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Vol 17, No 4 (2022)
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Wild at heart: multiple mechanisms of cocaine-induced myocardial infarction

Aneta Zontek1, Zofia Kampka1, Katarzyna Mizia-Stec2
Folia Cardiologica 2022;17(4):257-263.

Abstract

Introduction. Results of cocaine intake can be such cardiovascular complications as hypertension, myocardial infarction, arrhythmia, and cardiomyopathy. Anabolic androgenic steroids use is related to hypertension, cardiomyopathy and lipid metabolism derangements.
Case report. On admission to the cardiology department a 37-year-old man presented prolonged pain at rest located in the middle part of the chest, which occurred 2 days earlier. He was after the use of cocaine, tetrahydrocannabinol, and alcohol. Smoking and using the growth hormone and anabolic androgenic steroids (AAS) in the past were present in the patient’s medical history. Physical examination with no deviation, heart rate 72/min, and blood pressure 130/90 mm Hg. Features of anterior wall myocardial infarction (MI) were present in electrocardiogram — ST-elevation up to 3 mm in V2–V5. In laboratory tests, troponin T rise (1.99 ng/mL) and D-dimer (503 ng/mL) were observed. In echocardiography — apex hypokinesis and concentric left ventricular hypertrophy — max. thickness: 19 mm. No significant abnormalities were detected in an immediate coronary angiography. Heart damage of vascular aetiology involving an apical region and partial interventricular septum were confirmed in magnetic resonance imaging. No significant arrhythmias are present in electrocardiogram Holter monitoring. Conservative treatment was prescribed: beta blockers, atorvastatin, enoxaparin, captopril, acetyl salicylic acid (ASA), electrolytes i.v. and was released from hospital after 4 days. On discharge in a good general condition with a recommended further treatment.
Conclusions. The presented case is an example of ST-elevation myocardial infarction (STEMI) in a young patient with left ventricular hypertrophy of multifactorial aetiology (hypertrophic cardiomyopathy, athlete’s heart, hypertrophy due to anabolic steroids, and growth hormone intake). Immediate coronary angiography showed no significant abnormalities. The patient during STEMI was after ingestion of cocaine and other stimulants which, apart from pulmonary embolism, vasospastic angina, and Takotsubo cardiomyopathy, can be an aetiology factor. Elimination of all modifiable risk factors is the key factor influencing successful therapy in this case.

case report/PRACA kazuistyczna

Folia Cardiologica 2022

vol. 17, no. 4, pages 257–263

DOI: 10.5603/FC.a2022.0042

Copyright © 2022 Via Medica

ISSN 2353–7752

e-ISSN 2353–7760

Wild at heart: multiple mechanisms of cocaine-induced myocardial infarction

Pułapki diagnostyczne zawału mięśnia sercowego typu drugiego spowodowanego stosowaniem kokainy

Aneta Zontek1Zofia Kampka1Katarzyna Mizia-Stec2
1Students’ Scientific Society, 1st Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, Katowice, Poland
21st Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, Upper Silesia Medical Centre, Katowice, Poland

Address for correspondence: Aneta Zontek, Studenckie Towarzystwo Naukowe przy I Katedrze i Klinice Kardiologii Śląskiego Uniwersytetu Medycznego w Katowicach, ul. Ziołowa 47, 40–635 Katowice, Poland, e-mail: aneta114@gmail.com

This article is available in open access under Creative Common Attribution-Non-Commercial-No Derivatives 4.0 International (CC BY-NC-ND 4.0) license, allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.

