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Ruptured Left Ventricular Pseudoaneurysm: A Complication of Power Injector Assisted Ventricular Angiography


1 Department of Cardiology, Saint Michael’s Medical Center, New York Medical College, New York, United States
*Corresponding author: Amer Hawatmeh, Department of Cardiology, Saint Michael’s Medical Center, New York Medical College, 111 Central Avenue, Newark, New Jersey 07102, United States. Tel: +1-9738775000, Fax: +1-9738775124, E-mail: amer_hawatmeh@hotmail.com.
Research in Cardiovascular Medicine. 6(1): e34511 , DOI: 10.5812/cardiovascmed.34511
Article Type: Case Report; Received: Nov 9, 2015; Accepted: Nov 21, 2015; epub: May 28, 2016; collection: Jan 2017

Abstract


Introduction: Left ventricular pseudoaneurysm; also referred to as contained left ventricular wall rupture, is a rare complication that is reported in about 0.2 to 0.3 percent of all myocardial infarction patients. Since it has a high risk of fatal rupture, early surgical repair is recommended once pseudoaneurysm is diagnosed.

Case Presentation: In this case report, we are describing a case of a left ventricular inferior wall pseudoaneurysm which was diagnosed by angiography, and was complicated by rupture and cardiac tamponade shortly after the patient received a powered assisted left ventricular angiogram.

Conclusions: This case exemplifies that pseudoaneurysm represents a part of the ongoing process of ventricular rupture, that begins with a small tear in the endocardium and then extends to the myocardium and the pericardial cavity, causing hemopericardium and cardiac tamponade. Therefore, earlier recognition and urgent surgical repair can be lifesaving.

Keywords: Ventricular Pseudoaneurysm; Cardiac Rupture; Myocardial Infarction; Cardiac Tamponade; Powered Assisted Ventriculogram

1. Introduction


Left ventricular pseudoaneurysm; also referred to as contained left ventricular wall rupture, is a rare complication that is reported in about 0.2 to 0.3 percent of all myocardial infarction patients (1-3). Since it has a high risk of fatal rupture, early surgical repair is recommended once pseudoaneurysm is diagnosed (4).

2. Case Presentation


A 66- year-old male with a past medical history of diabetes mellitus and hypertension with no previous cardiac history, presented to our emergency department complaining of chest pain for two days that worsened the night before his presentation. Initial vital signs showed blood pressure of 110/60 mmHg, pulse rate of 109 beats per minute, and respiratory rate was 18 breaths per minute, oxygen saturation was 98 percent on room air. Physical examination was only significant for an irregularly irregular pulse, normal heart sounds with no murmurs or added sounds. Initial laboratory results showed a white blood cell count of 17.700/μL, hemoglobin of 15.4g/dL, platelets of 189,000/μL, creatinine of 1.26 mg/dL, troponin I of 3.79 ng/mL, creatinine kinase myocardial band: 10.6 ng/dU. Electrocardiogram (Figure 1) revealed Q-waves with ST-segment elevations in leads II, III and aVF, along with atrial fibrillation and right bundle branch block. A presumed diagnosis of inferior wall acute myocardial infarction (AMI) was made, and the patient was transferred immediately to the cardiac catheterization lab.


Figure 1.
12 leads Electrocardiogram Upon Presentation

Coronary angiography demonstrated 60% stenosis in the left anterior descending and 70% stenosis in the left circumflex artery, images of the right coronary artery showed a total occlusion of the posterior descending artery. Left ventricular angiogram (LV Gram) showed inferior wall hypokinesia and an ejection fraction of 40% and an inferior wall pseudoaneurysm (Figures 2 and 3). The neck of the pseudoaneurysm measured 12 mm in width and the aneurysmal sac measured 35 mm; the neck to sac ratio was less than 0.5, which is strongly suggestive of pseudoaneurysm. Cardiothoracic surgery team was immediately consulted for an urgent pseudoaneurysm repair and coronary artery bypass grafting. During cardiac catheterization the patient received two powered injection LV Grams via a 6 French Pigtail catheter; he received 24 mL of contrast at a rate of 12 mL/sec at the pressure of 450 psi which equals about 23,271 mmHg, a second LV gram was done for better visualization of the pseudoaneurysm. After that the second LV gram the patient became hypotensive and hemodynamically unstable, which then developed to cardiac arrest with pulseless electrical activity. Cardiopulmonary resuscitation was started, and an intra-aortic balloon pump was inserted. After resuscitation for about 10 minutes the patient recovered, and his rhythm was normal sinus with tachycardia, but he remained hypotensive. At this point the assumption was that the pseudoaneurysm ruptured, causing hemopericardium and cardiac tamponade, pericardiocentesis was immediately performed and a bedside echocardiogram confirmed the diagnosis and showed moderate to severe pericardial effusion with end diastolic collapse of the right atrium and ventricle (Figure 4). The patient’s blood pressure slightly improve after the pericardiocentesis and the removal of about 150 mL of bloody pericardial fluid. Then, the cardiothoracic surgeon was available and an emergent lower mini sternotomy surgery was performed, and bloody pericardial fluid with clots were seen in the pericardial cavity, which confirmed the diagnosis of cardiac rupture and pericardial tamponade. However, the patient had cardiac arrest again with pulseless electrical activity. Unfortunately, despite all the efforts which were made to resuscitate the patient, he remained pulseless with no recordable blood pressure, and was pronounced dead.


