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Surviving Left Ventricular Free Wall Rupture after Elective Left Heart Catheterization
Abstract
Cardiac catheterization with percutaneous coronary intervention carries a 0.4% risk of in-hospital
Q wave myocardial infarction, a 1.9% risk of urgent coronary artery bypass graft surgery, and a
1.4% risk of death (1). Acute myocardial infarction (AMI) result in less than 1% risk of
mechanical complications, including papillary muscle rupture, interventricular septal rupture,
and left ventricular free wall rupture (2). We present a patient who underwent elective left heart
catheterization complicated by AMI, which in turn was complicated by left ventricular free wall
rupture. The sudden onset of chest pain and pulseless electrical activity (PEA) in an elderly
woman with a recent virgin anterior AMI should raise a high index of suspicion for left
ventricular free wall rupture.
Case Report
A 75-year-old Caucasian female presented to her primary care provider (PCP) complaining of a
three-month history of nocturnal heartburn, fatigue, elevated blood pressure, axillary, and back
discomfort that occurred at rest but worsened with exertion. Her past medical history was
significant for hypertension, hyperlipidemia, and stage 3 chronic kidney disease. Given her risk
factors and symptoms concerning for coronary artery disease (CAD), her PCP performed a
baseline electrocardiogram (ECG) (Figure 1) which was normal. Exercise stress
echocardiography was equivocal due to lack of expected increase in ejection fraction at peak
stress from rest. Given her ongoing symptoms and equivocal stress test, the patient was referred
for an elective heart catheterization.
Heart catheterization revealed a focal 80% stenosis of the left anterior descending artery (LAD)
at the bifurcation of the first diagonal branch (D1) (Figure 2). A drug-eluting stent was deployed
in the LAD, but this resulted in plaque shift with total occlusion of D1 (Figure 3). Multiple
attempts to rescue D1 were made but were unsuccessful. The patient developed chest pain after
catheterization. Ischemic ECG changes ensued (Figure 4) and troponin I was elevated at 9.52
ng/mL, peaking at 36.63 ng/mL. No arrhythmias were noted and she was started on guidelinedirected medical therapy with Aspirin, Clopidogrel, high-intensity statin, beta-blocker, and
angiotensin receptor blocker. She was observed for 48 hours in the hospital.
The patient reported symptomatic improvement on hospital day three. She was ambulating
without difficulty and preparing for discharge later that day. While conversing with her
cardiologist that morning she developed severe acute substernal chest pain, clutched her chest,
and fell backward into bed. She became cyanotic and was noted to be in PEA. Advanced cardiac
life support (ACLS) was immediately initiated, and she received a total of two cycles of chest
compressions before regaining pulses. Bedside echo revealed a large hemopericardium with
organized thrombus associated with both systolic and diastolic inversion of the right ventricular
free wall consistent with tamponade (Figure 5). The patient was emergently taken to the
catheterization lab where she underwent pericardiocentesis with evacuation of 110 mL of blood
and rapid improvement in hemodynamics. A pericardial drain was left in place. Repeat left heart
catheterization revealed no evidence of coronary perforation or acute stent thrombosis. The
patient was transferred to the coronary care unit (CCU). She remained stable off all drips
throughout the night.
On hospital day 4, the patient felt better and ambulated to her commode to urinate. As she stood
up, she again developed severe acute substernal chest pain and went into PEA. ACLS was
initiated, and 80 mL of blood was aspirated through her pericardial drain. She rapidly regained
pulses. Given recurrent hemopericardium with tamponade, cardiothoracic surgery was consulted
and opted to perform a mediastinal exploration to elucidate the etiology of her hemopericardium.
The patient’s pericardium was opened and clotted blood predominantly around the lateral and
diaphragmatic aspect of the left ventricle was removed. Epicardial bruising and thrombus was
noted over the D1 infarct territory, and this was not disturbed. The pericardium was left open
after the chest was copiously irrigated with antibiotic solution. Two mediastinal drains were
placed prior to chest closure, and the patient was transferred to the cardiothoracic surgery
intensive care unit (CSICU). Immediately upon arrival to the CSICU, she had three liters of
bloody output through her mediastinal drains associated with hypotension prompting emergent
mediastinal re-exploration. Pulsatile extra-cardiac ejection of blood at the D1 infarct site was
noted consistent with left ventricular free wall rupture. Multiple topical sealant patches were
applied to the area and the rupture site was sutured.
After return to the CSICU and subsequent transfer to the CCU, the patient did very well. She was
weaned off pressors on hospital day 5, placed on beta-blocker therapy, and successfully
extubated on hospital day 15. Her follow up echocardiogram demonstrated no recurrent
pericardial effusion and preserved left ventricular systolic function.
Discussion
Left ventricular free wall rupture is exceedingly rare among AMI patients with an incidence of
less than 1% (2). Its incidence has declined with increased use of reperfusion therapies, antiplatelets, and adequate control of myocardial work load, oxygen demand and afterload. The
Multicenter Investigation of Limitation of Infarct Size (MILIS) study noted that rupture was 9.2
times more likely to occur in patients who had no prior history of myocardial infarction, STelevation or Q-wave development on initial ECG, and a peak CK-MB level greater than 150
IU/L (3). Several other studies have noted persistent ST-elevations on ECG, persistent or
recurrent chest pain, anterior AMI location, age greater than 70, and female sex to be significant
risk factors for rupture (4-6). Rupture occurs within the first five days after AMI in about 50% of
cases and within two weeks in over 90% of cases (7-10). Primary percutaneous coronary
intervention (PPCI) has significantly reduced the incidence of rupture. In a retrospective study of
2,209 patients with AMI treated with primary PPCI, reperfusion within 12 hours of presentation
had an incidence of rupture of 0.7% while reperfusion after 12 hours had a 0.9% incidence.
Failed reperfusion had a rupture incidence of 3.8% (11).
Survival hinges on the rapid recognition and immediate medical and surgical intervention.
Fluids, inotropes, vasopressors, and urgent pericardiocentesis should be performed if a patient
with rupture cannot urgently be taken to surgery. Rapid medical and surgical therapy portends
appreciable survival rates. In one study, 76% of patients with subacute rupture survived surgery
and 48% of subacute rupture patients were long-term survivors (12). We present a case of an
exceedingly rare and deadly mechanical complication of AMI. Our patient survived early left
ventricular free wall rupture only due to expeditious pericardiocentesis and surgical intervention.
Left ventricular free wall rupture should be considered especially in an elderly female patient
with a recent virgin anterior AMI who develops sudden chest pain and PEA.
IMAGING
Figure 1: Baseline ECG shows normal sinus rhythm with no pathologic Q waves or ST-T
abnormality.
Figure 2: RAO cranial projection shows a focal stenosis at the bifurcation of the LAD and
D1(Solid white arrow).
Figure 3: Post-stent deployment in the LAD, the D1 is jailed with no flow seen angiographically
(solid white arrow).
Figure 4: Ischemic ECG changes noted with development of ST-elevations in I, aVL and
reciprocal ST-depressions in the inferolateral leads. Note also the new development of Q-waves
in I and aVL.
Figure 5. Subcostal view of transthoracic echocardiogram demonstrating large hemopericardium
with organized thrombus (solid black arrow) and right ventricular free wall inversion (solid
white arrow) consistent with tamponade physiology.
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