Mural thrombi are thrombi that attach to the wall of a blood vessel and cardiac chamber. Mural thrombus occurrence in a normal or minimally atherosclerotic vessel is a rare entity in the absence of a hypercoagulative state or inflammatory, infectious, or familial aortic ailments. Mural thrombi can be seen in large vessels such as the heart and aorta and can restrict blood flow. They are mostly located in the descending aorta, and less commonly, in the aortic arch or the abdominal aorta. Mural thrombi can invade any cardiac chamber. Left ventricular thrombus is a frequent complication of acute myocardial infarction, mostly with the involvement of cardiac apex. This thrombus can separate from the ventricle and travel through arteries, blocking any blood vessels.
Virchow's triad describes the pathogenesis of thrombus formation. Endothelial injury initiates the process. It is induced by trauma to the endothelium of blood vessels. Abnormal laminar flow induced by turbulence in arteries propagates the process. Valvulitis or an aneurysm induces it. Then hypercoagulability further enhances the thrombosis. Leukemia or coagulation disorders induce hypercoagulability. These 3 factors create a cascade of events leading to the propagation of thrombus that ultimately occludes the vessels and produces complications.
Before the lytic and urgent interventional era, left ventricular thrombus occurred in 25% to 40% of patients after a first anteroapical myocardial infarction. With the advent of acute reperfusion strategies, there has been a decline in prevalence. The major risk of left ventricular thrombus is subsequent embolization with stroke or major organ loss. Historically, the likelihood of embolic events was greatest in the first 2 weeks after the acute event and tapered off over the ensuing 6 weeks. After this time, there was presumed endothelization of the thrombus with a reduction in its embolic potential. Now, with the use of thrombolytics and anticoagulants, the incidence of thrombi has diminished but not to a great extent.
Thrombus formation starts in response to injury, activating the hemostatic process. Platelets are activated by exposure of collagen or tissue factor. This causes a further cascade of platelet activation with the release of cytokines, ultimately causing thrombus formation. A number of cardiac conditions pose an increased risk of thrombus formation. These include atrial fibrillation, heart valve replacement, deep venous thrombosis, acute myocardial infarction, and genetic coagulation disorder. The whole process is regulated by thermoregulation. Large thrombus in a vessel can occlude a vessel and can induce ischemia, also termed as mural thrombi, resulting in the death of tissue. Sometimes thrombi are free-floating and can dislodge to the distal vessel. Embolization to the brain can lead to stroke. Embolization to the limb can lead to amputation.
They appear reddish-gray, representing bands of fibrin with entrapped white blood cells (WBC) and red blood cells (RBC). Thrombi are classified into 3 major groups depending on the relative amount of platelets and RBC. Three major groups are white thrombi, characterized by a predominance of platelets; red thrombi characterized by a predominance of RBC; and mixed with features of both white and red thrombi. Thrombi may be mobile, a characteristic that has been associated with a higher embolic potential. On occasion, fresh thrombi take on a cystic appearance. This is due to a combination of factors including varying degrees of maturity of the clot and results in acoustic boundaries between relatively fresh and more organized regions.
The mural thrombus may be symptomatic or may be diagnosed as an incidental finding. Symptoms are mainly related to the localization of thrombus. It can be incidentally detected lying in walls of the aorta in an asymptomatic patient. Its embolization to brain induces cerebrovascular events, causes mesenteric ischemia in the gut, and causes renal infarction, coronary ischemia in heart, pulmonary infarction, among others. Its presence in the distal part of the vessel can induce ischemia, which can result in limb loss.
Various modalities can help in a diagnosis, but the modality of choice for diagnosis of mural thrombi is CT or MRI angiography. These tools are best for determining the location and extent of mural thrombi. These modalities are costly but helpful in prognostication of disease. Transoesophageal echocardiography (TEE) is another, relatively noninvasive option and a good tool for diagnosis. TTE is an inexpensive, bedside procedure with a low risk of complications. TEE is also helpful in diagnosing left ventricle thrombus and aortic atheroma especially in ascending aorta. Both MRI and CT are more sensitive than TEE in detecting the thrombus in an entire thoracic aorta. Both are usually well tolerated. Other modalities like intravascular ultrasound or optical coherence tomography have opened up a new era of defining thrombi.
Treatment of thrombi could reduce the risk of stroke, myocardial infarction, and pulmonary embolism. There are no standardized guidelines for the treatment of mural thrombi. Heparin and warfarin are often used to inhibit the initiation and propagation of existing thrombi. Heparin binds to and activates the enzyme inhibitor antithrombin III, and warfarin inhibits vitamin K epoxide reductase, both enzymes needed to produce clotting factors. Heparin is a preferred drug for dissolving the clot. If thrombi do not resolve after 2 weeks of heparin therapy, then surgery is an option. Thrombolytic therapy is another option for clot dissolution. It includes streptokinase, urokinase, reteplase, and tenecteplase. These are usually administered intravenously. Surgical candidates include younger patients, those having a low risk of perioperative complications, those in whom conservative treatment is unsuccessful, and those who have a highly mobile thrombus with high embolic risk. The surgical procedure includes thrombectomy, segmental aortic resection, thromboaspiration, and endoluminal stent-grafts. No approach is definitively superior. Endoluminal stent grafting is the least invasive option, but it carries a high risk of distal embolization through wire manipulation and stent deployment.
Mural thrombi in the cardiac cavity can mimic a cardiac mass.
In the aortic wall, it can appear as mural hematoma or aortic dissection.
If left untreated the patients are at risk of embolization leading to a cerebrovascular infarction as the most feared complication. In general, with appropriate therapy, the prognosis related to mural thrombi is favorable.
Left ventricular thrombi can embolizes to the brain or any other body organ causing fatal events. Aortic mural thrombi have high chances of embolization and higher incidence of limb loss. Mesenteric ischemia, renal infarction, vision loss, myocardial infarction are other rare complications.
Anticoagulation is an effective means of controlling and preventing the further progression of mural thrombi.
The occurrence of mural thrombi has detrimental effects on morbidity and mortality of cardiac patients. Earlier detection and initiation of timely anticoagulation prevents many complications.
Early detection of mural thrombi is of great importance for preventing the complication arising from embolization of thrombi.
The diagnosis and management of mural thrombi is best done with an interprofessional team that includes an internist, cardiologist, neurologist, radiologist, vascular surgeon and a team of specialty nurses. It is vital to treat mural thrombi as this can lower the risk of stroke, myocardial infarction, and pulmonary embolism. There are no standardized guidelines for the treatment of mural thrombi. The type of treatment depends on the location of thrombi, patient symptoms, and urgency of the situation. Even after treatment, patients may have to remain on some type of anticoagulation until the cause of the thrombus has been identified and treated.
The prognosis for patients with mural thrombi is good but in the presence of emboli, the prognosis is guarded.
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