Left Ventricular Pseudoaneurysm: A Diagnostic Dilemma.

Cases of infective endocardits presenting per se as huge LV PA are rarely reported in the literature. A 30-year-old male with no cardiac risk factors presented with community-acquired pneumonia and sepsis and shock. Chest X-ray revealed bilateral consolidation. A huge bulge was noted on the left ventricular border. Electrocardiogram did not reveal any ischemia or infarction. A transthoracic echocardiogram showed an aneurysm-like structure communicating with the left ventricle free wall below the mitral valve suggestive of LV pseudoaneurysm with severe mitral regurgitation. This was confirmed by a computed tomography scan. No vegetation was noted. He was treated aggressively with intravenous broad-spectrum antibiotics and inotropes but was in persistent shock. Cardiac surgery was considered, but the patient and relatives refused. Finally, he went into refractory shock and expired. The dilemma was the cause for this presumably acute-onset PA. There was no clear-cut evidence of endocarditis, though this appears to be the etiology in this patient. Copyright:

INTRODUCTION

Most reported cases of left ventricular (LV) pseudoaneurysm (PA) are typically related to myocardial infarction (particularly inferior wall myocardial infarction), cardiac surgery, or congenital submitral aneurysm (SMA).[12]

Diagnosing LV PA is often difficult due to its atypical presentations. The standard noninvasive techniques for diagnosing LV PA are transthoracic echocardiography and chest computed tomography (CT). Here, we present a case of LV PA with severe mitral regurgitation (MR) and septic shock where etiology was a diagnostic dilemma.

CASE PRESENTATION

A 30-year-old Indian worker, nondiabetic, nonhypertensive, nonsmoker, was admitted to a regional hospital with a history of 1-week high-grade fever and purulent productive cough. He was diagnosed to have community-acquired pneumonia. On physical examination, he was toxic; febrile at 38°C temperature; tachycardic with heart rate of 115 bpm, regular; blood pressure of 68/39 mmHg on inotropes, tachypneic with RR 26/min; jugular venous pulse was raised; cardiac examination a grade 4/6 pansyatolic murmur was heard with S3 gallop. He had lung crepitations and bilateral pitting edema.

ECG [Figure 1] showed sinus tachycardia and no ST-T changes. CXR [Figure 2] revealed cardiomegaly with a huge bulge at the LV border.

Figure 1

Electrocardiography showed sinus tachycardia and no ST-T changes

Figure 2

Chest X-ray: Showing increased cardiomegaly and an abnormal bulge over the left cardiac border (arrow)

He was treated with IV tazozin 4.5 g every 8 hours and was transferred to our center for further management.

Transthocacic echocardiography [Figure 3a] showed an aneurysm-like structure measuring 5 cm × 4 cm, suggestive of a large SMA in the posterolateral LV just below the posterior mitral leaflet communicating with the LV. There was severe mitral regurgitation [Figure 3b]. There was no valvular vegetation.

Figure 3

(a) Two-dimensional echocardiogram in apical four-chamber view showed an aneurysm-like structure measuring (5 cm × 4 cm) suggestive of a large submitral aneurysm in the posterolateral left ventricular just below the posterior mitral leaflet communicating with the left ventricular with a relatively narrow neck (arrow) (PA: pseudoaneurysm). (b) There was severe mitral regurgitation. (MR) (LA: Left atrium, LV: Left ventricle, PA: Pseudoaneurysm (arrow), RA: Right atrium, RV: Right ventricle)

His LV ejection fraction was 50%. His laboratory data showed leukocytosis (white blood cell counts: 37.8 × 109/L and neutrophil counts: 32.9 × 109/L), hemoglobin: 13.2 g/dL, high inflammatory markers (erythrocyte sedimentation rate: 48 mm/h and C-reactive protein: 38.8 mg/L), deranged renal function test (RFT) (creatinine: 256 micmol/L, estimated glomerular filtration rate: 27 ml/min, urea 37 mmol/L, and Na+: 124) with severe acidosis (pH: 7.1, bicarbonate: 18 mmol/L, and lactate: 7.4 mmol/L), and derangement of liver functions tests (LFTs) (total bilirubin: 33 μmol/L, alanine transaminase: 1280 IU/L, and albumin: 23 g/L). Troponin T level was 69 ng/mL. Chest CT [Figure 4a and b] revealed bilateral parenchymal consolidation, moderate pleural effusion, and posterolateral LV wall PA (measuring 8 cm × 7 cm × 6 cm, neck 3.5 cm). Blood cultures were sent and later reported as no growth in the first set. The patient's sputum revealed Gram-positive cocci.

