Cocaine Abuse: An Attack to the Cardiovascular System—Insights from Cardiovascular MRI
Published Online:Jun 13 2019https://doi.org/10.1148/ryct.2019180031
Abstract
Cocaine is the most commonly used illicit drug in the European Union. Its cardiac effects are numerous and diverse, both in acute and chronic abuse, and include myocardial infarction, myocarditis, catecholamine-induced cardiomyopathy, and chronic cardiomyopathy (subclinical, hypertrophic, and dilated phases). Their clinical manifestations are vastly overlapping, and differential diagnosis should be performed using a thorough diagnostic workup featuring clinical history, laboratory tests, electrocardiography, stress test, noninvasive imaging modalities, and coronary angiography. Cardiac MRI has the unique ability of in vivo tissue characterization. This unique feature can play a pivotal role in the differential diagnosis through proper characterization of the myocardial tissue. Especially in acute settings, cardiac MRI makes it possible to distinguish between cocaine-induced myocardial infarction, cocaine-induced myocarditis, and catecholamine-induced cardiomyopathy. Conversely, in chronic cardiomyopathy, cardiac MRI permits evaluation of ventricular function and myocardial tissue, allowing the investigation of the underlying cause. On the one hand, assessing the ventricular function permits differentiation among subclinical, hypertrophic, and dilated phases of chronic cardiomyopathy; on the other hand, cardiac MRI could classify the causes underlying remodeling, including chronic ischemic injury, chronic myocarditis, and cardiac motion impairment. This review analyzes the relationship between pathophysiology, histology, and disease using the existing literature on cardiac MRI cocaine abuse evaluation.
© RSNA, 2019
Summary
Cardiac MRI has a pivotal role in the diagnostic workflow of cocaine-induced cardiovascular diseases in both acute and chronic settings.
Essentials
- ■ Cardiac MRI is able to depict cocaine effects on the cardiovascular system.
- ■ Cardiac MRI helps in the differential diagnosis between acute and chronic manifestations.
- ■ Cardiac MRI has a pivotal role in the differential diagnosis between cocaine-induced acute manifestations: myocardial infarction, myocarditis, and catecholamine-induced cardiomyopathy.
- ■ Cardiac MRI has diagnostic and prognostic implications in cocaine-induced chronic manifestations, which are divided into asymptomatic, hypertrophic, and dilated cardiomyopathies.
Introduction
According to the World Drug Report 2018 (1), 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. Cocaine is the main illicit psychostimulant drug in the European Union (2). In the European Union adult population (15–64 years old), prevalence of cocaine consumption was estimated to be around 3.4 million during 2017 (2). Throughout Europe, the most recent surveys reveal an increasing or stable trend of cocaine abuse, in contrast with the decreasing rate reported in previous years (2).
One of the organs most affected by cocaine abuse is the heart, with cardiovascular effects mostly depending on an uncontrolled stimulation of the sympathetic system, inducing arterial hypertension, intraventricular conduction disturbances, and chronotropic and inotropic uninhibited triggering.
This corresponds to a spectrum of clinical manifestations, including myocardial ischemia and infarction (cocaine-associated heart attack affects 0.7%–6% of those presenting with chest pain to the emergency department), coronary spasm, impairment in systolic and diastolic function, atherosclerosis, myocarditis, cardiomyopathy, arrhythmia, hypertension, and endocarditis (prevalence, 1%–5%) (3). As far as cardiovascular complications are concerned, cocaine abusers can have aortic dissection (incidence of 1%, as reported by the International Registry for Aortic Dissection), mesenteric ischemia, pulmonary edema, renal and testicular infarction, seizures, migraine, cerebral infarction and intracranial hemorrhage (associated with crack cocaine in 94% of the whole spectrum of cocaine-related cerebrovascular events), venous thrombosis, and thrombophlebitis (3).
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 (4).
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 (5), and the review is structured accordingly.
Recommended Protocol for Cocaine-induced Cardiac Manifestation at Cardiac MRI
Cardiac MRI assessment should focus on the complexity of cocaine-induced cardiac damage in both acute and chronic manifestations. Thus, biventricular function and myocardium characterization should be analyzed.
