Heart disease and substance addiction: what are the effects of cocaine on the heart?

By Cristiano Antonino On Jan 13, 2023

Cocaine use is an increasingly widespread phenomenon throughout the world. The apparent and temporary benefits offered by this substance, however, often lead to conditions of dependence and abuse with very serious, sometimes irreversible, clinical consequences

HOW WIDESPREAD IS COCAINE?

UNODC (the UN agency that monitors drug use worldwide) reports that cocaine use has been steadily increasing in recent years in some countries around the world, especially in North America and Western Europe.

The 2018 European Drugs Report agrees that cocaine is increasingly present in European markets, as documented also by analyses of wastewater in some large metropolitan cities.

Retail’ prices are stable while the purity of this drug is at its highest level in the last decade.

In Europe, there are two types of cocaine: the most common is cocaine powder (in the form of salts), while crack cocaine (free base), which is taken by inhaling smoke, is less readily available.

Historically, most cocaine arrives in Europe via the ports, by large container ships, of the Iberian peninsula, but recent seizures suggest that this route is no longer the only one.

Indeed, in 2016, Belgium overtook Spain as the country with the largest amount of cocaine seized at ports.

COCAINE: WHO USES IT AND HOW?

Cocaine, unlike other substances, is generally used in a compulsive (binge) manner followed by periods of non-use that, from a neurochemical point of view, correspond to a strong depletion of neurotransmitters.

The nasal route (snorting) is preferentially used and only rarely the parental route.

Recently, it has become more common to smoke cocaine in its basic form: crack

Cocaine is used by people from all social strata without ethnic differences, and there is also evidence that young women are more likely than their male peers to binge.

Cocaine use is closely related to the pharmacological properties of the substance, the characteristics of the individual and the environment.

This substance, perhaps more than any other drug, tends to be used in certain social contexts and by specific groups of people.

In fact, it has been proven that environmental factors are absolutely crucial in determining an amplification of use.

Still largely to be clarified is the influence of particular personality frameworks or how different personality structures may be more or less vulnerable to cocaine use.

HOW DOES COCAINE WORK?

The purer the substance, the greater the clinical effects procured.

In practice, however, cocaine is always adulterated with other compounds such as:

mannitol;
lactose or glucose to increase its volume;
caffeine;
lidocaine;
amphetamine to amplify its effects (Bastos, Hoffman, 1976).

Cocaine that is usually sold contains 10 to 50 per cent active ingredient and only very rarely reaches 70 per cent.

Pharmacologically, cocaine is able to block the neuronal reuptake of dopamine, noradrenaline and serotonin and to increase glutamatergic transmission.

CLINICAL EFFECTS ON THE BODY

The clinical effects of cocaine are directly proportional to the dose administered.

Doses between 25 and 125 mg result in what are the desired effects consisting of:

euphoria;
increased sociability and energy;
reduced need for sleep;
apparent and temporary increase in efficiency.

Higher doses of the substance, above 150 mg result in:

vasoconstriction;
increased heart rate and temperature;
dilation of the pupil of the eye in the absence of light (mydriasis)
if the substance is taken nasally, strong local anaesthesia.

Doses in excess of 300 mg may cause overdoses in even tolerant subjects with

stereotyped and repetitive behaviour
anxiety;
panic attacks;
paranoia;
hallucinations;
aggression;
violence;
cardiovascular problems such as myocardial infarction or angina; arrhythmias;
neurological accidents such as dizziness, headaches, blurred vision, ischaemia, heart attacks and haemorrhages.

Through the brain’s increase in dopamine it is also able to bring about an increase in sexual arousal.

Cocaine is normally abused for its psychostimulant abilities

It must be remembered that the central nervous system cannot be artificially stimulated beyond a certain limit because it tends to undergo metabolic exhaustion if over-excited in a relatively short time.

In fact, it is common to observe after real binges strong symptoms of

depression;
lack of motivation;
drowsiness;
paranoia;
irritability and psychosis (Gold, Verebey, 1984).

HOW LONG DO THE EFFECTS OF COCAINE LAST?

If taken nasally, the half-life – that is, the time required to halve the initial concentration or activity of a substance – is about 80 min, 60 min if administered parenterally and 50 min if ingested.

Metabolites detected in urine persist for about 1 week.

Cocaine, like many substances of abuse is capable of inducing tolerance, dependence and withdrawal once its administration is abruptly discontinued.

