathogenesis, and strategies for management of peripartum patients with MI, SCAD, and cocaine use.

Case Report. A 25-year-old African-American woman (gravida 2 para 2) was discharged home after an uncomplicated vaginal delivery of a healthy female baby. She was doing fine until 10 days postpartum, when she developed the sudden onset of a squeezing, non-radiating, left-sided chest pain associated with shortness of breath. The continuous and gradually worsening pain prompted her to come to the emergency room. Upon arrival, she complained of ongoing chest pain, but denied any fever, cough, palpitations, diaphoresis, dizziness, or lower extremity edema.  There was no prior history of coronary artery disease or connective tissue disorders. She admitted to smoking tobacco (one pack per day for 3 years) and using cocaine 3 days prior to presentation. She was using Depo-Provera for contraception. 

On physical examination, the patient appeared to be a healthy woman in moderate distress, afebrile with a pulse of 109 beats/min, respiratory rate of 25/min, blood pressure of 137/100 mm Hg in both upper extremities, and an oxygen saturation of 98% on 2 L oxygen inhalation via nasal cannula. A rise in jugular venous distension was noted, along with bibasilar crackles on auscultation. Heart rate was regular, S1, S2, and S4 were heard, along with a grade 2/6 systolic murmur in the mitral area. 

The electrocardiogram showed sinus tachycardia with deep symmetric T-wave inversions in the anterolateral leads (Figure 1). Chest radiograph was remarkable for a prominent cardiac silhouette with mild bilateral hilar congestion and small bilateral pleural effusions. Troponin I levels were elevated at 6.8 ng/mL and peaked up to 27ng/mL (normal, <0.04 ng/mL). Urine drug screen was positive for cocaine and cannabinoids. Echocardiography showed severe global left ventricular hypokinesis with an ejection fraction of 20%-25%, diastolic dysfunction, mild pulmonic insufficiency, moderate tricuspid regurgitation, severe mitral regurgitation, and pulmonary hypertension. She was given intravenous (IV) furosemide in the emergency room and started on IV nitroglycerin, IV eptifibatide, subcutaneous low molecular weight heparin, aspirin, clopidogrel, atorvastatin, and fosinopril. The patient underwent emergent coronary angiography due to persistent chest pain that revealed a hazy 80% lesion of the mid-LAD, with severe stenosis of the diagonal branch (Figure 2). To reverse any possible spasm, she received multiple doses of intracoronary nitroglycerin and verapamil, but no difference was seen on repeat angiography.  A Luge wire (Boston Scientific Scimed) was advanced and intravascular ultrasound (IVUS) of the LAD was performed that showed a soft plaque, dissection, with severe narrowing and no improvement after repeated intracoronary nitroglycerin (Figure 3). The patient continued to have refractory angina; at this point, the LAD lesion was primarily stented with a 3.5 x 18 mm Driver stent (Medtronic) at 12 atm. Post stent deployment was complicated by dissection of the proximal LAD extending to the major diagonal branch. A second 3.5 x 24 mm Driver stent was deployed in the proximal-mid LAD. At this time, there was a loss of flow in the diagonal (Figures 4 and 5). The diagonal was wired with a 0.014˝ Whisper guidewire (Abbott Vascular) and multiple balloon inflations were done with a 3.0 x 15 mm Voyager balloon (Abbott Vascular) to tag up the dissection with partial establishment of flow (Figure 6). Because of compromised flow, three overlapping stents (two 2.5 x 28 mm Minivision stents and one 3.0 x 28 mm Vision stent; Abbott Vascular) were deployed with restoration of diagonal flow. By using the Culotte technique, a 3.5 x 18 mm Vision stent was placed in the diagonal toward the mid-LAD at 12 atm. After rewiring the LAD through the diagonal stent struts, a 4.0 x 18 mm Vision stent was placed in the LAD at 12 atm and kissing-balloon inflations of the LAD and diagonal were done by 4.0 x 20 mm Quantum balloon (Boston Scientific Scimed) and 3.0 x 12 mm Maverick balloon (Boston Scientific), respectively, at 10 atm. Final angiogram showed TIMI 3 flow in the LAD and diagonal without any dissection or staining (Figure 7). 

Following the procedure, the patient was monitored closely in the coronary care unit and was placed on IV labetalol and nitroglycerin drips for blood pressure control. Gradually, the IV medications were weaned off and changed to oral formulation. Eptifibatide drip was discontinued and long-acting isosorbide mononitrate was initiated. On day 6 of hospitalization, the patient was discharged home on optimal medical therapy including aspirin and clopidogrel. The patient was counseled extensively on lifestyle modification including smoking cessation, quitting cocaine abuse, and avoidance of pregnancy and breastfeeding.

Echocardiogram that was done 3 months postpartum showed global hypokinesis with an ejection fraction of 20%-25%. The patient was readmitted 6 months later with recurrent angina. A coronary angiogram performed at that time showed 80%-90% diffuse in-stent restenosis in the proximal-to-mid LAD, proximal diagonal, and a completely occluded distal diagonal. The left main coronary, circumflex, and right coronary arteries were normal. Successful percutaneous coronary intervention (PCI) of the LAD and diagonal was performed with 4 drug-eluting stents (DESs).  Now 36 months postpartum, she has remained asymptomatic with improvement of left ventricular systolic function to 50% with mild mitral regurgitation.

