Ventricular septal rupture is a major mechanical complication of STEMI . Excruciating chest pain , is the sine qua non of any myocardial tear , dissection and rupture . It is surprising , VSR following STEMI is rarely a painful event . I can recall number of such events , when a stable patient with persistent ST elevation in the coronary care unit , wakes up next morning with a systolic murmur.And echo reveals a septal defect promptly.
Three reasons can be proposed for relatively pain free rupture of IVS in STEMI.
- Typically VSR occurs in 3rd or 4 th day of infarct . By this time myocardium can be as soft as an ice cream ! . There is not much stress and strain at the site. The necrotic debri just gives way to spikes of LV systolic pressure .
- For rupture to occur there must be transmural infarct .The pain nerve terminals also die in the process .
- Further , it is a cavity to cavity rupture (LV to RV ) . Direct pericardial stretch does not occur .
* Ventricular free wall tear is a near fatal event is extremely painful .This often occurs in the first 24 hours when the nerve terminals are alive . The free wall rupture is more of a tear in the plane of myocardium . The pericardial (epicardium) layer has rich somatic nerve supply .
In summary
Early myocardial tear involving the epicardial surface can be severely painful . Late giving way of softened , necrotic often hemorrhagic muscle ( especially in the IVS ) is less painful or totally painless.
Coming soon . . .
By the . . . what happens to pieces of septal myocardium as it gives way and enter the right ventricle ?
Burning question (have not found the perfect answer):
Why does pericarditis pain get worse on laying back but the rub get louder on sitting forward. Ie if leaning forward increases the rub should it not also increase the pain because in theory leaning forward increases the contact between the two pericardial surfaces?