Online Clinical Case Study (February 2016)
content of the February Cardiology Series is provided by:
Dr. KAM Ka Ho, Kevin MBChB(CUHK), MRCP(UK), FHKCP, FHKAM(Med), Specialist in Cardiology
Dr. CHEUNG Shing Him, Gary MBBS(HK), MRCP(UK), FHKCP, FHKAM(Med), Specialist in Cardiology
A 70-year-old man who was a retired construction site worker was admitted to A&E Department because of on and off chest pain for 2 days. He was a chronic smoker for decades with past history of hypertension and asymptomatic frequent premature ventricular ectopics (PVC). ECG (Diagram 1) was done at A&E which showed diffuse ST elevation at V2-3 leads. Diagnosis of anterior ST-elevation myocardial infarction (STEMI) was established and thrombolysis was given in view of persistent chest pain. Loading dose of aspirin, clopidogrel and enoxaparin were administered as well. Upon arrival to CCU, his blood pressure dropped to 70/49mmHg and pulse rose up to 120/min. He was sweating profusely but his temperature was still within normal range. Physical examination revealed an elevated JVP together with a harsh pansystolic murmur throughout the precordium. His periphery was cold and there was mild basal crepitation on chest examination. No evidence of tarry stool from per rectal examination. ECG did not show any serial change.
regard to the above scenario, what is the most likely reason of his shock?
a. Septic shock
b. Anaphylatic shock
c. Hypovolaemic shock
d. Cardiogenic shock
e. Neurogenic shock
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of the following could explain the development of his new murmur?
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held echocardiography (Diagram 2) was subsequently done in CCU. There was
evidence of infarct at left anterior descending artery territory and his
ejection fraction at that time was 40%. There was also a left to right shunt
across left ventricular mid to apical septum. Which is the most appropriate
treatment plan for this patient?
a. Percutaneous coronary intervention (PCI)
b. Consult cardiac surgeon for consideration of VSD patch repair and coronary artery bypass grafting (CABG) operation
c. Continue medical therapy and wait for the VSD to heal by itself
d. Referral to Heart Transplant Unit
e. None of the above
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from the treatment plan as above, is there any other therapeutic option
available for his scenario?
b. Yes, percutaneous closure of post infarct VSD
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The picture of anterior STEMI is clear-cut given the classical ECG change and new onset of chest pain. With background history of STEMI, cardiogenic shock is the most likely reason to explain his hypotension and cold sweaty periphery. The clinical history speaks against septic shock especially this patient has no fever. Absence of rash and allergic reaction basically ruled out the possibility of anaphylactic shock. Hypovolemic shock is also unlikely as patient is not suffering from acute fluid loss and no clinical sign of gastrointestinal bleeding.
Acute mitral regurgitation due to papillary muscle rupture, systolic anterior motion of mitral valve with dynamic left ventricular outflow tract obstruction and post infarct ventricular septal defect could explain the development of new murmur and cardiogenic shock. Acute mitral regurgitation caused by papillary muscle rupture is a rare but life-threatening complication of STEMI. It is postulated that the preserved contractility exerts extra stress on an ischemic papillary muscle which eventually leads to rupture. In the setting of anterior STEMI, left anterior descending artery occlusion per se unlikely infarct the entire anterolateral papillary muscle as its blood supply is coming from both the left anterior descending and circumflex arteries. Systolic anterior motion (SAM) of the mitral valve could be caused by the change in in left ventricular wall motion during the acute phase of myocardial infarction. Eccentric mitral regurgitation and dynamic left ventricular outflow tract obstruction are the subsequent consequence of SAM of mitral valve.
Post infarct ventricular septal defect (VSD) is a rare but lethal complication of STEMI. It occurs as a bimodal presentation with a higher incidence in the first 24 hours, especially after fibrinolytic agent given, and then again 3 to 5 days afterwards. The event occurs 2-8 days after an infarction and often results in cardiogenic shock. Infarction associated with a VSD is usually transmural and extensive. This is due to complete coronary artery occlusion with little or no collateral flow. Revascularization by PCI with VSD left behind is not going to reduce the overall mortality. On the other hand, medical therapy is largely ineffective and majority of patients may die within 1-2 weeks due to refractory heart failure or cardiogenic shock.
The American College of Cardiology and American Heart Association (ACC/AHA)1 advises immediate surgical closure. However, high mortality rates are not unexpected with advanced patient age, and other factors including comorbidities, hemodynamic instability, and technical challenges of the surgical procedure. Therefore, many surgeons prefer to delay surgical repair at least by two weeks to allow initial healing, firmer anchoring of suture and better support for patch material.
Percutaneous device implantation to post infarct VSD is another viable option for immediate complete defect closure or initial hemodynamic stabilization. This less invasive approach may improve survival rates in selected patients with suitable anatomy.
Since the first case report in 1998, a variety of devices have been used including atrial-septal-defect occluders, muscular VSD occluder and recently a specific post-infraction VSD (PIMVSD) occluder developed by Amplatzer2 (Diagram 3). The Amplatzer PIMVSD device is a nitinol construct with sizes ranging from 16 to 24 mm and a connecting waist of 10 mm in length. The LV and RV disks are 5 mm larger than the waist. According to the latest UK experience published3, the immediate success rate of implantation was 89%. Major immediate complications included procedural death (3.8%) and emergency cardiac surgery (7.5%). Even the overall outlook remains poor for such high risk patients, but those who survived and were discharged from the hospital had a good long-term prognosis.
In conclusion, post-infarction VSD are uncommon but associated with a high morbidity and mortality. Percutaneous closure of post infarct VSD is a challenging but reasonably effective treatment for these extremely high-risk patients.
Series for February 2016 is provided by:
Dr. CHAN Hau Ngai, Kingsley, Dr. TANG Yuk Ming, William, Dr. KWAN Chi Keung, Dr. LEUNG Wai Yiu and Dr. CHANG Mee, Mimi
Specialists in Dermatology & Venereology
A 28-year-old lady complained an itchy nodule over her right middle finger which was rapidly increasing in size for few months. She complained of occasional bleeding. She was otherwise well and there was no other similar lesion over other parts of her body. Physical examination showed a 0.8 cm size reddish nodular growth over right middle finger.
|1.||What are the differential diagnoses?|
|The differential diagnoses includes pyogenic granuloma, bacillary angiomatosis, angiolymphoid hyperplasia with eosinophilia, SCC, metastatic carcinoma, Kaposi sarcoma, etc.|
|2.||What is the diagnosis?|
|The diagnosis is pyogenic granuloma. It is a relatively common benign vascular lesion over the skin and mucosa area.|
|3.||What is the cause of this condition?|
|The cause of pyogenic granuloma is unknown. It occurs more commonly in children and young adults. There are several factors that have been identified may play a role in the development - including trauma, bacterial infection, pregnancy, etc.|
|4.||How is this skin condition diagnosed?|
|Diagnosis of pyogenic granuolma is usually made clinically from typical history and clinical presentation and no further investigation is needed. However, if skin cancer is suspected, skin biopsy is needed to confirm the diagnosis.|
|5.||What are the treatment options of this condition?|
|Different treatments can be used to treat the pyogenic granuloma. Cryotherapy, laser surgery, curettage and cauterisation and complete excision are the common treatments used to treat pyogenic granuloma depending on the size and location of the lesion. Since the feeding vessels usually extend deep into the dermis, recurrence after treatment may occur.|
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