Phosphocreatine (creatine phosphate, PCr, PC) is the phosphorylated form of endogenous creatine that serves as a rapidly mobilizable reserve of high-energy phosphates in skeletal muscle and the brain of vertebrates. Phosphocreatine is a key component in the intracellular system of energy buffering and transports from the site of energy production to the site of energy utilization to ensure that supply meets the high and dynamic demands of the heart. Phosphocreatine can anaerobically donate a phosphate group to ADP to form ATP during the first two to seven seconds following an intense muscular or neuronal effort. Conversely, excess ATP can be used during a period of low effort to convert creatine to phosphocreatine. The reversible phosphorylation of creatine is catalyzed by several creatine kinases. Particularly, PCr makes the energy of phosphoryl bonds of adenosine triphosphate (ATP) available at the myofibrillar creatine kinase that allows myocardium contraction. Supplementation with PCr was, therefore, suggested as potentially beneficial in patients with acute and chronic myocardial ischaemic injury. Phosphocreatine has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. Phosphocreatine is used intravenously in hospitals in some parts of the world for cardiovascular problems under the name Neoton and also used by some professional athletes, as it is not a controlled substance.

Prenylamine, a slow Ca2+ channel blocker, was used to treat patients with angina pectoris, but because of the QT prolongation, this drug was withdrawn from the market. Prenylamine binds to calmodulin section and inhibits myosin light chain kinase.

Cafedrine, also known as norephedrinoethyltheophylline, is a chemical linkage of norephedrine and theophylline and is a cardiac stimulant used to increase blood pressure in people with hypotension. There are few data available for cafedrine. Cafedrine has a half-life of 60 min following both oral and intravenous administration Cafedrine is metabolized to norephedrine and several minor metabolites, but nearly 90% of the administered norephedrine is excreted via the kidneys, mostly unchanged, within 24 h. The effects of cafedrine on cardiac output are believed to be mediated via β- adrenoceptors. Cafedrine has a positive inotropic effect in humans, and this can be abolished by administration of the non-selective β-adrenoceptor antagonist propranolol. A combination of cafedrine and theodrenaline called Akrinor® is used for the treatment of hypotension in adults that occurs during emergency situations, general anesthesia, and regional anesthesia, especially during cesarean sections. Cafedrine/theodrenaline may have advantages over other vasopressor drugs. For example, it can be administered via bolus while catecholamines normally need to be diluted and administered via syringe pumps. Bolus injection is faster, which may be beneficial in emergency situations, plus it is more cost efficient with respect to the disposables. Cafedrine/theodrenaline has been widely used in Germany since 1963

Etafenone is an antiarrhythmic and coronary vasodilator drug. Etafenone exerts negative inotropic action on myocardium. It is able to block calcium channels. As a coronary vasodilator which produces a decrease in the heart rate and myocardial oxygen consumption, etafenone has been used in the therapy of ischemic heart disease.

Linsidomine (SIN-1, chemically 3-morpholinosydnonimin), is a vasodilator and antianginal drug. It is the direct hepatic metabolite of molsidomine. The dosage recommended by its manufacturer for its initial purpose, coronary angiography, is 0.4-1 mg. Contrary to molsidomine, which is widely used as an antianginal drug, linsidomine is used only for coronary angiography. The plasma half-life of Linsidomine is about 1 hour. Linsidomine is nonenzymatically metabolized to SIN-1A which spontaneously releases NO. NO, probably released directly from nonadrenergic, noncholinergic (NANC) nerves in the penis, is believed to cause smooth muscle relaxation by stimulating the soluble form of guanylate cyclase leading to an increase of intracellular cyclic guanosine 3',5' monophosphate (cGMP) with subsequent smooth muscle relaxation. Linsidomine also hyperpolarizes the cell membrane, making the smooth muscle less susceptible to adrenergic stimulation. NO further interacts with platelets when released intraluminally causing an increase in cGMP that decreases platelet aggregation and adhesion

Bunaftine is a class III antiarrhythmic agent which has been found effective in treating or preventing both ventricular and supraventricular arrhythmias. The acute electrophysiologic effects of intravenous Bunaphtine 1,5 mg/kg body weight, were studied in 19 subjects with estimated normal impulse formation and conduction. Significant effects were sinus bradycardia, prolongation of atrial refractory periods, depression of intranodal and infranodal conduction and prolongation of His-Purkinje system refractory periods. These properties are compared with those of amiodarone and quinidine and form the basis for correct use of Bunaphtine in the management of arrhythmias

Etilefrine is a cardiac stimulant used as an antihypotensive. Intravenous infusion of this compound increases cardiac output, stroke volume, venous return and blood pressure in man and experimental animals, suggesting stimulation of both α and β adrenergic receptors. However, in vitro studies indicate that etilefrine has a much higher affinity for β1 (cardiac) than for β2 adrenoreceptors. Intravenous etilefrine increases the pulse rate, cardiac output, stroke volume, central venous pressure and mean arterial pressure of healthy individuals. Marked falls in pulse rate, cardiac output, stroke volume and peripheral bloodflow, accompanied by rises in mean arterial pressure, occur when etilefrine is infused after administration of intravenous propranolol 2,5 mg. These findings indicate that etilefrine has both β1 and α1 adrenergic effects in man. The French Health Products Agency concluded that etilefrine and heptaminol have an unfavourable harm-benefit balance, and also placed restrictions on the use of midodrine.

Neo-Gilurythmal (or prajmaline), an antiarrhythmic agent, which is used to treat angina pectoris, Wolff–Parkinson–White Syndrome and coronary artery disease. Neo-Gilurythmal found to be effective even in the case where other previously used antiarrhythmics were ineffective.

Creatinolfosfate (or creatinol-O-phosphate, or COP) possesses anti-ischemic and anti-arrhythmic activities associated with improved ionic balance and heart performance. This compound exerts its cardioprotective effect by action on anaerobic glycolysis. The results of the toxicological studies showed that creatinolfosfate didn’t have side effects.

Efloxate is a coronary vasodilator developed in 1959 in Italy by Recordati and used for the treatment of angina pectoris. The drug is no longer marketed.