Cocaine

Cocaine: History and Effects on the

 

Circulatory and Reproductive Systems

 

Jennifer Pearce

 

Kim Caldwell

 

Jason Scarabin

 

Todd Chelius

 

Running Head: COCAINE

 

BrighamYoungUniversity, English 315

 

March 28, 1995

 

I. HISTORY

 

Integral to the development of the healing arts has been man’s use of plants and other natural products to ease his lot in life- whether for shelter, food, alleviation of suffering, or recreation in the form of mind alteration. “Primitive” cultures have often been the true discoverers of particular compounds, while “modern” society exploits the peculiar attributes of certain plants for beneficial or perverse ends or both. Such has been the lot of the coca plant, the “divine plant of the Incas”.

 

A. THE ROOTS

 

“The Divine Plant” of the Incas was originally written by Dr. W. Golden Mortimer in 1901 and reprinted in 1974. Dr. Mortimer, a New York physician, devoted years to this text. It is written in the romantic style of his time and he outlines the origins of the use of the coca plant in South America:

 

During the early age, when this nature’s garden was unknown to the rest of the

world, the Incas, who were then the dominant people of this portion of the

continent, regarded this shrub as “the divine plant,” so all important and

complete in itself, that it was termed simply khoka, meaning the tree, beyond

which all other designation was unnecessary. This plant, which has been

described known as Coca, has appealed alike to the archaeologist, the botanist,

the historian, and traveler as well as to the physician. Its history is united with

the antiquity of centuries, while its traditions link it with a sacredness of the

past, the beginning of which is lost in the remoteness of time. So intimately

entwined is the story of Coca with these early associations – with religious

rites, with superstitious reverence, with false assertions and modern doubts –

that to unravel it is like to the disentanglement of a tropical vine in the

primitive jungles of its native home.

 

Coca’s use in the spiritual, political, and everyday life of the Incan Indians was well established and seemingly very structured. For centuries, the Incas had made a habit of inserting leaves from the coca plant between teeth and gums with “lime” -usually wood ashes or burnt crushed shells. In South and Central America, chewing of the leaf of the coca plant dates back to very ancient times. News of this plant and its properties was brought back to Europe by the early explorers and references to coca can be found in European medical texts dating from the 17th century. However, it was not until the 19th century that scientific and chemist, Dr. Albert Neimann, isolated cocaine in the pure alkaloid form from leaves brought to Europe. During the following twenty years or so, cocaine was used extensively by the medical profession as a stimulant, a local anesthetic, and as a “cure” for morphine dependence.

 

This era of unrestrained medical enthusiasm was short-lived, however, and by the end of the 19th century it had become very clear that the dangers of dependence developing with this drug had been greatly underestimated. There were many reports from both Europe and North America of physicians and nurses who had become dependent and of cases of cocaine dependence, associated with its use in treatment.

 

In the early part of the 20th century it also became clear that as a result of the uncontrolled availability of this drug it was being used, in certain circles, as a “recreational” drug. The extent of this recreational use, at that time, is difficult to ascertain, but it was certainly extensive enough to arouse concern and to stimulate calls for legislative control- the fact that cocaine is a drug with potential for misuse had become very firmly established.

 

The middle decades of the 20th century might be viewed as a rather quiescent period as far as cocaine is concerned- coca leaves continued to be chewed in the geographical areas traditionally associated with their use and there was a continuing low-level problem of cocaine misuse in the developed world. This period, however, saw an almost explosive increase in the misuse of synthetic stimulants (amphetamine and phenmetrazine) in many countries. The experiences of the countries where these “epidemics” of misuse occurred gave ample confirmation of the threat to public health posed by any type of central nervous system stimulant. Today it is the use of cocaine that threatens to erupt into just such an epidemic.

 

Central nervous system stimulants are very popular as drugs of misuse; new drug misusers are likely to be rapidly recruited, and stimulant use can be a substitute for, or be combined with, narcotic misuse. Furthermore, in the aftermath of a stimulant epidemic, th established demand may be easily transferred to opiates.

