Chronic hypertension, recreational cocaine use and a subsequent acute aortic dissection in a young adult

Abstract

Cocaine is a widely used illicit substance and has previously been described as a risk factor for aortic dissection. We present a case of a young recreational cocaine user with uncontrolled hypertension who presented to hospital with acute chest pain and was diagnosed with an acute aortic dissection. The patient’s last use of powdered cocaine was 3 days prior. A workup for secondary hypertension was negative and no other risk factors for aortic dissection were determined. In hospital, the patient was medically managed with multiple antihypertensive agents, was provided with education regarding the risk of ongoing stimulant use and resources to support his goal of abstinence. This case highlights the importance of considering a diagnosis of aortic dissection in a young patient presenting with acute chest pain, underscores the need for a thorough substance use history and provides a novel example of the potential danger of even recreational cocaine use.

Background

Though acute aortic dissection is an uncommon clinical presentation, early diagnosis and treatment are essential as mortality associated with this condition can approximate 25–30%.¹ Accurate diagnosis requires knowledge of signs and symptoms associated with its clinical presentation and familiarity with significant risk factors, which can vary substantially based on the age of the patient presenting. Among younger patients, this can be particularly challenging as aortic dissection may be associated with atypical presentations and occur as a result of unusual risk factors.^2–4 For example, one study by Januzzi et al using data from the International Registry of Aortic Dissection (IRAD) (a prospective database of patients diagnosed with an aortic dissection worldwide) demonstrated that patients <40 years of age with an aortic dissection were less likely to have pre-existing hypertension but more likely to have a diagnosis of Marfan’s syndrome, a bicuspid aortic valve or have undergone previous aortic surgery.⁵

Stimulants, particularly crack or powder cocaine, are a widely used substance of abuse and have previously been described as an important risk factor for aortic dissection, particularly among younger patients.^6–8 To our knowledge, no literature exists highlighting the risk of recreational stimulant use on aortic dissection among younger patients with concurrent chronic uncontrolled hypertension. Here, we report a case of a young patient with an aortic dissection who was a recreational cocaine user and had a past medical history significant for chronic untreated hypertension. Our case illustrates the need to consider aortic dissection in any young patient with poorly controlled chronic hypertension and a history of cocaine use who presents with acute chest pain and highlights several unanswered questions regarding this causal relationship.

Case presentation

A 34-year-old man presented to the emergency department (ED) of an urban hospital located in downtown Vancouver, Canada, with new, sudden onset severe central chest pain radiating to the mid lower back, accompanied by shortness of breath and diaphoresis. The onset of symptoms occurred at rest, 30 min prior to presenting for assessment. The patient’s past medical history was significant for hypertension, for which he had been non-compliant with his medication for an unknown period of time. His substance use history revealed he was an ex-cigarette smoker (having quit 1 year prior), a heavy alcohol consumer drinking approximately 4 beers 5 times per week and an occasional cocaine user (approximately twice per month mainly via nasal inhalation, but occasionally also smoking cocaine). His reported last use of cocaine was 1 g of powder, 3 days prior to presentation in the ED. He denied the use of any injection drugs or any other illicit substances.

On presentation to the ED, the patient was alert but in distress. He appeared pale, cool and clammy. His blood pressure was 262/134 mm Hg but was equal in both arms. He was afebrile, his heart rate was 71 beats per minute, respiratory rate was 22 breaths per minute and his oxygen saturation was 100% on 2 L nasal prongs. His cardiovascular examination revealed normal heart sounds with no murmurs or extra heart sounds. No pulse deficits were noted. His respiratory, abdominal and neurological examinations were all normal.

Investigations

His investigations revealed a normal complete blood count, electrolyte and renal profile and he had a negative troponin series. His ECG revealed normal sinus rhythm with moderate voltage criteria for left ventricular hypertrophy. His chest X-ray showed moderate cardiomegaly with a mild unfolding of the thoracic aorta (figure 1). No effusions or consolidations were seen. Given the patient’s presentation and preliminary investigations, a CT scan of the chest was ordered and revealed a descending (type B) dissection of the thoracic and abdominal aorta, extending into both common iliac arteries as well as the left renal artery (figures 2 and 3).

Figure 1.

Portable anterior-posterior (AP) chest X-ray of the patient sitting demonstrating mild unfolding of the thoracic aorta and moderate cardiomegaly.

Figure 2.

