Left ventricular rupture: a rare complication and an unusual presentation

Abstract

Myocardial infarction (MI) is a relatively common medical condition in the community. A rare complication of acute MI is left ventricular rupture (LV) rupture. This usually follows a transmural infarct. The incidence of this is 2%–4% and this usually happens within 3–7 days of MI. The anterolateral wall is involved in the majority of cases. Atypical presentations can occur several weeks after the initial event. Symptoms may mimic gastrointestinal disorder. The prognosis of this condition is very grim. However, with appropriate treatment, they can make an excellent recovery. The definitive treatment for this is surgical repair. We present the case of a 70-year-old man who had LV rupture and his clinical journey.

Background

Left ventricular (LV) rupture is a rare complication of myocardial infarction (MI). It usually happens within a few days of the initial event. Our patient had LV rupture nearly 8 weeks after his initial event. His presentation was atypical with predominantly gastrointestinal symptoms. He had a significantly difficult and tortuous clinical journey. Even though the general prognosis of this condition is very bleak, he made an excellent recovery in the end. This case report demonstrates that late presentation with atypical symptoms is possible with this rare complication of MI. With appropriate treatment despite its bad prognosis excellent recovery is possible.

Case presentation

A 70-year-old man presented to our emergency department (ED) with a history of feeling very weak and lethargic. He is a cycling enthusiast and he had done 80 km cycling competition over a weekend. Since then he was feeling very weak. He was not getting better after about 5 days. Hence he decided to present himself to our ED, which is a district general hospital in a rural setting in the UK.

He had a background history of hypertension and was on ramipril. He is retired and lives with his wife. He is a non-smoker and his alcohol consumption was minimal.

His ECG done at that time showed one segment ST elevation in LII, LIII, aVF and Q waves in LIII, aVF (inferior leads, figure 1). This was suggestive of a recent inferior wall MI. His highly sensitive troponin level came raised at 715 ng/L (nanograms/litre) (normal <15 ng/L).

Figure 1.

ECG showing ST elevation and Q waves in the inferior leads (LII,LIII,aVF).

He was diagnosed as having acute coronary syndrome (ACS). His condition and ECG were discussed with the cardiology team in the nearest tertiary centre. Cardiology team felt ECG changes were old and he is not suitable for emergency coronary intervention. Hence the patient was admitted under the care of the medical team locally.

When admitted he was treated with aspirin, clopidogrel and subcutaneous enoxaparin.

Six days later, he was transferred to the tertiary centre. There he underwent a coronary angiogram. This revealed proximal occlusion of the right coronary artery (RCA) with collaterals from left coronary artery. It was decided, the best treatment for the patient is optimising medical therapy. The patient was discharged from there on dispersible aspirin 75 mg per day, Clopidogrel 75 mg per day, atorvastatin 80 mg per day, bisoprolol 1.25 mg per day and glyceryl trinitrate spray as required. He was already on ramipril 5 mg two times a day.

Forty-eight days postadmission patient presented back with collapse. At home while on his way back from the toilet, he felt giddy and he collapsed on to the floor. There was no history of loss of consciousness. There may have been a very transient chest pain that lasted for less than a minute which he felt was insignificant. When picked up by the paramedics, his blood pressure was 67/47 and his pulse rate (PR) was 62/min. His abdomen looked distended and he vomited once. He was fluid resuscitated by the paramedics. In the ED, his BP was 81/62, PR was 69/min. His abdomen looked distended and he had tenderness all over the abdomen. He vomited again in the department.

Investigations

His ECG showed fixed changes from his previous admission.

Because of his tender abdomen and low blood pressure, a CT scan of the abdomen was done.

This showed blood in the pericardial sac suggesting cardiac tamponade (figure 2). There was blood seeping from LV into pericardial sac (figure 3). He had a suspected inferior wall aneurysm rupture.

Figure 2.

CT scan: large collection in the pericardial sac. Tip of the arrow shows collection in the pericardial sac.

Figure 3.

CT scan: blood seeping from left ventricle (LV) into the pericardial sac. Tip of the arrow shows blood seeping from LV into pericardial sac.

He went on to have a bedside transthoracic echocardiogram (TTE). This showed a collapsed right ventricle, aneurysm in the inferior basal wall of the left ventricle and moderate pericardial effusion.

Differential diagnosis

Taking into consideration his age and symptoms, the first diagnosis considered was a ruptured abdominal aortic aneurysm. Hence the reason for requesting a CT abdomen.

A cardiogenic shock or cardiogenic pulmonary oedema were also considered. Clinically, he had a clear chest and ECG did not show any acute changes.

Because of the high incidence in that age group, a septic shock also was a differential. However, other clinical features did not match this diagnosis.

Treatment

Initially, the patient had multiple 250 mL instalments of normal saline. After 750 mL of fluid, the further fluid challenge was stopped. Anaesthetic support was summoned. No active airway management was necessary. Later the patient was airlifted to the tertiary centre to the care of cardiac team.

Under the cardiac team, initially, he had a TTE-guided pericardiocentesis and it retrieved 150 mL of blood-stained fluid. With this, the patient’s clinical condition stabilised. The patient was admitted to cardiac intensive therapy unit (ITU). He was closely monitored. The clinical impression at this point was the patient had a contained rupture which may be sealed and is unlikely to bleed again. There was a chance that he may not need any surgical intervention at all.

Five days later, he went on to have another TTE. It showed a localised large basal LV aneurysm. There was no obvious flow seen into the pericardium and no thrombi were seen. There was some residual effusion around the right heart. Hence a cardiac MRI) was requested. The aim was to demonstrate a rupture if one exists and prepare the patient for semiurgent surgical repair if necessary.

