@entity460 -channel modulators for XXXX .

@entity8 @entity455 @entity64 @entity101 @entity712 @entity301 @entity39 @entity1283 @entity460 @entity731 @entity65
It is generally accepted that @entity101 doubles the risk of @entity65 , of which @entity301 is the most common and lethal. @entity101 is a predisposing factor for the development of @entity64 , peripheral @entity455 , @entity712 and end-state @entity8 . @entity731 -causing @entity301 is related to the severity of @entity101 . Inhibition of @entity460 entry reduces the active tone of vascular smooth muscle and produces vasodilatation. This pharmacological action has been the basis for the use of @entity460 -channel blockers (CCBs) for the management of @entity101 . Other drug families may achieve this: diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin-receptor antagonists. @entity65 and @entity731 are major complications related to @entity101 . @entity1283 is considered as an independent risk factor associated with abnormalities of diastolic function and can result in @entity712 . @entity731 is associated with activation of innate immunity. @entity731 is expressing itself not only as @entity301 , but as a cerebrovascular and peripheral @entity455 . By impairing physiological vasomotor function, @entity731 includes ultimately @entity39 of myocardium. CCBs reduce blood pressure. Do they prevent the progress of the main complications of @entity101 ? This major question is the matter of the present paper.
