|Year : 2017 | Volume
| Issue : 1 | Page : 41-44
Ventricular septal rupture, right ventricular free wall rupture, hemopericardium, cardiac tamponade, cardiogenic shock, and death in a patient with acute ST elevation myocardial infarction during transthoracic echocardiography
Osama A El Kady1, Hisham Soliman Abbas1, Surrinder Kumar Bakshi2, Mohammed Kamal Mahrous3, Nasser Rashid Al Shukeili3, Wasim Rauf Kadri3
1 Department of Cardiology, Rustaq Hospital, Sultanate of Oman, Rustaq, Oman
2 Department of Medicine, Oman Medical College, Sultanate of Oman, Sohar, Oman
3 Department of Medicine, Rustaq Hospital, Sultanate of Oman, Rustaq, Oman
|Date of Web Publication||8-Mar-2017|
Dr. Surrinder Kumar Bakshi
Oman Medical College, Sohar
Source of Support: None, Conflict of Interest: None
The incidence of mechanical complications related to myocardial infarction has decreased due to various factors over the last few decades. Patients admitted for acute ST segment elevation myocardial infarction (STEMI) may respond well to thrombolytic therapy before being taken up for coronary angiography and percutaneous coronary intervention depending on the facilities available at the specific center. Unfortunately, some patients develop complications of myocardial infarction during hospital stay or postdischarge. We present a patient admitted with acute STEMI responding well to thrombolytic therapy. During transthoracic echocardiography of the patient in Intensive Care Unit, the patient developed ventricular septal rupture, right ventricular free wall rupture, hemopericardium, cardiac tamponade, and cardiogenic shock and expired.
Keywords: Cardiac tamponade, hemopericardium, ST elevation myocardial infarction, ventricular free wall rupture, ventricular septal defect, ventricular septal rupture, transthoracic echocardiography
|How to cite this article:|
El Kady OA, Abbas HS, Bakshi SK, Mahrous MK, Al Shukeili NR, Kadri WR. Ventricular septal rupture, right ventricular free wall rupture, hemopericardium, cardiac tamponade, cardiogenic shock, and death in a patient with acute ST elevation myocardial infarction during transthoracic echocardiography. Heart India 2017;5:41-4
|How to cite this URL:|
El Kady OA, Abbas HS, Bakshi SK, Mahrous MK, Al Shukeili NR, Kadri WR. Ventricular septal rupture, right ventricular free wall rupture, hemopericardium, cardiac tamponade, cardiogenic shock, and death in a patient with acute ST elevation myocardial infarction during transthoracic echocardiography. Heart India [serial online] 2017 [cited 2019 Mar 24];5:41-4. Available from: http://www.heartindia.net/text.asp?2017/5/1/41/201738
| Introduction|| |
Coronary heart disease is the leading cause of death worldwide. It is on the rise and has become a true pandemic that respects no borders. Severe ventricular dysfunction or one of the other mechanical complications of acute myocardial infarction (AMI) causes most of the deaths following AMI. Complications of AMI include ischemic, mechanical, arrhythmic, left ventricular mural thrombus, and inflammatory sequelae. In addition to these broad categories, right ventricular (RV) infarction and cardiogenic shock are other common complications of AMI. The incidence of mechanical complications to myocardial infarction has decreased over the last decades, and prompt revascularization certainly plays a major role in this change. However, the mortality rate still remains high despite developments in medical and surgical sciences. A patient admitted to Intensive Care Unit with anterior myocardial infarction and managed with thrombolytic therapy developed ventricular septal rupture (VSR), RV free wall rupture (VFWR), hemopericardium, cardiac tamponade, cardiogenic shock, and cardiac arrest during transthoracic echocardiography (TTE) and expired.
| Case Report|| |
A 59-year-old man with diabetes was admitted with retrosternal chest pain radiating to left arm. The duration of pain was about 9 h and associated with vomiting and sweating. There was no history of shortness of breath, dizziness, or syncope. On admission, his general condition was fair with no pallor, no jaundice, and no cyanosis. He was maintained on 98% oxygen saturation at room air with facial mask. His body temperature was 36.2°C. Pulse was 96 bpm, regular, and good volume and blood pressure was 160/100 mmHg. Jugular venous pressure (JVP) was not raised. No lower limb edema was present. Respiratory and abdominal examinations were unremarkable. Cardiovascular system examination revealed pansystolic murmur at the left sternal edge (Grade IV/VI). S3 was absent, but S4 was heard. There was no pericardial rub. His laboratory investigations showed hemoglobin 162 g/L, white blood cell count 19.3 × 109/L, capillary blood glucose 163 mg/dL, and troponin T 1304 pg/mL. The renal, liver, electrolyte, and coagulation profiles were normal. Electrocardiogram showed ST segment elevation in V1-5, with T-wave inversion I, aVL, and q wave in V2-5.
