Rupture of the cardiac free wall after infarction confirmed by aortic CTA

doi:10.21203/rs.3.rs-4083476/v1

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Case Report

Rupture of the cardiac free wall after infarction confirmed by aortic CTA

https://doi.org/10.21203/rs.3.rs-4083476/v1

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Background

Free wall rupture is a rare complication of myocardial infarction, occurring as early as a few hours after myocardial infarction. It usually happens after transmural myocardial infarction and has a very high mortality rate. The diagnosis of free wall rupture requires echocardiographic evidence of pericardial leakage or pericardial tamponade. The patient's cause of death is often attributed to other causes such as cardiac arrhythmia unless determined by open heart surgery or autopsy. Diagnostic tools for post-infarction cardiac free wall rupture are limited to date.

Case presentation

We report a patient with myocardial infarction who presented with atypical chest pain. Subsequent coronary angiography suggested small vessel disease, but the patient's severe clinical presentation was not consistent with small vessel disease. Considering the patient's non-excluded aortic coarctation and the small size of the vascular lesion, no intervention was performed for the time being. Next, to further clarify the diagnosis, the patient underwent an aortic computed tomography angiography (CTA). In the aortic CTA a rupture of the free wall of the heart was detected and a large amount of bloody pericardial effusion was found. Unfortunately, the patient did not have a successful puncture and drainage, and died after resuscitation.

Conclusions

The diagnosis of cardiac rupture is a challenge. We need to be alert to the possibility of cardiac rupture even in small vascular lesions. When patients present with more severe clinical manifestations that are not consistent with myocardial infarction, it is important to be alert to the possibility of cardiac rupture in addition to identifying the possibility of aortic coarctation. Aortic CTA may be able to confirm the diagnosis when neither echocardiography nor coronary angiography is used to detect such occurrences of cardiac rupture.

Cardiac rupture

Free wall rupture

Aortic computed tomography angiography

Diagnosis

Cardiac rupture is one of the complications of myocardial infarction and is often characterized by acute episodes of shortness of breath, chest pain, shock, sweating, unexplained vomiting, cold clammy skin, and fainting[1]. Risk factors for cardiac rupture after myocardial infarction include older adults, women, hypertension[2–6], single-vessel disease, and first-time infarction[7, 8]. Pericardial effusion is the most common manifestation of cardiac rupture during acute myocardial infarction. It has extremely limited diagnostic tools and can often only be clarified by open-heart surgery or occasionally by echocardiography or angiography showing blood leakage into the pericardial cavity[9]. A ruptured heart can lead to rapid death, making prompt diagnosis and treatment crucial[1]. We will present a patient with myocardial infarction who had a rupture of the free wall of the heart detected not by cardiac ultrasound or coronary angiography but by aortic computed tomography angiography (CTA).

We report a 47-year-old middle-aged male admitted to the emergency department with severe posterior back and lumbar pain. The patient's general state was poor, characterized by agitation, dyspnea, inability to lie down, cyanosis, and clammy cold skin. Electrocardiogram showed ST-segment elevation in leads II, III and AVF (Fig. 1).

Based on the patient's symptoms and history of hypertension it was considered that aortic coarctation was not excluded and that the elevation of the ST segment in the inferior wall lead could be due to a cumulative right coronary artery opening. It was then decided to further identify the patient by drawing blood for laboratory tests. After waiting for 10 minutes, the laboratory results showed TroponinI 0.87 ng/ml (0.01–0.023), D-dimer: 978 ng/ml (80–500), N-Terminal Pro-Brain Natriuretic Peptide 599 ng/L (300–500), Lactate 25 mmol/L (0.5–1.6), Glucose 30 mmol/L (3.9–5.8), Potassium 2.7 mmol/L (3.4–4.5).

Considering that the patient's troponin was markedly elevated and his D-dimer was not, the decision was made to proceed with coronary arteriography. Coronary angiography of the patient showed the left anterior descending branch of the muscle bridge, systolic more than 70% stenosis, the diagonal branch of the middle about 50% stenosis, the left coronary artery cyclopean branch opening is normal, the main trunk does not see obvious stenosis, the distal occlusion, TIMI flow grade 0, the right coronary opening is normal, the middle can be seen 30–40% stenosis, the right coronary opening is normal, the middle can be seen 30–40% stenosis, the right coronary artery is normal, the right coronary artery is normal, the middle can be seen 30–40% stenosis (Fig. 2). During the procedure the patient experienced a drop in blood pressure and we gave antihypertensive drugs to maintain blood pressure combined with continuous noninvasive ventilator-assisted respiration.