Figure 4

(a) Chest computed tomography image showing a pseudoaneurysm over the left ventricular border (arrow). (b) A narrow orifice (neck) relative to the diameter of the pseudoaneurysm (arrow). (RV: Right ventricle, LV: Left ventricle, PA: Pseudoaneurysm)

He was dyspneic and in septic shock (on 3 inotropes), SPO2 was 80% even with an oxygen mask. The patient was discussed with a cardiothoracic surgeon for surgical intervention; however, it was not done as the patients' family refused to go with very high-risk surgery. His clinical (shock) and biochemical (sepsis, deranged LFT, and RFT) conditions were not improving despite maximum medical support, and finally, he died on the same day of transfer with asystole possibly due to the rupture of PA.

DISCUSSION

This 30-year-old male with no past medical history was shifted to our hospital with chest infection, sepsis, acute decompensated heart failure, severe MR, and an LV PA. The diagnosis of an LV PA was confirmed by transthoracic echocardiogram and CT chest. Possible causes of LV PA can include congenital SMA, myocardial infarction, cardiac surgery, infective endocarditis (IE) of the mitral valve (MV), and coronary spasm.

The patient had no previous cardiac surgery. He did not complain to severe chest pain or chest tightnesss. He had no previous rask factors for coronary artery disease. ECG showed no ST-T changes. Hence, myocardial infarction was excluded, although coronary angiography should have been done as gold standard to rule out coronary stenosis, it was not done due to his critical conditions.[3] He was not a drug abuser and other causes of coronary artery spasm were excluded. The ECG did not show any transient ST elevation oro depression.[4]

The intriguing issue in this unfortunate patient was the etiology. It was a dilemma whether he had pre-existing congenital LV PA or acquired due to IE. A SMA is a congenital outpouching of the LV wall adjacent to the posterior leaflet of the MV in the absence of ischemic, infective, or traumatic disease.[5] In this patient, there was no history of previous heart disease or trauma. A definite diagnosis of IE because blood cutures were negative and patient was given antibiotics so modified Duke's criteria could not be applied. Patient also had no minor criteria such as predisposing heart disease or IV drug abuse and vascular or immuological phenomenon phenomenon. However, a possible IE diagnosis could be made if an LV PA is taken as major criteria as per the European Society of Cardiology 2015 guidelines and temperature of 38°C as a minor criterion.[6] Recent studies show that patients diagnosed with staphylococcal endocarditis tend to have increased serum troponin levels,[78] and in our case, troponin T level was raised to 69 pg/mL.

LV PA can lead to very unstable hemodynamic conditions including severe acute pulmonary edema respiratory failure. In such type of emergency condition, heart status is usually assessed by portable two-dimensional (2D) echocardiography instead of by cardiac CT, as the patient's movement may increase the catastrophic consequences. Three LV PA characteristics that can be revealed by 2D echocardiography include (1) a sharp discontinuity of the endocardial image at the site of communication between the PA and the LV cavity, (2) a saccular or globular contour of the PA chamber, and (3) a relatively smaller diameter of the orifice in comparison with the PA.[9]

Frances et al. reported that the risk of rupture in LV PA is 30%–45% and that most cases are related to myocardial infarction or cardiac surgery.[1] Of the 290 cases of LV PA analyzed in that study, the etiology was related to MV IE in only two (1%) cases. Therefore, IE complicated by an LV PA is very rare but more difficult to treat compared to classic IE. The recent American Heart Association Scientific Statement reported that congestive heart failure increases mortality risk in IE,[10] especially if a patient does not undergo surgical intervention (MV replacement, wide resection, and patch closure of the defect) and the same consequence happened to our case. The family refused surgery.

CONCLUSION

LV PA presenting with sepsis is a diagnostic dilemma with regard to etiology. It could be due to preexisting congenital SMA or due to IE. Cases involving IE complicated by a huge LV PA are rarely reported in the literature. Transthoracic echocardiography is a useful diagnostic tool for diagnosing LV PA along with cardiac CT. In view of huge LV PA, surgical intervention must be considered early as there is a high risk of rupture and death as noted in this patient.

Declaration of patient consent

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.