Two Cases of Intramyocardial Dissecting Hematoma Diagnosed by Echocardiography

Abstract

Intramyocardial dissecting hematoma (IDH), a rare complication of myocardial infarction, was investigated through two unique clinical cases in this study. We demonstrate echocardiography’s pivotal role in emergency diagnostics by detailing its critical contribution to rapid identification. Furthermore, we propose a hypothesis regarding the anatomical subtypes of IDH, potentially offering new perspectives and insights into this rare cardiac condition.

1. Introduction

Intramyocardial dissecting hematoma (IDH) is a rare yet life-threatening complication of acute myocardial infarction, characterized by low incidence, complex clinical manifestations, and extremely poor prognosis. Currently, there remains a lack of unified standards for its diagnosis and management in clinical practice. This study aims to explore the value of echocardiography in the emergency diagnosis of such rare conditions by reporting two cases of IDH confirmed by echocardiography. One case involves a 73-year-old woman with a history of myocardial infarction, admitted with septic shock and left ventricular dysfunction; the other is a 69-year-old diabetic woman presenting with acute myocardial infarction complicated by metabolic acidosis. Both cases highlight the pivotal role of echocardiography (especially transthoracic echocardiography, TTE) in rapidly identifying lesions and dynamically monitoring hematoma changes (e.g., size, blood flow communication)—even in the absence of advanced imaging modalities like MRI, it can still provide timely evidence for clinical decision-making.

Furthermore, this study proposes a hypothesis regarding potential anatomical subtypes of IDH based on case characteristics, offering new insights into the pathological mechanisms of the disease and providing practical references for IDH diagnosis and treatment in primary hospitals or emergency scenarios.

2. Case 1

A 73-year-old woman with past history of myocardial infarction and coronary artery disease with stenting was admitted with diarrhea that had persisted for 26 days and fever that persisted during the last 7 days. Physical examination revealed jugular venous distension and moderate bilateral lower limb pitting edema. The apical impulse was palpable at the fifth intercostal space, 1.0 cm lateral to the left midclavicular line, spanning approximately 3.0 cm. No thrill or heave was noted. Bilateral basal pulmonary crackles were auscultated. Mild periumbilical tenderness was present. The skin and sclerae were anicteric, and no cyanosis was observed on the lips. Laboratory results showed hypokalemia (K+ 2.73 mmol/L), elevated BNP (10,338 pg/mL), and positive blood cultures (Salmonella and E. coli). The electrocardiogram (ECG) showed sinus rhythm with pathological Q waves, ST-segment elevation in leads V3–V4, and inverted T waves in leads V4–V5. (Fig. 1). Transthoracic echocardiography (TTE) showed a dilated left ventricle (LV, 53 mm). LV systolic function was impaired, with an ejection fraction of approximately 35 %, and LV apical aneurysm with possible thrombosis and LV intramyocardial dissection hematoma were observed (Fig. 2). Reexamination of TEE after 12 days revealed a dilated LV (58 mm), an LV ejection fraction of approximately 33 %, LV intramyocardial dissection hematoma hat has expanded compared with the first examination, LV apical pseudoaneurysm, and LV apical thrombosis (Fig. 3). Our clinical diagnoses were septic shock, sepsis, LV aneurysm with thrombosis, and LV intramyocardial dissection hematoma. The clinical course involved conservative management which initially improved symptoms, but sudden hemodynamic collapse occurred 20 days later. The ECG shows supraventricular tachycardia and significant ST segment elevation (Fig. 4). Despite cardioversion for supraventricular tachycardia, the family declined ICU transfer. The patient died after one week post-discharge.

Fig. 1.

The electrocardiogram of the first case showed sinus rhythm with pathological Q waves, ST segment elevation in leads V3–V4, and inverted T waves in leads V4–V5.

Fig. 2.

Echocardiogram images of Case 1. Intramyocardial dissecting hematoma at the apex of the heart is indicated by the white arrow. (A) Apical four-chamber view showed the formation of intramyocardial dissecting hematoma. (B) Two-chamber view showed that the blood flow enters the left ventricle and the interlayer capsule through the tear. (C) Apical ventricular aneurysm of the left ventricle, with thrombosis (indicated by the triangle).

Fig. 3.

