Step II Ventricular remodeling

[zenna]

What is actually ventricular remodeling? How do ACE inhibitors reduce it? How are B-blockers, ACE inhibitors, and diuretics mortality reducing drugs for HF?

 

[Fuzuli]

What is actually ventricular remodeling? How do ACE inhibitors reduce it? How are B-blockers, ACE inhibitors, and diuretics mortality reducing drugs for HF?

What would happen to your skin if you were to cut it deeply? There would be a scar tissue to remind you for the rest of your life to be careful 🙂 In the heart, however, the regeneration of the tissue is more complex after an infarction. The infarcted area may become thinner, become dilated and unable to contract and relax properly (so called "dyskinesis"). This process is named as remodelling.

How ACE inhibitors block this remodeling is not exactly known, but suffice to say that it's due to their inhibition of AT-II effect on myocytes, macrophages and fibroblasts.

Understanding why these drugs reduce mortality is based on understanding the pathophysiology of heart failure. Basically, heart failure means that heart cannot fulfill its duties as a pump. Or to say it in another term: the main problem in decompensated heart failure is decreased cardiac output. A decrease in CO means sympathetic NS activation as a compensatory mechanism. SNS will have direct effect on the heart and will activate RAAS. Ultimately RAAS will cause 1) vasoconstriction 2) Increase sodium and water reabsorption. So, both preload and afterload will increase as a result, which will be a further load on the already malfunctioning heart.

BB will decrease the adverse effect of SNS on the heart. ACE inhibitors will block RAAS. Diuretics will reduce sodium and water absorption. Although this is a simplification of these drug's effects, I hope it summarizes some of their main effects.

 

[Orange Man]

What is actually ventricular remodeling? How do ACE inhibitors reduce it? How are B-blockers, ACE inhibitors, and diuretics mortality reducing drugs for HF?

Re: ACEI's and remodeling. in the mid-90s, studies clearly showed that less available ang II is available to stimulate fibroblast AT(1) receptors in the interstitium, leading to less type II collagen deposition, less cardiac remodeling (and so less stiffening). Hope that helps.

 

[zenna]

Thank you both of you Fuzuli and Orange Man.
Preload in HF is increased to maintain the CO but too much of that isn't good for heart, right?
I never knew about ACEI stimulating fibroblasts, yes it makes sense now.

 

[turkeyjerky]

Thank you both of you Fuzuli and Orange Man.
Preload in HF is increased to maintain the CO but too much of that isn't good for heart, right?
I never knew about ACEI stimulating fibroblasts, yes it makes sense now.

also, keep in mind that diuretics don't prolong survival. They are a symptomatic treatment. Spiranolactone and eplernone reduce mortality not due to their diuretic effect (which is quite small, actually) but via their effect on inhibiting aldosterone's effects on cardiac fibroblasts.

 

[zenna]

Hey, thanks yes of course diuretics don't reduce mortality. Thank you so much

 

[nickolas]

It should be noted that there are two types of remodeling. The hypertrophic one (concentric) with thickening of the heart muscle, usually due to a history of hypertension-pressure overload (EF usually is normal) and the "dilative" one (eccentric) were the diastolic volume of the left ventricle is increased and EF usually is low. Treatment as far as BBs, CCBs, ACEI/ARB and spironolactone is exactly the same.
After a STEMI the damaged part of the heart becomes passive in a way that during systole it dilates and fills with blood which remains in the left ventricle cavity instead of going forward. This creates the "volume overload" that leads to eccentric hypertrophy (healthy walls do become hypertrophic in response).