CT scan, sagittal view showing a descending type aortic dissection of the thoracic aorta.

Figure 3.

CT scan, coronal view showing a type B descending dissection of the thoracic and abdominal aorta extending into both common iliac arteries as well as the left renal artery.

Outcome and follow-up

In hospital, the patient required aggressive medical treatment with multiple antihypertensive agents, along with a labetalol infusion, to reach and maintain a blood pressure target of 120 mm Hg systolic. Multiple attempts to wean off the labetalol infusion resulted in recurrent episodes of hypertension and symptom recurrence of chest pain and dyspnoea. As such, the patient remained in hospital for a total of 12 days until his blood pressure could be stabilised on oral medications. A workup for secondary causes of hypertension revealed no abnormalities, with a normal thyroid stimulating hormone (TSH), urine metanephrines, renin–aldosterone ratio and a normal dexamethasone suppression test. It was felt by the treating cardiologist that the patient’s aortic dissection most likely occurred secondary to untreated hypertension exacerbated by the patient’s recent cocaine use. As such, the inpatient addiction medicine service was consulted who provided information regarding the risks of ongoing stimulant use as well as community resources for helping support the patient’s goal of abstinence from both alcohol and cocaine. He was subsequently discharged home on oral ramipril, amlodipine, labetalol, hydralazine, spironolactone and a nitroglycerine patch and advised to attend a follow-up cardiology appointment a few weeks later.

Discussion

We have presented a case of a 34-year-old man with an aortic dissection that occurred in the context of recent cocaine use and untreated chronic hypertension. The patient was a recreational cocaine user, using approximately twice a month, having last insufflated cocaine 3 days prior to the acute onset of chest pain and dyspnoea for which he was evaluated for in the ED. He had a pre-existing diagnosis of hypertension and had been non-compliant with his antihypertensive medication for an unknown period of time. Further workup revealed no secondary cause for his hypertension. Furthermore, there was no history of Marfan’s syndrome, a bicuspid aorta, previous cardiac surgery, nor did the patient have a large proximal aorta. It was felt that the patient’s aortic dissection was secondary to untreated chronic hypertension exacerbated by recreational cocaine use.

Untreated or suboptimally treated hypertension has previously been demonstrated to be a significant risk factor for the development of an acute aortic dissection.1 2 9 10 This case illustrates that such a risk can exist among young adults and highlights the importance of prompt medical management among this patient population. Furthermore, though cocaine use has previously been shown to induce acute hypertension, it is unlikely to have been the cause for the patient’s chronic hypertension given two large-scale studies reported no such association.^{8 10–13} More likely, the patient’s reported heavy alcohol consumption either caused or contributed to his systemic hypertension given the known association between quantity of alcohol consumption and hypertensive risk (with one study demonstrating such a risk to exist at ≥1 drink per day among men).¹⁴

The primary inciting event of an aortic dissection is a tear to the intimal lining of the aorta.^{9 10} Though several studies have demonstrated systemic hypertension to be a significant risk factor, as stated previously, a paucity of literature currently exists examining its association with recreational cocaine use and the potential magnification of risk for an acute aortic dissection among young adults.^{1 2 10} In the setting of cocaine use, several pathogenic mechanisms have been proposed for the creation of such an intimal tear.^{8 11}First, cocaine blocks the reuptake of dopamine and norepinephrine at the presynaptic cleft in both the central and peripheral nervous systems. As a consequence, the activity of these neurotransmitters is enhanced resulting in an acute increase in blood pressure, heart rate and vasoconstriction.^{8 11 15} These acute changes may increase the shearing forces on a blood vessel’s walls, increasing the risk for an intimal tear and ultimately may result in the development of an acute aortic dissection.^{8 11} The rapid onset of cocaine’s haemodynamic effects, especially crack cocaine, further compounds this risk.⁸ At a cellular level, increased endothelin production, decreased nitrous oxide release, platelet aggregation and thrombus formation, all of which occur following cocaine use, can lead to further ischaemia, vasoconstriction and injury.¹⁶ Baseline vasoconstriction may already exist among cigarette smokers or individuals with untreated hypertension and, as such, concurrent cocaine use may further increase one’s risk for development of an acute aortic dissection.^{8 11}

