Myocardial Disease in Stimulant Abusers

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Clinical reports of dilated cardiomyopathy, where neither biopsies nor arteriograms are obtained, are impossible to interpret, and the real diagnosis must remain in question.35-39 But even in the absence of florid heart failure, certain types of morphologic alterations are frequently seen in the hearts of individuals dying from stimulant abuse. Most of the observed changes appear to be catecholamine mediated40-42. Chronic catecholamine toxicity is a well-recognized entity in animals and humans. Norepinephrine "myocarditis" was first described over 40 years ago.43,44 The histologic changes associated with norepinephrine treatment are indistinguishable from those seen in patients and animals with pheochromocytoma.45 Contraction band necrosis is the earliest recognizable lesion in both situations.46-49

Several features distinguish catecholamine necrosis from ischemic necrosis. The most obvious is the distribution of the lesions. In ischemic injury, all cells supplied by a given vessel are affected, leading to homogeneous zones of necrosis. In catecholamine injury, individual necrotic myocytes are found interspersed between normal cells, and the pattern of injury appears unrelated to the blood supply.49

The arrangement of the myofilaments also helps distinguish the two processes. In ischemia, myofilaments remain in register. In cases of catehcolamine-toxicity, the filaments are disrupted. After 12 or more hours have elapsed, a mononuclear infiltrate, predominantly lymphocytic, may be seen. Necrotic myocytes are eventually reabsorbed, and replaced by non-conducting fibrous tissue. After repeat bouts of necrosis, the myocardium becomes increasingly fibrotic. Fibrosis of this type alters ventricular function and, more importantly, may lead to abnormal impulse propagation40,50 (see Figures 2.2.2.1 and 2.2.2.2).

Biopsy findings in a group of cocaine users with recent onset of chest pain and congestive failure showed changes very similar to those described above, with microfocal interstitial

Figure 2.2.2.1. Contraction band necrosis in a 32-year-old cocaine abuser with arrhythmic sudden death. The dark cross banded lesions are a marker for intracytasolic calicum overload secondary to catecholamine excess. Cells with these lesions may or may not be viable. If severe, the cells are replaced by fibrous tissue with abnormal conduction properties.

Figure 2.2.2.1. Contraction band necrosis in a 32-year-old cocaine abuser with arrhythmic sudden death. The dark cross banded lesions are a marker for intracytasolic calicum overload secondary to catecholamine excess. Cells with these lesions may or may not be viable. If severe, the cells are replaced by fibrous tissue with abnormal conduction properties.

Figure 2.2.2.2 Patchy myocardial fibrosis in a 28-year-old cocaine abuser who died in a motor vechicle accident. Fibrosis is confined to focal areas, not corresponding to blood supply. This pattern is typically seen in cases of catecholamine excess, not just in instances of cocaine toxicity. The presence of such microfocal fibrosis may be an underlying cause of arrhythmic sudden death.

Figure 2.2.2.2 Patchy myocardial fibrosis in a 28-year-old cocaine abuser who died in a motor vechicle accident. Fibrosis is confined to focal areas, not corresponding to blood supply. This pattern is typically seen in cases of catecholamine excess, not just in instances of cocaine toxicity. The presence of such microfocal fibrosis may be an underlying cause of arrhythmic sudden death.

fibrosis evident in all cases.41 Lymphocytic infiltrates were seen in only two of the cases, and eosinophils were not seen at all. Identical changes have been described in chronic amphetamine abusers.51 Because contraction band necrosis is a prominent feature of all myocardial biopsies, regardless of the underlying cause, the presence of these lesions in biopsy material is difficult, but not impossible, to assess.52 The presence of nuclear pyknosis in damaged cells may be one way to distinguish preexisting contraction band lesions from those produced by the biopsy process itself. In some cases, Z-band remnants have been identified with electron microscopy. This particular finding is classically associated with dilated congestive cardiomyopathy and is not generally associated with the type of necrosis resulting from catecholamine toxicity.

Nonetheless, it has been documented in patients with amphetamine toxicity,51 where its presence probably signifies only that necrosis was very severe .

The first reports of contraction band-like lesions and cellular infiltrates in the heart of a cocaine users were published in the 1920s!53 However, more than half a century elapsed before another paper, describing similar findings, was published in 1986.54 A biopsy of one of the cocaine users described in that report disclosed eosinophilic infiltrates. Others have observed both lymphocytic and eosinophilic interstitial infiltrates.46'47,55-58

More often than not, when mononuclear infiltrates are present, there is no associated myocyte necrosis.47 According to generally accepted criteria, myocarditis cannot be diagnosed without necrosis.59 In the only study ever to directly address the issue, immunologic and histologic findings were tabulated in 15 HIV negative, intravenous drug abusers.58 Five cases demonstrated active myocarditis, and five others had borderline myocarditis. Antimyocardial antibodies were positive in 4 of the 15 cases, including patients with active, borderline, and absent myocarditis, and toxicology studies did not implicate any particular drug of abuse. Thus, intravenous drug abuse appears to be an independent risk factor for myocarditis, a factor which should be taken into consideration when evaluating possible cases of HIV-associated myocarditis.

The presence of eosinophilic infiltrates suggests that what is being described is not myocarditis at all, but rather a hypersensitivity phenomenon. Hypersensitivity myocarditis is distinguished from toxic myocarditis by the fact that its occurrence is not dose-related. Lesions are all of the same age, hemorrhages are rare, and there is no myocyte necrosis. The list of drugs causing hypersensitivity myocarditis is increasing.60 Eosinophilic myocarditis is a very rare disorder. When it is diagnosed, it is often an incidental finding or a surprise finding at autopsy or in biopsy specimens obtained to evaluate chest pain, heart failure, or arrhythmia.

Clinical manifestations of this disorder are so nonspecific that the diagnosis is rarely suspected during life.61 None of the cocaine users with eosinophilic infiltrates have had signs of extra cardiac involvement such as polyarteritis nodosa or eosinophilic leukemia. These patients do not match the picture classically associated with acute necrotizing myocarditis,62 nor do they resemble patients with eosinophilic coronary arteritis (Churg- Strauss syndrome, also called allergic granulomatosis angiitis), although one case of cocaine-associated Churg-Strauss has been reported.63

A heterogeneous group of agents can cause toxic myocarditis, and since cocaine can be adulterated with a very long list of agents, implicating cocaine as the cause of eosinophilic myocarditis is difficult. A review paper published in 1988 listed sugars (lactose, sucrose, and manitol) as the most common cocaine adulterants, followed by stimulant drugs (caffeine, amphetamines) and local anesthetic agents as the most common agents found mixed with cocaine samples.64 Eosinophilic infiltrates in the myocardium could be in response to any of these agents, alone or in combination. Furthermore, most adult drug abusers are polydrug abusers, which further enlarges the list of possible offenders.

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