Cine sequences (steady-state free precession) performed on the entire short-axis, four-chamber, and long-axis planes are crucial for evaluation of ventricular function abnormalities (6).
Tissue characterization should include short tau inversion-recovery (STIR) and T2 mapping for edema and T1 mapping, extracellular volume, and late gadolinium enhancement (LGE) sequences for fibrosis and necrosis assessment (6) (see Fig 1 for the detailed protocol).
Figure 1: Cardiac MRI in cocaine-related disease. The lower row is the suggested protocol; numbers are time in minutes. The upper row is the corresponding pathophysiologic change (see Fig 2 and Fig 4) and related cardiac MRI findings. CIAM = cocaine-induced acute myocarditis, CIMI = cocaine-induced myocardial infarction, CMP = cardiomyopathies, Gd = gadolinium, SSFP = steady-state free precession, STIR = short tau inversion-recovery, T2w = T2 weighted.
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 (7,8) (Fig 2a). 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 (9).
Figure 2a: (a) Mechanism of catecholamine reuptake inhibition in sympathetic nerve terminals. Cocaine (black squares) blocks the normal recycling process of catecholamines (yellow circles) by binding the dopamine transporter, causing dopamine accumulation in the intrasynaptic space. This leads to hyperstimulation of the postsynaptic receptor of norepinephrine and dopamine leading to several effects on the cardiovascular system (see text for detailed explanation). (b) Graph shows effects on cardiovascular system. NO = nitric oxide synthesis. (Fig 2a courtesy of Cinzia Catapano.)
Figure 2b: (a) Mechanism of catecholamine reuptake inhibition in sympathetic nerve terminals. Cocaine (black squares) blocks the normal recycling process of catecholamines (yellow circles) by binding the dopamine transporter, causing dopamine accumulation in the intrasynaptic space. This leads to hyperstimulation of the postsynaptic receptor of norepinephrine and dopamine leading to several effects on the cardiovascular system (see text for detailed explanation). (b) Graph shows effects on cardiovascular system. NO = nitric oxide synthesis. (Fig 2a courtesy of Cinzia Catapano.)
From a biochemical point of view, norepinephrine binds β1-adrenergic receptors and gives origin to a signaling cascade that eventually leads to an increase in calcium levels in cardiomyocytes (positive inotropic effect). In addition, cocaine improves pacemaker cells’ rate of depolarization, increasing the heart rate in a dose-related way (positive chronotropic effect) (7,10). Furthermore, cocaine causes coronary vasoconstriction, an effect of increased norepinephrine levels, stimulation of the production of endothelin, and inhibition of nitric oxide synthesis (7,11).
Cocaine also has a prothrombotic action, exerted by activating platelet aggregation and coagulation, which increases fibrinogen and tissue factor and decreases expression of tissue factor inhibitor, antithrombin III, and protein C. These events can lead to thrombus formation, endothelial damage, and accelerated atherosclerosis in patients with chronic abuse (11). Specifically, cocaine promotes thrombosis by increasing platelet activity and aggregation, elevating the levels of fibrinogen and von Willebrand factor and increasing plasminogen activator inhibitor activity (5). In addition, platelet aggregation is increased by activating the shear-dependent von Willebrand factor due to vasoconstriction-induced flow velocity augmentation (12). Last, autopsy studies have shown the presence of mast cells in the plaques of habitual cocaine users; these cells have a causal role in atheroma formation and progression in these patients (13).
To summarize, the increased oxygen demand by the myocardium caused by the positive inotropic and chronotropic effects, the decreased oxygen supply due to the contraction of coronary arteries’ smooth muscle cells, and the accelerated atherosclerosis and prothrombotic status lead to an imbalance in the demand-supply equilibrium (3,11). The alteration of this balance may underlie the acute manifestations of cocaine abuse (11) (Fig 2b).
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 (5,11). 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 (14).
Several possible manifestations of acute cocaine abuse involve the heart, including cocaine-induced myocardial infarction (CIMI) (15), cocaine-induced acute myocarditis (16), and catecholamine-induced cardiomyopathy (17). Even though the clinical manifestations are highly overlapping, cardiac MRI is able to inform differential diagnosis (18,19).
