Acute Severe Mitral Regurgitation Secondary to Ruptured Chordae Tendineae

Roberts., C William; Braunwald, Eugene; Morrow, Andrew G.

doi:10.1161/01.cir.33.1.58

Cited by 141 publications

(17 citation statements)

References 19 publications

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“…Thus, it is remarkable that the extreme severity of presentation related to the mechanical complication of MI does not affect long-term outcome of operative survivors who return to the expected outcome of patients with MI. This restoration of life expectancy by surgery is consistent with the limited extent of the infarcted area, 30,31 most often in the context of an inferior wall infarction causing PMR. 1,32 In addition, the frequently limited extent of obstructive CAD in patients suffering a PMR 2,31 observed in our study may contribute to restoration of life expectancy, particularly in patients who can be revascularized by simultaneous CABG.…”

Section: Long-term Outcomesupporting

confidence: 74%

Clinical Outcome After Surgical Correction of Mitral Regurgitation Due to Papillary Muscle Rupture

et al. 2008

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Background-Papillary muscle rupture (PMR) is an infrequent but catastrophic complication of acute myocardial infarction (MI). Although always considered, surgical treatment is often denied because of high operative mortality. Moreover, the effects of surgery for PMR on long-term outcome, particularly compared with expected outcome after MI, are undefined. Methods and Results-Fifty-four consecutive patients (age, 70Ϯ8 years; 74% male) underwent mitral surgery for post-MI PMR from January 1980 through December 2000. Severe presentation (cardiogenic shock, pulmonary edema, or cardiac arrest) was noted in 91% preoperatively. Performance of coronary artery bypass graft was associated with lower operative mortality (odds ratio, 0.18; 95% CI, 0.04 to 0.83; Pϭ0.011), whereas there was a trend for lower mortality after surgery after 1990 (odds ratio, 0.28; 95% CI, 0.06 to 1.3). Thus, operative mortality (overall, 18.5%) decreased from 67% up to 1990 without coronary artery bypass graft to 8.7% after 1990 with coronary artery bypass graft. Overall 5-year survival was 65Ϯ7%, and survival free of congestive heart failure was 52Ϯ7%. Five-year survival of 30-day operative survivors was 79Ϯ4%, identical (Pϭ0.24) to that of matched controls with MI (similar age, sex, ejection fraction, MI location, and MI year). Survival free of congestive heart failure was similar in PMR cases and MI controls (10-year survival, 28Ϯ8% versus 36Ϯ6%; Pϭ0.46). Conclusions-Surgery for post-MI PMR involves a notable operative mortality, but there are recent trends for lower operative risk, particularly with associated coronary artery bypass graft. Long term after surgery, outcome is restored to that of similar MI without PMR. These encouraging observations emphasize the importance of prompt diagnosis and aggressive therapeutic approach for patients incurring PMR after MI. (Circulation. 2008;118:1528-1534.)

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Section: Long-term Outcomesupporting

confidence: 74%

Clinical Outcome After Surgical Correction of Mitral Regurgitation Due to Papillary Muscle Rupture

et al. 2008

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“…The pathophysiology and clinical presentation in acute valve regurgitation is different from that of chronic regurgitation. In acute VHD, depending on the severity of the lesion and hemodynamic consequences, emergency surgery may be necessary [1,2,3,56,57]. …”

Section: Etiology Of Isolated Valve Diseasementioning

confidence: 99%

Etiology of Valvular Heart Disease in the 21st Century

Boudoulas

Borer²,

Boudoulas

2013

Cardiology

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“…2 Though the degree of hypertrophy was mild in the present study, a considerable thickening of the left atrial wall has been actually documented in autopsied patients who had had severe mitral regurgitation secondary to ruptured chordae tendineae. 40 In these cases, hypertrophy may well cause a decrease in compliance when hypertrophied myocardium is accompanied by an alteration in the material properties. The present model is not relevant to these pictures of clinical mitral regurgitation.…”

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confidence: 99%

Role of the left atrium in adaptation of the heart to chronic mitral regurgitation in conscious dogs.

Kihara

Sasayama

Miyazaki

et al. 1988

Circulation Research

112

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The manner in which the left atrium adapts to chronic mitral regurgitation and the role of the adapted left atrium as a modulator of excessive central blood volume were analyzed in seven conscious dogs, instrumented with high-fidelity pressure transducers and ultrasonic dimension gauges for measurement of left atrial and left ventricular pressure and cavity size. After obtaining data in a control situation, mitral regurgitation was produced by transventricular chordal sectioning. Heart rate was matched by right atrial pacing. In the "early" stage (7-14 days), left ventricular end-diastolic and mean left atrial pressures increased from 6 to 16 mm Hg and from 4 to 12 mm Hg, respectively. Both left ventricular end-diastolic segment length and left atrial diameter prior to atrial contraction increased by 7%. In the "late" stage (20-35 days), despite significant decreases in left ventricular filling pressure (11 mm Hg) and left atrial pressure (8 mm Hg), there was a continuous increase in left ventricular end-diastolic dimension (10%) and atrial end-diastolic diameter (10%). After the onset of mitral regurgitation, the left atrium performed greater work with a more enlarged cavity. Left atrial chamber stiffness was progressively decreased. These changes were associated with progressive increase in the left atrial diameter at zero stress, and there was a significant increase in the diameter of the left atrial myocyte. These results indicate that during chronic mitral regurgitation, the left atrium enlarges in size and mass, with a more potent booster action. The left atrial chamber becomes more compliant. Thus, the enlarged left atrium appears to exert an important compensatory mechanism in the case of T he left atrium, a muscular contractile chamber located in the inflow path to the left ventricle, functions both as a pump and as a reservoir for blood.1 During mitral regurgitation, the left ventricle decompresses into the left atrium as the mitral orifice, in parallel with the aortic valve, acts as a pressuredependent outlet for the ventricle. The physiological consequences to the left atrium are characterized by increases in left atrial size and pressure; however, the magnitude of these changes depends chiefly on the rapidity and severity with which the regurgitation develops. In animal experiments, we observed that the atrial diameter suddenly increased following the onset of acute mitral regurgitation. Hence, atrial shortening was initially augmented, in accord with the FrankStarling mechanism in atrial muscle. However, progressive increase in regurgitation was associated with further increases in atrial size but diminished atrial stroke; hence, the atrial chamber was rendered less compliant.2 These changes in left atrial compliance were postulated as follows: the atrium subjected to From the Third Division, Department of Internal Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan, and the Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan.Presented in pa...

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Acute Severe Mitral Regurgitation Secondary to Ruptured Chordae Tendineae

Cited by 141 publications

References 19 publications

Clinical Outcome After Surgical Correction of Mitral Regurgitation Due to Papillary Muscle Rupture

Clinical Outcome After Surgical Correction of Mitral Regurgitation Due to Papillary Muscle Rupture

Etiology of Valvular Heart Disease in the 21st Century

Role of the left atrium in adaptation of the heart to chronic mitral regurgitation in conscious dogs.

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