Sotagexal, tablets 80 mg 20 pcs

Beta1-, beta2-adrenoblocker. Sotalol is a non-selective blocker of β1-, β2-adrenoreceptors that has no sympathomimetic and membrane-stabilizing activity of its own. Like other beta-adrenoblockers, sotalol suppresses renin secretion, and this effect is pronounced both at rest and during exercise. The beta-adrenoblocking effect of the drug causes a decrease in heart rate (negative chronotropic effect) and a limited decrease in heart force (negative inotropic effect). These changes in cardiac function reduce myocardial oxygen demand and cardiac workload.

The antiarrhythmic properties of sotalol are associated with both blockade of β-adrenoreceptors and prolongation of myocardial action potential. The main effect of sotalol is to increase the duration of effective refractory periods in atrial, ventricular and accessory pulse conduction pathways.

Pharmacokinetics

Intake

The bioavailability when taken orally is almost complete (more than 90%). Cmax in plasma is reached 2.5-4 hours after oral administration. Absorption is reduced by approximately 20% with food compared to fasting. In the dose range from 40 to 640 mg/day the plasma concentration of Sotalol is proportional to the dose taken.

Distribution

Distribution occurs in plasma and in peripheral organs and tissues. It occurs within 2 to 3 days. Sotalol does not bind to plasma proteins.

It penetrates poorly through the GEB, and its concentration in cerebrospinal fluid is only 10% of that in blood plasma.

Metabolism

It is not metabolized. The pharmacokinetics of the d- and l-enantiomers of sotalol are virtually identical.

Elevation

The primary route of excretion is through the kidneys. From 80 to 90% of the administered dose is excreted unchanged in the urine, and the rest in the feces. T1/2 is 10-20 h.

Pharmacokinetics in special clinical cases

Patients with impaired renal function should be prescribed lower doses of the drug.

The pharmacokinetics do not change much with age, although impaired renal function in elderly patients reduces the excretion rate, which leads to increased accumulation of the drug in the body.

Indications

Symptomatic and chronic heart rhythm disturbances:

ventricular tachycardia, incl. supraventricular tachycardia in Wolff-Parkinson-White syndrome;
ventricular extrasystole;
paroxysmal form of atrial fibrillation.

Pharmacological effect

Beta1-, beta2-adrenergic blocker. Sotalol is a non-selective blocker of β1-, β2-adrenergic receptors that does not have its own sympathomimetic and membrane-stabilizing activity. Like other beta blockers, sotalol suppresses renin secretion, and this effect is pronounced both at rest and during exercise. The beta-adrenergic blocking effect of the drug causes a decrease in heart rate (negative chronotropic effect) and a limited decrease in the force of heart contractions (negative inotropic effect). These changes in cardiac function reduce myocardial oxygen demand and the amount of workload on the heart.

The antiarrhythmic properties of sotalol are associated both with the blockade of β-adrenergic receptors and with the prolongation of the myocardial action potential. The main effect of sotalol is to increase the duration of effective refractory periods in the atrial, ventricular and accessory impulse pathways.

Pharmacokinetics

Suction

Bioavailability when taken orally is almost complete (more than 90%). Cmax in blood plasma is achieved 2.5-4 hours after oral administration. Absorption of the drug is reduced by approximately 20% when taken with food compared to when taken on an empty stomach. In the dose range from 40 to 640 mg/day, the concentration of sotalol in the blood plasma is proportional to the dose taken.

Distribution

Distribution occurs in the plasma, as well as in peripheral organs and tissues. Css is achieved within 2-3 days. Sotalol does not bind to plasma proteins.

It penetrates the BBB poorly, and its concentration in the cerebrospinal fluid is only 10% of the concentration in the blood plasma.

Metabolism

Not metabolized. The pharmacokinetics of the d- and l-enantiomers of sotalol are almost the same.

Removal

The main route of elimination from the body is excretion through the kidneys. From 80 to 90% of the administered dose is excreted unchanged in the urine, and the rest in the feces. T1/2 is 10-20 hours.

Pharmacokinetics in special clinical situations

Patients with impaired renal function should be prescribed lower doses of the drug.

With age, pharmacokinetics change slightly, although impaired renal function in elderly patients reduces the rate of excretion, which leads to increased accumulation of the drug in the body.

