Cocaine and aortic dissection: the need for collaboration to overcome the underreporting bias

The incidence of acute aortic dissection is not common in clinical practice, and early diagnosis is essential considering that the mortality rate is 25–30% [15,16,17,18]. Jannuzzi et al. published a retrospective study using data from the International Registry of Aortic Dissection (IRAD), a retrospective database collecting data of patients diagnosed with aortic dissection worldwide [19].

The abuse of stimulants, especially cocaine, is described in scientific literature as a significant risk factor for the onset of aortic dissection, particularly in young people [20,21,22]. Cocaine exerts its cardiotoxic effect also at the level of cardiac muscle, leading to various forms of cardiomyopathy [23, 24].

Hsue et al. [21] published a retrospective study based on 20 years’ experience in the field of acute aortic dissection. Results indicate that 37% of patients treated for acute aortic dissection (14 out of a total of 38) reported cocaine use in the minutes or hours immediately preceding the event. Cocaine, especially crack, seems to play a crucial role in aortic dissection in the study group (with a mean age of 41 ± 8.8 years), especially among white individuals (11 out of 14, 79% of total) and those affected by hypertension (11 out of 14, 79% of total). The mortality rate in hospital was 29% (4 patients out of 14).

Dewar and Nolan reported a non-fatal case of aortic dissection in a 34-year-old man who arrived at the emergency department with severe chest pain radiating to the back, accompanied by dyspnea. Cardiac, respiratory, abdominal, and neurological examinations were normal. However, the man admitted cocaine use, with the last assumption three days before the chest pain [25].

From an anamnestic perspective, the here discussed case fits the history of a substance abuse for at least a year when compared to other cases that have been reported in the literature, especially the review by Greve et al. [25]. Authors evidenced as the percentage of tobacco smokers in all reviewed case series ranged from 61 to 100%. Prior research has also revealed a higher incidence of cocaine-related aortic dissection in young male smokers suffering from hypertension [25].

In the presented case the personal history of alcohol consumption is a key element, while no history of smoking is reported, and toxicological analyses resulted negative to nicotine/cotinine. Alcohol is a cardiotoxic substance [24,25,26,27] although other research has not reported on such exposure in fatal cases involving aortic dissection in cocaine addicts. The combined use of cocaine and alcohol has been reviewed in relation to violent behavior, but not in fatalities [28], with only one non-fatal reported case of associate heavy consumption of cocaine and alcohol [29]. Apart from the deliberate exposures, it should be mentioned that for the here case discussed, the deceased presented a diagnosis of hypertension and was under pharmacological treatment. However, there was no information available regarding treatment responsiveness, in contrast to another case report in which hypertension was reported under proper pharmacological control [30]. The deceased was diagnosed with a type A aneurysm under the Standford classification, which is the least represented subclassification from the perspectives of cardiac surgery and anatomy-pathology [20,21,22, 31, 32]. As in the cases already mentioned, the patient here presented was male and fell perfectly within the age ranges of the other case reports in the literature. One of the most interesting aspects to be highlighted in the presented case is the evidence of high urinary cocaine metabolite levels as well as blood concentration, indicating chronic exposure over time to the substance, with a previous residual metabolism of the substance itself. The patient has had a recent alcohol intake, as evidenced by ethyl glucuronate positivity, despite blood alcohol resulted negative. Such evidence, also confirmed by circumstantial datum of a past alcohol abuse reported by his relatives, could have played a key role in determining a vulnerability of the patient to the occurrence of the acute and fatal event.

Regardless of cocaine cardiotoxicity, its possible role in increasing the risk for aortic dissection is still debated, especially due to a lack of epidemiological correlation [25]. Data from case series available in literature [20, 21, 22, 25, 3132] show features that increase the risk for aortic dissection: young male patients, hypertension, smokers, apart from already mentioned history of cocaine abuse. Difficulties in outlining a correlation between cocaine abuse and aortic dissection on an epidemiological base are mainly related to the low prevalence of AD in cocaine abusers with respect to the general population, accounted for 1.8% (63 cocaine positive out of 3584 patients) according to IRAD data collected from 1996 to 2012 [20]. Cocaine use is associated to the most severe type of aortic dissection according to Stanford classification (B type): data from Dean et al. evidenced a prevalence of 1.4% of cocaine abusers suffering from type A aortic dissection (33/2232), with 2.4% among patients with type B (30/1252) [20]. A reliable explanation of such low prevalence could be a significative underestimation of drug’ use/abuse among patients. Due to the low prevalence of toxicological analyses not often present in diagnostic protocols, data from individual habits are mainly derived from self-reports at clinical history collection. Consequently, the so-called “self-reported bias” could represent a serious issue in limiting the accuracy of the exact prevalence of drugs abuse among patients with AD. A complete toxicological screening should be included in clinical practice, as a unique tool to highlight the real patient status, thus overcoming his/her reticence to self-admit the use. Moreover, the overall differential diagnosis process would benefit, both in terms of prompt and resolutive patients’ management and possible malpractice allegations in case of fatal outcomes. To balance the patient’ right to self-determination and the due to ensure best therapeutic management, an effective information should be offered, with particular emphasis on consequences related to all risk factors, among which cocaine use/abuse could lead to the most fatal outcome, making the patient aware of the real value of a complete and truthful anamnesis. In non-fatal cases the patient awareness about possible future and potentially more severe consequences could positively impact on his/her habits.

The correct estimation of aortic dissection prevalence could benefit from forensic reports about fatal cases not-related to hospitalization. At present such portion of individuals is totally unknown, since such cases are not recorded in IRAD, thus missing critical information in the most severe cases of AD. To cover such a gap, information collected from case reports like the one discussed here could be a starting point for a solid collaboration between clinicians and forensic scientists aimed to comprehensively describe the extent of the phenomenon.

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