Cocaine-induced myocardial infarction.—Chest pain and ST segment electrocardiographic abnormalities are very common among cocaine abusers, but only 6% of them are caused by myocardial infarction (5,20). However, as shown by Schwartz et al (5), in patients with CIMI, angiographic findings revealed one- or two-vessel disease in 31%–66% of the cases and three-vessel disease in 13%–15%. CIMI involves the anterior wall in 77% of cases (7); within 12 hours of onset, it is associated with lower incidence of complications such as ventricular arrhythmias, congestive heart failure, and death (2% of cases) when compared with non–cocaine-related myocardial infarction. In non–cocaine-related acute myocardial infarction, myocardial necrosis is usually associated with plaque rupture, whereas in cocaine abusers, atherosclerotic lesions displayed neither plaque rupture nor hemorrhage. In fact, CIMI is most frequently associated with the altered oxygen supply-demand balance due to increased inotropism and chronotropism, coronary vasospasm, and prothrombotic state (20).
The classic pathologic theory of myocardial infarction consists of a wave-front ischemic injury rising from the subendocardial layer with a progressive extension to the subepicardium (18,21). From a histologic point of view, within 4 hours of the myocardial infarction, interstitial edema can be seen at light microscopy; within 7 days prolonged coagulative necrosis, granulation tissue, and fibroblasts can be detected (22). All of these histologic changes can be identified with high sensitivity at cardiac MRI (23). The myocardial edema, arising from ischemia-induced inflammation, can be depicted with a T2-weighted STIR sequence (24,25) (Fig 3). The postischemic fibrosis can be depicted with T1-weighted LGE sequences. Edema and fibrosis should be distributed in the so-called ischemic pattern, consisting of the involvement of the subendocardial layer with a progressive extension to the subepicardium and an injured area consistent with one or more coronary artery supply territories. Moreover, patients with CIMI had a higher prevalence of microvascular obstruction (26) (Fig 3, D), a well-known independent predictor of left ventricular (LV) remodeling, compared with the control group as assessed both with coronary angiography (27) and cardiac MRI (24) (Fig 4, A).
Figure 3: A, B, MR images of aborted myocardial infarction in a 44-year-old woman with acute chest pain, chronic cocaine abuse (>10 years), troponin elevation, and ST elevation at admission electrocardiography. A,Short-axis T2-weighted short tau inversion-recovery image demonstrates the presence of transmural edema (arrows) in the anteroseptal and inferoseptal myocardial segments (left descending artery’s vascular territory).B, Late gadolinium enhancement (LGE) sequence in the same cardiac plane did not show deposition of gadolinium inside the myocardium. C, D, MR images show an anteroseptal infarction with microvascular obstruction in a 38-year-old man with long-standing abuse of cocaine and troponin elevation. C, Edema in anteroseptal wall (arrow). D, The short-axis LGE sequence highlighted transmural hyperintensity of the anteroseptal wall (arrow) with linear hypointensity (arrowhead) inside the microvascular obstruction.
Figure 4: Diagnostic flowcharts of, A, acute and, B, chronic manifestations. CIAM = cocaine-induced acute myocarditis, CIC = cocaine-induced cardiomyopathies, CIMI = cocaine-induced myocardial infarction, ECV = extracellular volume, LGE = late gadolinium enhancement, STIR = short tau inversion-recovery.
