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Figure 3: Q waves in V1, V2, and resolved T wave inversion in inferior leads with poor R wave progression in lateral leads.

A few days later, the patient stabilized clinically therefore, a Computed Tomography Coronary Angiogram (CTCA) and a repeat ECHO were requested. Repeat ECHO showed a normal-sized heart with hyperdynamic LV systolic function. The visual LVEF was 70% +/-5%, an improved function compared to the previous ECHO. CTCA showed a normal coronary artery, no coronary stenosis or plaques, and a calcium score of 0, which raised the likelihood the patient had Stress Cardiomyopathy (Takatsubo).

The patient was deemed medically stable for discharge. A follow-up in the cardiology outpatient clinic was arranged along with a cardiac MRI. Another out-patient follow-up with the ENT team has been also arranged.

Discussion

Cocaine is a tropane alkaloid that blocks the reuptake of amines, it acts as a sympathomimetic agent, central nervous system (CNS) stimulant, local anesthetic, and vasoconstrictive agent [4,5].

Systemic side effects of the administration of cocaine are well-known, such as arrhythmias, cardiac ischemia, cerebral ischemia, convulsions, hypertension, hyperthermia, loss of consciousness, renal failure, respiratory depression, and rhabdomyolysis [6-8]. In our patient, she experienced a severe cardiovascular collapse shortly after the use of cocaine intranasally.

Acute coronary syndrome (ACS) or MI are well-known complication of cocaine use, however, most of the reported cardiac complications of cocaine were secondary to the recreational use of cocaine until the 1980s when cocaine started being used as a topical anaesthetic more cases of MI secondary to medical use have been published [9]. Even with the current common use of cocaine in sinonasal surgeries, cardiac events secondary to the medical use of cocaine are significantly lower than cardiac complications due to recreational use [7]. However, our patient was unfortunate to suffer from clear cardiac ischemic changes along with severe LV dysfunction leading to hemodynamic instability.

Cocaine increases the risk of acute coronary syndrome (ACS) in multiple ways. Firstly, due to its sympathomimetic effects leading to increased heart rate and blood pressure, cocaine increases the myocardial oxygen demand [5,10]. Secondly, due to its alpha-adrenergic effects, cocaine causes coronary vasoconstriction and therefore decreases the myocardial oxygen supply [5,10].

It was widely reported that 200 mg is the maximum safe dose of topical intranasal cocaine [2]. However, there are multiple reports of significant adverse reactions and even deaths due to the administration of doses as low as 10 mg of cocaine, which raises the suspicion of the possibility of cocaine toxicity being dose-independent [2]. Recent studies suggest that topical cocaine doses should not exceed 100 mg or 1.5 mg/kg [7]. The highest concentration of cocaine in the bloodstream following nasal administration typically occurs within 15 to 60 minutes after application [11]. This is the same period during which our patient shows signs of hemodynamic deterioration.

The evidence of cardiac complications of intraoperative topical cocaine use is mainly based on case reports. However, a population study in 2020 studied the difference in perioperative cardiac complications between patients who have sinonasal surgery in institutions that use cocaine versus patients who have their surgeries in institutions that use alternative agents in sinonasal surgeries. They found no statistically significant difference in the rate of major cardiac events or death between patients treated with topical cocaine and those treated with alternatives [12]. Moreover, the overall rate of cardiac events and mortality within 48 hours of use was very low, ≤0.2% with no statistically significant difference in comparison to alternative agents.

The metabolism of cocaine is complex and varies significantly across different populations due to genetic differences. These genetic variations can impact the efficacy and safety of cocaine when used medicinally. Cocaine is primarily metabolized by the cytochrome P450 (CYP) enzyme system, particularly CYP3A4 and CYP2D6 [13]. Variations in the genes coding for these enzymes can lead to differences in how individuals process the drug.

Genetic polymorphisms in CYP enzymes are distributed differently among racial and ethnic groups. For instance, certain variants of CYP2D6 that lead to poor metabolism are more prevalent in Caucasians compared to Asians and Africans [14]. This means that individuals with these variants may have higher plasma concentrations of cocaine, increasing the risk of adverse effects.

Some populations have a higher prevalence of enzyme deficiencies that can affect cocaine metabolism. For example, pseudocholinesterase deficiency, which can slow the breakdown of cocaine, is more common in certain ethnic groups. This deficiency can lead to prolonged effects and increased toxicity [15].

Conclusion

This article aims to highlight a severe cardiovascular event, likely due to cocaine-induced myocardial infarction and stress cardiomyopathy, following the use of medical cocaine during surgery. It underscores the risks associated with cocaine, even in controlled settings, and the importance of personalised medicine, including genetic screening, to identify patients at higher risk of adverse reactions. The study advocates for cautious use of cocaine, considering safer alternatives in sinonasal surgeries, and calls for further research to better understand cocaine toxicity. Understanding the genetic factors is vital for personalised medicine, as it can help tailor treatments to minimize risks and optimize the safe use of cocaine in medical contexts. It emphasizes the need for thorough patient screening and ongoing vigilance to manage potential complications.