 

The dangers of cocaine were initially underestimated and this mistake should not be repeated. The early experiences with cocaine and the problems of stimulant misuse in the middle of this century provide a warning of the potential public health problems associated with the misuse of cocaine-type drugs. What is more, the present level of cocaine misuse signals a resurgence of stimulant misuse in epidemic proportions with all the associated dangers.

 

B. THE SPREAD OF COCAINE

 

After the isolation of cocaine from coca leaf, events began to occur at such a blinding pace that it’s difficult to elaborate them in chronological fashion. In April 1884, Sigmund Freud obtained cocaine from the Merck Company and took small amounts himself and felt a “sudden exhilaration and a feeling of ease.” He persuaded his bride-to-be to try and also doomed a friend to lifetime cocaine habituation by prescribing the drug to cure his morphine addiction.

 

Meanwhile across the Atlantic cocaine was being first used as an anesthetic in the first nerve block in 1884. Both Freud and this doctor became addicted to cocaine. Cocaine continued to find legitimate medicinal uses as time passed but possibly as a result of the enthusiasm of Freud and other well-intentioned researchers, cocaine left the scientific arena and captured the souls of the public in Europe and North America.

 

The new wonder drug caught the fancy of the public during the latter part of the 19th century and was hailed as a cure for asthma, cancer, conjunctivitis, dyspepsia, edema, nosebleed, broken bones, headache, hypochondria, itch, melancholy, nausea, nervous disorders, hemorrhoids, rheumatism, stomachache, and fainting spells, among others. It was also sold in many forms.

 

 

Commercial and street chemistry of coca derivatives

 

 

 

 

 

 

 

Coca leaf

 

acid/solvent extraction ® flavorings

 

(Plus multiple other compounds

 

and residual plant flavor)

 

 

 

ecgonine alkaloids

 

ecgonine

 

cocaine (benzoylmethylecgonine)

 

benzolecgonine

 

cinnamylcocaine

 

alpha- and beta-truzilline

 

 

 

hydrolysis

 

 

 

ecgonine

 

(plus other hydrolysis products)

 

 

 

methanol/benzoic acid esterification

 

 

 

cocaine hydrochloride

 

 

 

base/solvent extraction

 

 

 

neutral free-base cocaine

 

 

 

 

 

 

 

 

 

 

C. COCA AND ITS COMPONENTS

 

Coca is the dried leaf of Erythroxylon coca and the commercial drug is derived from three plant varieties found in Bolivia, Peru, Java, and Colombia. Cocaine has been grown in botanical gardens and private collections throughout the world. Many countries have experimented with coca as a cultivated crop, including Indonesia, India, Sri Lanka, and Japan. Most coca is now grown in Peru and Bolivia.

 

Coca is a small, bushy tree with oval leaves, fragrant white flowers, and scarlet fruit. The plant may reach a height of 18 ft. at lower elevations but heights decrease to 6 ft. or so with increasing altitude. Leaves are harvested three times during the year and are processed by alternating drying and fermentation for three to four days before being collected. Cocaine is extracted from the leaves with dilute sulfuric acid and solvents.

 

D. COCAINE ON THE STREETS

 

Cocaine may be relatively pure or may by cut, or diluted, with a variety of harmless or toxic compounds once it enters into the channels of illicit commerce. Cocaine can also be injected and used as a local anesthetics.

 

Nomenclature

 

snow

 

the pimp’s drug

 

the Cadillac of drugs

 

flake

 

gold dust

 

green gold

 

coke

 

speedball (heroin and cocaine)

 

blow

 

liquid lady (alcohol and cocaine)

 

toot

 

crack

 

Street measures

 

hit

 

snort

 

line

 

dose

 

Adulterants

 

local anesthetics: procaine, lidocaine, tetracaine, benzocaine

 

stimulants: amphetamine, caffeine, methylphenidate, ergotamine, aminophylline

 

hallucinogens: LSD, hashish, marijuana, PCP

 

opioids: codeine, heroin (speedball)

