Etiology and differential diagnosis of acute mitral regurgitation

Sanders, Charles A.; Armstrong, Paul W.; Willerson, James T.; Dinsmore, Robert E.

doi:10.1016/0033-0620(71)90051-x

Cited by 46 publications

(10 citation statements)

References 100 publications

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“…Unlike some authors (Orlando et al, 1964;Robinson et al, 1965;Morrow et al, 1968;Heikkila, 1971;Sanders et al, 1971), but in agreement with Heikkila (1967), we did not find a higher incidence of mitral regurgitation in patients with posteroinferior myocardial infarction than in those with anterior infarction. This distribution corresponded well with the frequency of valvar regurgitation in various patterns of coronary arterial disease.…”

Section: Discussionsupporting

confidence: 90%

“…This may also hold for the varying character, intensity, and localisation of the systolic murmur. In common with other authors Phillips et al, 1963), we have found that the 'diamond shaped' or ejection type murmur, as well as panor late systolic murmurs, occurred with mitral regurgitation, but no type of murmur correlated with the grade of reflux on angiography (Heikkila, 1967(Heikkila, , 1971Shelburne et al, 1968;Sanders et al, 1971;Shelburne and Gorlin, 1972), nor did the intensity and character of the systolic murmur strictly correspond with any particular mechanism of valvar regurgitation (De Busk and Harrison, 1969;Heikkila, 1971). 'Silent' mitral regurgitation (Aravanis, 1965;Forrester et al, 1971) has been reported, and 15 of our 39 patients with angiographically demonstrable mitral regurgitation had no murmur.…”

Section: Discussionsupporting

confidence: 87%

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Mitral regurgitation in coronary heart disease.

Gahl¹,

Sutton²,

Pearson³

et al. 1977

Heart

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Mitral regurgitation is a relatively common finding in coronary heart disease. In this series of 127 patients, selected with a view to coronary or left ventricular surgery on the basis of severity of symptoms, the incidence was 39 (31%). Mitral regurgitation is significantly more common in patients with a history or electrocardiographic evidence ofprevious myocardial infarction. Clinically it may present as a pan-or late systolic or even a mid-systolic, ejection type murmur at the apex or at the left sternal edge; but in 39 per cent of the patients with angiographic mitral regurgitation no murmur was present. Angiographically important mitral regurgitation (grades 2-4/4) was usually associated with a systolic murmur; this finding was independent of ejection fractions. Left ventricular enlargement clinically or radiographically is likely to accompany mitral regurgitation but left atrial enlargement (electrocardiographically or on chest x-ray) is a more reliable pointer to mitral regurgitation and pulmonary venous hypertension is even more strongly suggestive of its presence. The electrocardiographic signs of papillary muscle infarction were rare in this series (15%) and were not related to angiographic mitral regurgitation. There was no difference in the incidence of mitral regurgitation in association with anterior or inferior myocardial infarction or in distribution of coronary artery disease. There is, however, a higher incidence of mitral regurgitation in more severe coronary arterial disease (P<005).The incidence of mitral regurgitation is significantly higher with reduction in left ventricular ejection fraction (P< 0001), with rise in the left ventricular end-diastolic pressure (P<0'02), and with abnormalcontraction patterns, but the severity of mitral regurgitation is not significantly related to these findings.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 87%

Mitral regurgitation in coronary heart disease.

Gahl¹,

Sutton²,

Pearson³

et al. 1977

Heart

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“…Involvement of the posterior papillary muscle usually results from occlusion of a branch of a dominant right coronary system (Heikkila, 1967). The anterior papillary muscle is less frequently affected (Craddock and Mahe, 1953;Sanders et al, 1957;Sanders, Armstrong, Willerson, and Dinsmore, 1971). Reported cases of papillary muscle rupture complicating myocardial infarction have been reviewed (Davison, 1948;Craddock and Mahe, 1953;Sanders et al, 1957).…”

Section: Discussionmentioning

confidence: 99%

“…Unless further myocardial infarction occurs, and apart from the subsequent development of left atrial or ventricular strain, electrocardiography was not reported to show specific changes (Breneman and Drake, 1962;Phillips, De Pasquale, and Burch, 1963). Chest films might reveal pulmonary vascular congestion with a near normal left atrial size and normal cardiothoracic ratio (DeBusk et al, 1970;Sanders et al, 1971).…”

Section: Discussionmentioning

confidence: 99%

Papillary muscle rupture following myocardial infarction: Successful treatment by resection of akinetic left ventricular area, mitral valve replacement, and aorta to coronary artery bypass graft

Mary¹,

Pakrashi²,

Ionescu³

1973

Thorax

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A patient is reported in whom rupture of the posterior papillary muscle of the left ventricle occurred following myocardial infarction. The intractable pulmonary oedema that followed responded to the combined surgical approach of mitral valve replacement, resection of the akinetic area of the left ventricular wall, and saphenous vein aortocoronary bypass. This combination of surgical procedures has not been reported to date, and was considered to have preserved adequate left ventricular performance.

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“…Hemodynamic (and thus, radiographic) sequelae of ischemic mitral regurgitation depends upon the degree of severity and the rapidity of onset. Acute severe mitral regurgitation is most commonly caused by rupture of the chordae tendineae (usually involving the posterior mitral leaflet) resulting in a flail mitral leaflet as a spontaneous event in patients with no apparent heart disease [9,10,11].…”

Section: Left Ventricular Ischemiamentioning

confidence: 99%

Imaging of ischemic heart disease

et al. 2002

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Despite advances in the understanding and treatment of ischemic cardiomyopathy, characterized by extensive coronary artery disease and left ventricular (LV) dysfunction, the prognosis remains poor with only a 50-60% 5-year survival rate. The composition of atherosclerotic lesions is currently regarded as being more important than the degree of stenosis in determining acute events. If imaging techniques could distinguish vulnerable from stable plaques, then high-risk patient subgroups could be identified. Another important concept is that LV dysfunction may be the result of either scarring due to necrosis or to the presence of myocardial hibernation, in which there is sufficient blood flow to sustain viable myocytes, but insufficient to maintain systolic contraction. This concept of myocardial viability is critical for making optimal clinical management decisions. This review describes how noninvasive imaging methods can be used to distinguish regions of irreversibly injured myocardium from viable but hibernating segments. Technical advances in CT and MR have made imaging of the beating heart possible. Considerable clinical progress has already been made and further cardiac applications are expected. Radiologists therefore have new opportunities for involvement in cardiac imaging but must recognize the political implications as well as the diagnostic potential of these modalities not only for the heart, but also for the whole vascular system. This review focuses on imaging myocardial injury. It compares state-of-the-art CT and MR with more established yet contemporary echocardiography and nuclear scintigraphy.

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Etiology and differential diagnosis of acute mitral regurgitation

Cited by 46 publications

References 100 publications

Mitral regurgitation in coronary heart disease.

Mitral regurgitation in coronary heart disease.

Papillary muscle rupture following myocardial infarction: Successful treatment by resection of akinetic left ventricular area, mitral valve replacement, and aorta to coronary artery bypass graft

Imaging of ischemic heart disease

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