Left ventricular dissecting haematoma and aneurysm formation in a patient who uses methamphetamines: a case report

Abstract

Introduction

Myocardial dissection is a rare complication of ischaemic heart disease. It occurs when a haematoma forms within the cardiac muscle, either due to an endocardial rupture or rupture of an intra-myocardial vessel. Higher ventricular wall tension and reduced myocardial tensile strength increase the risk of dissection. We describe a young male who developed a myocardial dissection following an ST elevation infarction. We explore the possible pathophysiological connection between myocardial dissection and his amphetamine use.

Case presentation

A 37-year-old Sri Lankan patient presented with progressively worsening heart failure for two weeks. One month before the presentation, he had developed an ischaemic chest pain, for which he had not sought medical advice. He was abusing inhalational heroin, crystal methamphetamines and cigarette smoke daily for five years. On examination, the patient had a blood pressure of 90/60 mmHg and a pulse rate of 110 beats per minute. The cardiac apex was deviated. The jugular venous pressure was elevated, bilateral pitting ankle and pulmonary oedema were present. The ECG had Q-ST elevations in the lateral leads. Serum troponin was elevated. A transthoracic echocardiogram revealed a poorly functioning dilated left ventricle with a mass within the myocardial apex. Cardiac MRI established that the mass was an intra-myocardial haematoma. A coronary angiogram demonstrated a critical plaque stenosis at the mid left-anterior-descending artery with poor distal flow. The patient did not have HIV or infective endocarditis. We treated the patient with diuretics and guideline-directed medical therapy for heart failure with reduced ejection fraction. We did not attempt surgical repair as the dissection was non-expanding, and the patient was at a high risk of operative complications.

Conclusions

Myocardial dissection with aneurysm formation is a rare complication of ischaemic heart disease. Methamphetamines enhance the risk of myocardial dissection by inducing myocardial inflammation, causing a dilated cardiomyopathy and increasing the left ventricular pressures.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12872-024-04382-0.

Introduction

Myocardial dissection, which results in a haematoma within the myocardium (with or without aneurysm formation), is a rare complication of myocardial infarction [1]. It differs from cardiac rupture, in which blood traverses the full thickness of the myocardium from the ventricle and enters the pericardium [2]. Such myocardial rupture can cause sudden death or, if contained, result in a pseudo aneurysm. We describe a patient who presented with progressive dyspnoea, and the echocardiogram showed a large left ventricle myocardial dissecting hematoma with aneurysmal dilation and left ventricular (LV) dysfunction. He was a long-term amphetamine abuser. We explore the potential patho-mechanistic relationship between amphetamine use and myocardial dissection.

Case presentation

A 37-year-old Sri Lankan male presented with a two-week history of progressively worsening exertional dyspnoea and ankle oedema. He had developed orthopnoea and paroxysmal nocturnal dyspnoea over the same period. One month before the presentation, he had developed a constricting central chest pain, which radiated to the left shoulder, associated with autonomic symptoms. He had not sought medical advice at the time. The chest pain had subsided after 4 h. The patient has been abusing inhalational heroin, crystal methamphetamines and cigarette smoke, daily for five years. There was no history of fever or loss of appetite. The rest of the systemic inquiry was unremarkable. He did not have diabetes, hypertension, dyslipidaemia, a family history of cardiomyopathy, premature atherosclerotic cardiovascular disease or collagen vascular diseases.

The patient had a blood pressure of 90/60 mmHg, a pulse rate of 110 beats per minute and cold clammy peripheries. The cardiac apex was at the 7th intercostal space in the anterior axillary line. The apical impulse was diffuse. The first and second heart sounds were normal, without additional heart sounds or murmurs. All peripheral pulses were present. Jugular venous pressure was elevated 8cm above the manubrial-sternal junction. There were fine crepitations in the bilateral lung bases. Abdominal and neurological examinations were normal.

The electrocardiogram demonstrated left axis deviation, biphasic p waves in V1 and V2, Q-ST elevations in V5 and V6, and T inversions in lead I, aVL and lead V4 to V6 (Fig. 1 – Panel E). The electrocardiogram (ECG) changes were non-dynamic. The serum troponin I was positive (5.83 ng/ml). The other biochemical and haematological investigations are given in Table 1.

Fig. 1.

The angiographic view of the coronary arteries. A – Right anterior oblique (RAO) (1°) cranial (40°). B – PA caudal 45°. C – Left anterior oblique (LAO) 42°. There is critical plaque stenosis in the mid left anterior descending artery (LAD) [Arrow] with faint filling of the distal artery. Panel D depicts the electrocardiogram with left axis deviation, biphasic p waves in V1 and V2, Q-ST elevations in V5 and V6, and T inversions in lead I, aVL and lead V4 to V6

Table 1.

