Correspondence Address: Dr. Bharat Rathi E-1, 160, Phase 3, Roop Rajat Township, Pal Road, Jodhpur - 342 001, Rajasthan India
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The case describes a rare mechanical complication of myocardial infarction in the form of right ventricular free wall rupture leading to cardiogenic shock and death. The patient had no cardiac high-risk factors and had short-lasting symptoms of the chest pain but presented in the emergency department in a semi-conscious state. The condition was diagnosed on transthoracic echocardiography and during the course of investigation, the patient instantaneously deteriorated and succumbed to the condition.
How to cite this article: Rathi B, Inaniya R, Agarwal R. Right Ventricular Free Wall Rupture: A Catastrophic Sequela of Myocardial Ischemia. J Indian Acad Echocardiogr Cardiovasc Imaging 2020;4:213-6
How to cite this URL: Rathi B, Inaniya R, Agarwal R. Right Ventricular Free Wall Rupture: A Catastrophic Sequela of Myocardial Ischemia. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2020 [cited 2021 Dec 5];4:213-6. Available from: https://www.jiaecho.org/text.asp?2020/4/2/213/292634
Coronary heart disease and related complications are the leading cause of death all over the word. The incidence of acute cardiac events continues to rise but with the advent of successful diagnostic and therapeutic interventions, the mortality has reduced significantly. Several mechanical complications of acute myocardial infarction (AMI) are known which include cardiogenic shock, ventricular septal rupture, acute mitral regurgitation, right ventricular infarction, and very rarely ventricular free wall rupture (VFWR). Besides, the mechanical complications, arrhythmic, and inflammatory complications are also well known. VFWR is one of the rarest and most catastrophic complications of AMI which almost always proves fatal if not diagnosed and treated in time., The condition can present with subtle symptoms and misguiding hemodynamic parameters in a previously asymptomatic and low-risk patient. We hereby present a case of the right VFWR (RVFWR) leading to cardiac tamponade, cardiogenic shock and death in an elderly male with no cardiac high-risk factors.
A 72-year-old male presented to our emergency department with complaints of chest pain for the past 10 h along with syncope and dizziness for the past 3 h. The patient was brought in a semi-conscious state and was poorly responding to verbal commands. There was no history of diabetes mellitus, hypertension, or dyslipidemia or history of chest pain or cardiac interventions in the past. On physical examination, the patient had tachycardia, blood pressure was 130/90 mm Hg, respiratory rate was 22/min, and oxygen saturation was 92%. Chest auscultation revealed no significant abnormality except that the heart sounds were feeble with no appreciable pericardial rub or murmur. Electrocardiography (ECG) showed ST depression in the anterior leads (V1, V2, and V3) with tachycardia (heart rate of 130 beats/min). To confirm the diagnosis of non-ST elevation myocardial infarction (NSTEMI), cardiac markers were sent and while waiting for the report of cardiac markers, the patient underwent computed tomography (CT) of the head because of the compromised neurological state. The CT head revealed no abnormality but the cardiac markers were markedly raised (Troponin I level was 25 ng/ml, and creatinine phosphokinase-muscle and brain (CPK-MB) was 194 IU/L), hence, the diagnosis of acute coronary syndrome (ACS) (NSTEMI) was established. His bedside transthoracic echocardiography (TTE) revealed regional wall motion abnormality of the inferior and posterior wall along with large pericardial effusion [Figure 1] with a smooth layer of echo-dense substance suggestive of blood [Figure 2] with ejection fraction of 40%. Right atrium (RA) and right ventricle (RV) were seen collapsed during the diastole [Figure 3] and in the right ventricular free wall, a slit-like defect was seen which was around 4–5 mm in size [Video 1 and [Figure 4]. There was no septal or apical rupture or any valvular regurgitation. Normal aortic and pulmonary valve flow was noted. Left atrial, right atrial, and RV diameters were normal. Cardiac tamponade was confirmed with the typical signs of systolic RA collapse and diastolic RV collapse. Repeat blood pressure was found to be 70/40 mmHg with worsening oxygen saturation of 86% on face mask. The patient was intubated immediately, and inotropic support was started with fluid replacement in view of cardiogenic shock. Within a short span of 15 min, the patient developed cardiac arrest and cardiopulmonary resuscitation was started but the patient could not be revived despite best of efforts.