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 (16). However, in an autopsy study by Virmani et al (28), 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 (16). 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 (10). Autopsy studies support the concept that cocaine may induce scattered foci of necrosis and loss of cardiac myofibrils (10,29). 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 (30). Following these histologic findings, Friedrich et al (31) 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 (32). In particular, the classic Lake Louise criteria considered, for myocarditis diagnosis, the presence of at least two of three of the following criteria: regional or global edema (T2-weighted STIR), hyperemia and capillary leakage (early gadolinium enhancement), and necrosis and fibrosis (LGE). The new criteria are still linked to the pathophysiology of myocardial inflammation but are now configured as “two of two” instead of “two of three” (32). In particular, to reach a sufficient accuracy for the diagnosis of myocarditis, T2-based imaging and T1-based imaging criteria are both necessary (32) (Fig 5). The T2-based imaging criterion aims to detect edema in the myocardium with at least one of the following parameters: regional high T2 signal intensity or global T2 signal intensity ratio between myocardium and skeletal muscle ≥ 2 standard deviations on T2-weighted images or regional or global increase of myocardial T2 relaxation time. The T1-based imaging criterion deals with the presence of edema, hyperemia, capillary leak, necrosis, and fibrosis. Such criterion can be fulfilled by increased regional or global native myocardial T1 relaxation time or expanded extracellular volume or areas with high signal intensity in a nonischemic distribution pattern on LGE images. The nonischemic pattern was defined as an injured area not consistent with coronary artery supply territories and without the involvement of the subendocardial layer (32). The performance of the updated Lake Louise criteria depends on which parameter was selected in both criteria (T1- and T2-based imaging). The accuracy ranges from 76% (71%–89% for LGE and T2-weighted) to 96% (82%–97% for LGE and T2 mapping). Aquaro et al (33) demonstrated that myocardial edema (positive on T2-weighted STIR images) is correlated with the acute consumption of cocaine reflecting an early marker of silent cardiac damage. In addition, although considering the original Lake Louise criteria, Francone et al (34) analyzed the cardiac MRI diagnostic performance based on different clinical presentations (sensitivity of 80% for infarct-like pattern, 57% for cardiomyopathy pattern, and 40% for arrhythmic pattern). Considering all these data and the most common clinical presentation of cocaine abuse (chest pain) (35), cardiac MRI stands out as a crucial tool in the differential diagnosis between ischemic and nonischemic forms and should be considered in symptomatic patients with elevated troponin level following cocaine abuse (16) (Fig 4, A).
Figure 5: Acute myocarditis in a 34-year-old man with acute chest pain and runs of ventricular tachycardia, elevated troponin level, ST elevation at electrocardiography, and no stenosis at coronary artery angiography. Reported 8 years of intense cocaine abuse. A, Short-axis short tau inversion-recovery sequence (T2-based imaging) shows edema (arrow) distributed as nonischemic pattern in the free wall of the left ventricle. B, Late gadolinium enhancement (T1-based imaging) image confirms nonischemic pattern with subepicardial band (arrow). C, Histologic specimen from endomyocardial biopsy shows edematous myocardial tissue and remarkable mononuclear infiltration surrounding the cardiomyocytes (black arrows). (Histologic image courtesy of A. Frustaci, Rome.)
Catecholamine-induced cardiomyopathies.—In an autopsy study, Tazelaar et al (36) showed that the presence of contractile bands is more frequent in cocaine-abuse myocardium with respect to the control group (28 [93%] of 34 and nine [45%] of 20, respectively, P < .01). Contractile bands are a typical sign of catecholamine-induced cardiomyopathy (37). This finding is mainly linked to the preganglionic inhibition of norepinephrine reuptake, potentiating the catecholamine effects on the heart and inducing catecholamine-induced cardiomyopathy. This pharmacologic effect causes an LV dysfunction due to cocaine’s direct inotropic effect and due to excessive catecholamine levels, which induce toxicity and cardiomyocyte apoptosis, as seen in pheochromocytoma-induced cardiomyopathy (10,38). Cardiac MRI is essential in catecholamine-induced cardiomyopathy diagnosis to rule out CIMI and cocaine-induced myocarditis and to analyze the contractile abnormalities, a true hallmark of the disease (39). The wall-motion abnormalities consist of dyskinesia, akinesia, or hypokinesia of the midplane of the LV, without coronary vascular distribution, leading to an apical ballooning motion pattern that can be detected with cine cardiac MRI (40).
Positive T2-weighted STIR images reflecting an acute inflammatory insult of the myocardium are most commonly midapical, with diffuse or transmural edema distribution and a noncoronary pattern (40) (Figs 4, A; 6).