The incidence of acute aortic dissection associated with cocaine use varies depending on the patient population being studied. Among 3584 acute aortic dissections registered in the IRAD database between 1996 and 2012, 1.8% were associated with the use of cocaine.⁶ Comparatively, the incidence of cocaine-associated acute aortic dissections reported by two retrospective studies of inner city populations ranged between 28% and 37%.^{7 8} Several studies have described cocaine-associated acute aortic dissections to occur more commonly among younger, black, men who are cigarette smokers.^6–8 Furthermore, type B aortic dissections were more common among those related to cocaine use^{6 8} and though one retrospective study did report untreated hypertension to be a risk factor for the development of an acute aortic dissection in the context of cocaine use,⁷ these results have not subsequently been replicated (though two larger studies did confirm cocaine-using patients were more likely to be hypertensive at clinical presentation).^{6 8}

Despite this, several knowledge gaps regarding this relationship remain. More specifically, the study’s inclusion of only those individuals ‘who use cocaine to the detriment of his/her health and social functioning’ excludes those who may use cocaine in a recreational fashion and may result in significant reporting bias.⁶ Furthermore, the study’s lack of urine drug screening combined with very high rates of hypertension at the time of clinical presentation among those labelled as cocaine users (92.6%) makes the temporal and causal association of one’s cocaine use with their subsequent aortic dissection particularly challenging. Lastly, no data was collected regarding the type of cocaine used (ie, crack versus powder) or timing of use in relation to symptom onset.

Beyond the IRAD database results, existing literature of cocaine-associated acute aortic dissections comprise primarily of individual case reports or small retrospective studies.2–4 8 10 11 17 18 As such, adequately addressing these knowledge gaps proves problematic. Our case report adds to the existing literature in a number of ways. First, we report the development of an acute aortic dissection in a young recreational cocaine user with concurrent uncontrolled hypertension. A review by Rashid et al of 12 cocaine-associated acute aortic dissections revealed the majority were chronic or daily users in the years prior to presentation with only one case occurring among young women who reported cocaine insufflation approximately 1–2 times per week.^{17 18} Furthermore, the temporal relationship of cocaine use to symptom onset has previously been described in several case reports and retrospective studies and ranges from immediate to 48 hours.^{7 8 17} Our case highlights the importance of considering a diagnosis of acute aortic dissection among individuals reporting or suspected of cocaine use beyond this time frame, given symptom onset did not occur until over 72 hours after cocaine use in our case. Lastly, our patient’s use of powder cocaine and the subsequent development of an acute aortic dissection is unique. The results from two retrospective studies indicate a predominance of crack use among cocaine-associated acute aortic dissections.^{7 8} Similar findings have been reported among existing case reports with only four cases (out of a review of 12) being attributable to the use of powder cocaine.¹⁷ Such findings are likely explained by the pharmacokinetics of both crack and powder cocaine. Crack cocaine, which is not water soluble and vaporises at low temperatures, is rapidly absorbed upon inhalation. As such, peak plasma concentration occurs after just 2 min with its euphoric effects lasting only between 30 and 45 min. In contrast, powder cocaine is a water-soluble crystalline salt that can be insufflated or injected. Its peak plasma concentration occurs after approximately 30 min and its euphoric effects last roughly twice as long as that of crack cocaine.¹⁹ Given crack cocaine’s shorter duration of action and subsequent euphoria, repeated administration (often in a binge pattern) can occur resulting in haemodynamic effects that may be more accentuated, acute in onset and repetitive giving rise to an increased risk for the development of an acute aortic dissection.⁷

The current case illustrates a young patient with untreated hypertension and acute aortic dissection in the context of recent recreational powder cocaine use and highlights the importance of considering such a diagnosis among individuals with reported or suspected cocaine use presenting with symptoms given its high associated mortality rate. Future research should examine in further detail the underlying nature of cocaine use and its association with aortic dissection. including the risk conferred by the type of cocaine used (eg, crack vs powder), timing and chronicity of use and the degree of additional risk conferred by untreated hypertension.

Learning points.

• Systemic hypertension is an important risk factor for aortic dissection, even among younger patients.^6–8

• Concurrent cocaine use can exacerbate uncontrolled hypertension. As such a thorough substance use history is essential for any patient presenting with acute chest pain; this is of particular importance among young adults.

• Future research should evaluate in detail the association between cocaine use and aortic dissection. including the type of cocaine used (eg, crack vs powder), timing and chronicity of use and the degree of additional risk conferred by untreated hypertension.