about 60 y old patient without typical clinical afflictions of myocardial ischemia (Diabetes type 2 is known: silent ischemia? or only indolent aptient?). The patient was admitted to our ER with
weakness and diarrhoea.
In ECG we found a sign of myocardial infarction stadium I-II in inferior leads, no signs of disturbance in V1-V6. Also we heard a new heard murmur (holosystolic murmur in Erb-point). Blood-sample
showed us distinct elevated liver enzymes (GOT > 1000 U/l, GPT > 800 U/L) and severe disturbance of electrolytes (Na 115 mmol/l, K 5,8 mmol/l); lactate was elevated with 4,8 mmol/l with
In TTE I found a inferior (pseudo-)aneurysm with perforation (VSD) in right ventricle (inferior-septale) with acute leading pressure and secundary volume overload of right ventricle. Overall signs of
acute RV-failure (maybe a myocardial infarction of right ventricle too).
Definitely NO clinical afflictions; NO haemodynamic instability.
This TTE clip demonstrates what is meant by myocardium that is 'moving' but not 'thickening'. You can see how the inferior wall seems to come nearer to the anterior, but it does
not thicken which is indicative of ischemia or scar. In this case, the patient was admitted with an acute coronary syndrome and was found to have profound multivessel CAD including disease resulting
in inferior wall ischemia.
about 50 y old man with distinct dyspnoea in context of lung oedema. In TTE and TEE we found a severe mitral valve insufficiency with regurgitation in pulmonary veins caused by mitral valve prolapse
in context of rupture of chorda tendinea. The reason of the ruptur of chorda tendinea is not clear: no myocardial ischemia (no elevated troponin, no coronary occlusion in cardiac catheter) and no sign
of endocarditis (no elevated values of inflammation). Some idea?
After recompensation the patient was admitted to cardiac surgery for mitral valve reconstruction.