THE 2 PHASES OF WITHDRAWAL

The withdrawal symptoms induced by cocaine, especially in chronic users, are particularly intense.

It is characterised by three phases.

The first, defined as the crash phase, which appears a few days after cessation of use (1-3 days) is characterised by depression, difficulty sleeping and only moderate craving – that is, the intense and incoercible desire to take the substance.
The second, which appears 2 to 10 days after discontinuation, recognises the peak of withdrawal symptoms with dysphoria, lack of energy, increased appetite, widespread pain and headache, anxiety, paranoia, hallucinations, delusions, strong mood swings, drowsiness and intense craving.

The third phase appears after the first week and can last up to months and is characterised by episodic craving, insomnia, irritability, agitation.

Of particular interest from a neurobiological and clinical perspective is one of the most important symptoms of cocaine addiction: craving.

EFFECTS ON THE HEART

Ischaemia and acute myocardial infarction are the most frequently described pathologies in cocaine abuse, but the effects of this substance on the cardiovascular system are many and complex, and may lead to a wide range of complications, ranging from acute coronary syndromes to aortic dissection and sudden death from arrhythmic causes.

The main mechanism, but not the only one, is an increased level of circulating catecholamines and prolonged stimulation of adrenergic receptors in the heart.

This alteration leads to various effects, including an increase in heart rate, systemic blood pressure and cardiac cell contractility, all of which lead to an increased demand for oxygen from the myocardium.

Conversely, at the coronary level, cocaine induces vasoconstriction and thus a reduction in blood flow to the heart muscle, leading to an imbalance between oxygen demand and oxygen supply and consequent ischaemic suffering.

Alterations in coagulation

In addition to the haemodynamic effects, cocaine use also leads to alterations in coagulation in a prothrombotic sense; there are numerous cases of acute thrombosis myocardial infarction related to cocaine use even in the absence of significant coronary artery stenosis.

Cocaine promotes thrombosis by altering the expression of molecules involved in platelet activation and aggregation, with pro-inflammatory action and involved in the biochemical process of coagulation.

Among the main pro-thrombotic mechanisms related to cocaine use is endothelial dysfunction: the endothelium is the ’tissue’ that lines the inner surface of blood vessels and the endocardium and plays a fundamental role in the proper regulation of vascular tone (vasodilation and vasoconstriction), in inflammatory processes, atherosclerosis and coagulation.

Cocaine, by altering the production by the cells of the endothelium of substances that regulate all these processes, promotes the formation of clots and accelerates the process of atherosclerosis. (3)(4)(8)

Myocardial infarction

Subjects with angor or ongoing myocardial infarction due to cocaine abuse at the time of admission to the Emergency-Urgency Departments may be indistinguishable from the general population in terms of the characteristics and duration of pain and the coexistence of other cardiovascular risk factors (smoking, family history, diabetes, dyslipidaemia, etc.), although on average they are younger than the average for subjects with coronary artery disease due to other causes.

In cocaine infarction, the time of onset of symptoms from the last intake of the substance varies from 30 minutes to several hours (sometimes more than 15 hours after intake) with a peak incidence approximately one hour after use; the onset of symptoms is not always related to the dose taken or the type of administration. (3)

Case reports on cocaine-addicted patients who have developed an acute heart attack show that on angiographic study both normal coronary arteries and stenosing lesions can be seen.

It must be emphasised, however, that in cocaine-abusing patients a picture of marked and widespread atherosclerosis is predominantly observed despite a young age and even in the absence of additional cardiovascular risk factors.

In the long term, a progressive deterioration of cardiac function may be observed, even in the absence of previous symptomatic ischaemic events, with a significant reduction in ‘pump function’ and the development of chronic heart failure.

This cardiac dysfunction appears to be the result of several factors such as:

asymptomatic subendocardial ischaemia;
recurrent exposure to excess catecholamines;
increased apoptosis (death) of myocytes;
induction of changes in the structure of cardiac cells themselves.

In addition to ischaemic damage mediated by catecholamines or thrombosis phenomena, cocaine can cause direct damage to myocardial cells by increasing the production of reactive oxygen species involved in oxidative stress processes. (5)

Cocaine and arrhythmias

Cocaine abuse is also related to arrhythmic phenomena of varying degrees:

tachycardia and/or bradycardia;
onset of conduction disturbances;
supraventricular tachycardias;
ventricular tachycardia and fibrillation;
peak torsion;
appearance of electrocardiographic patterns mimicking Brugada syndrome (sudden death related syndrome).

