An interpretation of the incidence of mural thrombi in the left auricle and appendage with particular reference to mitral commissurotomy

Wallach, John R.; Lukash, Leslie; Angrist, Alfred

doi:10.1016/0002-8703(53)90185-9

Cited by 56 publications

(5 citation statements)

References 6 publications

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“…The proportion of thrombi located in the LAC was 56% (95% CI 53% to 60%; table 1) , 22% (95% CI 19% to 25%; table 2) and 11% (95% CI 6% to 15%; table 3) in the valvular, mixed and non-valvular AF cohorts, respectively 9 10 13–44. These data are further evaluated as shown in the Forest plot (figure 2), which presents the point estimate of thrombus location outside the LAA in all the studies.…”

Section: Resultsmentioning

confidence: 99%

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Importance of the underlying substrate in determining thrombus location in atrial fibrillation: implications for left atrial appendage closure

Mahajan

Brooks

Sullivan

et al. 2012

Heart

113

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The location of atrial thrombus in patients with AF is dependent on the underlying substrate. In valvular AF, more than half the thrombi are located in the left atrial cavity. In the non-valvular AF group, a smaller proportion of thrombi were located outside the appendage. However, in certain subgroups (ie. non anti-coagulated, left ventricular dysfunction or prior stroke) the chances of left atrial cavity thrombus are higher.

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Section: Resultsmentioning

confidence: 99%

“…Two additional references were included from reference list screening. Both these references had the selected keywords within them 9 10. Studies that were follow-ups of other included studies or a sub-study of the same cohort were also excluded.…”

Section: Methodsmentioning

confidence: 99%

Importance of the underlying substrate in determining thrombus location in atrial fibrillation: implications for left atrial appendage closure

Mahajan

Brooks

Sullivan

et al. 2012

Heart

113

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“…Previous reports [9, [14][15][16][17] have shown that dilated LAA and poor LAA contractile function are associated with a higher inci dence of LAA thrombus formation. Our re port was the first study to demonstrate that, both in sinus rhythm and atrial fibrillation, LAA function in patients with rheumatic mi tral valve disease was poorer than that in patients without rheumatic heart disease.…”

Section: Laa Function In Rheumatic Mitral Valve Diseasementioning

confidence: 99%

Left Atrial Appendage Function Determined by Transesophageal Echocardiography in Patients with Rheumatic Mitral Valve Disease

Hwang

Lin

et al. 1994

Cardiology

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Left atrial thrombi have been considered to be the major source of systemic arterial embolization in patients with rheumatic mitral valve disease. Almost half of the left atrial thrombi are found in the left atrial appendage (LAA). To investigate LAA size and LAA contractile function in patients with rheumatic mitral valve disease, transesophageal echocardiographic and Doppler studies were performed in 61 patients. Among them, 46 patients were in atrial fibrillation (group 1), while the other 15 were in sinus rhythm (group 2). Thirty-six patients with nonrheumatic atrial fibrillation were chosen as control to group 1. Another 22 patients with various cardiovascular diseases and sinus rhythm served as control to group 2. When compared to the patients with nonrheumatic atrial fibrillation (control group), group 1 patients tended to have a larger LAA maximal area (9.7 ± 5.2 vs. 5.9 ± 2.8 cm²; p < 0.001). LAA ejection fraction and LAA peak emptying velocity were also lower. A significantly higher incidence of LAA spontaneous echo contrast (SEC) and thrombus formation was also found in these patients. Group 2 patients were also found to have a larger LAA maximal area when compared to the control group (8.8 ± 3.7 vs. 5.2 ± 3.0 cm²; p < 0.001). LAA ejection fraction and LAA peak emptying velocity were lower in this group, too. A higher incidence of LAA SEC formation was found in these patients with rheumatic mitral valve disease (4/15 vs. 0/22; p = 0.021). There was no significant difference, however, in LAA thrombus formation between group 2 and its control group (1/15 vs. 1/22; p = NS). Thus, patients with rheumatic mitral valve disease tend to have larger LAA size and poorer LAA contractile function. These promote the formation of LAA SEC and thrombus, especially when the patients have atrial fibrillation. Whether the poor LAA function predisposes these patients to future systemic arterial embolization still needs further investigation.

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“…The vast literature on systemic embolism in rheumatic heart disease was largely compiled before the introduction of surgery in the treatment of mitral valve disease. Some of the recent papers, such as those of Jordan, Scheifley, and Edwards (1951), and of Wallach, Lukash, and Angrist (1953), were based on necropsy findings and must have included a number of cases which would have been too advanced or too complicated for surgery. The incidence of embolism and auricular thrombosis may well be different in the fatal and in the operable cases.…”

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confidence: 99%

Systemic Embolism and Left Auricular Thrombosis in Relation to Mitral Valvotomy

Belcher¹,

Somerville²

1955

BMJ

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An interpretation of the incidence of mural thrombi in the left auricle and appendage with particular reference to mitral commissurotomy

Cited by 56 publications

References 6 publications

Importance of the underlying substrate in determining thrombus location in atrial fibrillation: implications for left atrial appendage closure

Importance of the underlying substrate in determining thrombus location in atrial fibrillation: implications for left atrial appendage closure

Left Atrial Appendage Function Determined by Transesophageal Echocardiography in Patients with Rheumatic Mitral Valve Disease

Systemic Embolism and Left Auricular Thrombosis in Relation to Mitral Valvotomy

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