 

depressants: alcohol (liquid lady), methapyrilene

 

others: quinine, thiamine, thyarmine

 

Cocaine substitutes

 

sugars

 

caffeine

 

procaine

 

tobacco

 

lidocaine

 

caryanthine

 

E. ABSORPTION

 

As a topical anthesthetic in opthamological procedures, cocaine was used. It has been thought of as rapidly absorbing across the mucus membranes but they have found this not to be true. “Cocaine is relatively rapidly absorbed from almost any vascular surface, even skin and denuded or inflamed urinary muscosa, when used as a topical anesthetic.”(1) A high comes over the user within a minute or so of snorting. Furthermore, injection or smoking free-base cocaine increases the absorption rate 10-fold over snorting. It was amazing to find though that “free-base smoking induced more intense effects than did injection, even with less free-base inhaled than cocaine hydrochloride injected.”(1)

 

It has been thought that cocaine is not absorbed in the digestive tract, if at all very little. It is not absorbed until it reaches the duodenum because of the increase of alkaline that reacts with the pKa of the cocaine. Results show that ingested cocaine is in the range of 30% compared to 60% for the snorted drug. Therefore, orally can be effective if the user is willing to double the price for the effect. One problem associated with gastrointestinal absorption is the high mortality rate of smugglers who have swallowed packets of cocaine and they have ruptured which releases an overdose into the body.

 

 

 

1. Pharmacologic Mechanisms

 

Cocaine has the ability to show 3 main pharmacological effects. They are: (1) local anesthetic effect, (2) central nervous system stimulation, and (3) inhibition of neuronal uptake of catecholamines. The feeling of euphoria and an increase is alertness are the primary reasons people abuse this drug. The toxicity, however, come from the these effects mentioned above. Furthermore, “street” cocaine is usually not used alone and mixed with other toxic drugs or chemicals. This causes a mixed overdose that the user may not even be aware of.

 

2. Toxic Effects

 

The central nervous system is stimulated when cocaine is used. This is the primary cause of most user’s deaths because it results in seizures, hypothermia, ventricular fibrillation, or respiratory arrest. When someone overdoses on cocaine they are rarely treated in emergency centers, they are usually found dead.

 

Specific effects from a stimulated CNS are excitement, anxiety, severe agitation and overt paranoid psychosis.

 

The route of administration and a large degree of stimulant exposure appear to predispose some people to become habitual users. A rapid decline of cocaine results in spite of its continued presence in plasma. Users have commented that the satisfactory euphoria feeling they experienced the first time has not ever been captured again by other subsequent trials.

 

As mentioned before, seizures may occur. If there are multiple seizures, a risk of hypothermia and death is likely. It has been reported that intra cranial hemorrhage and stroke have occurred.

 

“Cardiovascular effects of cocaine include arrhythmia (both arrial and ventricular) , severe hypertension (including a case of aortic rupture), and both coronary and peripheral vasoconstriction. Myocardial infarction may result from coronary spasm, with or without pre-existing coronary artery disease. Cardiomuyopathy has been reported, as have several cases each of intestinal ischemia.”

 

Some of the pulmonary complications reported have been pulmonary edemas and respiratory arrest. A forced Valsalax maneuver during crack smoking have caused Pneumomediastinum and pneumothorax.

 

Metabolic complications also occur which result in hypothermia, rhabdomyolysis, renal failure, hepatotoxicity, and disseminated intra vascular coagulation.

 

Persistent rhinorrhea, epistaxis, anosmia, atrophy or nasal septum mucosa, and necrosis of the nasal septum are side effects of chronic intranasal cocaine use.

 

Similar to tobacco use, free-base smoking results in significant carbon monoxide-diffusing capacity reduction and can irritate the large and small airways.

 

Withdrawal from cocaine is a very painful process. There is a phase called the “crash” which can last from several hours to several days. Symptoms are depression, hyper somnolence, and hyperphagia. Up to four days afterward, an increase in rapid eye movement sleep will occur. The second phase consisted primarily of depression and decreased energy follows. Those who have abused cocaine may continue to have psychological craving for the drug up to ten years after their withdrawal process.

