[Pharmacological correction of heart rate in myocardial ischemia]

Cardiovascular diseases is one of the key causes of lethality in developed countries. Coronary heart disease and arterial hypertension make significant contribution to this lethality. The above two diseases are often accompanied with compensatory acceleration of the heart rate (HR). At the same time long-term tachycardia is an independent risk factor of complications resultant from high consumption of oxygen, disturbed energy metabolism in cardiomyocytes, regress of heart contractility, development of cardiac failure. Heart contraction rhythm depends on electric activity of the sinus node cells which spontaneously generate action potentials (4P) present in all heart compartments and triggering contractile activity of cardiomyocytes. The study of the pacemaker cells (pC) discovered not only mechanisms responsible for AP rise and HR physiological regulation but revealed new ionic channels -f-channels involved in acceleration and lowering of the heart rate. Reduction of current along the f-channels (If-current) lowers AP generation in PC and, therefore, HR. Three groups of medicines are now used for HR lowering: beta-adrenoblockers, non-dihydropyridine calcium antagonists and recently introduced into clinical practice innovative drug ivabradin (coraxan) selectively suppressing activity of f-channels of sinus node cells and thus lowering HR. The review analyses differences in mechanisms of a negative chronotropic effect of these drugs.