Abstract
Introduction. Results of cocaine intake can be such cardiovascular complications as hypertension, myocardial infarction, arrhythmia, and cardiomyopathy. Anabolic androgenic steroids use is related to hypertension, cardiomyopathy and lipid metabolism derangements.
Case report. On admission to the cardiology department a 37-year-old man presented prolonged pain at rest located in the middle part of the chest, which occurred 2 days earlier. He was after the use of cocaine, tetrahydrocannabinol, and alcohol. Smoking and using the growth hormone and anabolic androgenic steroids (AAS) in the past were present in the patient’s medical history. Physical examination with no deviation, heart rate 72/min, and blood pressure 130/90 mm Hg. Features of anterior wall myocardial infarction (MI) were present in electrocardiogram — ST-elevation up to 3 mm in V2–V5. In laboratory tests, troponin T rise (1.99 ng/mL) and D-dimer (503 ng/mL) were observed. In echocardiography — apex hypokinesis and concentric left ventricular hypertrophy — max. thickness: 19 mm. No significant abnormalities were detected in an immediate coronary angiography. Heart damage of vascular aetiology involving an apical region and partial interventricular septum were confirmed in magnetic resonance imaging. No significant arrhythmias are present in electrocardiogram Holter monitoring. Conservative treatment was prescribed: beta blockers, atorvastatin, enoxaparin, captopril, acetyl salicylic acid (ASA), electrolytes i.v. and was released from hospital after 4 days. On discharge in a good general condition with a recommended further treatment.
Conclusions. The presented case is an example of ST-elevation myocardial infarction (STEMI) in a young patient with left ventricular hypertrophy of multifactorial aetiology (hypertrophic cardiomyopathy, athlete’s heart, hypertrophy due to anabolic steroids, and growth hormone intake). Immediate coronary angiography showed no significant abnormalities. The patient during STEMI was after ingestion of cocaine and other stimulants which, apart from pulmonary embolism, vasospastic angina, and Takotsubo cardiomyopathy, can be an aetiology factor. Elimination of all modifiable risk factors is the key factor influencing successful therapy in this case.
Key words: acute coronary syndrome, cocaine, growth hormone, anabolic steroids, hypertrophic cardiomyopathy
Folia Cardiologica 2022; 17, 4: 257–263

Introduction

A 37-years-old patient was admitted to the hospital to the cardiology department 48 hours after an occurrence of prolonged retrosternal resting chest pain. The patient was after ingestion of cocaine, alcohol, and tetrahydrocannabinol. Medical history embraced smoking, using growth hormone (GH) and anabolic androgenic steroids (AAS). The man suffered from celiac disease and underwent cervical neck surgery. In physical examination, no significant abnormalities were found. Blood pressure was 130/90 mm Hg and heart rate was 72/min.

Initial diagnosis

Because of the presented symptoms and history of cocaine, GH and AAS intake, myocardial infarction (MI) type II was suspected.

Differential diagnosis

The differential diagnosis that should be taken into consideration in the presented patient is in Table 1 [1].

Table 1. Differential diagnosis

Probable causes of LV hypertrophy

For

Against

Hypertrophic cardiomyopathy

LV concentric hypertrophy

Diagnosis has to be confirmed by genetic test

Athlete’s heart

Medical history

Diagnosis has to be confirmed by imaging test 3 months after a detraining

Hypertrophy due to anabolic steroids, GH intake

Medical history of presented substances intake

Probable causes of ACS

For

Against

I type of MI

Majority of ST-elevation MI are associated with atherosclerotic plaque rupture, MRI results support vascular aetiology of heart damage

no significant changes in coronary angiography

MINOCA — myocardial infarction with non-obstructive coronary arteries in presented case — no detection of coronary occlusion due to atherosclerosis — non-obstructive coronary arteries as per angiographic guidelines, with no lesions ≥ 50% in a major epicardial vessel detection of elevated cardiac biomarkers (cardiac troponin > 99th percentile of the upper reference level), clinical symptoms
of myocardial ischaemia, new ECG changes, evidence of new regional wall motion abnormality, identification of new loss of viable
myo­cardium on MRI

Coronary causes

Takotsubo cardiomyopathy

Transient LV apical ballooning

Left ventricular apical hypokinesis detected using echocardiography

Significant rise in troponin level

In presented case MRI results support vascular aetiology of heart damage

Variant angina (Prinzmetal angina) — vasospastic angina

Probable coronary artery spasm due to cocaine intake

Transient changes in ECG during variant angina episode the lack of vasoactive (provocative) test that could confirm or exclude this diagnosis (acetylcholine or ergonovine testing)

Microvascular angina — coronary microvascular dysfunction

No evidence of coronary occlusion

The lack of intracoronary provocative testing (acetylcholine or ergonovine tests)

Non-coronary causes

Myocarditis

Clinical manifestations include prolonged retrosternal chest pain

No significant elevation of inflammation parameters

No evident clinical symptoms of inflammation

Alternative diagnosis

Pulmonary embolism

Co-occurrence of risk factors

No significant elevation of D-dimer concentration

Hypertensive crisis

Cocaine intake according to medical history

No evidence of hypertension in physical examination

Tachyarrhythmias

Cocaine intake according to medical history

No detection of specific supraventricular and ventricular arrhythmias in ECG Holter monitoring

