|Year : 2019 | Volume
| Issue : 1 | Page : 55-57
Surgical ventricular restoration of the dilated left ventricle with large left ventricular thrombus following acute decompensated heart failure: A late complication of anterior wall myocardial infarction: “Tomb of Dead Myocardium!”
Pankaj Jariwala, Sridhar Kale Satya
Department of Cardiology and Cardio-Thoracic Surgery, Yashoda Hospitals, Somajiguda, Hyderabad, Telangana, India
|Date of Web Publication||10-May-2019|
Dr. Pankaj Jariwala
Department of Cardiology and Cardio-Thoracic Surgery, Yashoda Hospitals, Somajiguda, Raj Bhavan Road, Hyderabad - 500 082, Telangana
Source of Support: None, Conflict of Interest: None
There are various case reports and the original article in the literature about the formation of a left ventricular thrombus (LVT) after acute myocardial infarction as an early to a late sequel. However, there are no guidelines available for their management, as the clinical presentation of LVT is variable and there is no consensus about its management. Furthermore, there are no randomized controlled trials comparing different treatment strategies. Here, we present a case of a large LVT who presented as acute decompensated heart failure. After stabilization, he underwent surgical repair of left ventricular aneurysm and retrieval of a thrombus.
Keywords: Acute decompensated heart failure, acute myocardial infarction, left ventricular thrombus, surgical ventricular restoration
|How to cite this article:|
Jariwala P, Satya S. Surgical ventricular restoration of the dilated left ventricle with large left ventricular thrombus following acute decompensated heart failure: A late complication of anterior wall myocardial infarction: “Tomb of Dead Myocardium!”. J Indian coll cardiol 2019;9:55-7
|How to cite this URL:|
Jariwala P, Satya S. Surgical ventricular restoration of the dilated left ventricle with large left ventricular thrombus following acute decompensated heart failure: A late complication of anterior wall myocardial infarction: “Tomb of Dead Myocardium!”. J Indian coll cardiol [serial online] 2019 [cited 2021 Apr 12];9:55-7. Available from: https://www.joicc.org/text.asp?2019/9/1/55/257954
| Introduction|| |
The anterior wall myocardial infarction leads to various late manifestations such as left ventricular thrombus (LVT) formation, arrhythmias, and sudden cardiac death. Over time, the formation of LVT has decreased from 30%–40% to 5%–15%, with the availability of early revascularization strategies., The formation of LVT leads to various late clinical manifestations such as embolic phenomenon and acute decompensated heart failure. Embolic events in these patients are common without anticoagulation occurring in 10%–40% of patients. Since large and mobile thrombi are relatively rare, there are no studies to address the real risk of embolization of such clots. Moreover, the literature provides little guidance on best approaches to management of such patients, especially those with low left ventricular ejection fraction (LVEF).
| Case Report|| |
A 66-year-old male was brought to an emergency room with complaints of acute onset of breathlessness at rest for the past 2 h. Clinical diagnosis of acute left ventricular (LV) failure was made. On examination, his pulse rate was 122/min, respiratory rate was 32/min, and blood pressure was 100/60 mmHg. There were peripheral signs of hypoperfusion such as cold and clammy extremities. Cardiovascular examination revealed elevated jugular venous pressure, enlarged apical impulse, muffled heart sounds, and no murmur. Bilateral lung fields revealed basal rales and rhonchi. Blood chemistry revealed no abnormalities. Arterial blood-gas analysis showed mild hypoxemia with normal PCO2 suggestive of Type I respiratory failure. Electrocardiography showed sinus tachycardia, poor “R” wave progression, and QS pattern in V1-4 with persistent ST-T segment elevation. Chest X-ray revealed cardiomegaly with increased bronchovascular markings.
His room air saturation was 77%, which improved marginally with 10 L of oxygen using a mask; hence, noninvasive ventilation in the form of intermittent positive-pressure ventilation started. Furthermore, pharmacological measures in the form of intravenous dobutamine, furosemide, and noradrenaline were started. This improved his vital parameters, and the patient was shifted to the intensive cardiac care unit for further observation and stabilization.
Bedside two-dimensional echocardiography revealed large organized “horseshoe” crescent-shaped laminar thrombus occupying the apex and adjacent portion LV cavity. There were LV regional wall motion abnormalities (RWMA) in the form of akinetic, scarred, and thinned-out mid- and distal interventricular septal, mid, and distal anterior segments with an apical aneurysm, while other areas had hypokinesia. Overall, his LVEF was 28% with mild mitral regurgitation [Figure 1]a and [Figure 1]b.
|Figure 1: Transthoracic echocardiogram (apical four-chamber view, [a]; short-axis view, [b]) showed a large thrombus filling almost half of the left ventricle. It extended into the apical and mid segments of the left ventricle assuming a crescent shape. There was a dense spontaneous echo contrast in the rest of the left ventricular cavity. We could appreciate an echo-dense, older organized thrombus toward the apex and a layer of fresh thrombi deposited over it, which was brighter toward the left ventricular cavity|
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He had anterior wall myocardial infarction 8 months back. At that time, echocardiography demonstrated moderate LV dysfunction (ejection fraction – 38%) with regional wall abnormality involving the anterior wall and no LVT. Coronary angiography revealed a recanalized left anterior descending artery, and other coronary arteries were normal. He was prescribed aspirin 150 mg, high-intensity atorvastatin 80 mg, ramipril 2.5 mg, and metoprolol 25 mg as per the American College of Cardiology/American Heart Association (ACC/AHA) Guidelines for the secondary prevention of the coronary artery disease. Magnetic resonance cardiac imaging was not performed, as the patient was hemodynamically unstable. His workup for the hypercoagulable state did not reveal any abnormality.
