What is the MOA of calcium channel blockers in stable angina?

[arossm]

Package insert for nifedipine says "dilation of coronary arteries is not an important factor in classical angina.", which seems to contradict all other sources (guidelines, textbooks, etc.). Who is right?

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[sahell]

Dihydropyridines have a greater effect on arterioles. Verapamil has a greater effect on the heart.

Dihydropyridines in stable angina would reduce myocardial oxygen demand by reducing after load.

 

[arossm]

Dihydropyridines have a greater effect on arterioles. Verapamil has a greater effect on the heart.

Dihydropyridines in stable angina would reduce myocardial oxygen demand by reducing after load.

You evaded the question.
I feel like medical school is just memorization.

Nifedipine is a DHP CCB. Academic sources confidently say that CCBs work on both the demand and supply sides of the equation. But when you probe further, you find conflicting information.

DHPs cause peripheral vasodilation, therefore reduce afterload, therefore reduce oxygen demand of the heart.
Non-DHPs cause both vasodilation and cardiodepression. Vasodilation component = reduced demand. Cardiodepression = reduced demand.

The question is whether either class causes coronary vasodilation (increased supply)?

package insert says no while guidelines says yes. Which is correct?

 

[sahell]

I just kept it simple. A lot of times that's what's needed to answer a question. I haven't seen a single question on this specifically nor has it come up in any of the review materials I used, but I would go with the guidelines because that's what I would have guessed.

 

[greenleaves]

Arossm it seems like it's memorization but you got to have a clear concept in order to memorize. To answer your question, Diltiazem is the one CCB whose action on coronary dilation is more potent than on the arterioles. Otherwise where in the literature does it say the primary mechanisms by which these drugs effect angina relief is by coronary vasodialation? The contribution of the vasodialation is so minimal to the other primary mechanisms, that it could be considered negligible and hence not an important factor.

 

[arcus]

Arossm it seems like it's memorization but you got to have a clear concept in order to memorize. To answer your question, Diltiazem is the one CCB whose action on coronary dilation is more potent than on the arterioles. Otherwise where in the literature does it say the primary mechanisms by which these drugs effect angina relief is by coronary vasodialation? The contribution of the vasodialation is so minimal to the other primary mechanisms, that it could be considered negligible and hence not an important factor.

OP is misquoting and misinterpreting the Pfizer Label. The Pfizer label does not state what OP claims.
Besides, OP is missing the big picture here.

Who is administering the Step 1 board Exam, Pfizer or NBME?
For Step 1 prep purposes UWorld is the definitive arbiter.

UW indicates:

dihydropyridines (Amlodipine, felodipine, nifedipine) location MOA is vascular/arterial smooth muscle and their physiological effect is peripheral vasodilation

Non-dihydropyridines (verapamil) MOA location is myocardium and their physiological effect is to reduce contractility (negative inotropic effect) and reduce HR (negative chronotropic effect).

Diltiazem (also a non-dihyropyridine) MOA location is both vascular smooth muscle and myocardium which means it has combined effects - peripheral vasodilation & reduced heart rate /myocardial contractility

UW >>>> textbooks/PI labels/guidelines/FA for Step 1 purposes