Diagnostic process

Electrocardiogram revealed ST-elevation up to 3 mm in V2–V5 and negative T-wave in V3 and aVF — features of anterior wall MI (Figure 1). Laboratory tests demonstrated microcytic anaemia (erythrocytes — 4.32 × 106/uL, haemoglobin — 11.50 g/dL, hematocrit — 34.20%, mean corpuscular volume — 79.2 fl), lowered serum creatinine level (0.58 mg/dL) and high sensitivity troponin T rise (1.840 ng/mL). Other parameters were normal. Transthoracic echocardiography showed concentric left ventricular (LV) hypertrophy (interventricular septum thickness up to 19 mm and posterior wall thickness up to 12 mm), apical hypokinesis and presence of LV false tendon. LV ejection fraction was 58% (Figure 2).

Z_1A.jpg
Z_1B.jpg
Figure 1. 12-lead electrocardiogram: Normal axis, sinus rhythm, heart rate about 70/min., J point and upward ST-segment elevation in V2–V4 (about 0.2 mV), horizontal ST elevation in V5 about 0.1 mV. “rS” morphology of QRS complex in V1–V4, and “RS” in V5. Biphasic
T waves with initial deflection positive and terminal deflection negative in V3–V4, negative T waves in V5, and slightly negative T waves in III and V6. Interventricular conduction disturbances in III. PR interval — 180 ms, QT interval 420 ms, QTc interval 454 ms, QRS complex time about 90 ms

141213.png

The patient underwent immediate coronary angiogra­phy that showed no significant abnormalities in both right and left coronary arteries (Figure 3). Magnetic resonance imaging (results available after the patient’s discharge) revealed abnormalities (Figure 4). No significant supraventricular and ventricular arrhythmias were present during electrocardiogram Holter monitoring.

Z_3.jpg
Figure 3. Coronary angiography; the dominance of the left coronary artery (LCA), narrowing and irregular outlines of left anterior descending artery (LAD), suspected intramuscular course of LAD

141236.png

Therapeutic procedure

Coronarography results were ambiguous so interventional procedures were not performed. Conservative treatment was implemented: enoxaparin, acetyl salicylic acid (ASA), atorvastatin, captopril, protein-protein interactions (PPIs), beta-blockers (bisoprolol, nebivolol). The patient responded well to the therapy, but an increased concentration of serum troponin was observed (1.990 ng/mL). The patient was discharged after 4 days in good general condition with recommendations for further treatment: ASA, atorvastatin, nebivolol, PPIs, zofenopril, a control appointment in the cardiology clinic in 2–3 weeks, and contraindications to smoking, drugs, and alcohol.

Final diagnosis

Considering the past medical history and the results of the diagnostic process, MI type II was diagnosed. It was caused by decreased oxygen supply due to the coronary artery spasm and increased oxygen demand because of myocardial hypertrophy.

Discussion

When searching for aetiology of acute coronary syndromes (ACS) among young patients, apart from the genetic background and metabolic disorders, stimulant drugs and muscle growth stimulants need to be considered.

The influence of particular substances (cocaine, tetrahydrocannabinol, AAS) on the cardiovascular system is visible in lipid metabolism derangements, endothelial damage, excessive production of free radicals. These lead to earlier atherosclerosis, affecting coronary arteries [2].

Molecular cocaine effects embrace adrenergic stimulation because of blocking noradrenaline reuptake which causes various cardiovascular complications. They can be both acute cardiac arrhythmia, a sudden increase in blood pressure, ACS and chronic LV hypertrophy, earlier atherosclerosis. ACS occurs from a few minutes to a few hours after cocaine intake [2, 3].

The influence of GH on the cardiovascular system embraces heightened angiogenesis in the heart, cardiac myo­cytes growth promotion, antiapoptotic activity, increased NO production. GH stimulates the proliferation of endothelial cells by activating the expression of eNOS, promoting angiogenesis. It can also increase vascular resistance and inflammation [4].

Anabolic androgenic steroids cause lipid derangement, elevated blood pressure, coagulation alterations, atherosclerosis promotion, heart muscle hypertrophy. These changes can increase the risk of cardiovascular disorders — coronary artery disease, arrhythmias, and congestive heart failure [2, 5].