The images of the follow-up echocardiogram in Case 1. Intramyocardial dissection hematoma at the apex is shown by white arrow. (A) Fourcavity core section, the interlayer area has an expansion trend compared with 2A. (B) Left ventricular blood flow into the anechoic dark area, and the torn endocardium has a tendency to expand compared with 2B. (C) Pseudo ventricular aneurysm at the apex of the left ventricle and thrombosis at the apex (triangle shown).

Fig. 4.

The electrocardiogram of the first case 20 days after the initial showed supraventricular tachycardia with ST segment significantly elevated in leads V1–V5.

3. Case 2

A 69-year-old woman with diabetes was admitted to our hospital due to chest pain for 10 days and sudden loss of consciousness for 4 h. On physical examination, our patient had deep breathing, a fetid odor resembling that of rotten apples, and urinary and fecal incontinence. Blood pressure was low (84/60 mmHg) and heart rate was 106 beats per minute. No jugular venous distension was observed. Peripheral perfusion was impaired, with cold and mottled extremities. The patient was comatose, appeared dyspneic with an apathetic expression, and was admitted to the ward via stretcher, demonstrating poor cooperation with physical examination. Corneal reflexes were intact. Limbs showed symmetric withdrawal to painful stimuli, without pathological reflexes or meningeal irritation signs. No significant cardiac murmurs were auscultated.

Laboratory results revealed cTn-I: 0.718 ng/mL, CK-MB: 27.1 ng/mL, Myoglobin: 797 ng/mL, BNP: 1502.00 pg/mL. ECG showed sinus rhythm, Q waves combined with ST segment elevation in II, III, and aVF, inverted T waves in III and aVF, and ST segment depression in leads V1–V5 (Fig. 5). TEE revealed LV systolic function was impaired, with an ejection fraction of approximately 45 %, and intramyocardial dissection hematoma in the basal segment of the inferior posterior wall of the LV, pericardial effusion (Fig. 6). Our clinical diagnoses was acute myocardial infarction (Killip class III), intramyocardial dissection hematoma, and metabolic acidosis. After a period of conservative management, the patient’s condition improved. Therefore, the patient refused to undergo further cardiac magnetic resonance imaging (MRI) examination. However, unexpectedly, the patient died approximately 1 week after discharge from the hospital.

Fig. 5.

Echocardiogram images of Case 2. (A) The epicardium is intact, and intramyocardial dissecting hematoma at the apex of the heart is formed (indicated by the white arrow). (B) Subepicardial and intramyocardial hematomas are formed (indicated by the pentagram), and there is pericardial effusion (indicated by the triangle); The epicardium is intact (indicated by the white arrow). (C) Three-dimensional imaging of intramyocardial hematoma and pericardial effusion is observed at the apex of the heart; The epicardium is intact (indicated by the white arrow). (D) Three-dimensional imaging shows that there are intramyocardial hematoma and pericardial effusion on the lateral wall of the left ventricle.

Fig. 6.

The electrocardiogram of the second case shows sinus rhythm, Q waves combined with ST segment elevation in II, III, and aVF, inverted T waves in III and aVF, and ST segment depression in leads V1–V5.

4. Discussion

Intramyocardial dissecting hematoma (IDH) is a pathological manifestation of blood accumulation in the myocardium (subepicardial) caused by myocardial hemorrhage or coronary artery rupture due to various reasons, followed by the pathological manifestation of a hematoma that forms in the myocardium.1

Echocardiography is the preferred method for noninvasive diagnosis of suspected IDH. IDH can be diagnosed on the basis of three or more of the following characteristics: (1) The formation of one or more neocavitations in the myocardial tissue, an echogenic center, and the cavity is enlarged in systole and decreased in diastole; (2) thin-walled and mobile endocardium surrounding the cavity; (3) the cavity is surrounded by normal myocardial tissue; (4) Spiral channels are observed when the dissection is in the ventricular septum; (5) The echo of the newly formed cavity is consistent with that of the blood; (6) the cavity communicates with the ventricle through a tear; (7) The dissection is partially or completely absorbed during follow-up, and may be combined with other cardiac rupture manifestations, such as pericardial effusion or pseudoaneurysm.2 Case 1 was consistent with manifestations 1, 2, 3, 5, and 6. Case 2 was consistent with manifestations 1,3,5. In Case 2, the hematoma was located between the epicardium and the myocardium, which was different from the commonly reported “endocardial - myocardial separation” in the literatures.3,4 This anatomical difference suggests that the pathological mechanism of IDH may be more complex and might be related to the distribution of shear stress between myocardial layers or the pattern of local ischemic injury.

