Ventricular remodeling follows large myocardial infarction .This term denotes to change in size , shape and function of the ventricle due to altered myocyte geometry .It is now believed , this process begins to occur very early following a STEMI.(less than 24hours)
In which MI remodeling is more common ?
Any MI of large size , especially anterior and lateral MI. Inferior and posterior MI are less affected by adverse remodeling.The incidence is up to 20% of all myocardial infarction , if left untreated. Ventricular aneurysm formation and dyskinetic segments can be termed as the worst form of remodeling. The old terminologies of infarct extension and expansion could by synonymous with ventrilar remodeling . (Note : Every patient with STEMI undergoes some form of physiological remodeling that should not be confused with progressive pathological remodeling , we are discussing here ! )
What is the clinical impact of remodeling ? How to prevent it ?
Progressive cardiac failure and a poor outcome . It may provoke ventricular arrhythmias. ACE inhibitors (CONSENSUS study 1992 ) has since revolutionized the pharmacological prevention of adverse remodeling.
How to recognise left ventricular remodeling ?
Many methods are available .
2 D Echocardiography
These imaging methods diagnose remodeling only after it manifest* .We know remodeling is a cellular and molecular process .The earliest trigger for remodeling is the mechanical stretch and wall stress on the ventricles.Large areas of necrosed myocardium and the adjacent normal myocardium sets a perfect stage for eccentric pulling of myocardial segments and unregulated slippage of myocytes.
* Diagnosing fully established ventricular remodeling serves , no great purpose as it is very difficult to reverse it by pharmacological methods.it requires complex surgery.
What is the effect of mechanical stretch on cellular function ?
It is well known myocyte granules secrete Type B -Naturetic peptide in response to stretch. It could be a very early sign of adverse remodeling. So monitoring of BNP may give us an opportunity to intensively treat those patients who are likely to land in progressive cardiac failure.
A baseline level of NT-proBNP >120 pmol/L identified patients prone for adverse remodeling .Serial measurements showed further increase.It is possible to identify adverse remodeling of LV by documenting fresh elevation of BNP following MI .