Initial blood investigations

Parameter	Value
White blood cells (x 103μl)	13.19 (4 – 10)
Neutrophils	74% (50 −70)
Lymphocytes	19.4% (20 – 40)
Eosinophils	4.6% (3 – 12)
Haemoglobin (g/dl)	12.2 (11 – 16)
Platelets (x 103μl)	281 (150—450)
Na + (mmol//l)	136 (136 – 145)
K + (mmol//l)	4.1 (3.5 – 5.1)
Serum creatinine (mg/dl)	1.0 (0.72 – 1.25)
Serum lactate (mmol//l)	4.3 mmol/l (0 – 4)
Serum glucose (mg/dl)	116 mg/dl (80 – 180)
Aspartate transaminase (IU/l)	125 (5 – 34)
Alanine transaminase (IU/l)	447 (0 – 55)
Total bilirubin (mg/dl)	1.9 (0.2 – 1.2)
INR	1.11

The 2D echocardiogram, cardiac computed tomography (CT) and magnetic resonance imaging (MRI) findings are in Table 2 and Fig. 2. The echocardiogram and cardiac MRI videos are in Supplementary Materials 1 and 2, respectively.

Table 2.

The radiological characteristics of the myocardial haematoma

Imaging modality	Findings
2D echo	Dilated left ventricle with a large mass within the apical myocardium. Global hypokinesia with an ejection fraction of 25% No pleural or pericardial effusions
Contrast-enhanced cardiac CT	Enlarged left ventricle with a large crescentic shaped, smoothly margined non-enhancing area (6cm) in the apex of the left ventricle Other cardiac chambers are normal
Cardiac MRI	Large crescentic intra-myocardial mass in the left ventricular apex (6cm × 10 cm) Layering of signal within the lesion (high T1 and dark T2 signal) without contrast enhancement The myocardium is thinned out with poor contractility and very poor ejection fraction

Fig. 2.

Radiological appearances of the heart and the left ventricle A. – T2 weighted MRI of the sagittal section (A) and transverse sections (E) of the heart across the LV. 2D echocardiographic views of the heart in the parasternal short axis (B) and apical four-chamber (C) views. Contrast-enhanced computed tomography view (D). The grey arrows indicate the intramyocardial haematoma. The antero (A) -posterior (P)  axis is indicated by the white Arrow.

The invasive coronary angiogram showed critical plaque stenosis in the mid-left anterior descending artery (LAD), and the distal artery was faintly filling. The left circumflex (LCX) and right coronary arteries (RCA) were normal.

We made a diagnosis of intra-myocardial dissecting hematoma and aneurysm of the left ventricle following an anterior ST elevation myocardial infarction (STEMI). We hypothesised that the pathogenesis was related to recreational amphetamine abuse.

We managed the patient with intravenous furosemide and oral empagliflozin in the acute phase. We treated the coronary artery disease with dual antiplatelets, high-intensity statins and subcutaneous low molecular weight heparin (LMWH). We assumed that the acute coronary syndrome related to the occluded LAD would have occurred 4 weeks ago (based on the history of chest pain) and the cardiac muscle was already infarcted (based on the ECG and cardiac imaging). There was no evidence of ongoing ischaemia. Therefore, we did not attempt revascularisation as per the findings of the OAT trial [3] and ESC guidelines on acute coronary syndrome [4]. After the acute heart failure was resolved, we added enalapril, spironolactone, and bisoprolol to treat the heart failure with reduced ejection fraction. Surgical evacuation of the clot and repair of the myocardium was deemed high risk by the cardiothoracic team, and a conservative follow-up was planned. Given the risk of possible clot expansion via the dissection route, we did not initiate long-term anticoagulation to dissolve the myocardial clot. We expected the haematoma to be organised with time. We followed up the patient with echocardiograms every two days for two weeks and established that the dissection was not expanding. We review the patient every three months to screen for left ventricular aneurysm expansion and clot dissolution.

Discussion and conclusions

We describe a patient who presented with worsening heart failure and was found to have an intra-myocardial haematoma. He had evidence of a STEMI that possibly happened one month before the presentation. The patient has been abusing tobacco, methamphetamines and heroin for the last five years. We describe the cardiac effects of stimulant psychotropic drugs and explore the possibility of an association with myocardial dissection.

Myocardial dissection with haematoma formation has been described following myocardial infarction [1, 5–8], aortic arch replacement (in a patient with sarcoidosis)[9] and trauma [10], Dissection occurs along the natural dissection planes between spiral muscle fibres [11]. This is either due to blood in the left ventricle entering the myocardium through the ruptured endocardium or a rupture of a penetrating coronary artery within the cardiac muscle[12].

Myocardial dissection likely occurs when the necrotic tissue is weakest following a myocardial infarction; with tissue liquefaction but before scar tissue formation. Therefore, it can be assumed that the risk of myocardial dissection is highest in the weeks following a myocardial infarction. Revascularisation can increase the risk of myocardial dissection by enhancing tissue liquefaction (reperfusion injury) [2] and increasing the luminal pressure within the infarct-related artery.

Myocardial remodelling after infarction is an inflammatory process: Immune cells infiltrate the necrotic tissue, and the cytokine levels (tumour necrosis factor, interleukin 1 and 6) increase [13, 14]. Oxidative stress augments the inflammation [15]. Inflammation and remodelling reduce myocardial contractility and lead to ventricular dilatation. Ventricular dilatation and the thinning of the myocardium lead to increased wall tension, as per Laplace law, predisposing to dissection (Fig. 3).