The patient was thrombolysed with reteplase and was also given statins, aspirin, clopidogrel, angiotensin-converting enzyme inhibitors, and insulin as per sliding scale.
The patient underwent TTE (ECHO) which showed borderline dilated left ventricle with ejection fraction 40%. Apico-septal, apical, and apico-lateral wall thinning with aneurysmal dilatation was also seen. There was an apical ventricular septal defect (VSD) about 7 mm with left-to-right shunt [Figure 1]. No mitral regurgitation or tricuspid regurgitation was seen. Normal aortic and pulmonary valve flow was noted. Left atrial, right atrial, and RV diameters were normal. Suddenly, the left ventricle became smaller in size. Apical VFWR was also seen [Figure 2] and [Video 1],[Video 2],[Video 3],[Video 4]. Apical VFWR with rapidly accumulating pericardial effusion (cardiac tamponade), systolic RA collapse, and diastolic RV collapse was noticed [Figure 3],[Figure 4],[Figure 5] and [Video 5],[Video 6],[Video 7]. The patient became breathless with cardiogenic shock and could not be reviewed.
|Figure 1: Apical ventricular septal rupture (ventricular septal defect) with left-to-right shunt (color jet)|
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|Figure 2: Apical ventricular septal rupture (ventricular septal defect) and apical ventricular free wall rupture (color jet)|
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|Figure 3: Apical ventricular free wall rupture with right atrial and right ventricular collapse|
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|Figure 4: Apical ventricular free wall rupture with massive pericardial effusion and systolic right atrial collapse|
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|Figure 5: Ventricular free wall rupture with massive pericardial effusion (cardiac tamponade), right ventricular collapse, and right atrial collapse|
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| Discussion|| |
VFWR is a serious complication of anterior myocardial infarction. Acute VFWR is defined as an abrupt transmural rupture of the infarcted area, causing hemopericardium and death within 30 min. Subacute VFWR is defined as a gradual or incomplete rupture of the infarcted area with slow or recurrent bleeding into the pericardial sac, causing progressive or recurrent cardiac tamponade. VSR is diagnosed on the basis of abnormal shunting through the interventricular septum on color Doppler echocardiography or a significant increase in oxygen saturation in the right ventricle.
The VFWR is reported in 4% of all myocardial infarction and 12%–21% of anterior myocardial infarction patients. Within a period of 1st week of AMI, the ventricular free wall may rupture and present with profound cardiogenic shock and cardiac tamponade. Plasmin, which is activated by thrombolytic agents, can break down collagen and this may cause wall rupture.,, Well-known risk factors for free wall rupture include old age, female sex, hypertensive patients, and a first lateral or anterior wall AMI. Some authors have reported about a predilection to first myocardial infarction and even single-vessel disease due to a lack of collateral vessels.
The common indicators of impending rupture are loss of consciousness, bradycardia, cyanosis, and hypotension due to entry of blood into the pericardial cavity. Such patients may also complain of chest pain which is usually resistant even to opiates and may be associated with muffled heart sounds, pulsus paradoxus, raised JVP, hypotension, cardiac tamponade, shock, or asystole., Many patients with free wall rupture die suddenly, often even without a diagnosis. Abreu Filho et al. observed 98 (77.2%) patients in these conditions, of which only 5 (5.1%) underwent surgery with one (20%) survived. Free wall rupture after AMI is approximately 10 times less frequent than septum rupture and papillary muscle rupture. Left ventricular rupture is 8 times more common than RV rupture.
VSR with RV free wall dissection is an extremely rare complication, with 100% mortality without urgent surgical treatment. The main cases of RV rupture are myocardial infarction, accidental, therapeutic, mechanical trauma, myocarditis, mediastinitis, surgical complications, and other pathologies.
The incidence of cardiac rupture has decreased from 3.3% to 2.8% to 1.7% (corresponding year periods 1977–1989, 1990–2000, 2001–2011), with the use of reperfusion therapy. The mortality rate of cardiac rupture has also decreased from 90% to 56% to 50% during the above corresponding periods due to an increase in the rate of emergent surgery. The surgical approach for management is the only salvaging procedure in such cases provided the facilities are available.
| Conclusion|| |
VSR with RV free wall dissection is a rare complication of AMI with 100% mortality without urgent surgical treatment. The purpose of presentation of this case report is the presence of events noticed during echocardiography, for example, VSD, RV wall rupture, hemopericardium, cardiac tamponade, and cardiogenic shock. In our patient, progression of coronary artery disease with pressure overload on the right heart did not allow the right ventricle to reshape into aneurysm, but unfortunately caused rupture of the RV wall and associated features leading to instantaneous death. The recognition of the complications at an early stage, management of such patients, and transfer to cardiovascular surgery for urgent intervention may save such patients.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]