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].

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).

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

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.

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

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.