The patient had a small vessel in the occluded segment of the systolic branch, and an urgent aortic CTA was performed, considering that the patient's symptoms were more inclined to aortic coarctation. Bedside ultrasound during this period visualized only moderate amounts of pericardial effusion due to irresistible factors such as the patient's obesity, irritability, and the level of the ultrasound operator. The aortic CTA showed a large amount of bloody pericardial effusion, right ventricular collapse, incomplete closure of the vena cava valve or valve agenesis, and blood flow was seen to be shuttling through the myocardium into the pericardium by careful observation, but no obvious aortic coarctation was seen (Fig. 3).

After ruling out aortic coarctation, the patient was returned to the catheterization laboratory for further management of distal systolic branch occlusion and pericardiocentesis: the guidewire was sent along the catheter to successfully pass the distal end of the occluded segmental branch of the pirouette branch, and the balloon was sent to the occluded segment of the pirouette branch to dilate it at 6–8 atmospheres, and the distal end of the pirouette branch was seen on the angiogram, with a fine diameter of the tube, about 70% stenosis, and a grade of 3 on the TIMI (Fig. 4). Due to unsuccessful pericardiocentesis, the patient was transferred to the cardiac care unit (CCU) for proposed ultrasound-guided pericardiocentesis. The patient's generalized cyanosis and dyspnea increased throughout.

After transfer to the CCU, the patient's ultrasound-guided pericardiocentesis remained unsuccessful due to massive gas interference in the chest cavity. Consider the possibility of a pneumothorax, the patient undergoes a Computed tomography (CT) of the lung (Fig. 5). Lung CT suggests pneumothorax, increased pericardial effusion as well as more collapse of the right ventricle. After being transferred back to the CCU the patient suddenly developed respiratory arrest, unconsciousness, decreased heart rate, and undetectable blood pressure. The patient was declared clinically dead after ineffective resuscitation.

Cardiac rupture is one of the most serious complications of acute myocardial infarction. Although its incidence is only 2–4%, the mortality rate is as high as 90%. This higher mortality rate is closely related to pericardial tamponade[9].

Cardiac rupture is not a sudden full-layer rupture of the myocardium. Instead, a rupture occurs in the endocardium first, and blood flows from the rupture into the myocardium to form a myocardial entrapment hematoma, which gradually penetrates to the epicardium, and ultimately ruptures the whole layer to occur pericardial pressure occlusion. Once a heart rupture has occurred, timely and accurate diagnosis is important[1]. Patients presenting with acute catastrophic rupture usually die immediately and are often diagnosed by autopsy[10]. In some patients, the clinical manifestation of the subacute process is accompanied by persistent or recurrent severe chest pain after acute myocardial infarction, with entrapment hematoma in the myocardium, and a drop in blood pressure and deterioration of the condition. The blood pressure continues to remain at a low level for several hours to more than ten hours, with a gradual accumulation of seeping blood in the pericardial cavity, followed by the phenomenon of pericardial tamponade. Early diagnosis and timely emergency surgical treatment of such patients can be expected to be successful.Although echocardiography has moderate sensitivity (70%) and high specificity (90%) in the diagnosis of cardiac rupture, it is a great challenge for both operator skill and patient cooperation[11].

In our case, the patient was not found to have extravasation of contrast medium during coronary angiography, but demonstrated a clinical picture that was not consistent with coronary vascular lesions. However, we accidentally made a definitive diagnosis by aortic CTA in order to rule out aortic coarctation. This suggests that we may be able to make a definitive diagnosis with aortic CTA when cardiac rupture is not detected by either coronary angiography or cardiac ultrasound, especially if there are high-risk factors for cardiac rupture. We can even diagnose the area of rupture by the amount of contrast and the rate of outflow.

CTA: Computed tomography angiography

CCU: Cardiac care unit

CT: Computed tomography

Ethics approval and consent to participate

This case report was approved by the Medical Ethics Committee of the China-Japan Union Hospital of Jilin University. The patient consented to participate the study.

Consent for publication

Written informed consent was obtained from the patients for publication.

Availability of data and materials

All the data discussed in the manuscript are included in this published article.

Competing interests

The authors have no conflicts of interest to disclose.

Funding

Not applicable.

Authors' contributions

JL cared for the patient and drafted the manuscript. WC assisted in writing the manuscript. ZL critically revised the manuscript. NL performed the literature search. CM provided consultation and coordination of the manuscript. All authors reviewed and approved the final manuscript.

Acknowledgements

Not applicable.

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No competing interests reported.

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Rupture of the cardiac free wall after infarction confirmed by aortic CTA

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Abstract

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Background

Case presentation

Discussion and Conclusions

Abbreviations

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References

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