However, if several factors, such as high doses, male sex and a fall in pH (such as a seizure) occurred simultaneously, the free cocaine concentrations near the Ki of sodium channels are possible. In a reported case, a 41 year old male individual exhibited violent, aggressive, and threatening behavior in a public place, which led to his admission to the emergency department after experiencing a cardiac arrest. Upon admission to the emergency department, a urine screening test was performed, which revealed positive results for cocaine. During his hospitalization, he was treated with pharmacological interventions, including the administration of inotropes and rehydration therapy. Despite these efforts, the patient died suddenly due to cardiac arrest approximately 14 hours after his admission to the emergency department.
The methods were in compliance with the ethical standards for medical research and the principles of good clinical practice in accordance with the World Medical Association’s Declaration of Helsinki. In all patients, blood samples were drawn for biochemical and hematological parameters, and for serologic testing for human immunodeficiency virus (HIV) infection and hepatitis C virus (HCV) infection. In 2015, the UNODC, with support from the US Department of State, partnered with Pakistan’s Ministry of Interior and Narcotics Control to launch a drug prevention campaign across nine cities in the Sindh Province. This initiative included strategic billboard placements, local language awareness messages on FM radio and local TV stations, community-based activities in schools and colleges, and the establishment of a hotline to raise awareness about drug abuse 15.
1. Mechanisms of Acute Toxicity
Amphetamines, similar to cocaine, can elevate catecholamine release and hinder catecholamine reuptake, potentially leading to myocardial ischemia due to increased oxygen consumption from tachycardia and systemic hypertension. Acute myocardial damage is also observed with heroin abuse, which is of significant concern 12, given Pakistan’s high addiction rates 13. The data items extracted from each paper included summary measures such as prevalence, odd ratios, risk ratios, and standardized mean difference (SMD). We used Hedges’ g for SMDs as it contains a correction for small sample sizes and allows groups with unequal acute and chronic effects of cocaine on cardiovascular health pmc variances and size. If a study did not report these effect sizes, or their confidence intervals, we attempted to extract enough primary data to calculate the effect sizes ourselves.
- Cocaine produced significant dose-dependent increases in median HR, BP, CO, and +dP/dt (a measure of cardiac contractility) and a significant dose-dependent reduction in median SVR.
- In addition, cocaine blocks the reuptake of serotonin by interacting with the serotonin transporter, inducing leptin-dependent anorexic effect 107,108.
- Cocaine users often consume other substances concurrently, exacerbating the impact on coronary arteries’ narrowing.
- Finally, the Nexfin device may not always perfectly agree with the gold standard of CO measurement11 and those disagreements are likely to have more influence in a smaller patient population.
Table 2.
The left ventriculography showed mild dyskinesia at the apex and a significant increase in contraction at the base depicting TCM (Figure 4). On echocardiography (done on admission day 2), the LV was dilated with normal wall thickness and severely depressed systolic function. As a result of global hypokinesis, LV relaxation was decreased during early diastole, resulting in an estimated left ventricular ejection fraction (LVEF) of 5%-10%.
The effects of acute and chronic cocaine use on the heart
The availability of so few studies does however make it difficult to draw any firm conclusions regarding the specific benefits or risks of beta-blocker therapy in chronic cocaine users. Patients with acute cocaine poisoning present with life-threatening symptoms involving several organ systems. While the effects of cocaine are myriad, they are the result of a limited number of cocaine-protein interactions, including monoamine transporters, neurotransmitter receptors and voltage-gated ion channels. These primary interactions trigger a cascade of events that ultimately produce the clinical effects. The purpose of this article is to review the primary interactions of cocaine and the effects that these interactions trigger. We also describe the progression of symptoms observed in cocaine poisoning as they relate to serum cocaine concentrations.
- People who feel compelled to keep using cocaine should see a compassionate medical professional who specializes in addiction.
- No use, distribution or reproduction is permitted which does not comply with these terms.
- Finally, and perhaps most importantly, cocaine abstinence or even reduced use promotes reduction in endothelial-1 damage 45,46.
- As such, cocaine induces acute MI by directly affecting myocardial tissues in the heart and indirectly enhancing thrombosis in vessels.
- He had transaminitis with an ALT of 467 and an AST of 493, deemed to be likely multifactorial in the setting of rhabdomyolysis, cocaine use, and respiratory failure.