Figure 6: Catecholamine-induced cardiomyopathy in a 37-year-old woman admitted in the emergency department for acute chest pain and troponin elevation following acute cocaine intake. A, T2-weighted short tau inversion-recovery image on a two-chamber long axis shows myocardial edema with typical apical distribution (arrow). This finding was confirmed by, B, late gadolinium enhancement image in the same plane that highlights the presence of the late accumulation of gadolinium in the same territory (arrowhead). (Images courtesy of Luigi Natale, Rome.) C, Histologic specimen shows contraction-band necrosis and fibrosis found at endomyocardial biopsy. Inflammatory cells can be seen infiltrating the necrotic tissue.
Chronic Cardiovascular Effects of Cocaine: Cocaine-related Cardiomyopathy
Clinical and Cardiac MRI Manifestations in Chronic Abuse
Several direct and indirect effects of cocaine are implicated in the genesis of the chronic manifestations of cocaine abuse, including impaired calcium handling, oxidative myocardial damage, catecholamine surplus, and myocardial ischemia (20,41). These features may lead to chronic hypertension and LV dysfunction. The dose-related increase in blood pressure provoked by the general vasoconstriction represents an additional risk factor for cardiac long-term events (ie, dilated cardiomyopathy) and heart failure (10,42). Histologic findings from endomyocardial biopsies and autopsies revealed that cocaine abuse is linked to the presence of foci of cardiomyocytes being either dead (necrosis or apoptosis) or damaged (severe myofibrillolysis, contracted residual myofibrils, dilated mitochondria, and fragmented sarcoplasmic reticulum) (41). Frustaci et al (41) also found sparse lymphocytic infiltrates, possibly associated with the inflammatory reaction activated by damaged cells. Another histologic finding is areas of fibrosis representing districts of healed contraction-band necrosis, which can lead to severe ventricular arrhythmias (10).
Fibrosis, necrosis, and inflammatory infiltrate are similar in appearance to the cardiac lesions described during prolonged catecholamine exposure (especially pheochromocytoma) (5). In fact, cardiomyopathy and cocaine cardiotoxicity are strongly related to myocardial oxidative stress and mitochondrial dysfunction. Catecholamines induce formation of aminochromes and redox cycling molecules, which activate NADPH oxidase and xanthine oxidase and promote generation of reactive oxygen species. Different studies performed with cardiac MRI revealed that cocaine users are characterized by ventricular dilatation and hypertrophy (8), associated with systolic dysfunction, reduction of ejection fraction, and LV remodeling (both eccentric and concentric). In addition, the impairment of regional myocardial contraction could play a role in the pathophysiologic mechanism of heart overwhelming as described using cardiac MRI strain by Ren et al (43). These findings are related to several interacting mechanisms: ischemia, sympathetic stimulation, cardiotoxicity, and myocarditis caused by chronic cocaine use (44).
The phenotypic manifestations of long-standing use of cocaine are hypertrophic and/or dilated cardiomyopathies (42); the broad spectrum of this is called cocaine-related cardiomyopathy (CCM). Rajab et al (45), in an autopsy study, observed that 85% of the deceased had cardiovascular disease, specifically LV hypertrophy in 46%, multifocal non–infarctlike fibrosis in 21%, and LV dilatation in heart failure in 18%. The hypothetical pathophysiologic process could be summarized as subclinical → hypertrophy → dilatation → heart failure (44).
These findings suggest a possible role of cardiac MRI in the evaluation of chronic abusers; however, no data were present in the literature regarding impact on primary and secondary cardiovascular prevention in this set of patients.
CCM: Asymptomatic phase.—In recent years, the new concept of subclinical CCM has received considerable interest. Aquaro et al (46) 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 (47) 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 (47) (Fig 7).
Figure 7: Early stage cocaine-related cardiomyopathy. MR images in a 31-year-old man with recurrent arrhythmia and a 6-year history of cocaine use. A, Short-axis cine steady-state free precession sequence demonstrates no motion alteration. B, Short-axis T2-weighted short tau inversion-recovery sequence shows the absence of myocardial edema. C, Short-axis native T1 mapping highlights diffuse myocardial fibrosis, with a native T1 greater than 1100 msec. D, Histologic specimen.
