By Ahmed Adlan
03 September 2018
A seventy two year old man presents to the local hospital with 5 days of chest pain and acute breathlessness. Past medical history included metastatic bowel cancer, treated hypertension and dyslipidaemia.
Admission ECG is shown in Figure 1.
Clinical examination revealed normal heart sounds with a systolic murmur and signs of fluid overload (elevated jugular venous pressure, bibasal crackles within the chest and peripheral oedema to mid shins). Vital signs as follows: blood pressure 89/55 mmHg, heart rate 98 beats per minute, oxygen saturations 96 % on 6 Litres of oxygen, afebrile.
He was discussed with the local cardiac centre who declined primary angioplasty on the basis of clinical status and malignancy. Medical therapy was initiated with Aspirin, Clopidogrel, Enoxaparin, intravenous loop diuretic, morphine and sublingual glyceryl trinitrate. Chest radiograph confirmed pulmonary oedema. He was transferred to the coronary care unit and a bedside transthoracic echocardiogram was performed (Video 1). He developed cardiogenic shock and unfortunately did not survive.
Learning points
Late presentation inferior ST-elevation myocardial infarction with ventricular septal defect/rupture
ST-elevation myocardial infarction (STEMI) is a medical emergency and should be treated with immediate primary angioplasty to restore coronary blood flow [1]. A 12 lead ECG should be undertaken immediately in patients presenting with acute chest pain, and once the diagnosis has been made an urgent referral should be made to the local cardiac centre for consideration of primary angioplasty. However primary angioplasty may not be appropriate in all patients and hence patients should be assessed prior to the procedure. Patients with significant comorbidity (such as metastatic cancer) may not be suitable candidates for angioplasty as the risks of the procedure may outweigh the potential benefits of revascularisation. In addition patients with completed myocardial infarcts (e.g. delayed presentation STEMI) may not benefit from revascularisation if the myocardium is not viable. A myocardial viability study (i.e. cardiac magnetic resonance imaging) may be necessary to dmeonstrate viability prior to revascularisation as attempts to restore blood flow to a dead myocardium would certainly be futile. In this case the echocardiogram demonstrates a thinned out, akinetic inferior wall with evidence of a ventricular septal defect.
Post myocardial infarction ventricular septal defect/rupture
Ventricular septal defect (VSD) or rupture (VSR), an abnormal connection between the left and right ventricle, is a rare complication following myocardial infarction and is associated with a substantially high mortality [2]. Acute VSD/VSR post myocardial infarction is a cardiothoracic surgical emergency however intervention carries a high mortality risk (18-54 %).
References
1. Steg G, James S, Atar D., et al. ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2012; 33: 2569-2619.
2. Arnaoutakis G, Zhao Y, George T., et al. Surgical repair of ventricular septal defect after myocardial infarction: outcomes from the society of thoracic surgeons national database. Ann Thorac Surg 2012; 94: 436-43.
03 September 2018
A seventy two year old man presents to the local hospital with 5 days of chest pain and acute breathlessness. Past medical history included metastatic bowel cancer, treated hypertension and dyslipidaemia.
Admission ECG is shown in Figure 1.
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| Figure 1. ECG (Open in another window) |
Clinical examination revealed normal heart sounds with a systolic murmur and signs of fluid overload (elevated jugular venous pressure, bibasal crackles within the chest and peripheral oedema to mid shins). Vital signs as follows: blood pressure 89/55 mmHg, heart rate 98 beats per minute, oxygen saturations 96 % on 6 Litres of oxygen, afebrile.
He was discussed with the local cardiac centre who declined primary angioplasty on the basis of clinical status and malignancy. Medical therapy was initiated with Aspirin, Clopidogrel, Enoxaparin, intravenous loop diuretic, morphine and sublingual glyceryl trinitrate. Chest radiograph confirmed pulmonary oedema. He was transferred to the coronary care unit and a bedside transthoracic echocardiogram was performed (Video 1). He developed cardiogenic shock and unfortunately did not survive.
Video 1. Transthoracic echocardiogram (parasternal short axis view at the level of the mitral valve).
Learning points
ECG
The ECG demonstrates ST elevation in the inferior leads (III, aVF) with reciprocal ST depression in the lateral leads (I, aVL, V5, V6). Q waves can be seen in leads III and aVF indicating a full thickness myocardial infarction i.e. established infarct. Late presentation inferior ST-elevation myocardial infarction with ventricular septal defect/rupture
ST-elevation myocardial infarction (STEMI) is a medical emergency and should be treated with immediate primary angioplasty to restore coronary blood flow [1]. A 12 lead ECG should be undertaken immediately in patients presenting with acute chest pain, and once the diagnosis has been made an urgent referral should be made to the local cardiac centre for consideration of primary angioplasty. However primary angioplasty may not be appropriate in all patients and hence patients should be assessed prior to the procedure. Patients with significant comorbidity (such as metastatic cancer) may not be suitable candidates for angioplasty as the risks of the procedure may outweigh the potential benefits of revascularisation. In addition patients with completed myocardial infarcts (e.g. delayed presentation STEMI) may not benefit from revascularisation if the myocardium is not viable. A myocardial viability study (i.e. cardiac magnetic resonance imaging) may be necessary to dmeonstrate viability prior to revascularisation as attempts to restore blood flow to a dead myocardium would certainly be futile. In this case the echocardiogram demonstrates a thinned out, akinetic inferior wall with evidence of a ventricular septal defect.
Post myocardial infarction ventricular septal defect/rupture
Ventricular septal defect (VSD) or rupture (VSR), an abnormal connection between the left and right ventricle, is a rare complication following myocardial infarction and is associated with a substantially high mortality [2]. Acute VSD/VSR post myocardial infarction is a cardiothoracic surgical emergency however intervention carries a high mortality risk (18-54 %).
1. Steg G, James S, Atar D., et al. ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2012; 33: 2569-2619.
2. Arnaoutakis G, Zhao Y, George T., et al. Surgical repair of ventricular septal defect after myocardial infarction: outcomes from the society of thoracic surgeons national database. Ann Thorac Surg 2012; 94: 436-43.
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