At the time, the patient refused further follow-up with an MRI scan and left the hospital AMA. Had this possible abscess been followed up with an MRI at an earlier time, it is theorized that it could have been more effectively characterized and treated. Patient education by case managers and social workers plays a major role in addressing the underlying substance use disorder, aiming to prevent recurrent hospitalizations and improve overall outcomes for patients in similar situations as this gentleman.
Statistical analysis
While data are limited, this suggests that cocaine use may have a role in impairing systolic ventricular function among patients with symptomatic cardiac disease. A mechanism for LV dysfunction could be cocaine-induced small vessel coronary disease or direct myocardial damage32. Cocaine is one of the most widely consumed recreational drugs in the world with the number of global users estimated at around 18 million1. In the United States, cocaine use is regarded as a major source of morbidity and mortality with effects ranging from long-term cognitive impairment to early death2–5. The cardiovascular effects of cocaine are of particular interest to researchers and clinicians as they account for more than 64,000 presentations of chest pain every year and an estimated $155—$226 million in annual healthcare costs6,7.
A small 2014 study found that cocaine users who were otherwise young and healthy had enlarged left ventricles compared with non-users. Treatment for cocaine-induced acute vascular events may be similar to indications in patients with traditional risk-factors, with few exceptions. In addition to cocaine-specific effects, there are secondary harms resulting from synergetic effects between multiple environmental, psychosocial and behavioral factors comprising the addiction phenomenology that could in turn enhance potential vascular damage. These factors include the life-course and complexity of CUD, comprised of years (often, decades) of concomitant alcohol and/or tobacco and/or other drug use, potentiating vascular toxicity. The issue is complicated further by the fact that contaminants such as procainamide, quinidine and antihistamines, which are often mixed with the cocaine, may contribute to the effects seen and influence the underlying pathophysiology 30. The prevailing low socio-economic status, limited awareness of health issues, lack of sleep, and poor nutrition, could further hasten vascular disease 43,44.
Damage to the structure of the heart
As such, cocaine-induced changes in food intake patterns and the metabolic process can lead to cardiovascular complications during addiction as well as cessation periods. It was interesting to confirm that medical comorbidity was the only predictor of death in this cohort with a high prevalence of polysubstance use. Some studies on CUD indicate that the risk of death is higher in men, in those with a history of injected drugs, in those with an early onset of use, in those who drink alcohol, or in those with psychiatric comorbidity (Arendt et al., 2011; de la Fuente et al., 2014). However, there are hardly any studies on the medical comorbidity of CUD other than HIV infection and HCV infection. VACS Index analyzes kidney and liver function in addition to age, hemoglobin and HIV and HCV infections, thus reflecting the general health status.
Cardiac effects of cocaine: a review.
When vessels are stressed, endothelin-1 (a vasoconstrictor protein produced by vascular endothelial cells) is elevated and nitric oxide (a blood vessel dilator) decreases, leading to vasoconstriction 35,36. It was recently demonstrated that cocaine elicits autophagy involving nitric oxide and glyceraldehyde-3-phosphate dehydrogenase signaling cascade 48. Additional mechanisms implicated in cocaine induced vasoconstriction include increases in calcium 49. This cascade reduces blood flow following cocaine use and can lead to acute organ damage. Maceira et al. 45 found that cocaine abusers had increased LV end-systolic volume, LV mass index, and right ventricular (RV) end-systolic volume, with decreased LV ejection fraction and RV ejection fraction.
In summary, cocaine use affects eating behavior and suppresses appetite, leading to malnutrition and anorexia through disruption of the metabolic process and neuroendocrine regulation. Also, cocaine uptake in the body can lead to mesenteric vasoconstriction and focal tissue ischemia, and alter lipid as well as glucose profiles, presumably resulting in increased risk for metabolic and cardiovascular problems in cocaine users. Notably, the cessation of cocaine use causes sudden/excess weight gain during the recovery period/process, leading to increased cardiovascular and cardio-metabolic risks.
Chronic cocaine users have altered regional density of several neurotransmitter receptors and monoamine transporters compared to non-cocaine users 94–96;96–98;98. This group has suggested that these changes increase the susceptibility of chronic users to severe cocaine toxicity. While some toxic effects of cocaine are mediated by the DAT, the SERT also contributes to cocaine toxicity. In a mouse model, pretreatment with fluoxetine, a potent inhibitor of the SERT, decreased the latency of cocaine-induced convulsions by 53% and increased the occurrence of seizures in a dose-dependent manner 58. As cocaine has a very low affinity for serotonin (5HT) receptors 29 ,the effects of 5HT2 and 5HT3 antagonists cannot be due to inhibition of cocaine binding.