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Cocaine

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Cocaine
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posted:
11/10/2011
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Rami Khouzam, MD

Which one of the following tests

would be POSITIVE:



a- BNP

b- Troponin I

c- Urine Na+

d- UDS

e- Urine Ca++ and Mg++

INDEX CASE 1

• 50 yo AA gentleman presents with:

– One month hx of  LEs edema

– 3 days hx of SOB &  DOE

– Non-compliance with meds. (lately)





PMHx:

– CHF

– HTN

Meds:

– Aldactone

– Lasix

– Diltiazem





PE:

– Remarkable for: RR; 28, P:101, BP: 196/110,

O2 Sat: 93% on 4L

– S1 S2 S4. PMI @ ant. axillary line

– Bilat. diffuse lung crackles & wheezes

– 2+ edema bilat. in LEs.

CXR:

–  Interstitial markings consistent with

pulmonary edema

– Cardiomegaly

INDEX CASE 2

• 54 yo AA gentleman with 3-4 hrs. hx. of CP,

SOB, diaphoresis & palpitations



• Admits to not taking his meds x 3 days because

he was more busy drinking whisky and smoking

cocaine & marijuana



PHMX:

– CHF

– HTN

– Gout

Meds:

– Lasix

– KCl

– Aldactone





PE:

– Remarkable for P: 220, RR: 32, BP: 113/60,

S1 S2. PMI laterally displaced

Adenosine 6mg, 12mg, 12mg



HR: 160 then 220 SVT (called @ 2:00 AM

from Med. ER)



Vagal maneuvers



Amiodarone 150mg IV over 10 minutes

• Cardizem 10mg IV

• HR: 105

Hospital day # 4:

• Left hospital AMA

• Called @ 3:00 AM from VA

• Patient found by EMT

• HR: 180

INDEX CASE 3

• 45 Yo AA lady presented with CP, substernal,

8/10, pressure-like, radiating to left arm,

accompanied with SOB, nausea & diaphoresis



PMHx:

• CAD.. MI x 2 in the past



Meds:

- ASA

- Metoprolol

- Zocor

PE:

• Remarkable for:

S1 S2, RR @ 110



EKG:

• Sinus tachycardia

• ST in I, aVL, V5, V6



Labs:

• Trop: 1.8  2,4  8.0



Cath. Lab:

• Lt. Cx: 80% Stenosis  Stent

Which one of the following tests

was POSITIVE:

(in the previous 3 cases)

a- BNP

b- Troponin I

c- Urine Na+

d- UDS

e- Urine Ca++ and Mg++

• Index case 1: Hypertensive emergency

• Index case 2: Life-threatening dysrhythmia

• Index case 3: NSTEMI



Correct answer: d

UDS + for COCAINE

HISTORY OF COCAINE

• In pre-Columbian times,

the coca leaf was officially

reserved for Inca royalty.

The natives used coca for

mystical, religious, social,

nutritional and medicinal

purposes



• Coca was initially banned

by the Spanish



• 1551: the Bishop of Cuzco

outlawed coca use on pain

of death because it was "an

evil agent of the Devil"

• The invaders discovered that

without the Incan "gift of the

gods", the natives could barely

work the fields - or mine gold



• So it came to be cultivated even

by the Catholic Church



• Coca leaves were distributed

three or four times a day to the

workers during brief rest breaks



• Returning Spanish

conquistadores introduced coca

to Europe





• It is told that even Shakespeare

may have smoked it

• 1814: an editorial in Gentleman's

Magazine urged researchers to

begin experimentation so that coca

could be used as "a substitute for

food so that people could live a

month, now and then, without

eating..."



• Around 1860: the active ingredient of

the coca plant was first isolated in

the West by Albert Niemann



• To Sherlock Holmes, cocaine was

"so transcendentally stimulating and

clarifying to the mind that its

secondary action is a matter of small

moment”



• Robert Louis Stephenson wrote The

Strange Case of Dr Jekyll and Mr

Hyde during a six-day cocaine-binge

• Cocaine was soon sold

over-the-counter. Until

1916, one could buy it at

Harrods



• Cocaine was widely used in

tonics, toothache cure and

patent medicines; in coca

cigarettes "guaranteed to lift

depression”; and in

chocolate cocaine tablets



• When combined with

alcohol, the cocaine alkaloid

yields a further potently

reinforcing compound, now

known to be cocaethylene

• Cocaine was a popular

ingredient in wines, notably

Vin Mariani



• Coca wine received

endorsement from prime-

ministers, royalty and even

the Pope



• Architect Frédérick-Auguste

Bartholdi remarked that if

only he had used Vin

Mariani earlier in his life,

then he would have

engineered the Statue of

Liberty a few hundred

meters higher

Cocaine & The Heart



• 1911: the earliest report of cocaine

damaging the heart



• Price & Leaky reported that cocaine use

for local dental anesthesia could induce

severe myocardial damage leading to

death

(Braunwald)

