Myocardial Hypertrophy

Stimulant abusers are prone to modest degrees of myocardial hypertrophy, and there is some evidence that opiate abusers may also share this tendency. Increased left ventricular mass is an independent risk factor for sudden cardiac death.11,12 As ventricular mass increases, coronary artery reserve declines,13 and myocardial contractility becomes impaired.14 Increased mass makes ventricular arrhythmias, and sudden death, more likely,15 even in the absence of relative myocardial ischemia provoked by the decline in coronary artery reserve.16 This combination of effects may well explain many cases of cocaine-related sudden death.

The mechanism by which stimulant abuse causes myocyte hypertrophy is not known. In general, stimuli associated with myocardial hypertrophy activate G-proteins, and either adenyl cyclase or phospholipase C. When one of the latter is activated, genes needed to make the proteins necessary for cell growth are also activated.17 After myocardial infarction, there is activation of early expression genes such as c-fos, c jun, and c-myc. Whether the same process also occurs in cocaine and methamphetamine users is not known, but c-fos activation has been observed in the aortas of cocaine-treated rabbits.10 In laboratory experiments, rats and rabbits chronically treated with cocaine have larger left ventricles than controls.10,18-20 They also have increased collagen content, higher levels of atrial naturetic hormone, and increased expression of the low ATPase myosin isoform V3,21 In clinical studies, hypertrophy has been confirmed by comparing electrocardiograms of age-sex matched controls to those of asymptomatic cocaine users in rehabilitation, and with symptomatic cocaine users with chest pain.22,23 Echocardiographic studies have yielded conflicting results. Studies of asymptomatic users in rehabilitation have found significant increases in left ventricular mass and posterior wall thickness,24,25 although others have failed to confirm this finding.26,27

Autopsy evidence has shown that the increase in heart size is modest,28 but quite real.28-31 When heart weights of asymptomatic cocaine using trauma fatalities were compared with drug-free trauma victims, the hearts of the cocaine users were found to be 10% heavier than those of controls, even though the heart weights of both groups fell within ranges generally considered to be normal.28 A related study compared the heart weights of individuals dying of drug toxicity (either cocaine, methamphetamine, or heroin) with heart weights of drug-free trauma victims. Heart weights for the drug users were significantly greater than those observed in the controls.32

Changes in heart weight that amount to less than 10% are likely to go unrecognized at autopsy. Even if wall thickness is fastidiously measured, which is not always the case, the increase would most likely go undetected. Yet it is important that the increase be detected because it very likely is the cause of death, and may well be the only abnormality detected at autopsy.

Such small changes go unnoticed because several different systems for determining normal heart weight are in use. Some pathologists still believe that arbitrary cutoffs can be used: 380 or 400 grams for men and 350 grams for women. Others determine normality by using a formula: heart weights less than 0.4% of the body weight (0.45% for women) are considered normal.32 Hearts weighing more than those percentages are considered enlarged. Neither of these approaches has proven accurate or reliable. A normalized weight nomogram is the most accurate tool for detecting modest degrees of enlargement. The Mayo Clinic nomogram relates heart weight to body weight (see Appendix III for nomogram). It is based on measurements made in hundreds of autopsies of individuals found to be free of heart disease.33 If a heart weighs significantly more than predicted by the nomogram, it is abnormal, even if the heart weighs less than the 400 grams.

Similar weight increases are to be expected in methamphetamine-related deaths, though methamphetamine toxicity has not received nearly the attention devoted to cocaine.31 Surprisingly, there is evidence that similar increases in heart size are to be seen in heroin abusers. The results of several, as yet unpublished, preliminary studies, indicate that increases comparable to those produced by cocaine may occur.31,34 Hypertrophy in stimulant abusers is thought to be catecholamine related. There is, however, no satisfactory explanation for the changes in the opiate abusers. The injection practices of heroin users can, of course, lead to pulmonary granulomas and pulmonary hypertension, but preliminary data suggest that the observed increases are not related to that mechanism.

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