CCM: Hypertrophic phase.—The hypertrophic phenotype has already been observed by Brickner et al (48) in the early 1990s (LV mass of 103 g/m2 ± 24 [standard deviation] vs 77 g/m2 ± 14, P < .01). These findings were confirmed by a study by Kozor et al (49) in 2014, showing that “otherwise healthy individuals” who abuse cocaine had a higher systolic blood pressure and LV mass and a lower aortic compliance when compared with control subjects (134 mm Hg ± 11 vs 126 mm Hg ± 11; 124 g ± 25 vs 105 g ± 16; 1.3 cm2 × 10-2 mm Hg-1 ± 0.2 vs 1.7 cm2 × 10-2 mm Hg-1 ± 0.5, respectively; P < .05). LV hypertrophy was found in 50% of long-standing cocaine abusers, and statistically significant differences were observed between cocaine abusing and control groups regarding LV end-systolic volume index, LV stroke volume index, and LV mass index (30 mL/m2± 9 vs 26 mL/m2 ± 5; 45 ± 9 vs 51 ± 6; 76 ± 15 vs 69 ± 4, respectively; P < .05) (8) (Fig 8). Both eccentric and concentric LV remodeling were present among patients with CCM, suggesting a multifactorial underlying mechanism (33% and 77%, respectively) (8,48). Interestingly, the right ventricle was also involved with a hypertrophic trend. Maceira et al (8) observed that the right ventricular end-systolic volume of cocaine abusers was significantly higher when compared with that of the control group (36 mL/m2 ± 9 vs 28 mL/m2 ± 4, P < .01); on the contrary, right ventricular ejection fraction was decreased (56% ± 5 vs 65% ± 5, P < .01) (Fig 4, B).
Figure 8: MR images in a 47-year-old man with a long-standing history of cocaine abuse. Images show hypertrophic cardiomyopathy after 6 years of cocaine use. A, Four-chamber cine steady-state free precession image shows moderate thickening of the ventricle wall (14 mm). B, Short-axis T2-weighted short tau inversion-recovery sequence demonstrates the absence of signal alteration. C, Phase-sensitive inversion-recovery sequence shows a fibrosis replacement in the inferior wall on middle plane (arrow) confirmed by an elevation at, D, native T1 mapping. Left ventricle function: End-diastolic volume indexed to body surface area, 203 mL/m2; end-systolic volume indexed to body surface area, 163.7 mL/m2; mass indexed to body surface area, 150.1 g/m2. E, Histologic specimen.
CCM: Dilated phase.—The dilated phase of CCM is clinically indistinguishable from idiopathic dilated cardiomyopathies (41). 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) (41). Even though no differences were found between CCM and idiopathic dilated cardiomyopathies using cardiac MRI in ventricular function (41), 31% of long-standing cocaine abusers showed LV dilatation (8). 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) (8). The LGE patterns found in the dilated phase of CCM were nodular subepicardial, linear subepicardial, junctional, and subendocardial (8) (Fig 9). All of these LGE patterns could potentially represent the multifactorial pathogenesis of CCM (50). More precisely, nodular subepicardial and linear subepicardial involvement may represent the results of chronic myocarditis (51), junctional pattern arises from focal replacement fibrosis due to hypertrophy and desynchrony between the two ventricles (52), and subendocardial pattern is the classic appearance of ischemic cardiomyopathies (44) (Fig 4, B).
Figure 9: MR images in a 55-year-old woman with 15 years of cocaine abuse admitted to the hospital for dyspnea. A, Four-chamber cine steady-state free precession image shows severe ventricle dilatation (end-diastolic volume indexed to body surface area, 297 mL/m2) with compromised ejection fraction (12%) and pericardial effusion. B, No signal alteration was depicted with short tau inversion-recovery, on the contrary. C,Phase-sensitive inversion-recovery after 15 minutes of gadolinium-based injection shows focal replacement fibrosis at the level of inferior interventricular junction (arrow).
Conclusion
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).
Disclosures of Conflicts of Interest: G.D.R. disclosed no relevant relationships. F.C. disclosed no relevant relationships. G.C. disclosed no relevant relationships. A.A. disclosed no relevant relationships. N.G. disclosed no relevant relationships. C.C. disclosed no relevant relationships. M.F. disclosed no relevant relationships.
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