Cocaine Pharmacology by

Route of Administration

ROUTE FORMULA ONSET OF PEAK DURATION

ACTION EFFECT

Inhalation “Crack” 8 seconds 2-5 minutes 10-20 minutes

Intranasal Cocaine HCl 2-5 minutes 5-10 minutes 30 minutes

Intravenous Cocaine HCl Seconds 2-5 minutes 10-20 minutes

Oral Cocaine HCl 10 minutes 30-60 minutes 60 minutes







(Braunwald)

• Exploited by humans for at least 5000

years



• Except for medicinal purposes, the drug

is illegal in North America

Cocaine

• 2nd. most commonly used illicit drug in

the US (after Marijuana)



• ~ 30 million (~ 11%) persons in the US

have used cocaine at some time



• 5-6 million on regular basis

Adulterants

• Sugars



• Stimulants (ephedrine, caffeine,

amphetamines)



• Quinine, strychnine



• Local anesthetics

Review of Simple Physiology

• Caliber of the coronary arteries is

controlled by a complex interplay between:

– Local metabolic factors

AND

– Neural input





• Oxygen delivery to the myocardium is

achieved through changes in coronary

artery caliber

A) Sympathetic

• Norepinephrine from presynaptic vesicles

onto alpha-and B2- receptors

•   coronary v.c.

• 2  coronary v.d. (mild)



B) Parasympathetic:

• Acetylcholine on M3 Cholinergic receptors

 v.d.

(Gutterman DG. The heart and cardiovascular system. 2nd ed. 1991)

Cocaine, more than just an illicit drug



• Pharmacological effects:

– Blocking reuptake of cathecholamines in the

presynaptic neurons:  Norepinephrine

–  Dopamine and Serotonin

– Cholinergic stimulation

– Blocking sodium channels :

Local anesthetic

Class I antiarrhythmic

Effects of cocaine on

Hemodynamics

•  HR,

•  BP

•  myocardial contractility  cardiac output

•  Cardiac function (Direct myocardial

toxicity)

• CVS toxicity:



– Hypertensive emergency/ Pulmonary edema

– Arrhythmias

– Myocardial ischemia and infarction



– Acute aortic dissection or rupture to stroke

– Sudden death

– Acute reversible myocarditis

– Dilated cardiomyopathy



(Pasternack, PF Am J Cardiol 1985)

Hypertensive Emergencies

• Phentolamine or direct -adrenergic

antagonist: the antihypertensive of choice



• Should -B be avoided with cocaine

because of paradoxical hypertension ?

(class IIa for SBP > 150 or HR > 100)



• IV NTG or nitroprusside can be used

Dysrhythmias

• Atrial or ventricular



• Sinus tachycardia: most common

• A. fib, SVT (sympathetic stimulation)



• Respond to sedation with benzodiadepines



• Other standard therapies to slow rate

Cardiac Dysrhythmia

Cocaine (lidocaine-like effect) Rhabdomyolysis & ischemia

 

Blockade of fast Na+ channels Hyperkalemia



slowing depolarization









Wide complex tachycardia



(Braunwald)

• Wide complex tachycardia from cocaine of

unknown etiology  iv bolus of sodium

bicarbonate, 1-2 mEq/kg will empirically

treat sodium channel blockade as well as

cardiotoxicity from hyperkalemia



(Braunwald)

Mechanism of Myocarditis

1) Direct effect on lymphocyte activity



2)  natural killer cell activity in blood 

cytotoxic to myocardial cells



3) Cocaine-related eosinophilic infiltrate 

hypersensitivity reaction



4) Focal myocarditis also direct, negative

inotropic effect on cardiac muscle

• Cathecolamine excess  Contraction

band necrosis  anatomic substrate for

ventricular dysrhythmias



• Autopsy support scattered foci of

necrosis, myocarditis independent of

CAD

(Braunwald)