The patient underwent LV aneurysmectomy with surgical ventricular restoration (SVR), which involved the removal of a giant LVT (surgical thrombectomy) with repair of the left ventricle to restore the LV geometry. In the operating room, the LV apex was opened, which revealed the presence of a large amount of organized thrombus attached to the apex, septum, and anterior wall that were carefully removed. It weighed 406 g and on inspection, there were red- to brown-colored layers of thrombosis with patchy areas of fibrosis [Figure 2]. The patient did well postoperatively and was discharged in the stable condition.
|Figure 2: Postsurgical photo of a large left ventricular thrombus removed from the left ventricular apical aneurysm which extended till the mid of the left ventricular cavity. There were layers of old thrombus, which was brown in color mixed with white bands of collagen tissue. The fresh thrombus deposition was seen toward the left ventricular cavity, which was red in color|
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He was discharged on optimal medical management in the form of aspirin, ramipril, eplerenone, metoprolol, statin, and warfarin for the period of 6 months. LVEF improved to 50%, as SVR reduced the LV volume and “restored” a more normal elliptical ventricular shape in dilated hearts after anterior infarction [Figure 3].
|Figure 3: Follow-up two-dimensional echocardiography at 6 months in parasternal long-axis view demonstrated the improvement in the left ventricular ejection fraction to 50% with the restoration of normal elliptical shape and reduction of left ventricular size|
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Thereafter, he was advised regular follow-up and was asymptomatic till the last follow-up visit at the completion of 1 year.
| Discussion|| |
The incidence of LVT was very high in different series for 20%–50%, but in recent times, it has come down to <1.8%–2.5%. This reduced incidence was secondary to the early diagnosis of acute myocardial infarction (AMI), and reperfusion strategies including primary angioplasty or newer thrombolytic agents, use of anticoagulation, angiotensin-converting-enzyme inhibitors, which leads to improved LV remodeling secondary to smaller size of the myocardial infarction.
Further, the ease of availability of advanced imaging techniques such as 3D echocardiography, contrast echocardiography and magnetic resonance angiography for the cases with a high index of suspicion about LV aneurysm and screening for the LVT contributed to the early diagnosis and reduced incidence of LVT.
Despite all, there is an occurrence of the LVT in the modern era. Jiang et al. studied 13,732 AMI cases retrospectively and found that the lower LVEF, extensive anterior myocardial infarction, severe RWMA, and left ventricular aneurysm are the independent risk factors for the development of LVT after AMI, and 91.2% of the LVT masses were formed within a ventricular aneurysm or dyskinetic segments. The incidence of LVT after AMI was 0.7% in their study.
Earlier studies reported that the occurrence of LVT is rare after the 3-month post-AMI. However, in our case, the formation of LVT was noticed after 8 months of the AMI, which is a rare phenomenon. Increased hyperviscosity of the blood inside the LV cavity due to dehydration, stasis, and decreased intracardiac blood flow, particularly with global or RWMA, may be associated with hypercoagulable disorders such as protein C or S deficiency in a normally functioning heart.
LVT is an amorphous echogenic structure with varying shape and is adherent to the endocardium. Currently, no studies are available to choose the best strategy in such cases. Thrombolytic agents such as urokinase have been tried, but they carry a high risk of embolism, and hence contraindicated as a routine practice. Vitamin K antagonist (VKA) has robust evidence and also recommended by the European Society of Cardiology and ACC/AHA Guidelines in patients with an LV thrombus after myocardial infarction for the prevention of systemic embolism, though not useful for the resolution of LVT.
The addition of VKA along with dual-antiplatelet therapy (DAPT) leads to increased incidence of fatal and nonfatal bleeding to 12% versus the risk of cardioembolic cerebral infarction to 0.75%–1.2% postprimary angioplasty. Triple therapy of VKA and DAPT is not strongly recommended. There are no randomized controlled trials for the use of newer oral anticoagulants in patients with LVT except for the few case reports where they used apixaban.,
For large mural nonpedunculated LVT as in our case, surgical thrombectomy is the treatment of choice than conservative management using anticoagulants. In a study measuring the long-term outcomes of treatment strategies, the overall risk of systemic thromboembolism tended to be higher in those treated with anticoagulation versus those that underwent surgical resection (17.7% vs. 0%).
| Conclusion|| |
The occurrence of LVT after myocardial infarction is at the cost of dead myocardium and leads to high morbidity and mortality. Its early identification and treatment can be lifesaving. There are no definite guidelines for their management, and one should use experiences based on earlier published case reports and institutional peer discussion for the management of such cases of large LVT.
Informed consent was obtained from all individual participants included in the study, and additional informed consent was obtained from all individual participants whose information is included in this article.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]