 

F. METABOLISM

 

Metabolism and elimination of the cocaine after absorption is done through several different routes. Cocaine is primarily metabolized through the esterases in the blood and liver. Depending upon the Ph of the urine, cocaine may be unchanged in small amounts ranging from 1 to 9%. Most urine screening looks for benzoylecogonine and not the cocaine itself. Benzolyecogonine is the major urinary elimination product-35 to 54% of the total dose from this drug. Cocaine may be found in the urine up to 8 hours after use. And benzolyecogonine will remain present for two days.

 

G. BIOLOGICAL EFFECTS

 

Cocaine in the past was used for local anesthesia. This drug has the ability to cause axon membranes to stabilize and can block the nerve impulses in the area of initiation and conduction. The sympathetic nervous system is very affected by cocaine. As the same as other sympathomimetic drugs, cocaine prevents the neuronal re uptake of epinephrine and norepineephrine after they are released. This result in a net increase in available neurotransmitters, which can add to the subsequent stimulatous effect. Also, cocaine may hasten the releasing of catecholamines which originate from achenergic nerve terminals.

 

H. Clinical Effects

 

Human response to cocaine is predictable within certain limits. As with any drug, however, variables such as dosage, chronically of use, route of administration, and individual susceptibility must be considered. Most important when discussing catastrophic effects is the discrimination between the massive one-time overdose in an intravenous user or a body packer and the “wired” or “amped” chronic user on a “run,” or prolonged binge.

 

The effect upon the user’s central nervous system will generally follow the rostral-caudral progression, will a feeling of euphoric pleasure-the “rush”-being the earliest and most desirable effect. As doses increase, hyperactivity ensues and may be a visible sign to observers, as may the accompanying mydriasis. Pleasure gives way to negative sensations, particularly if the “set” and “setting” of the drug experience are adverse. Emotional ability and paranoia are signs of impending advanced toxicity, as are tactile hallucinations, such as “cocaine bugs,” visual hallucinations, such as “snow lights,” and other sensory hallucinations effects, terminating in overt cocaine psychosis with all its paranoid ideations and risk of physical harm to the user and those about him. Nausea, vertigo, and headache may precede later profound effects, as may tremors, tics, twitches, and jerks–“cocaine leaps”–associated with severe agitation.

 

Advanced stimulation may result in generalized hyperreflexia in the face of decreasing responsiveness, terminating in individual seizures and status epilepticus. Terminally, a depressive phase ensues, with loss of reflexes, coma, and loss of vital functions, ending in death.

 

Cardiovascular effects include a very early slowing the pulse, followed by an increase in the pulse and blood pressure. Pressures may rise sufficiently to cause intracranial hemorrhage or high-out-put congestive heart failure. Ventricular dysrhythmias may result form direct myocardial damage, evidenced anatomically by contraction ban necrosis, which promotes malignant reentry arrhythmias, eventual ventricular fibrillation, and cardiac arrest.

 

The picture of evolving malignant hyperthermia may be evidenced initially by a slight rise in body temperature with even a single snorted dose. The rise in core temperature is progressive through the stimulatory phases and is aggravated by seizure activity and progressive central effects.

 

The chronically “over-amped” individual is likely to present with restlessness, paranoia and hallucinations, hyperreflexia, and stereotyped movements, such as repetitive picking, lip-biting, and bruxism. The massive-overdose victim is more likely to present with advanced cardio respiratory distress and seizures.

 

Physical examinations of a chronic user may reveal lesions self-inflicted because of the urge to scrape out “cocaine bugs” crawling under the skin. Lesions may also be caused by the repetitive picking of the weird individual or may be the result of “coke burns” caused by cocaine injections.

 

In addition to nausea, vomiting, and diarrhea as a result of overamping, an interesting cas of pseudomemebranous colitis associated with cocaine addiction has recently been reported. It was thought to be due to a catecholamine-induced mucosal ischemia.

