Pharmocotherapy of Ischaemic Heart Disease. Ischaemic Heart Disease. Causes of IHD aren´t totally clear No satisfactory causal treatment, we eliminate only symptoms and treat complications. IHD.
Pharmocotherapy of Ischaemic Heart Disease
Causes of IHD aren´t totally clear
No satisfactory causal treatment, we eliminate only symptoms and treat complications
Is condition/disease, at which requirements of myocardium exceed possibilities of its supply with oxydized blood. The cause of this imbalance is wide spectrum of patophysiologic mechanisms and reasons.
Acute – unstable angina pectoris
acute myocardial infarction
sudden heart death
Chronic – asymptomatic IHD
angina pectoris- after excercise
state after MI
chronic heart failure
Deffects of blood perfusion can develop slowly and progressively (chronic) or can develop abruptly (acute form; even MI).
Changes caused by ischaemia can be temporary or permanent (irreparable damage of myocard). Conditions are usually interconnected, without sharp limits and IHD needs to be understood dynamically and individually.
AP was the first time described in the second half of 18th century by Wiliam Heberden and treated with nitroglycerin in the year 1879.
Organ damage – embolia, vasculitis
Function impairment – spasms, defects in relaxation of arteriolas
Changes of lifestyle (nicotine, food) → lowering lipids
Psychosocial factors (excercise, taking care of oneself) → primary and secondary prevention
CAN BE INFLUENCED
Active monitoring and searching for persons having risk factors with the goal to prevent formation of atherosclerosis
!! Low doses of acetylsalicylic acid!!
Males – accorcing to clinical studies taking aspirin din´t decrease mortlity, decreased occurrence of MI, increased cerebral bleeding (US Physician´s Health Study)
females even more unclear – prospective study 1991 showed that occurrence of the first MI decreased, but overall or cardiovascular mortality didn´t decrease
HST – postmenopausal women
Women´s Health Initiative Study proved, that among women in the first year of using HST significantly increases risk of coronary event occurrence
Consistent pharmacologic intervention to influence all risk factors among persons with clinically manifested IHD, among persons after MI, with the goal to prevent or at least slower disease progression
Antiaggregatory therapy decreases among patients with AP risk of complications (MI, sudden heart death) by 23 %.
- stimulation of adenylatcyclase (prostacyclin)
- inhibition of receptor for ADP on thrombocyte membrane (thienopyridines – ticlopidine, clopidogrel)
- inhibition of receptor for fibrinogen on thrombocyte membrane – glykoprotein IIb/IIIa (fibans, abciximab)
Lower intensity and also frequency of episodes, but according to EBM doesn´t influence morbidity and mortality
- dihydropyridins (amlodipine, felodipine, lacidipine, nifedipine, isradipine)
- phenylalkylamins (verapamil, gallopamil)
- benzothiazepins (diltiazem)
Block influx of calcium to cell through slow L-type channels, lower its intracellular concentration what causes relaxation of smooth muscle in vessel wall, decrease of contractility, decrease of electrical irritability and conductivity
Direct dilation of coronary arteries and so increased oxygen supply
Decreased demand of myocardium to oxygen with systemic arterial dilation, with subsequent decrease of peripheral vascular resistance, decrease of
contractility and decrease of frequency
AV blocks II., III. degree
Lowers renal excretion of digoxin
Marker of increased cardiovaskular risk, no its reason
Preventive taking of niacin has no proven benefit
No pharmacologic proofs, that lowering of homocysteinaemia is connected with lower risk of CVD occurance
Is disorder of plasmatic protein metabolism, can have different manifestation. Disorder can have genetic or dietetic reason, or connected disease.
- fibrates – fenofibrate
- derivates of nicotinic acid – lower synthesis of VLDL in liver and so also formation of LDL
Inhibit enzyme HMGCoA reductase, and so decreases intracellular synthesis of new cholesterol a decreases concentration of LDL
Bind as ligand for PPAR α – receptor activated with peroxisome proliferator
Increase lipolysis of lipoprotein lipases