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
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
