According to the World Drug Report 2018, the drug market is constantly expanding. Cocaine consumption in 2016 is estimated to have increased by almost 7% from the previous year, and global consumption is increasing among individuals of every socioeconomic strata. The Americas rank first among cocaine users at approximately more than half, mostly North America (34% of the global total).
Almost one-quarter of all cocaine users reside in western and central Europe, while Africa and, to a lesser extent, Asia and Oceania, together may account for the remaining quarter, although there is lack of data in many countries in Africa and Asia. In this context, cardiac MRI seems to be the most promising noninvasive imaging modality to investigate the involvement of the heart, with its unique ability of in vivo tissue characterization. This article aims to provide an overview of current and future cardiac MRI perspectives focusing on what has been called an attack on the cardiovascular system.
Following a clinical approach, cardiovascular manifestations of cocaine abuse have been classified into acute and chronic effects, and the review is structured accordingly.
Acute Cardiovascular Effects of Cocaine
Pharmacology in the Acute Phase: Effects on Myocardium, Coronary Arteries, and Platelets
Cocaine blocks the reuptake of catecholamines such as norepinephrine and dopamine, both in the central nervous system and at peripheral sites, leading to a sympathomimetic action mediated by α- and β-adrenergic receptors. In addition, cocaine acts as a class I antiarrhythmic agent (local anesthetic) causing depression of the cardiovascular system. Cardiovascular effects are often worsened by concomitant alcohol consumption; the abuse of these two substances together leads to the metabolism of cocaethylene in the liver, blocking the reuptake of dopamine and extending cocaine cardiovascular action.
Clinical and Cardiac MRI Manifestations in Acute Abuse
Acute manifestations of cocaine abuse can occur minutes or days after cocaine administration, but the risk is higher in the first 60 minutes after its intake. The most common clinical manifestation is chest pain, with more than 500 000 patients admitted to the emergency department every year in the United States. Several possible manifestations of acute cocaine abuse involve the heart, including cocaine-induced myocardial infarction (CIMI), cocaine-induced acute myocarditis and catecholamine-induced cardiomyopathy. Even though the clinical manifestations are highly overlapping, cardiac MRI is able to inform differential diagnosis.
Cocaine-induced acute myocarditis.—The pathophysiology of cocaine-induced myocarditis is still unclear. Moreover, the temporal change of cardiac effects following cocaine intake is not completely understood in the literature. However, in an autopsy study by Virmani et al, it was shown that mononuclear infiltration was present in 20% of dying patients with a detectable level of cocaine in the blood. Acute myocarditis is nearly 10 times more common than CIMI and was observed in 20% of patients who had died of cocaine abuse and had no signs of coronary artery disease. It has been postulated that the mononuclear cellular infiltrate in cocaine-induced acute myocarditis may be caused by a hypersensitivity reaction leading to an inflammatory response in the myocardium.
Autopsy studies support the concept that cocaine may induce scattered foci of necrosis and loss of cardiac myofibrils. In accordance with the Dallas criteria and the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases, myocarditis is histologically defined as myocyte degeneration, edema, and necrosis not explained by ischemic causes. Following these histologic findings, Friedrich et al published a pivotal article on the cardiac MRI diagnosis of myocarditis, addressing it as the reference standard technique and establishing the Lake Louise criteria, which were updated in 2018.
CCM: Asymptomatic phase—In recent years, the new concept of subclinical CCM has received considerable interest. Aquaro et al found 16 (53%) of 30 patients with subtle electrocardiographic abnormalities but negative finding for ischemia with stress test and pressure Holter monitoring. However, at cardiac MRI, 14 (47%) of 30 subjects showed edema and 22 (73%) of 30 were LGE positive (15 [68%] of 22 ischemic and seven [32%] of 22 nonischemic pattern). A recent study by Radunski et al using cardiac MRI found statistically significant differences between asymptomatic cocaine-abusing patients and a control group in terms of presence of LGE, nonischemic LGE pattern, and midmyocardial LGE (eight [40%] of 20 vs zero [0%] of 20; eight [40%] of 20 vs zero [0%] of 20; six [30%] of 20 vs zero [0%] of 20, respectively; P < .01). However, in this phase, no differences emerged regarding ventricular function and mapping tissue characterization between cocaine abusers and control subjects.
CCM: Dilated phase—The dilated phase of CCM is clinically indistinguishable from idiopathic dilated cardiomyopathies. However, several histologic differences were found in terms of cardiomyocyte diameters, nitric oxide synthase, and necrosis (20.4 μm ± 1.3 vs 17.5 μm ± 0.7; 1.8 ± 0.9 vs 0.5 ± 0.5; 18827 nuclei/106 ± 14442 vs 2949 nuclei/106 ± 1989, respectively; P < .05). Even though no differences were found between CCM and idiopathic dilated cardiomyopathies using cardiac MRI in ventricular function, 31% of long-standing cocaine abusers showed LV dilatation. Both LV and right ventricular ejection fractions were less in the cocaine abuser group versus the control group (59% ± 5 vs 68% ± 4; 56% ± 5 vs 65% ± 5, respectively; P < .05). The LGE patterns found in the dilated phase of CCM were nodular subepicardial, linear subepicardial, junctional, and subendocardial. All of these LGE patterns could potentially represent the multifactorial pathogenesis of CCM. More precisely, nodular subepicardial and linear subepicardial involvement may represent the results of chronic myocarditis, junctional pattern arises from focal replacement fibrosis due to hypertrophy and desynchrony between the two ventricles, and subendocardial pattern is the classic appearance of ischemic cardiomyopathies.
In conclusion, as shown, cardiac MRI can distinguish between acute cardiac manifestations of cocaine abuse, including CIMI, cocaine-induced myocarditis, and catecholamine-induced cardiomyopathy. Moreover, thanks to its unique ability of in vivo tissue characterization, cardiac MRI is also able to differentiate the multiple facets of CCM and to recognize underlying pathophysiologic processes. However, no radiologic and anatomopathologic differences were found between cocaine-induced and non–cocaine-induced cardiac manifestations. Therefore, diagnosis should be carried out by integrating epidemiologic data (younger patients, sex, etc), clinical assessment (history of drug abuse), laboratory findings, and imaging findings (cardiovascular MRI).