Beta blockers(BBs) have become key drugs in management of CHF .It helps by blocking toxic effects of inappropriately elevated catecholamine , which is actually a compensatory response(A fight and survival reaction ) from the sympathetic system to a failing heart . This process becomes a liability in the long run as the adrenergic receptors either down regulate or even promote apoptosis and cell death .Along with RASS-ACE it affects every cell in the body promoting neuro- humoral catabolic state.
By trial and error methodology we have found blocking the sympathetic system by BBs confer consistent benefits in CHF .This is in contrary to the days we were ignorantly stimulating the beta receptors with positive inotropic agents and wary to give BBs in cardiac failure .This is one the most dramatic 180 degree turn around in the annals of clinical cardiac therapeutics last century.
Is all BBs same ? Is it the class effect ?
It is tempting to think all BBs are equal and to conclude they simply represent a class effect.But carvidilol seems to be the flag bearer , for whatever reason . (Apart from the outcome of landmark studies , there is a pharmacological basis for it’s superiority COMET/COPERNICUS)
What is the secret of carvidilol’s superiority in CHF than other BBs ?
We know CHF is a systemic syndrome as do the sympathetic activation .Hence , In CHF , it would require a non selective , systemically acting beta blocker to reverse and reset the adverse effects of catechlamine.surge.(Does that mean Propronolol (Inderal ) could be the best ?)
Carvidilol being a non selective BB fits perfectly for the job . Of course , additionally it has alpha blocking action that reduce the after-load reliving he LV wall stress during systole enabling further lowering of MVO2 and promoting regression of LV size as well.
Having said that prototype cardioselctive agents like Metoprolol , Bisoprolol are also backed by robust evidence for survival benefit in CHF . How to explain this paradox ? (CIBIS/MERIT )
“Thinking wildly(Evidence would come later ) it is possible the benefits from cardio selective agents are accrued much later as the dosage is titrated upwards . I would believe the “inflection point” of benefit could be same time they lose the cardioselectivity”
Cardioselectivity is boasted as a gifted property of BBs .It may be true in HT, arrhythmia and angina , but in cardiac failure it plays a different ball game .The simple logic is the target receptors need to be blocked in systemic fashion.