Thrombosis may occur in any cardiac chamber and evolve from acute masses formed primarily of fibrin, platelets, and entrapped blood to fibrotic, organized, masses. The majority of mural thrombi occur in association with underlying heart disease. Left atrial thrombi are frequently associated with mitral valvular disease, especially mitral stenosis,¹ and thrombi occur in either atrium in patients with atrial fibrillation and/or cardiac amyloidosis.² There is an increased risk for their development after cardiac surgery.³

Right atrial thrombi are frequently incidental findings at autopsy in patients with indwelling catheters or pacemakers and may occur in the setting of right heart failure, tricuspid regurgitation, or underlying coagulopathy. Rarely, they are the result of atrial infarctions, either isolated or with ventricular infarctions.⁴ When occurring without underlying heart disease, atrial thrombi may be misdiagnosed as myxomas.⁵

In the majority of patients with mural thrombus and no structural heart disease, a coagulation defect is either suspected or documented.

Complications of mural thrombi include embolization, either pulmonary or systemic. Left-sided thrombi may be a source of transient ischemic attacks or stroke.

Mural thrombi are occasionally removed surgically, if mistaken for a neoplastic process, or if there is no response to anticoagulation. In one surgical series of heart tumors, 13 of 84 resected tumors were thrombi that clinically mimicked neoplasms.⁶

Grossly, mural thrombi may be broad based and organized with little risk for embolization or polypoid and friable imparting higher risk for embolic phenomena. The former have been termed membranous thrombi and histologically are smooth muscle cell rich with variable proteoglycan matrix and fibroelastic tissue at the base. Polypoid thrombi are rich in fibrin and platelets, are more friable, and often superimposed on membranous type. The site of either type is usually within left atrial appendage, especially if there is atrial fibrillation⁷ (Fig. 179.1).

Histologic findings in atrial thrombi are variable (Figs. 179.2, 179.3, 179.4). They are composed of fibrin, platelets, and entrapped blood cells, especially near the surface. Ingrowth of endothelium may result in a hemangioma-like appearance. Organization, often occurring at the base, usually has a fibroblastic appearance, which, in concert with a myxoid matrix, may mimic a myxoma. Importantly, vasocentric rings, and Gamna-Gandy bodies are not typically seen in organizing thrombus. Layering of thrombus (lines of Zahn) may be seen in early thrombi without organization. In later stages, the surface is endothelialized.

Aggregates of entrapped leukocytes (including neutrophils) may be encountered and should not be necessarily interpreted as infection. Septic thrombi are generally diagnosed clinically and will histologically demonstrate microabscesses and bacterial organisms.⁸ The presence of leukocyte necrosis and debris often raises suspicion for underlying infection and helps to differentiate such from entrapped leukocytes in a noninfected thrombus.

Calcified amorphous tumor was initially described as pseudotumor, clinically mistaken for a neoplasm that occurred in adults in all four chambers.⁹ Patients are usually symptomatic adults and suffer cardiorespiratory complaints or complications of embolism, such as stroke or digital gangrene.¹⁰

Grossly, resected specimens are often fragmented (Fig. 179.5) and usually have areas of dense calcification. Histologically, they consist of paucicellular eosinophilic material, with areas of dense calcification and admixed chronic inflammation and hemosiderin (Fig. 179.6), often with surface fibrin. Surgery is generally curative.⁹

Calcified amorphous tumors are generally considered a form of degenerating calcified thrombi.⁶ They may be associated with chronic renal failure and antiphospholipid syndrome.¹⁰ Those adjacent to the mitral annulus may be extensions of mitral annular calcification.^11,12,13