The mechanisms by which cocaine exerts its pro-arrhythmogenic effects are also multiple.

By acting at the level of ion channels (sodium, potassium, calcium), it can alter the normal formation and conduction of the electrical impulse, and the increased ‘instability’ of cardiac cells, induced by the ischaemic state, determines a favourable substrate for the onset of both atrial and ventricular arrhythmias.

In addition, a left ventricular hypertrophy picture is frequently observed in patients who assiduously take cocaine, a phenomenon that, in addition to being associated with infarction, also increases the risk of cardiac arrhythmias. (6,7)

Inflammation of the heart

The occurrence of endocarditis and myocarditis is not uncommon in cocaine addicts, to a greater extent in intravenous users.

Intravenous drug use is a risk factor for the entry of pathogens into the blood stream, increasing the risk of infectious disease of cardiac and valvular tissue, but from the statistics, cocaine itself appears to be an independent risk factor compared to other intravenous substances.

It is likely that the increase in heart rate and systolic blood pressure and the picture of endothelial dysfunction may lead to vascular and valvular damage that may favour the entry of pathogens into the tissue.

A higher incidence of vascular pathologies such as phlebitis and thrombophlebitis is also observed in cocaine addicts.

The incidence of aortic pathologies (dissection, rupture) and strokes (both ischaemic and haemorrhagic) is also statistically higher in cocaine addicts than in the general population.

COCAINE, SMOKING AND ALCOHOL

All cardiovascular effects of cocaine are amplified in individuals whose cocaine abuse is combined with cigarette smoking.

The concomitant use of alcohol also amplifies the effects of cocaine, by slowing its clearance and through the formation of cocaethylene, a methyl ester structurally similar to cocaine and with biological activity on dopaminergic neurons similar to cocaine, which is formed in the liver when cocaine and ethyl alcohol are in the circulation at the same time.

TREATMENT OF COCAINE USE DISORDER

Based on existing theories of addiction, a wide range of treatments of cocaine use disorder have been developed.

Cocaine addiction offers less availability of effective pharmacological protocols, so psychotherapeutic intervention, and in particular cognitive-behavioural intervention, assumes a pivotal role.

This model of psychotherapy has enabled the structuring of treatments that more frequently than others have been subjected to scientific verification of efficacy.

Within the behavioural approach, goals and therapeutic actions are articulated according to the individual’s unique characteristics, family, relational and work environment, treatment phase and concomitant pharmacological treatments.

Compared to other models of psychotherapy, cognitive-behavioural approaches place special emphasis on matching a person’s needs with the goals to be achieved.

Moreover, therapy is organised according to short-term treatment steps with goals that are agreed upon with the patient from time to time.

Among these, the first, in chronological order, is the gradual achievement of abstinence, especially when serious health risks are evident.

The first step in behavioural therapies, however, is aimed at developing a good therapeutic alliance to enhance the person’s adherence also to any pharmacological treatments that may be necessary.

Once the therapeutic alliance is achieved, the climate of trust created will facilitate the initial containment of the abusive behaviour.

The next step will then be therapeutic work aimed at increasing the person’s motivation to change with respect to progressively achieving abstinence.

Being able to see different choices than those made so far and learning to pursue them.

Change in addiction-related behaviour is therefore to be understood as a process, rather than an event, and motivation cannot be regarded as either entirely present or entirely absent.

FUNCTIONAL ANALYSIS OF CONSUMPTION BEHAVIOUR

Another important therapeutic step is the functional analysis of consumption behaviour and the factors that trigger and maintain it over time.

This is an in-depth assessment that aims to identify both the stimuli that the individual has learned to associate with substances and any protective factors that need to be enhanced.

The information that emerges from this functional analysis will then make it possible to prepare ‘training’ protocols aimed at supporting individuals when substance-taking has become, for them over time, the sole and generalised mode of response to internal emotional states, stressful situations or particular relational contexts.

Early recognition of high-risk situations of use or situations that trigger ‘memories’ of use is a major therapeutic goal for the cocaine user.

The individual who has already achieved cessation of use should then be helped by the therapeutic team to avoid high-risk situations, to implement self-control strategies and to choose alternative behaviours to substance use.

Given the centrality that the substance tends to play in the user’s life, an important objective is to encourage the development of alternative activities to the consumption behaviour that are satisfying for the person.

This is achieved by establishing a highly collaborative working climate between the treatment team and the patient.

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