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She was subsequently diagnosed with hypoxic brain injury and life support was withdrawn.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.
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.
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?