Long-term survival after mitral valve surgery for post-myocardial infarction papillary muscle rupture

Bouma, Wobbe; Hamer, Inez J. Wijdh-den; Koene, Bart M.; Kuijpers, Michiel; Erasmus, Michiel E.; Jainandunsing, Jayant S.; Horst, Iwan C. C. van der; Gorman, Joseph H.; Gorman, Robert C.; Mariani, Massimo A.

doi:10.1186/s13019-015-0213-1

Cited by 35 publications

(38 citation statements)

References 25 publications

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“…These findings are supported by the fact that preservation of the sub-valvular apparatus and papillary muscle continuity contributes to the improvement of the prognosis in patients with ischemic mitral regurgitation [19]. Consequently, LGE-MRI could be a suitable approach for identifying patients at risk for the development of ischemic mitral valve regurgitation, based on the extent of PM involvement [11].…”

Section: Discussionmentioning

confidence: 82%

“…Due to the vascular anatomy of the PM, the anterior PM is much less frequently affected [11,27]. The posterior PM was also more frequently affected, with nine patients compared to four with anterior PM involvement.…”

Section: Discussionmentioning

confidence: 99%

“…In comparison to intraoperative findings, the extent of PM damage is frequently underestimated by echocardiography [11]. Thus, patients with ischemic mitral regurgitation may benefit from magnetic resonance imaging (MRI) prior to mitral valve repair or replacement as it provides reliable information on left ventricular function, myocardial viability and PM morphology [8, 12 -14].…”

Section: Introductionmentioning

confidence: 99%

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Impact of Papillary Muscle Infarction on Ischemic Mitral Regurgitation Assessed by Magnetic Resonance Imaging

Bretschneider

Heinrich

Seeger

et al. 2017

Fortschr Röntgenstr

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This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited.the development of mitral regurgitation in patients with chronic myocardial infarction (MI). The aim of the present study was to assess the correlation of PM infarction depicted by MRI with mitral regurgitation and left ventricular function.Methods and Materials 48 patients with chronic MI and recent MRI and echocardiography were retrospectively included. The location and extent of MI depicted by MRI were correlated with left ventricular function assessed by MRI and mitral regurgitation assessed by echocardiography. The presence, location and extent of PM infarction depicted by late gadolinium enhancement (LGE-) MRI were correlated with functional parameters and compared with patients with chronic MI but no PM involvement.Results PM infarction was found in 11 of 48 patients (23 %) using LGE-MRI. 8/11 patients (73 %) with PM infarction and 22/37 patients (59 %) without PM involvement in MI had ischemic mitral regurgitation. There was no significant difference between location, extent of MI and presence of mitral regurgitation between patients with and without PM involvement in myocardial infarction. In 4/4 patients with complete and in 4/7 patients with partial PM infarction, mitral regurgitation was present. The normalized mean left ventricular enddiastolic volume was increased in patients with ischemic mitral regurgitation. ConclusionThe presence of PM infarction does not correlate with ischemic mitral regurgitation. In patients with complete PM infarction and consequent discontinuity of viable tissue in the PM-chorda-mitral valve complex, the probability of developing ischemic mitral regurgitation seems to be increased. However, the severity of mitral regurgitation is not increased compared to patients with partial or no PM infarction.

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Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Impact of Papillary Muscle Infarction on Ischemic Mitral Regurgitation Assessed by Magnetic Resonance Imaging

Bretschneider

Heinrich

Seeger

et al. 2017

Fortschr Röntgenstr

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“…[4][5][6] In the vast majority (90%), rupture involves the posteromedial papillary muscle, presumably a consequence of its single source blood supply from either the RCA or LCX coronary artery. 7 In contrast, the anterolateral papillary muscle has a dual source blood supply emanating from both the LAD and LCX coronary arteries, thus providing protection from ischemic rupture.…”

Section: N Discussionmentioning

confidence: 99%

Solving a Hemodynamic Enigma

Sharkey¹,

Burke²,

Samara³

et al. 2017

Journal of the Minneapolis Heart Institute Foundation

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This case illustrates the successful implementation of advanced circulatory support in a critically ill patient with acute ST-segment elevation myocardial infarction. The hemodynamic recordings demonstrate the effects of mechanical cardiopulmonary resuscitation, venoarterial extracorporeal membrane oxygenation, and acute severe mitral regurgitation. KEY WORDScardiogenic shock, ST-segment elevation myocardial infarction, ruptured papillary muscle, extracorporeal membrane oxygenation n CASE PRESENTATION A 53-year-old female presented to the emergency department with acute chest pain. The patient experienced the sudden onset of central chest pain radiating into the back with diaphoresis and dyspnea while at work. She called 911 and was transported by emergency medical services to the emergency department. Intermittent chest pain had been present for 2 weeks with sudden worsening on the day of admission. Risk factor profile included 1-pack/day cigarette smoking for 37 years, hypertension, and untreated hyperlipidemia (low-density lipoprotein: 192 mg/dL). Family history was negative for premature coronary events. Past medical history was notable for hypothyroidism and asymptomatic prolonged QT interval. The patient was not receiving antiplatelet agents.Emergency Department Course 9:23 AM. Initial evaluation revealed a diaphoretic acutely ill female with the following vitals: blood pressure, 63/28 mm Hg; heart rate, 86 beats/min; respiratory rate, 14/min; oxygen saturation, 96%; weight, 179 lbs. Figure 1) demonstrated lateral ST-segment elevation. The patient deteriorated rapidly with occurrence of clinical cardiogenic shock and pulseless electrical activity. 9:43 AM. An electrocardiogram (ECG;9:59 AM. The patient was intubated and cardiopulmonary resuscitation (CPR) was initiated with an automatic chest compression system. Epinephrine, dopamine, heparin, aspirin, and ticagrelor were administered. A bedside ultrasound was technically difficult and reported as unremarkable. The initial troponin I was 11.69 ng/mL (99th percentile, 0.033 ng/mL).10:13 AM. The level 1 ST-elevation myocardial infarction (STEMI) system 1,2 was activated and the patient was transported emergently to the cardiac catheterization laboratory.10:25-10:44 AM. Upon arrival in the catheterization laboratory, the patient was intubated and placed on an automatic chest compression system at 100 compressions/min, right femoral artery and vein sheaths were inserted. Initial blood pressure was 85/35 mm Hg, heart rate was 39 beats/min (Figure 2a). Epinephrine, norepinephrine, dopamine, sodium bicarbonate, and heparin were administered.10:44-10:55 AM. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) was initiated via the left femoral vein and right femoral artery. Circulation

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“…PMR is most common with an inferior myocardial infarction, and the posteromedial papillary muscle is most often involved (6 to 12 times more frequently than anterolateral papillary muscle); that's because of its single blood supply through the posterior descending coronary artery (anterolateral papillary has a dual blood supply, instead, from the left anterior descending and left circumflex arteries) [36,37,39].…”

Section: Papillary Muscle Rupturementioning

confidence: 99%