We report a case of successful survival from ventricular free wall rupture without surgery, which was not overt rupture but micro-rupture. The patient was diagnosed with acute myocardial infarction (AMI) and underwent primary percutaneous coronary intervention (PCI). Myocardial blood leakage could be detected on transthoracic echocardiography with intravenous infusion of contrast dye 3 days after PCI. This examination revealed that there was not overt perforation but diffuse fissure. Because of his critical condition, he was treated conservatively without surgery. Nevertheless, he survived eventually.
Ventricular free wall rupture is a disastrous complication of acute myocardial infarction (AMI). Rupture of ventricular free wall occurs in 0.8 percent to 6.2 percent of AMI patients and is a major cause of in-hospital death for ST segment elevation myocardial infarction (STEMI) [
A 65-year-old male patient visited the emergency department due to chest pain of abrupt onset. He was a current smoker. The initial ECG showed an inferior wall ST elevation and initial cardiac enzyme levels were within normal limits. However, 5 hours after arrival, CK level was 42 IU/L and Troponin-I was positive. Therefore, he underwent emergent coronary angiography. During the procedure, heart rate decreased to 48 beats per minute on the ECG, which made us implant a temporary pacemaker. Coronary angiography showed total thrombotic occlusion of the proximal right coronary artery (RCA) (
Cypher stent was implanted successfully. Although final angiography showed trapped thrombi in the stent, antegrade flow grade was TIMI 3 (
Early in the next morning, shock with decreased urine output was developed. Despite the support of inotropics, he remained in shock state. Transthoracic echocardiographic examination demonstrated cardiac tamponade without definite myocardial rupture (
Two days after PCC, cardiac arrest was developed after an abrupt decrease in blood pressure. Cardiopulmonary resuscitation (CPR) was performed immediately. At the same time, the drainage amount of PCC increased abruptly. Echocardiography showed redevelopment of pericardial effusion and severely depressed RV systolic function. However, once again, we failed to detect any myocardial rupture site. Instead, we observed abnormal movement of the RV free wall. It seemed that there was asynchronous movement between mid ventricular level and apical level of myocardium. Even with agitated saline test, no blood leakage around this point was observed on two-dimensional echocardiography. Finally, we injected radiocontrast (Iodixanol, Visipaque®) via an antecubital vein and found diffuse leakage of contrast through the RV free wall (
Ventricular free wall rupture after acute myocardial infarction is a catastrophic condition. The free wall rupture usually leads to hemopericardium, cardiac tamponade
and death. Patients’ survival depends on the early detection, hemodynamic stabilization and especially prompt surgical intervention.
In the case of our patient, there was a shock from cardiac tamponade on the next morning after PCI. However, on two-dimensional echocardiography, we could not find any demonstrable rupture site or color jet flow. We thought that free wall rupture, pacemaker tip injury, post infarction pericarditis and arterial perforation might be potential cause of pericardial effusion. First, the possibility of free wall rupture was not high, because there was no evidence for communication between the ventricle and pericardial space on echocardiographic examination. Second, although the pacemaker lead tip moved slightly in concordance with heart beat during PCI, we were convinced it was minimal and not traumatic. Third, post infarction pericarditis was not well consistent with his fulminant course. Fourth, on index PCI procedure and relook coronary angiography, no arterial perforation was detected. Hence, we could not elucidate definite cause of pericardial effusion at that time.
Ventricular free wall rupture could be diagnosed by pericardiocentesis, echocardiography, or cardiac catheterization, depending on the situation [
In our case, routine echocardiographic examination did not show overt perforation of ventricular free wall rupture. However, contrast echocardiography demonstrated sequential opacification of right ventricle and pericardial space. Therefore, it would be reasonable to assume that there was not overt perforation but diffuse fissure or micro-ruptures in myocardium, through which blood could leak and ooze. IV abciximab infusion might interfere with the healing process of diffuse myocardial fissure. However, 2 days after discontinuation of IV abxicimab, we were faced up with abrupt increase of pericardial effusion.
There are two types of contrast agents for echocardiography [
Both left and right ventricular free wall rupture occur with similar presentation and pathophysiology. Therefore, the treatment could be discussed together [
In the case of our patients, surgery was not undertaken in agreement with the surgical team. The calculated logistic Euroscore was more than 70 percent, which suggested extremely high risk surgery [
In conclusion, it is significant to note 3 points: 1) Myocardial blood leakage through diffuse fissure, or micro-rupture, could occur on the early stage of AMI. 2) Myocardial blood leakage through right ventricular free wall could be detected on transthoracic echocardiogramphy using intravenous infusion of contrast dye. 3) If there is no overt perforation, and micro-rupture is suspected, intensive supportive care could be the better alternative to surgical approach.