Figure 1: Four-chambered view showing large pericardial effusion
RVFWR is a rare complication of AMI because of two reasons: (1) inferior wall MI is less common than anterior wall MI and (2) RVFWR is an extremely catastrophic complication of AMI, leading to death even before the patient reaches a specialty care, and hence, this entity may be underreported. Only a handful of cases of RVFWR as a consequence of an ischemic event are reported till date.,, The outcome of RVFWR is mostly dismal in acute settings wherein it leads to hemopericardium and cardiogenic shock. Rarely, RVFWR can present in subacute settings with no concerning symptoms or hemodynamic instability, as the cardiac tamponade develops slowly if the rupture site is small. The mechanism assumed for masquerading clinical picture is thought to be due to spontaneous sealing of the tear site which can occur secondary to clotting of the leaked blood, but the patient remains at risk of sudden cardiac events due to progressive bleeding in the pericardial sac. Following an untreated AMI, the ventricular free wall may rupture within a week's time secondary to wall ischemia and necrosis. Typical patient profile for this complication is an elderly female with medical comorbidities such as hypertension, diabetes mellitus, and prior history of myocardial infarction or recent history of some cardiac intervention.
Most patients with VFWR are symptomatic with chest pain, altered consciousness, syncope, dizziness, bradycardia, and hypotension secondary to depressed cardiac contractility due to pericardial effusion of blood from the site of rupture. Examination findings can be subtle in subacute settings but can deteriorate MB-creatine kinase in no time. Chest auscultation can reveal obscured or feeble heart sounds, systolic murmurs, and pericardial rub. Pohjola-Sintonen et al. studied left ventricular rupture in 849 patients with AMI, they documented rupture in only 14 cases (1.7%) but it accounted for 14% of in-hospital mortality. Seven of the 14 ruptures occurred within 2 days and 10 within 4 days of the MB-creatine kinase determined the onset of infarction. The authors proposed that rupture was 9.2 times more likely to occur in patients with all of the following characteristics than in the remaining patients: (1) no history of previous angina or myocardial infarction, (2) ST segment elevation or signs of Q wave development on the initial ECG, and (3) peak MB-creatine kinase value (≥150 IU/L). They concluded that although these predictors are likely to be of little therapeutic value for free wall rupture since most patients with that complication die within minutes of its onset, they may aid in alerting physicians to the early diagnosis and timely surgical correction of ventricular septal rupture. In the present case, there was a short history of chest pain with NSTEMI and markedly raised CPK-MB levels.
Abreu Filho et al. observed 98 patients with ventricular rupture, of which only 5 (5.1%) were diagnosed in time to undergo surgical repair but only one patient could survive following surgical management. Septal rupture and papillary muscle rupture is comparatively more frequent than free wall rupture following AMI. RVFWR as described in the present case is eight times less common than the left ventricular rupture mainly because the inferior wall MI is less frequent than anterior wall MI, and the rupture site in the RV is difficult to localize on TTE.
Echocardiography is the most ubiquitous and easily accessed investigation used these days in patients presenting with acute or chronic cardiac symptoms. Echocardiography has established its role in the diagnosis of VFWR with typical signs on imaging. Pericardial effusion is the most frequent echocardiographic finding, with a sensitivity as high as 100%; however, the specificity might be lower, because the causes of pericardial effusion after MI include pericarditis, hemorrhage from postinfarcted myocardium, coronary perforation, and myocardial rupture. It is important to note that the absence of effusion does not exclude the diagnosis of left ventricular free wall rupture (LVFWR). Other signs are echogenic layering in the pericardium that indicates a pericardial thrombus or clot, regional myocardial dilation, and an abnormally thin and akinetic myocardium. During color flow Doppler echocardiographic evaluation, a color flow jet through a visible wall defect is diagnostic of LVFWR but it can be absent in RVFWR, also the jet might be absent when pericardial thrombus plugs the rupture site.
The management of VFWR is immediate surgery and repair of the defect. The surgical techniques involved are infarctectomy with patch repair, suturing of an overlay patch to the defect, or a patch-and-glue repair. Patients with a milder form of VFWR can be managed conservatively, but the bleeding can continue from the small tear and turn into a larger defect which can lead to emergency cardiac events such as massive tamponade and cardiac arrest. More recently with patch-and-glue techniques, avoiding cardiopulmonary bypass, short- and mid-term survival rates have improved to 60%–80% in studies of consecutive patients' series.
RVFWR is one of the rare complications of AMI and presents with almost 100% mortality if not diagnosed and treated in time. A high index of suspicion is needed in the settings of AMI with compromised hemodynamic status is the key to improved morbidity. The present case documents a very rare case of RVFWR in a patient with no comorbidities and NSTEMI. Echocardiography played a crucial role in the diagnosis but the patient deteriorated and succumbed to this catastrophe. These mechanical complications must be sought after in patients dying instantly in the settings of AMI, and the cardiac care team must be trained in handling such acute emergencies. The patients must be counseled about the warning symptoms of ACS so that they present in time, and coronary revascularization is timely achieved.
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The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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