Authors

• Dora Fabijanović — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0003-2633-3439
• Vlatka Rešković Lukšić — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-4721-3236
• Željko Baričević — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-5420-2324
• Hrvoje Jurin — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-2599-553X
• Maja Čikeš — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-4772-5549
• Boško Skorić — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0001-5979-2346
• Ivan Burcar — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia
• Sandra Večerić — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-8070-1012
• Jadranka Šeparović Hanževački — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-3437-6407
• Davor Miličić — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0001-9101-1570

Keywords

acute myocardial infarction, pulmonary edema, papillary muscle rupture, diabetic ketoacidosis

DOI

Full Text

**Introduction**: In the first few days following acute myocardial infarction mechanical complications such as septal defects, papillary muscle rupture or dysfunction, cardiac free wall rupture or ventricular aneurysms may occur. Incidence of these complications is rather low yet they are all life-threatening and need prompt detection and management. (1, 2) **Case report**: A 64-year-old healthy female was admitted due to acute posterolateral myocardial infarction. During the initial examination, the patient was hemodynamically stable, presenting with a holosystolic murmur heard best at the apex. Initial work up demonstrated newly discovered diabetes with high blood glucose levels (29 mmol/L). Urgent coronary angiography was performed revealing proximal left circumflex artery occlusion and drug eluting stent was put in place at the site. Following the intervention the patient became progressively dyspneic with signs of pulmonary edema, arterial hypotension and sinus tachycardia. Bedside transthoracic echocardiography was performed and despite the poor echo window significant mitral regurgitation (MR) with hyperdynamic left ventricular contraction and left ventricular ejection fraction of 60% was verified. Due to the extremely high values of blood glucose with elements of diabetic ketoacidosis, continuous perfusion of rapid-acting insulin was initiated. Careful titration of intravenous diuretics and nitrates gradually stabilized the hemodynamic status. Although diabetic ketoacidosis is described as a potential cause of noncardiac pulmonary edema, after stabilization was achieved, transesophageal echocardiography was performed. The study showed rupture of the anterolateral papillary muscle resulting in acute, massive and highly eccentric MR due to posterior leaflet "flail" (**Figures 1****,****2** and **3**). Patient underwent urgent mitral mechanical valve replacement surgery and was discharged from the hospital after a total of 14 days. Figure 1. Multiplane transesophageal echocardiogram showing massive, highly eccentric anterior mitral regurgitation jet. Figure 2. 3D transesophageal echocardiogram. Arrows showing flail posterior leaflet in the left atrium and ruptured papillary muscle head in the left ventricle. Figure 3. 2D transesophageal echocardiogram showing flail posterior mitral leaflet, wide mitral valve non-coaptation zone and floating ruptured head of the anterolateral papillary muscle in the left ventricle. **Conclusion**: Differential diagnosis of pulmonary edema during the early postinfarction period is extensive and demanding, particularly in patients with comorbidities that can mask the clinical picture. Although mechanical complications are rare, it is necessary to identify and treat them early on, which is possible only with continuous monitoring and constant search for the causes of new onset hemodynamic instability.

Literature

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2. Hochman JS, Buller CE, Sleeper LA, Boland J, Dzavik V, Sanborn TA, et al. Cardiogenic shock complicating acute myocardial infarction--etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol. 2000;36(3) Suppl A:1063–70. https://doi.org/10.1016/S0735-1097(00)00879-2