 

Various vascular complications of cocaine use in addiction to cerebrovascular accidents have now been reported, including renal infarction and rupture of an ascending aorta. Acute myocardial infarction was reported in 1985 in a 28-year-old woman without known previous heart disease, who had snorted 1.5 gm of cocaine over a five-hour period.

 

EFFECTS ON THE CIRCULATORY SYSTEM

 

There are basically three areas that I would like to cover within the effects of cocaine on the circulatory system: the cardiovascular, blood flow, and heart disease. These three areas are dominant parts of the circulatory system which should be addressed.

 

Cardiovascular

 

First of all, the cardiovascular may take more hits from the use of cocaine than any other part of the system being discussed. There are three phases of body reaction when cocaine is used. The three phases are 1)initial stimulation, 2)progressing stimulation, and 3)depression (Higgins, 1989).

 

The first of these is the initial stimulation phase. During this phase, the blood pressure and pulse increase rapidly accompanied by premature ventricular contractions. In addition, the person may feel “hot” as if with a fever. A cold sweat may accompany the “fever.” Vasoconstriction may be followed by skin pallor.

 

During the second phase of progressing stimulation, the pulse and blood pressure increase at an alarming rate. The pulse not only skyrockets, but it gets weak, speedy and rather abnormal. Because of decreased cardiac output and hypotension, there is a high risk during this stage for a cerebral hemorrhage.(Higgins, 1989).

 

Phase Effects

 

 

 

 

 

 

 

Initial stimulation

 

Variable pulse

 

Increased blood pressure

 

Premature ventricular contractions

 

Progressing stimulation

 

Cerebral hemorrhage

 

Decreased cardiac output

 

Hypotension

 

Ventricular fibrillation

 

Depression

 

Circulatory collapse

 

Cardiac arrest

 

Death

 

 

 

 

 

 

 

Depression is certainly the final stage usually resulting in death. However, before death overtakes the body, a few things happen. There is ventricular fibrillation, generalized cyanosis, and circulatory collapse. Naturally, cardiac arrest happens after the collapse of the circulatory system.

 

Perhaps one of the reasons for such a response to cocaine from the circulatory system, is the overwhelming adrenaline-like stimulation that is administered by the drug. Symptoms show up in the cardiovascular system because of the “tachycardia and hypertension produced by this sympathetic stimulation. Initial management of cocaine-induced agitation includes ventilatory and circulatory support, physical restraint, and correction of hyperthermia.” (Higgins, 1989).

 

Two other cardiovascular responses to cocaine are cardiomyopathy and coronary vasospasm. The abuser may complain of chest pain or other nonspecific symptoms.

 

Blood Flow

 

Research has shown that even tiny amounts of cocaine can constrict the arteries and reduce the flow of blood to the heart. In addition, cocaine “inhibits nerve blood flow by effects on nerve prostaglandin metabolites.” (Kalichman, Sanicolas, Jorge, and Roux, 1994).

 

Cocaine exerts its reinforcing actions by clinging on to the dopamine transporter. (Pearlson, Jeffrey, Harris, Ross, Fischman, and Camargo, 1993). “Chronic cocaine abusers demonstrated decreased relative cerebral blood flow (CBF) in prefrontal cortex immediately after stopping use and increased global brain metabolism.” (Pearlson, et al., 1993).

 

In a study of eight abstinent cocaine users, the subjects reported significant increases in several self-ratings of drug effect. “Significant drug-induced blood flow decreases were seen in selected frontal and basal ganglia regions, and significant negative correlations existed between these decreases and self-report measures.” (Pearlson, et al., 1993).

 

This study shows more than “80% first-pass extraction with an estimated 90-second time window reflecting regional CBF changes. This is considerably shorter than the 40-minute uptake period for labeled 2-deoxyglucose in humans and corresponds more closely to the time of peak subjective effects, which for intravenous cocaine is 3-5 minutes.” (Pearlson, et al., 1993).

