Leaking heart: ticking time bomb!

CONTEXT: Cardiac rupture is a very important but under-recognized complication of acute myocardial infarction and usually happens within a week of the event. Sometimes it can be subacute and may not be typical of an acute blow out rupture. Hence careful evaluation is needed as a missed or delayed diagnosis can be fatal. An emergent echocardiogram may aid in immediate diagnosis. Surgery is the only treatment option and is mandatory despite the high mortality risk. CASE REPORT: An elderly male presented with dizziness and hypotension. Based on the timeline of his symptomatology, electrocardiographic abnormalities and labs, a subacute cardiac rupture was suspected in the emergency room itself. A high index of suspicion is needed to diagnose cardiac rupture.
CONCLUSION: Subacute cases can be missed easily as presentation may not be dramatic. They can rapidly progress to a blowout rupture increasing mortality risk heavily even with surgical treatment.

Introduction

Cardiac rupture occurs in approximately 2-4% of patients after an acute myocardial infarction.[123] It accounts for at least 20% of mortality of patients with an acute myocardial infarction.[13] It can manifest as a blowout rupture or a subacute rupture. Contrast echocardiography, computerized tomography and magnetic resonance imaging can help in the diagnosis. In some cases, emergent surgery is the only option for diagnosis and treatment. Mortality risk can be very high despite timely surgery.

Case Presentation

A 72-year old male with hypertension presented to emergency room with light headedness and hypotension. Initial blood pressure was 80/50 mmHg and heart rate was 70 beats/minute. Electrocardiogram revealed evidence of tall R waves in lead V1-2 [Figure 1]. Troponin I level was 11.9 ng/mL. An emergent echocardiogram revealed a large pericardial effusion with fibrinous material [Figure 2]. Patient denied any other complaints including chest pain or dyspnea and wished to be discharged home. He did mention that he had an episode of chest pain 1 week earlier that resolved spontaneously and he did not seek medical care. Based on electrocardiogram and echocardiogram findings, we suspected patient suffered a posterior myocardial infarction which was complicated by contained free wall rupture and pericardial effusion. Based on the high index of suspicion, patient was taken for emergent coronary angiography which revealed 100% circumflex occlusion and right heart catheterization was consistent with tamponade physiology. Left ventriculogram showed an ejection fraction of 40% with staining of postero-basal wall suggestive of possible cardiac rupture. Patient underwent emergent percutaneous coronary intervention to the left circumflex along with placement of an intraaortic balloon pump, and emergent pericardiocentesis with removal of 50cc of hemorrhagic fluid. This led to hemodynamic stabilization. Limited pericardiocentesis was done to prevent dislodgement of the clot which may be tamponading the ruptured site. Patient was then taken to operating room immediately. Intraoperative a large amount of hemorrhagic fluid with clot was removed. The infarcted posterior myocardium showed necrosis and hemorrhage with multiple puncture sites leaking/oozing blood. A large patch was created with combination of Bio Glue and patient's own pericardium. This was glued onto the posterior wall and then sewn with a running 5-0 Prolene reinforced with multiple pledgeted 5-0 Prolene circumferentially around the posterior wall in the area of the circumflex distribution with care taken to avoid the circumflex artery itself. This appeared to completely stop all the bleeding. Post-operatively, patient did well in the intensive care unit for three days. However, on the fourth day patient suddenly developed pulseless electrical activity due to repeat free wall rupture and died.

Figure 1

Twelve lead electrocardiogram showing prominent R waves in leads v1 and v2 with ST segment depressions (arrows) suggestive of posterior myocardial infarction

Figure 2

Transthoracic echocardiogram apical two chamber view showing the pericardial effusion

Discussion

Cardiac free wall rupture is one of the most dreaded complications of acute myocardial infarction (MI) and is the second most important cause of mortality after cardiogenic shock in acute MI. Incidence is approximately 4% after an acute MI and causes 4-21% of deaths.[3] It can be sub-acute, ongoing for a few days after acute MI or could turn out to be an acute blow out rupture. Typically it can happen anywhere from 2-7 days after acute MI. Typical presenting symptoms and signs are chest pain, syncope, cyanosis, hypotension, bradycardia, pulsus paradoxus, elevated venous pressures, very feeble heart sounds, electromechanical dissociation and cardiogenic shock.[3] Cardiogenic shock can sometimes be transient as the hemopericardium could plug and prevent further leak from the rupture.[4] This was the likelihood scenario in our patient where he suffered a myocardial infarction a few days ago and the akinetic posterior wall developed multiple areas of micro perforation causing hemopericardium resulting in hypotension but with a relatively benign clinical presentation. Although the exact risk factors are unclear, some common characteristics have been noted in patients with cardiac rupture. Patients were noted to be older than 55 years of age and with preexisting hypertension.[56] In majority of cases it happened after first episode of myocardial infarction and there was a strong association with single vessel coronary artery disease.[78] This could suggest relation of rupture to lack of collaterals in newly developed coronary artery disease. Echocardiogram is the usual first line of diagnostic tool. A high index of suspicion is needed especially if there is ventricular wall thinning on echocardiogram and pericardial effusion particularly with echo dense masses within the effusion.[9] It is important to recognize the condition early as many of them show initially an oozing pattern without tamponade signs and could progress to a blowout rupture anytime at which time surgery carries an even higher mortality risk.[9] The only treatment for cardiac rupture is surgery, but there are no clear cut guidelines as to which is the best surgical approach so far. The standard technique involves removal of the infarcted area with reconstruction of the ventricle.[4] The recent popular sutureless techniques with pericardial patch closure do not use cardiopulmonary bypass.[10] It is to be realized that most of the patients with cardiac rupture have underlying severe coronary artery disease and benefit from revascularization.[10]

Although many cardiac rupture cases have been reported, our case is very interesting as the diagnosis was made on high index of suspicion based on electrocardiogram and echocardiogram findings despite the very benign clinical presentation by the patient. The findings on echocardiogram are very striking and an early diagnosis helped in emergent interventions. Unfortunately these patients are at high mortality risk even with surgery. Despite a successful pericardial patch repair our patient had a repeat free wall rupture and died. No clear cut guidelines have been established so far regarding the management of these extremely high risk patients due to lack of thorough experience as cases are very scattered. We are presenting this case to enhance the basic knowledge of identification of this condition which is very important to any physician or cardiologist as early diagnosis could expedite appropriate management and possibly aid patient survival.