THE ORIGIN OF COCAINE

• Erythroxylon coca is a densely-

leafed plant native to the

eastern slopes of the Andes



• Coca is widely cultivated in

Bolivia, Peru and Ecuador, but

the lead producer is Colombia,

currently the source of 80% of

the world's cocaine



• There are around 250 species

of erythroxylon plants. At least

20 produce cocaine. Only 2 of

them typically yield enough

cocaine to justify commercial

cultivation

• Typically, coca thrives in

warm, moist, frost-free

valleys between 1500 and

6000 metres above sea level



• The plant grows to a height

of up to 8 feet and can be

harvested 4 times a year



• The leaves are rich in

vitamins, protein, calcium,

iron and fiber



• The cocaine content of the

leaves ranges from O.1% to

0.9%

CRACK-COCAINE

• To obtain crack-cocaine,

ordinary cocaine hydrochloride

is concentrated by heating the

drug in a solution of baking

soda until the water

evaporates.



• This type of base-cocaine

makes a cracking sound when

heated; hence the name

“Crack”



• Base-cocaine vaporizes at a

low temperature, so it can be

easily inhaled via a heated

pipe

CHEMISTRY OF COCAINE

• C17H21NO4





• Cocaine can be

manufactured by converting

tropinone into

2-carbomethoxytropinone,

reducing this to ecgonine,

and then converting the

ecgonine to cocaine



• This isn't as easy as it

sounds

Cocaine Body Packers

• Cocaine is smuggled by a variety of

techniques



• Body packers ingest cocaine wrapped

tightly into condoms or other latex products

before crossing international borders



• Each packet can contain up to 10g of

cocaine and packers may swallow as many

as 150 packets

• On arrival at their destination: cathartic



• Unfortunately rupture of cocaine packet

can result in death, as each packet

contains close to 10 times the lethal

dose

(Braunwald)

Mechanisms of AMI

1)  HR +  BP   myocardial oxygen

demand



2)  coronary artery flow, coronary

vasospasm or thrombosis



3) Active myocarditis (hypersensitivity or

toxicity)

• A recreational dose of cocaine:

– HR ~ 30 beats/min.

– Also BP by 20/10 mm Hg.(equivalent to mild

exercise)





• Not sufficient to result in myocardial

ischemia

[I] VASOCONSTRICTION

A- Animal Studies

• Hale et al: anesthetized dogs: IV bolus

cocaine 10 mg/kg  15%  in circumflex

artery diameter



(This dose ~ 5 times the dose used

recreationally by humans)

(Hale SL, Am Heart J 1989)

• Kuhn et al: cocaine 2mg/kg in a dog model

 LAD diameter by 19% &  coronary blood

flow of 55%



– Attenuation of the effects of cocaine:

pretreating with phentolamine:  VC



– Potentiation of the effects of cocaine:

pretreating with propanolol:  VC

(Kuhn FE, J Am Coll Cardiol 1990)

• Egashira et al: a swine model



– Significant  in v.c. associated with denuded

coronaries compared with native ones (59%

cross-sectional area reduction vs 48%)



– Vasoreactivity to cocaine may be greater in

diseased coronaries

Egashira K, J Clin Invest 1991

B- Human Studies

• Human coronary arteries differ from animal

arteries in a number of ways



• Difference in the density and distribution of

alpha-and beta-receptors



• Most human studies have documented a  in

coronary artery diameter ranging from 4% to

29% associated with cocaine use

• Lange et al: phentolamine  abolishment

of cocaine-induced V.C.







• Flores et al: 13% reduction in coronary

caliber was observed in disease-free

coronary arteries, a 29% reduction in

caliber in coronary arteries with significant

stenoses (>50%)

• Moliterno et al: cigarette smoking + cocaine

 significant v.c.



(19% decrease in coronary diameter in

cocaine plus cigarette smoking versus 7%

in cocaine alone)

(Flores ED, J Am Coll Cardiol 1990)

Time factor

• Brogan et al:

– At 30 minutes: 17%  in coronary artery caliber

(maximal serum concentration of cocaine)



– At 60 minutes: coronary diameter returns to

baseline



– At 90 minutes: 21%  in diameter

(Serum concentrations of cocaine’s metabolites,

benzoylecgonine, ethyl methyl ecgonine)



(Brogan WC, Ann Int Med 1992)

[II] VASOCONSTRICTION

A- Animal Studies



• Friedrichs et al: coronary v.d. within the

first minute of I.V. cocaine

• A 13% and 68%  in coronary perfusion

pressure were measured, respectively, with

2mg/kg and 10mg/kg intravenous cocaine



• Same with lidocaine (of the same class as

cocaine) similar decreases in coronary

perfusion pressure (vasodilatory effects ?

due to the anesthetic properties of cocaine)



(Friedrichs GS, J Physiol Pharmacol 1990)

• Zimring et al: early increase in coronary

blood flow by 30% within the first 2

minutes of administration

(Zimring HJ, Circulation 1994)





– Dual effect:

a- Early v.d.

b- Followed by a more sustained v.c.