 

The researchers noted significant correlations between drug craving and frontal metabolic activity. In addition, it is noted that there are also significant correlations between “lesser cocaine-induced euphoriant effects (“rush” and “high”) and selected frontal and basal ganglia blood flow decreases. These data suggest that 48 mg of intravenous cocaine in humans produces regional decreases in CBF corresponding to sites enriched in dopaminergic terminals.” (Pearlson, et al., 1993).

 

Heart disease

 

Not only are a high fat diet, inactivity, high blood pressure and smoking contributing factors to heart disease, but now, cocaine abuse has been added to the list by doctors. In one study of individuals, average age 25, who had recently died from a variety of causes, researchers found the presence of “more atherosclerotic plaque in the aortas of those who had been cocaine users.” (McCarthy, 1991).

 

“Plaque buildup begins in most of us at this time of life,” explains Renu Virmani, M.D., chairperson of cardiovascular pathology at the Armed Forces Institute of Pathology in Washington, DC, who headed the study. “But in cocaine users, it appears to be much, much greater. It’s possible that by stopping cocaine use early enough, one could repair some of the damage, in the same way that stopping smoking can reverse problems.” Currently, about 20 million Americans say they have tried cocaine; about five million are chronic abusers. (McCarthy, 1991).

 

“The optimal medical regimen for the treatment of cocaine associated with myocardial ischemia has not been defined. While animal and human data demonstrate the risks of beta-adrenergic blockade, studies in the cardiac catheterization laboratory suggest a beneficial role of nitroglycerin. We performed a prospective multicenter observational study to evaluate the clinical safety and efficacy of nitroglycerin in the treatment of cocaine associated chest pain at six municipal hospital centers. Of 246 patients presenting with cocaine associated chest pain, 83 patients were treated with nitroglycerin at the discretion of the treating physician. Relief of chest pain and/or adverse hemodynamic outcome were the primary endpoints. Baseline comparisons of patients treated with nitroglycerin to those not treated with it found that the treated patients were at higher risk of ischemic heart disease.” (Hollander, Hoffman, Gennis, Fairweather, DiSano, Schumb, Feldman, Fish, Dyer, and Wax, 1994).

 

MYOCARDIAL ISCHEMIA

 

“Ischemia of the myocardium develops when the myocardial demand for oxygen-bearing coronary arterial blood exceeds the supply. In normal coronary arteries, ischemia can be induced by spasm. Cocaine use can lead to myocardial ischemia through these mechanisms.” (Bunn and Giannini, 1992).

 

“Cocaine potentiates the physiologic response to catecholamines. This action is produced by inhibition of the reuptake of norepinephrine into storage sites in adrenergic neurons, as well as by potentiation of tyramine-facilitated release of norepinephrine from these sites. The catecholamine response accelerates the pulse and elevates the blood pressure, increasing myocardial oxygen demand.” (Bunn and Giannini, 1992).

 

“Normally, increased myocardial oxygen demand results in dilation of the coronary arteries to allow more blood flow. However, cocaine has a direct vasoconstrictor effect on vascular smooth muscle.” (Bunn and Giannini, 1992).

 

“This effect is independent of alpha-adrenergic stimulation but is dependent on calcium. Thus, vasoconstriction occurs despite the increase in myocardial oxygen demand. If coronary artery disease is present, the problem is compounded by vasoconstriction can even occur in normal coronary arteries. This may overwhelm other auto-regulatory mechanisms that preserve coronary blood flow during exercise or during exposure to cold.” (Bunn and Giannini, 1992).

 

Chest pain, presumably due to myocardial ischemia, is a fairly frequent complaint in cocaine users and may precipitate a visit to the emergency department. While vasoconstriction may occur with small doses of cocaine, considerable variability exists among individuals; therefore, the occurrence of symptoms is unpredictable. Also, the “concomitant use of other drugs, such as alcohol, may enhance the cardiotoxic effects of cocaine.” (Bunn and Giannini, 1992).

 

“Holter monitor studies have demonstrated episodes of silent myocardial ischemia even during cocaine withdrawal, particularly during the first week of abstinence.” (Bunn and Giannini, 1992).

