ATC Group: C01E Other cardiac preparations

Adenosine is a purine nucleoside which is present in all cells of the body. Animal pharmacology studies have in several species shown that adenosine has a negative dromotropic effect on the atrioventricular (AV) node.

Alprostadil is chemically identical to prostaglandin E₁, the actions of which include vasodilatation of blood vessels in the erectile tissues of the corpora cavernosa and increase in cavernosal artery blood flow, causing penile rigidity.

Ibuprofen is a propionic acid derivative NSAID that has demonstrated its efficacy by inhibition of prostaglandin synthesis. In humans ibuprofen reduces inflammatory pain, swellings and fever. Furthermore, ibuprofen reversibly inhibits platelet aggregation.

Indometacin has anti-inflammatory, antipyretic, and analgesic effects, it is an inhibitor of prostaglandin synthetase.

Ivabradine is a pure heart rate lowering agent, acting by selective and specific inhibition of the cardiac pacemaker I_f current that controls the spontaneous diastolic depolarisation in the sinus node and regulates heart rate. The cardiac effects are specific to the sinus node with no effect on intra-atrial, atrioventricular or intraventricular conduction times, nor on myocardial contractility or ventricular repolarisation.

Mavacamten is a selective, allosteric, and reversible cardiac myosin inhibitor. Mavacamten modulates the number of myosin heads that can enter power-generating states, thus reducing (or in HCM normalizing) the probability of force-producing systolic and residual diastolic cross-bridge formation. Mavacamten also shifts the overall myosin population towards an energy-sparing, but recruitable, super-relaxed state. In HCM patients, cardiac myosin inhibition with mavacamten normalises contractility, reduces dynamic LVOT obstruction, and improves cardiac filling pressures.

Meldonium is a structural analogue of a precursor of carnitine, gamma-butyrobetaine (GBB), which has one carbon atom replaced by nitrogen atom. Meldonium, by reversibly inhibiting the activity of gamma butyrobetainhydroxylase, causes a decrease of carnitine biosynthesis and thus prevents long-chain fatty acid transport through the cell membranes. Accordingly, it prevents the accumulation of strong detergents, activated forms of un-oxidised fatty acids, in cells thus diminishing damage of the cells membranes.

Ranolazine may have some antianginal effects by inhibition of the late sodium current in cardiac cells. This reduces intracellular sodium accumulation and consequently decreases intracellular calcium overload. Ranolazine, via its action to decrease the late sodium current, is considered to reduce these intracellular ionic imbalances during ischaemia. This reduction in cellular calcium overload is expected to improve myocardial relaxation and thereby decrease left ventricular diastolic stiffness.

Regadenoson is a low affinity agonist (Ki ≈ 1.3 μM) for the A_2A adenosine receptor, with at least 10-fold lower affinity for the A₁ adenosine receptor (Ki >16.5 μM), and very low, if any, affinity for the A_2B and A₃ adenosine receptors. Activation of the A_2A adenosine receptor produces coronary vasodilation and increases coronary blood flow (CBF).

In patients with ischaemic heart disease, trimetazidine acts as a metabolic agent, preserving the myocardial high-energy phosphate intracellular levels.