( Dose dependent and Different

pharmacological properties)

B- Human Studies







Similar Results

IS IT ALL ABOUT

CORONARY DIAMETER?

Effects of Cocaine on

Platelets and Thrombostasis

• Intravascular thrombosis:

– Coronary

– Pulmonary circulation

– Peripheral venous circulation

– Skin

– Renal vasculature



• Composed of platelet rich-aggregates or in the

setting of atypical atheromatous lesions

(Minor RL, Ann Int Med 1991)

• Echhorn et al: aortic segment of rabbits,

daily IV cocaine (2 mg/kg) 6-12 weeks



• Endothelium produced high levels of

thromboxane A2



• In humans: Moliterno et al: intranasal

cocaine (2 mg/kg)   in the level of

plasminogen activator inhibitor

(Moliterno DJ, Am J Med 1994)

• Cocaine  166%  in platelet fibrinogen binding



(Kugelmass AD, Circulation 1993)







• Prothrombogenic & Antibibrilolytic

Treatment of cocaine-induced

ischemia/infarction

– Benzodiazepines, ASA, & Nitrates

– Ca.ch Blockers

Cocaine and -B ??

• -B ( including labetalol), should be

avoided during acute cocaine toxicity



• Patients with previously documented

coronary insufficiency who present without

acute intoxication may be candidates for

-B beginning with low doses

Coronary Atherosclerosis and LV

Hypertrophy Associated with

Cocaine



• Kolodgie et al: Autopsy: 495 patients, 6

(1.2%) had total thrombotic occlusion of a

major coronary a.



•  number of adventitial mast cells

• Proliferation of coronary mast cells 

accelerated atherosclerosis and the

promotion of thrombosis

(Kolodgie FD, J Am Coll Cardiol 1991)







• Cocaine also associated with  LV mass:

substrate for development of ischemia



(Chakko S, J Am Coll Cardiol 1992)

SUMMARY

• Cocaine: Many adverse effects



• CVS and CNS toxicity (among others…)



• Cocaine-induced myocardial ischemia and

infarction : multiple and distinct pathogenic

mechanisms beyond v.c.

•  myocardial oxygen demand by  HR & 

BP +  in coronary artery diameter (V.C.)



• Directly or indirectly activates platelets



• Shift in endothelial prostaglandin balance 

milieu that is favorable to thrombosis



• Long-term cocaine use  accelerated and

often more severe coronary artery

atherosclerosis and LV hypertrophy

• 1886: Coca-Cola was introduced as

"a valuable brain-tonic and cure for

all nervous afflictions".



• Coca-cola was promoted as a

temperance drink "offering the

virtues of coca without the vices of

alcohol".



• Until 1903, a typical serving

contained around 60mg of cocaine



• Today, it still contains an extract of

coca-leaves only for flavoring since

the drug has been removed





• The Coca-Cola Company imports 8

tons from South America each year

My name is Cocaine - call me Coke for short

I entered this country without a passport

Ever since then I've made lots of scum rich

Some have been murdered and found in a ditch

I'm more valued than diamonds, more treasured than gold

Use me just once and you too will be sold

I'll make a schoolboy forget his books

I'll make a beauty queen forget her looks

I'll make a schoolteacher forget how to teach

I'll make a preacher not want to preach

I'll take all your rent money and you'll get evicted

I'll murder your babies or they'll be born addicted

I'll make you rob and steal and kill

When you're under my power you have no will

Remember my friend my name is " Big C "

If you try me just one time you may never be free

I've destroyed actors, politicians and many a hero

I've decreased bank accounts from millions to zero

Now that you know me what will you do ?

You'll have to decide, It's all up to you

The day you agree to sit in my saddle

The decision is one that no one can straddle

Listen to me, and please listen well

When you ride with cocaine you are headed for hell !!!



(Anonymous)


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