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I have got a ques ... where it said CCB is contraindicated in ACS ... as ccb causes vasodilation ... thus reflex tachycardia ... may worsen ischemia .... But we use GTN tho diff mechanism .. it also cause vasodilate thus can increase HR and ischemia .... GTN in initial drug in chest pain if suspect ACS ... why GTN is not contraindicated ..... as it may worsen ischemia too .... if someone know this , pls tell ......
 

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Who said CCBs CIed in ACS!

Calcium Channel Blockers are not contraindicated in the treatment of Angina. They are contraindicated in heart failure but not ACS.
 

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I'm not 100% sure, but I think that nifedipine (I suppose that by SSBs you mean dihydropyridines, not verapamil/diltizem) exerts its effect mainly on arteries (not the veins, as nitrates do). Thus, when there is already a compromise to a coronary branch due to ACS, adding an arterial dilator will evoke coronary steal phenomenon.
 

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CCBs and Agnina

The main drugs used in angina are Nitrates and Beta blockers. The pharmacodynamic idea behind both of them is to decrease myocardial oxygen demand.

Calcium channel blockers are also used in angina for the same effect, however the spectrum of CCB differ, on one end you have Nifedipine which affects mainly blood vessels and therefore its action is more similar to nitrates and on the other end you have verapamil which affects mainly the heart muscle and therefore its action is more similar to beta blockers as far as treatment of angina is concerned.

CCBs are not contraindicated in angina. But they are less effective than nitrates or beta blockers. However, should you have a patient with heart failure then they are contraindicated as they have negative inotropic effect.

Remember that Hydralazine and Minoxidil (they are not CCBs) are absolutely contraindicated in angina because of the severe reflex tachycardia expected. Also remember that Pindolol and Acebutolol (beta blockers) are also contraindicated in angina because they are partial agonists.
 

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The AC syndrome is ischemia of the heart muscle expressing itself
this ischemia is due to increased demands with less suuply so all drugs used play on this axis :
1) BB --> inhibit all cardiac properties --> saving of fuel --- > ttt the increaded demand
2)Nitrates ---> potent venodilator---> decrease the preload ---> decresed
demand + also it is coronary dilator-- > increased supply
3)ACEI : arteriodilator (without reflex tachycardia )---> decreased afterload --> decreased demand
4)CCB ---> act like BB by inhibition of all cardiac proprties and coronary dilator + ?
peripheral VD which differ according to subgroups e.g : short acting dihydropyridines e.g short acting nifedipine is potent peripheral VD-- > + of baroreceptors --> reflex Sypmathetic stimulation --> overcome the inhibition on heart--> reflex tachcardia ---> increased demand ---> preciptate and worsen ischemia
this can be avoided by use of additon of BB or using long actind nifedipine or other new generations in dihydropyridines or use other CCB groups:)
 

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2)Nitrates ---> potent venodilator---> decrease the preload ---> decresed
demand + also it is coronary dilator-- > increased supply
We have to mention, though, that the caronary dilatory effect of nitrates is exerted only on normal coronaries. If there is damage on the endothelium (like when there is a stable or unstable atheromatic plaque), this effect is rather negative, because the normal coronaries dilate and increase blood supply to their assigned myocardial area in the detriment of non-responding damaged coronaries.
 

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We have to mention, though, that the caronary dilatory effect of nitrates is exerted only on normal coronaries. If there is damage on the endothelium (like when there is a stable or unstable atheromatic plaque), this effect is rather negative, because the normal coronaries dilate and increase blood supply to their assigned myocardial area in the detriment of non-responding damaged coronaries.
coronary steal syndrome.........
 
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