Figure 2.
Left Ventricular Angiogram in the Right Anterior Oblique View, Showing Inferior Wall Pseudoaneurysm

Figure 3.
Left Ventricular Angiogram in the Left Anterior Oblique View, Showing Inferior Wall Pseudoaneurysm

Figure 4.
Bedside Echocardiogram Showing Moderate to Severe Pericardial Effusion

3. Discussion


Left ventricular pseudoaneurysm (LVPA) is a rare complication of acute myocardial infarction (MI), which often has dreadful consequences. It usually develops when the free wall rupture is contained by the adjacent pericardium, organizing thrombus, and hematoma (1). Pseudoaneurysm (PA) is distinguished from true ventricular aneurysm by that it has no myocardial or endocardial tissue in its wall and maintains communication with the LV cavity through a relatively narrow neck, as opposed to true aneurysm, which involves the full thickness of the cardiac wall, has a wider neck and less likely to rupture (2).


The incidence of LVPA after MI is 0.2 to 0.3% (3). It occurs more frequently in elderly and in male patients. MI is the most common cause, particularly the posterior and the inferior wall of the left ventricle, following occlusion of the right coronary or left anterior descending arteries. Other causes include cardiac surgery, trauma and infective endocarditis (5). Because untreated LVPA has a 30 to 45 percent risk of rupture, early surgical intervention is recommended (4).


PA represents a part of the ongoing process of ventricular rupture, which begins with a small tear in the endocardium which then extends to the myocardium and pericardial cavity, causing hemopericardium and cardiac tamponade (6, 7). Risk factors for ventricular wall rupture and the development of a PA in the setting of acute MI include: a relatively small first acute MI, age of > 60 years, hypertension, pericarditis, post-infarct angina, high CK-MB levels, elevated peak serum C-reactive protein, decreased collateral flow, use of nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids during the acute phase of MI and late thrombolytic therapy (after 7 hours) (8).


PA presentation can be dramatic with tamponade and shock, or it can be subacute with arrhythmia, prolonged or recurrent chest pain, embolic events, and heart failure. However, 12% of the patients appear asymptomatic at the time of diagnosis, and 3% of the patients have sudden death as a presenting symptom (5).


LVPA diagnosis can be challenging given its nonspecific presentation and physical findings. Physical examination may show a systolic, diastolic or to-and-fro murmurs related to blood flow across the narrow neck of the PA during systole and diastole. Most of the patients have nonspecific ST-T wave changes, and only 20% shows ST-segment elevation (2).


Cardiac imaging has an important role in diagnosis and many cardiac diagnostic modalities are available, including echocardiography, cardiac magnetic resonance imaging, computerized tomography and left ventricular angiogram. Transthoracic echocardiogram is an important non-invasive test for diagnosing PA, and should be used in the initial assessment of patients with suspected PA. The ratio between the width of the neck and the maximal internal diameter of the aneurysmal sac is < 0.5, or the presence of bidirectional flow through the neck using color and pulsed Doppler are suggestive of PA (9). MRI has a high sensitivity and specificity for diagnosis (10), it usually demonstrates focal bulging of the pericardium with a dyskinetic segment. In some cases, delayed enhancement of the PA might be seen.


Left ventricular angiography usually shows a narrow neck connecting the ventricle to the cavity, where contrast remains for several beats following the injection (11). Although left ventricular angiography is considered the best diagnostic modality and has a high accuracy of about 85 percent, its use as a primary diagnostic test is limited because of the concern for thrombus dislodgment (12).


The optimum choice of treatment is surgical repair. Timing of surgery depends on the time period from MI to diagnosis. Urgent surgery is recommended for LVPA detected in the first 2 - 3 months after MI, because the risk of fatal rupture is higher than the operative mortality, which was reported to be between 7% - 29% (13). For high-risk surgical candidates transcatheter closure of the LVPA is a feasible alternative with good outcomes (14, 15).


Asymptomatic PA which are detected incidentally are usually stable under 3 cm, and they can be managed conservatively (16). Moreno et al. reported a cumulative survival of 74.1% at 4 years with conservative management of patients with chronic LVPA (17).


In our patient, the fact that the LVPA rupture occurred shortly after the two powered injection LV Grams with high pressures of 450 psi (23,271 mmHg). Although this pressure reflects the pressure within the power injection pump, but this can cause dramatic increase in LV pressure. We believe that the power injector assisted ventricular angiogram may have contributed to the PA rupture either by causing thrombus dislodgment or by increasing the pressure forces on the LV wall.


This case illustrates that pseudoaneurysm is a part of the ongoing process of ventricular rupture. And the final outcome raises questions about the need to use other safer and quick, noninvasive diagnostic imaging methods beyond coronary angiography and ventriculography for diagnosis and providing information for surgery.


3.1. Conclusion

Fatal rupture, hemopericardium, and tamponade are among the most important complications of pseudoaneurysm. Although no literature is available concerning the safety of left ventriculography in patients who presents acutely with left ventricular pseudoaneurysm, we suggest that care should be taken while performing left ventriculography to avoid fatal rupture.

Footnotes

Authors’ Contribution: All authors participated in the management of the patient. Amer Hawatmeh and Ahmad Abu Arqoub: acquisition, analysis, interpretation of the data and drafting of the manuscript; Ahmad Isbitan and Ashraf Jmeian: acquisition, interpretation of the data and critical revision of the manuscript; Fayez Shamoon: interpretation of the data and critical revision of the manuscript.
Financial Disclosure: Authors have no conflict of interest to declare. This manuscript has not been published in another journal and is not under consideration by another journal. The final manuscript has been seen and approved by all authors.

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Figure 1.

12 leads Electrocardiogram Upon Presentation

Figure 2.

Left Ventricular Angiogram in the Right Anterior Oblique View, Showing Inferior Wall Pseudoaneurysm

Figure 3.

Left Ventricular Angiogram in the Left Anterior Oblique View, Showing Inferior Wall Pseudoaneurysm

Figure 4.

Bedside Echocardiogram Showing Moderate to Severe Pericardial Effusion