Discussion. Pregnancy-associated MI is considered rare; the reported prevalence in the United States is 1 in 16,000 births.^3,4 The risk factors for peripartum MI include child-bearing age of 33 years or older, multiparity, and smoking. Other risk factors are obesity, family history of heart disease, hypertension, diabetes mellitus, hyperlipidemia, and cocaine use.^3,6,8 The incidence of cocaine-induced MI in pregnancy is unknown. Physiologic, metabolic, and hemodynamic changes of pregnancy may predispose pregnant cocaine users to MI.⁹ Cocaine abuse may lead to premature atherosclerosis.⁹ Cocaine-related MI might occur as a result of coronary artery spasm and/or thrombus.¹⁰ Spontaneous coronary artery dissection, which is infrequent in the general population, can account for up to 27% of pregnancy-related MIs.^6,7  

The usual time for presentation of MI is during pregnancy or up to 10 weeks postpartum, and the LAD is the most common culprit vessel.¹¹ There are case reports involving multiple arteries, circumflex and also left main.^12,13 Maternal mortality remains at approximately 11%.⁶ 

The pathogenesis of SCAD is believed to be multifactorial. During pregnancy, there is smooth muscle proliferation, reduction in collagen synthesis in the arterial wall, and additional parturition-induced shear stress that is blamed for the intimal tear and SCAD.¹¹ It is also postulated that eosinophilic granules that contain lytic substances, such as collagenase and peroxidase, may break the medial layer, leading to dissection.^14,15 The increased arterial blood pressure from cocaine’s inotropic and chronotropic effects, combined with its direct vasoconstrictive properties, may be responsible for the formation of intimal tear.¹⁶

In the past, diagnosis was mostly based on autopsy findings; however, angiography is the current gold-standard modality. Desai et al examined postmortem findings of 6 young women and 3 young men who had sudden cardiac death with SCAD; histology showed a split in the media of the artery, with blood and fibrin in the fissure.¹³ In this series, there was 1 postpartum patient and 1 man with history of cocaine use.  

Given the rarity of this condition and the wide variety of clinical presentation scenarios, the optimal therapy is less well defined. Postpartum SCAD patients with no evidence of ischemia can be treated medically, but in patients with ongoing signs of ischemia with hemodynamic instability, PCI or surgery need to be considered. Stenting effectively scaffolds the vessel wall and seals the dissection and protects against further dissection. There are technical difficulties during PCI to these vessels, such as placing the wire in the true lumen, vessel sizing¹⁴ and as seen in our case, chance of propagation of dissection in the proximal main vessel and further spiraling down to the branch vessels from the barotrauma of stent deployment.^17-19 The propagation of dissection after LAD stenting can be extensive and may reach to the left main and circumflex arteries.¹⁹ As a result of barotrauma, most patients require multiple stents placed. We do not have enough data to speculate if the amount of pressure used during deployment played a role in propagation of dissection in those cases. However, it might be reasonable to consider using nominal pressures in initial deployment of the stents with postdilatation when needed. Bare-metal stents have been used successfully¹⁴ in the past and there are more published case reports with successful use of DESs.^17-19 Although IVUS may be crucial to assess underlying etiology, there is still a possibility of unexpected propagation of these dissections proximally and distally in the setting of a frail arterial wall, which started the dissection in the first place. 

We undertook a comprehensive review of the literature since SCAD was first described 81 years ago.²⁰ We searched Medline, Pubmed, and Google using the medical subject headings, “pregnancy-related myocardial infarction” and “spontaneous coronary artery dissection” and “cocaine-related spontaneous coronary artery dissection.” A total of 162 case reports have been published between 1952 and 2012 on peripartum SCAD. None of these cases were related to cocaine exposure.^21-23 We found two cases of cocaine-induced SCAD in men^16,24 and two cases of cocaine-related peripartum MI.^25,26 These peripartum patients did not undergo coronary angiography. Our patient had a history of cocaine abuse and her MI was temporally related to smoking cocaine. We suspect a subintimal tear due to increased endothelial shear stress as caused by the inotropic, chronotropic, and vasoconstrictive effects of cocaine on the parturient heart. Our patient did have evidence of atherosclerotic coronary disease and spasm by coronary angiogram and evidence of dissection by IVUS. This led us to consider the link between postpartum coronary dissection and cocaine use. 

Conclusion. The diagnosis of SCAD should be considered in any postpartum patient who presents with MI, particularly in the setting of cocaine use. Urgent coronary angiography is indicated to establish the diagnosis and to determine the appropriate therapeutic approach. Although a clear correlation between cocaine use and coronary dissection is not yet known, we suggest that it be considered as a potential risk factor of postpartum SCAD.

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From the ¹Department of Cardiology, Louisiana State University Health Sciences Center in Shreveport and ²the Department of Cardiology, Overton-Brooks VA Medical Center, Shreveport, Louisiana.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted November 16, 2012 and accepted January 3, 2013.

Address for correspondence: Pavan K. Katikaneni, MD, Department of Cardiology, Louisiana State University Health Sciences Center, 1501 Kings Hwy, Shreveport, LA 71103. Email: pkatik@lsuhsc.edu