105 An intriguing case of pericardial effusion after acute coronary syndrome

Aims Left ventricular free wall rupture is one of the mechanical complications of myocardial infarction with an incidence of 2–4%. Sometimes the myocardial rupture hasn’t an immediate fatal evolution, nor is easy to be diagnosed because it is contained by the pericardium and thrombus formation, leading to pseudoaneurysm of the left ventricle. Pseudoaneurysms need a prompt surgical correction for their high risk of rupture both in the acute phase and later. Methods and results A 57 years old, smoker, woman with no previous cardiological history was admitted to our cardiological department for acute coronary syndrome with persistent ST segment elevation involving the postero-lateral wall (door to balloon time about 10 h, Killip class I and peak hs-TnI value was 27.67 ng/ml n.v. ˂0.02 ng/ml). The echocardiography showed mild left ventricular disfunction (LV EF 45%), postero lateral akinesia and moderate mitral regurgitation; ubiquitous pericardial effusion (1 cm) was present, particularly along the anterior left ventricular wall, with irregular echo-dense aspect. She underwent urgent coronarography that showed a critical stenosis of the distal third of the left circumflex and a thrombotic occlusion of the first marginal branch. The distal circumflex was treated with angioplasty and stent implantation but we couldn’t obtain the reperfusion of the marginal branch. Post procedural echocardiogram was unchanged and no free wall rupture was detected. 7 days after the admission, the patient showed persistent elevation of white blood count and CRP and developed fever, promptly empirically treated with a cephalosporin (blood cultures collected before were negative). After two new episode of fever with persisting biochemical flogistic parameters, a rheumatologic cause of the pericardial effusion was considered in the presence of positive antinuclear antibodies suggesting the diagnosis of Systemic Lupus Erythematosus. Steroidal therapy was prescribed which caused clinical improvement without complete resolution of the pericardial effusion. On day 20 of hospital stay a new echocardiographic evaluation showed a discontinuation of the postero lateral myocardial wall (Figure 1), about 1 cm in width, widely communicating with the left ventricular cavity and suggestive for a left postero-lateral ventricular pseudoaneurysm. The patient underwent surgical intervention and it was possible to expose a big clot occluding the pseudoaneurysmatic cavity communicating with the left ventricular chamber through an inlet about 1 cm in diameter, that was repaired with a bovine pericardial patch (Bard Sauvage technique). After surgery the patient was supported with an IABP and inotropes and was discharged to a rehabilitation structure on day 29 of hospital stay. Four months after the hospital discharge the patient died for a recently diagnosed pancreatic cancer. Conclusions Pseudoaneurisms are life-threatening complications of myocardial infarction that sometimes are hardly diagnosed. When correctly recognized surgical correction can lead to a good prognosis.

Left ventricular free wall rupture after myocardial infarction: a case report with rare live diagnostic record

Left ventricular free wall rupture is one of the most catastrophic and lethal mechanical complications associated with myocardial infarction. Its diagnosis in a patient still alive is rare, and its only therapeutic option is open surgical treatment. We report the case of an 82-year-old male patient who presented with an acute ST-segment elevation myocardial infarction, within more than 24 hours of onset, in which it was possible to record, in real time, the rupture of the left ventricular free wall by means of ventriculography.

Successful Low-Dose tPA for Mechanical Mitral Valve Thrombosis in a Patient with Postinfarction Contained Left Ventricular Free Wall Rupture

Prosthetic valve thrombosis is a potentially life-threatening complication diagnosed by a combination of clinical features and imaging modalities, but the optimal management in high bleeding risk patients remains controversial. Current treatment options for prosthetic valve thrombosis included surgery, thrombolytic therapy, and anticoagulation. We present a very unusual case of a patient with a recent ST-elevation myocardial infarction complicated by contained left ventricle free wall rupture and mechanical mitral valve thrombosis. Deemed a high surgical risk candidate, low-dose tissue plasminogen activator was used despite significant bleeding risk from contained left ventricle free wall rupture, which resulted in resolution of the thrombus. To the best of our knowledge, this is the first report of successful thrombolytic therapy for prosthetic mechanical mitral valve thrombosis in a patient with recent postmyocardial infarction contained left ventricular free wall rupture.

Neutrophil Counts Help Predict Free Wall Rupture Following St-elevation Myocardial Infarction

Purpose: Free wall rupture (FWR) is a lethal complication after acute myocardial infarction; however, the un-derlying mechanisms of FWR are unclear. This study analyzes the relationship between neutrophil counts and FWR following ST-elevation myocardial infarction (STEMI). Methods: The case group was STEMI patients with FWR and the control group was STEMI patients without FWR (case-control ratio was 1:4). The demographic data, clinical manifestation and laboratory test results were retrospectively collected and analyzed. Results: Of a total of 6,712 consecutive STEMI patients, 78 patients (1.2%) had FWR. Compared with STEMI patients, patients with FWR were older and more likely to be female with an anterior infarct. White blood cell (WBC) counts were significantly higher in the FWR group. Moreover, we found that the elevated neutrophil counts mainly accounted for the elevated WBC counts. There was also a correlation between the age and neu-trophil counts (P=0.0109); as patient age increased, neutrophil counts decreased (P=0.0387). We also found no correlation between neutrophil counts and the time between myocardial infarction attack and FWR; however, when dividing these patients into FWR ≤48 h after admission to hospital for STEMI and FWR >48 h, there was a significant difference in neutrophil counts (P=0.0196). Furthermore, the results of logistic regression analy-sis showed that increased neutrophil was an independent risk factor for FWR (odds ratio: 2.404, confidence interval: 1.055-5.477). Conclusion: Elevated neutrophil counts were found to be the main cause of differences in WBC counts be-tween FWR and STEMI. Elevated neutrophil was an independent risk factor for FWR. This study provided clues for further research and development of therapeutics for the prevention of FWR.