 

MYOCARDIAL INFARCTION

 

Since 1982, the medical literature has contained reports of patients with acute myocardial infarction temporally related to the use of cocaine. Cregler studied 36 such patients. The average age of these patients was 33 years, and 25 percent had no recognized risk factors for coronary artery disease. The infarcts in these patients were usually transmural, and they occured in first-time users as well as in chronic users. The mortality rate was 10 percent. (Bunn and Giannini, 1992).

 

“The pathophysiologic mechanisms for cocaine-induced myocardial infarction are usually multiple. These mechanisms include increased myocardial oxygen demand due to increased heart rate and blood pressure and coronary vasospasm induced by the direct effect of cocaine on vascular smooth muscle. In addition, cocaine’s effect on platelets causes increased thromboxane production and platelet aggregation, with a greater potential for intracoronary thrombosis.” (Bunn and Giannini, 1992).

 

“Finally, cocaine may induce procoagulant effects through transient depletion of protein C and antithrombin III.” (Bunn and Giannini, 1992).

 

Acute chest pain related to cocaine use is very similar to that produced by acute myocardial ischemia. “Although the degree of coronary artery narrowing is distinctly greater in the cocaine-addicted population than in comparable nonaddicted populations, the incidence of acute myocardial infarction is low.” Many young cocaine abusers, particularly in the black population, may have a normal-variant pattern of early repolarization on electrocardiograms. This pattern can simulate changes seen in acute myocardial injury and may cause difficulties in the emergency department. (Bunn and Giannini, 1992).

 

MYOCARDITIS AND CARDIOMYOPATHY

 

“Myocarditis and dilated cardiomyopathy are frequently found at autopsy in patients with a history of chronic cocaine use. In a series of 40 patients, the incidence of myocarditis was 20 percent. Foci of lymphocytes and/or eosinophils were seen on pathology specimens. The etiology of the myocarditis was unknown, but several mechanisms were postulated. Cocaine may have have a direct cytotoxic effect on cardiac myocytes. The presence of eosinophils in some biopsy specimens suggests the possibility of a hypersensitivity mechanism. Alternatively, sustained high levels of catecholamines may produce focal myocarditis. Chronic use of cocaine may lead to myocardial fibrosis.” (Bunn and Giannini, 1992).

 

“Reversible cardio myopathy also has been associated with cocaine intoxication. The acute dilated cardiomyopathy associated with cocaine intoxication runs a clinical course similar to that reported in patients with pheochromocytoma. In both situations, the depressed systolic function is probably attributable to the direct toxic effect of high levels of circulating catecholamines on myocytes. It is paradoxic that cocaine has a primary depressant effect on the myocardium and concurrently produces intense adrenergic stimulation.” (Bunn and Giannini, 1992).

 

Bunn, W.H. & Giannini, A.J. (1992). Cardiovascular complications of cocaine abuse.

American Family Physician, 46, 769-773.

 

Higgins, R. (1989). Cocaine abuse: what every emergency nurse should know.

Journal of Emergency Nursing, 15, 318-323.

 

Hollander, J.E., Hoffman, R.S., Gennis, P., Fairweather, P., DiSano, M.J., Schumb, D.A., Feldman, J.A., Fish, S.S., Dyer, S. & Wax, P. (1994). Nitroglycerin in the treatment of cocaine associated chest pain–clinical safety and efficacy. Journal of Toxicology, 32, 243-256.

 

Kalichman, M.W., Sanicolas, M.T., Jorge, M.C., & Roux, L. (1994). Effects of cocaine on blood flow and prostaglandin metabolites in rat sciatic nerve. American Journal of Physiology, 35, H2515-H2519.

 

McCarthy, L.F. (1991). Better body knowledge. Harper’s Bazaar, 124, 127-128.

 

Pearlson, G.D., Jeffrey, P.J., Harris, G.J., Ross, C.A., Fischman, M.W., & Camargo, E.E. (1993). Correlation of acute cocaine-induced changes in local cerebral blood flow with subjective effects.

American Journal of Psychiatry, 150, 495-497.

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