here is a case query for us to ponder
as always do post your thoughts
kim suvarna
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kind regards
Kim Suvarna
two new cases for interest and discussion
2018 cardiac EQA
hello
here are the digitised slides for the EQA, in case you have not seen the glass sections…. please copy and paste into your browser
for those of you attending the meeting later this month, please have a look over the cases. please complete a return (word file attached) to dr goddard if you need a certificate for the EQA.
please email me or dr goddard if there any problems
2018 Cardiac EQA question and answer sheet
kind regards
kim suvarna
Annual meeting and training day.
Happy New Year !
I look forward to seeing you in Sheffield in March
Here is the programme. Remember trainees go free !! and Consultants/equivalent have a basic registration fee payable to the UK Cardiac Pathology Network.
UK-CPN-2018-Meeeting-programme
The EQA slides should be available 1 month before the meeting on the website via link
best wishes
Kim Suvarna
UK CPN training meeting 16th March 2018
The next UK CPN training meeting will take place on 16/03/2018.
It will be at: The Circle, 33 Rockingham Ln, Sheffield S1 4FW (www.thecirclesheffield.org.uk )
09.00 – 16.30
Trainees – Free; Consultants – £70
5 CPD points
The programme and application form will be available in the New Year, to include :
Aortic disease, Valve pathology, Cardiac failure from the pathology perspective, Cardiac therapeutic medication overview, Case presentations, Cardiac EQA, Panel discussion of “What is normal”
two pathologies ?
here is an odd case that I came across recently
I hope it is of interest, and would be interested if anyone has had a similar pathology combination
a vascular problem
A heart with fibrosis and some myocyte changes
Case history 46 year old female.
Past medical history of sharp pain in her chest for 3 years. Pain sharp, restricting full inspiration and associated with bilateral arm heaviness and aching. Attended chronic pain clinic, where ECG, CXR and bloods were performed, all said to be normal. Diagnosed with costochondritis and treated with celecoxib and pregabalin. Other past medical history includes anxiety and low BMI..
Out of hospital unwitnessed cardiac arrest recently. She had CPR and was in VF, a shock was given and there was spontaneous return of circulation. Subsequent ECG showed ST depression and no prolonged QTc interval. Two hour troponin was 76. Echo showed preserved biventricular function and mild mitral regurgitation.
Urine toxicology screen on admission was positive for cannabinoids and negative for opiates, ethanol, methadone, cocaine, benzodiazepines and amphetamines.
She was subsequently diagnosed with hypoxic brain injury and life support was withdrawn. She died 15/9/17.
At post mortem, the BMI was 17.1. There were features of recent medical intervention.
A heart with fibrosis and some myocye changes
On examination of the heart – Pericardial sac intact and appears normal. Heart weighed 320 g and showed a normal configuration. Normal arteries, with up to 20% occlusion of the LAD and RCA by atheromatous plaque, with no superimposed thrombi.
LV showed mild myocardial pallor circumferentially. LV 10mm thick. RV 4mm thick. No ventricular dilatation. Cardiac valves unremarkable, no vegetations present. Normal circumferences of the valves. Foramen ovale is closed.
No significant pulmonary artery atheroma. No PE. Lungs heavy and congested.
Other organs normal externally and on histology.
Micro from both lungs bases has grown strep pneumoniae.
On histo – cardiac conduction system appears normal.
Patchy established replacement fibrosis of the LV myocardium. No evidence of active myocarditis (multiple blocks examined). No features of acute ischaemia.
Some myocyte nuclear hypertrophy. Some myocytolysis and vacuolar change in the region of the fibrosis but elsewhere the myocardium appears normal. RV shows some fatty infiltration but not associated with fibrosis.
Questions
Has there has been previous myocardial damage (unknown cause, possibly previous myocarditis (viral or toxic) ?
Or is this ischaemia from microvascular cause, vasculitis) and these areas of fibrosis have acted as a substrate for the generation of an arrhythmia?
Whilst there are changes within the myocytes that can be seen in cardiomyopathy, these tend to be seen in the region of the fibrosis?
There is fat within the RV, this is not thinned and there is no discrete associated fibrosis. I would be very grateful for your opinion?
A case with cardiac lupus ?
another interesting case of cardiac disease in the context of lupus