Fig. 3.

The pathophysiology of methamphetamine-induced myocardial dissection. Methamphetamines increase the sympathetic outflow to the heart. Furthermore, it causes direct cardiotoxicity (A). This leads to myocardial inflammation (B), dilated cardiomyopathy (C), myocardial infarction (D) and electrical remodelling of the heart (E). Laplace's law is given in subset F. Myocardial failure and amphetamine-induced hypertension increase the intra-ventricular pressure (P). Cardiac dilatation increases the ventricular radius (r). Myocardial ischaemia, necrosis and dilatation thin out the myocardial wall (t). The cumulative effect is increased myocardial wall tension (Subset G). Increased wall tension in the presence of weak myocardium (due to inflammation and ischemia/infarction) predisposes to dissection. (Designed using BioRender.com)

Methamphetamines are potent central nervous system stimulants that increase the release and reduce the reuptake of monoamine neurotransmitters (such as serotonin, dopamine, and norepinephrine) from the pre-synaptic nerve terminals[16]. Methamphetamines exert myriad effects on the myocardium, including eosinophilic degeneration, atrophy, hypertrophy, cellular infiltration, myolysis, fibrosis, and vacuolisation [17–19]. Cardiomyocyte T tubule and sarcoplasmic reticulum dilatation, accumulation of glycogen granules and fat droplets are ultrastructural features of methamphetamine exposure [17]. Methamphetamines decrease the cardiac contractility [20, 21] and induce myocyte apoptosis [22]. Therefore, we hypothesise that the weakened myocardium, dilatation of the heart and acute hypertension with methamphetamine use predisposed the patient to develop myocardial dissection.

Compared to amphetamines, the cardiac effects of heroin abuse are less well studied. Heroin can cause acute myocardial injury [23], myocardial necrosis and fibrosis [24] (in addition to the well-known electrophysiological and negative ionotropic effects). The cardiac remodelling enzyme levels were higher in patients who used both heroin and amphetamines[25]. Therefore, heroin use would have contributed to the weakening of the myocardium, predisposing to dissection. Cigarette smoke enhances atherosclerosis and would have contributed to myocardial infarction[26].

We hypothesise that methamphetamines (and heroin to a lesser degree) weakened the myocardium, causing a dilated cardiomyopathy. The myocardial infarction caused a second hit by further weakening and thinning out the left ventricular wall. Increased left ventricular chamber size and methamphetamine-induced hypertension would have caused an increased left ventricular pressure (Laplace's law) [27]. Because the myocardium was thinned out, the wall tension per unit area would have been high. During the process of post-infarction repair, when the infarcted tissue was weakest, the myocardium would have dissected, leading to the haematoma (Fig. 3).

Myocardial dissection can lead to death [2], aneurysm formation [1], myocardial rupture with pseudoaneurysm [28] formation, ventricular septal defects [29], or spontaneous closure with thrombus organisation [30]. There are no established guidelines for the management of intramyocardial dissection. It has been managed conservatively [7, 31–33], with anticoagulation [34], and surgically [35, 6].

Diagnosing dissecting myocardial aneurysm is anchored on the radiological findings; a few decades ago, it was a post-mortem diagnosis [36]. As the echogenicity of the clot was more or less similar to the myocardium in our patient, we considered intra-ventricular clot, ventricular pseudoaneurysm, apical hypertrophic cardiomyopathy and cardiac tumour as the initial differential diagnoses. As the immediate subendocardial myocardium was contracting (Supplementary material 1), we considered an intra-mural clot less likely. The pericardium and the thin pericardial space were visible separately, and the enlargement was restricted to the left ventricular wall, which supported the diagnosis of an intra-myocardial lesion compared to an extra-cardiac pseudoaneurysm. There was no colour Doppler signals of blood flow within the myocardium. Therefore, we excluded a vascular tumour. Cardiac MRI confirmed the diagnosis of intra-myocardial haematoma.

In conclusion, myocardial dissection with intra-myocardial haematoma formation is a rare complication of myocardial infarction. We hypothesise that methamphetamine use might be causatively associated with myocardial dissection in this patient, who presented late after an acute STEMI. The diagnosis is based on echocardiography and cardiac MRI. There are no established guidelines on managing myocardial dissections and intra-myocardial hematoma, and surgical, anticoagulation and conservative management are described in the literature.

Abbreviations

CT

Computed tomography

ECG

Electrocardiogram

LAD

Left anterior descending

LCx

Left circumflex

LMHW

Low molecular weight heparin

LV

Left ventricular

MRI

Magnetic resonance imaging

RCA

Right coronary artery

STEMI

ST-elevation myocardial infarction

Authors’ contributions

PR, SP, GD, DA and GG conceptualised. PR drafted the manuscript. GG critically revised it.

Funding

No funding involved.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

Approval from an ethics review committee was not sought as the publication is a case report per institutional policy.

Consent for publication

Written informed consent was obtained from the patient to publish this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare no competing interests.