Most ACS with ST-elevation are MI type I [6]. The STEMI in the presented case had a different aetiology. The lack of occlusion in coronary angiography allowed the diagnosis of MI type II. In differential diagnosis, we take into consideration transient coronary vasospasm, an arterial embolism because of possible hypercoagulability after AAS use, dehydration after alcohol and chronic inflammation due to celiac disease [5].

Concentric LV hypertrophy could be caused by several factors: physiological adaptation due to physical exercises, AAS and GH intake, as well as unrecognised before hypertrophic cardiomyopathy [4, 5, 8]. Left ventricular hypertrophy heightens heart’s oxygen demand and alongside coronary artery spasm, hyperkinetic circulation due to anaemia, tachycardia can lead to myocardial supply-demand imbalance [7]. Elimination of all reversible risk factors is crucial for further treatment of the patient.

Conflict of interest

Authors declare no conflict of interest.

Funding

None.

Streszczenie

Wstęp. Kokaina stanowi drugą pod względem popularności substancję narkotyczną. Jej zażywanie może skutkować chorobą niedokrwienną serca w postaci ostrych zespołów wieńcowych, arytmii, kardiomiopatii czy nadciśnienia tętniczego. Przyjmowanie steroidów anabolicznych związane jest z rozwojem nadciśnienia tętniczego, kardiomiopatii oraz zaburzeń w gospodarce lipidowej.

Opis przypadku. 37-letni mężczyzna został przyjęty na oddział kardiologii z powodu przedłużającego się od dwóch dni epizodu bólu w klatce piersiowej o charakterze dławicowym bez objawów towarzyszących. Stwierdzono stan po spożyciu kokainy, tetrahydrokannabinolu, alkoholu, w przeszłości palenie tytoniu, przyjmowanie steroidów anabolicznych, hormonu wzrostu. W wywiadzie obecność celiakii, stan po operacji w obrębie kręgosłupa szyjnego. W badaniu fizykalnym nie stwierdzono odchyleń od normy (ciśnienie krwi 130/90 mm Hg, rytm serca 72/min). W badaniu elektrokardiograficznym (EKG) zaobserwowano uniesienie odcinka ST do 3 mm w V2–V5, ujemne załamki T w V3, aVF (niedokrwienie przedniej ściany mięśnia sercowego). W badaniach laboratoryjnych stwierdzono znaczący wzrost stężenia hsTnT, obniżone stężenie kreatyniny, anemię mikrocytarną. Podczas badania echokardiograficznego uwidoczniono koncentryczny przerost lewej komory (LV), hipokinezę okolicy koniuszka LV, frakcja wyrzutowa LV 58%. Wykonano koronarografię w trybie pilnym, nie stwierdzono istotnych zmian. W MRI zaobserwowano zmiany sugerujące zawał koniuszka oraz dystalnej części IVS. Monitorowanie EKG metodą Holtera nie ujawniło arytmii. Wdrożono standardową terapię OZW: enoksaparyna, ASA, atorwastatyna, kaptopryl, IPP, bisoprolol, nebiwolol, NaCl, PWE. Po 4 dniach hospitalizacji pacjent w dobrym stanie ogólnym został wypisany z oddziału z zaleceniem kontynuacji leczenia za pomocą ASA, atorwastatyny, nebiwololu, IPP, zofenoprylu, oraz kontrolą w poradni w ciągu 2–3 tygodni.

Wnioski. Prezentowany przypadek stanowi przykład STEMI u młodego pacjenta z przerostem lewej komory o wieloczynnikowym podłożu (HCM, serce sportowca, wtórny przerost w wyniku stosowania steroidów anabolicznych i hormonu wzrostu). Wykonana w trybie pilnym koronarografia nie wykazała zmian w naczyniach wieńcowych. Chory w momencie STEMI był pod wpływem kokainy oraz innych używek, co może stanowić czynnik etiologiczny obok zakrzepicy tętniczej, dławicy wazospastycznej, kardiomiopatii Takotsubo. Eliminacja wszystkich modyfikowalnych czynników ryzyka jest kluczowa w leczeniu tego chorego.

Słowa kluczowe: ostry zespół wieńcowy, kokaina, hormon wzrostu, sterydy anaboliczne, kardiomiopatia przerostowa

Folia Cardiologica 2022; 17, 4: 257–263

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