While awaiting this, 10 days from admission, the patient had a further collapse and went into pulseless electrical activity (PEA) cardiac arrest. He was actively resuscitated. TTE done during this resuscitation showed a large pericardial collection. Attempt to drain this percutaneously failed. With full cardiopulmonary resuscitation (CPR), the patient had a return of spontaneous circulation. The patient was intubated and ventilated at this stage. He was started on inotropes and with this patient stabilised haemodynamically with a blood pressure of 110/60 mm Hg and satisfactory arterial blood gas. A further TTE was done, which showed large pericardial effusion with organised clot causing tamponade.

A decision was made to take him to the theatre and do salvage drainage of the pericardium through a subxiphoid approach. In the theatre, on attempting to drain the pericardium through the subxiphoid approach, significant clots were noted. On evacuating the clots, active bleeding was encountered. Hence it was decided to proceed with a full sternotomy. Through this approach, pericardial sac was entered into. There was a significant amount of fresh and old clots. This was evacuated. A salvage repair of the inferior wall of LV with teflon strip was carried out. This was further reinforced by biological glue. He had coronary artery bypass grafting (CABG) done with vein graft to the distal RCA and diagonal artery. He had very prolonged haemostasis with blood products and other adjuncts. His chest was packed with a large pack over three drains. His sternum was left open.

Postoperatively, he remained unstable with acidosis and high lactate levels. He had gone into coagulopathy following massive blood transfusion. A transoesophageal echo (TEE) showed compression of right ventricle (RV) by the pack. Nine hours after the initial surgery, his chest was opened in the cardiac ITU. The removal of the pack was carried out. A further TEE showed a better RV function. Clinically, the patient became more stable.

Outcome and follow-up

He had a difficult course at the ITU. He needed high doses of inotropes which resulted in the gangrene of his toes. He went on to have Clostridium difficile colitis, which was successfully treated. He developed melaena and this was managed conservatively without endoscopy. He needed a tracheostomy and also he needed continuous veno venous haemofiltration for acute renal failure. He developed pleural effusion which was drained with a chest tube. He slowly and progressively got better. After 2 months of ITU care, he was repatriated to base hospital with good neurological function. He spent another month in the local hospital before discharging home.

Currently, he is doing well. He had a recent TTE, which showed good LV function. He is followed up by the podiatry team for his gangrenous toes. He is fully mobile and spends his time doing quiz shows locally. He is getting back to cycling slowly.

Timeline of events at local hospital

• Day 0—80 km cycling event.

• Day 5—ED presentation, ACS diagnosed, admission under the medical team.

• Day 17—coronary angiogram at the tertiary centre and discharge home.

• Day 53—ED presentation with collapse, LV rupture diagnosed, transferred to the tertiary centre.

Timeline of events at tertiary centre

• Day 0—percutaneous aspiration of the pericardium.

• Day 5—TTE, basal LV aneurysm, no flow into pericardium noted.

• Day 10—PEA cardiac arrest. CPR and resuscitation. Emergency repair of LV and CABG.

• Day 67—patient discharged to the local hospital.

Discussion

LV rupture is a rare complication of acute MI.^1–3 This usually follows a transmural infarct.1 2 4–6 The incidence of this is 2%–4%^{1–3 7} and this usually happens within 3–7 days of MI.^{3 7–11} Anterolateral wall^{7 9} is involved in the majority of cases.

The classical risk factors for LV rupture are elderly (≥55 years and commonly in-between 65 and 70 years), first anterior or lateral transmural infarction, persistent or recurrent chest pain, persistent ST elevation in ECG¹ and also female gender.^{2 4 9}

A typical presentation of acute rupture is a sudden collapse with hypotension or PEA arrest.^{1 7 8}

Transthoracic echocardiogram (TTE) is the gold standard for diagnosing LV rupture.^{7 12 13} Pericardial effusion is the usual finding. Less commonly, a right-sided heart collapse may be seen. TTE offers a 100% sensitivity and 93% specificity for diagnosis.¹³ In the case of a diagnostic dilemma, a CT scan is useful.¹² Cardiac MRI is a useful investigation to do in a non-acute setting to prepare the patient for surgery.^{12 14 15}

Fluid resuscitation and administration of inotropes are the cornerstones of initial management¹ until definitive management is planned. Pericardiocentesis is indicated in patients who are haemodynamically unstable as a desperate measure. It may cause further injuries and also may decompensate the tamponade effect.^{12 16 17} The definitive treatment for this condition is surgical repair.^{1 12 18}Various surgical techniques like patching, surgical reconstruction of LV and sutureless technique with glue, for example, gelatin–resorcin–formalin glue exists.

The prognosis of this condition is very grim with up to 82% mortality rate.^{1–3 19}

What was different in our patient?

Usually, LV rupture happens early after MI and it more commonly occurs in women. Our patient was a male and had this rupture 53 days after the initial event. The clinical symptom which goes with the rupture are chest pain and collapse. Our patient did not have any significant chest pain at all. His symptoms were more gastrointestinal in nature. He had vomiting and had tenderness all over the abdomen.

Common sites of LV rupture are the anterolateral wall. He had a rupture of the inferior wall.

He had the most difficult clinical course imaginable. He had an emergency thoracotomy following cardiac arrest, and 9 hours later, his chest had to be opened for another tamponade. He had a string of complications, which include sepsis, pleural effusion, renal failure, upper gastro intestinal bleed and others any one of them could have killed anybody. But he overcame all of these, one by one.

Even though in general prognosis of his condition is very grim, he recovered extremely well.

Learning points.

• A patient with left ventricular rupture can present late (weeks) after the initial event

• Symptoms of this need not be clear cut. Gastrointestinal symptoms and signs do not rule out this condition.

• Even though the prognosis of this condition is bleak, with appropriate management, a very good outcome is possible.