Other imaging modalities for diagnosing IDH include LV angiography, transesophageal echocardiography, CT, and MRI. LV angiography can also provide more diagnostic information, display the location and size of the rupture, observe hemodynamic changes in real time, observe myocardial perfusion and determine whether the dissection is blind, and distinguish it from other cardiac space-occupying diseases.5 Esophageal echocardiography can provide higher image resolution and accuracy. MRI is the gold standard for the diagnosis of IDH and has high tissue resolution.6 Neither of the two cases was diagnosed by MRI. However, early identification was achieved through dynamic echocardiographic monitoring (such as the trend of hematoma expansion and the communicating blood flow between the cardiac cavity and the hematoma), which supports the crucial role of TTE in emergency situations. Therefore, when hemodynamic instability is present or resources are limited, TTE, as the preferred tool, is crucial for the early identification of IDH, for explaining the illness condition and avoiding doctor - patient disputes. In contrast, magnetic resonance imaging (MRI) should be employed as a subsequent means for definitive diagnosis.

Important differential diagnoses include pseudoaneurysm, intracavitary thrombus, prominent ventricular trabeculations, and cardiac space-occupying lesions. A pseudoaneurysm is a cyst cavity formed by surrounding tissues, such as the pericardium and thrombus, after the complete rupture of the myocardial wall7(Table 1). The intracavitary thrombus and prominent ventricular trabeculations are located in the ventricular cavity, with an intact endocardium.8 Whether the echo-free cavity at the apical cap location in Case 1 is a myocardial dissection or a pseudoaneurysm is controversial. When rupture of the epicardial myocardium cannot be determined by echocardiography, it is necessary to combine it with MRI examinations for diagnosis. However, the patient and his family did not request follow-up cardiac MRI, LV angiography, and other examinations, and a chest CT only revealed cardiac enlargement (especially in the LV); therefore, the diagnosis could not be further confirmed by other imaging data.

Table 1.

Comparison of Pseudoaneurysm vs. Intramyocardial Dissecting Hematoma.

Characteristics	Pseudoaneurysm	Intramyocardial Dissecting Hematoma
Etiology	Full-thickness myocardial rupture, encapsulated by pericardium and thrombus.	Intramyocardial hemorrhage or coronary rupture causing hematoma dissection.
Anatomy	Epicardial rupture, wall lacks myocardium, bidirectional flow via narrow neck (<50 % diameter), Sac expands in systole.	Epicardium is intact, hematoma is connected to the ventricular cavity through the tear (if any exists), dynamic expansion in systole.

IDH is an entity with very low incidence and high mortality. Previous case reports have described that low left ventricular ejection fraction, late diagnosis, pericardial effusion, and age over 60 years are associated with worse prognosis.9 Note-worthily, a recent study reported that all patients with comparable conditions died.10 The presence of pericardial effusion increases the risk of mortality by 3.92 times.11 Even if the patient’s symptoms improve temporarily (as in Case 2), there remains a risk of delayed rupture in IDH complicated with pericardial effusion, necessitating close echocardiographic follow-up.

5. Conclusion

Current evidence suggests that early surgical intervention may reduce mortality in IDH patients with large hematomas, hemodynamic instability, or LVEF <40 %.12 The patients with a small lesion localized to the apex, and with stable hemodynamics, especially in subjects whom the culprit artery had been opened, may benefit from conservative management.13 However, limited data from case reports preclude definitive guidelines. The best treatment for IDH in each clinical scenario is not clearly defined.14 Further multicenter studies are needed to refine management strategies. Our cases highlight echocardiography’s role in urgent diagnosis and dynamic monitoring, especially when MRI is unavailable.

Funding Statement

This work was supported by grants from the National Natural Science Foundation of China (No. 82100244), China Postdoctoral Science Foundation (No. 2022M712012), Shandong Province Medical and Health Science and Technology Development Project (No. 202003040648), Binzhou Medical University Scientific Foundation (No. BYFY2020KYQD40).