Special instructions

Caution should be exercised when prescribing Sotahexal to patients:
– with a history of diabetes mellitus with pronounced fluctuations in blood glucose levels, as well as following strict diets;
— for pheochromocytoma (simultaneous administration of alpha-blockers is necessary);
– if you have a history or family history of psoriasis;
— in case of impaired renal function;
– elderly.
Treatment with the drug is carried out under the control of heart rate, blood pressure, and ECG. If there is a pronounced decrease in blood pressure or a decrease in heart rate, the daily dose should be reduced.
Patients with impaired renal function require dosage adjustment.
Cancellation of Sotahexal should be done under the supervision of the attending physician and gradually (especially after long-term use).
Sotahexal should not be used in patients with hypokalemia or hypomagnesemia until the existing disorders are corrected. These conditions may increase the degree of QT prolongation and increase the likelihood of torsade de pointes (TdP). Monitoring of electrolyte balance and acid-base status is necessary in patients with severe or prolonged diarrhea and in patients receiving medications that cause a decrease in magnesium and/or potassium levels in the body.
In thyrotoxicosis, sotalol may mask certain clinical signs of thyrotoxicosis (eg, tachycardia). Abrupt withdrawal in patients with thyretoxicosis is contraindicated because it can increase the symptoms of the disease.
When prescribing beta-blockers to patients receiving hypoglycemic agents, caution should be exercised, since during long breaks in food intake, hypoglycemia may develop, and its symptoms, such as tachycardia or tremor, may be masked by the action of the drug.

Active ingredient

Sotalol

Composition

Active ingredient: sotalol hydrochloride 80 mg;

Excipients: corn starch; lactose; hydroxypropylcellulose; sodium starch glycolate; silicon dioxide; magnesium stearate

Contraindications

chronic heart failure stage IIB-III;
cardiogenic shock;
AV block II or III degree;
sinoatrial block;
sick sinus syndrome;
severe bradycardia (heart rate less than 50 beats/min);
congenital or acquired long QT syndrome;
arterial hypotension (systolic blood pressure less than 90 mm Hg);
obliterating vascular diseases;
bronchial asthma or COPD;
metabolic acidosis;
pheochromocytoma without simultaneous administration of alpha-blockers;
acute myocardial infarction;
renal failure (creatinine clearance less than 10 ml/min);
general anesthesia that causes suppression of myocardial function (for example, cyclopropane or trichlorethylene);
tachycardia of the “pirouette” type;
severe allergic rhinitis;
simultaneous use of MAO inhibitors;
lactation period;
age under 18 years (efficacy and safety have not been established);
hypersensitivity to sotalol, sulfonamides and other components of the drug.

Caution should be exercised when prescribing Sotahexal to patients who have recently suffered a myocardial infarction, with diabetes mellitus, psoriasis, impaired renal function, AV blockade of the first degree, with water-electrolyte imbalance (hypomagnesemia, hypokalemia), thyrotoxicosis, depression (including a history of depression), with prolongation of the QT interval, in elderly patients.

Use with extreme caution when there is a history of allergic reactions, as well as against the background of desensitizing therapy, because sotalol suppresses sensitivity to allergens.

Side Effects

From the nervous system and sensory organs: dizziness, headache, feeling of fatigue, sleep disturbance, confusion, paresthesia, depression. Inflammation of the cornea and conjunctiva (should be taken into account when wearing contact lenses), blurred vision (extremely rare), decreased tear production.

From the cardiovascular system and blood (hematopoiesis, hemostasis): heart failure, bradycardia, AV block, angina pectoris (in rare cases), hypotension.

From the respiratory system: bronchospasm.

From the gastrointestinal tract: nausea, diarrhea, constipation, dry mouth.

Metabolism: hypoglycemia (more often in patients with diabetes mellitus or with strict adherence to a diet).

From the genitourinary system: decreased potency.

From the musculoskeletal system: a feeling of coldness in the extremities, muscle weakness or cramps.

From the skin: skin rash, itching (rare); redness, psoriasiform dermatosis, alopecia.

Interaction

When taking slow calcium channel blockers such as verapamil and diltiazem simultaneously, a decrease in blood pressure may occur as a result of worsening contractility. IV administration of these drugs should be avoided while using sotalol (except in emergency situations).
The combined use of class I A antiarrhythmic drugs (especially quinidine type: disopyramide, quinidine, procainamide) or class III (for example, amiodarone) can cause a pronounced prolongation of the QT interval. Drugs that prolong the QT interval should be used with caution with drugs that prolong the QT interval, such as class I antiarrhythmics, phenothiazines, tricyclic antidepressants, terfenadine and astemizole, and some quinolone antibiotics.
When taking nifedipine and other 1,4-dihydropyridine derivatives simultaneously, a decrease in blood pressure is possible.
The simultaneous administration of norepinephrine or MAO inhibitors, as well as abrupt withdrawal of clonidine, can cause arterial hypertension. In this case, withdrawal of clonidine should be carried out gradually and only a few days after stopping Sotahexal.
Tricyclic antidepressants, barbiturates, phenothiazines, opioids and antihypertensives, diuretics and vasodilators can cause a sharp decrease in blood pressure.
The use of inhalation anesthesia, incl. tubocurarine while taking Sotahexal increases the risk of depression of myocardial function and the development of arterial hypotension.
With simultaneous use of Sotahexal with reserpine, clonidine, alpha-methyldopa, guanfacine and cardiac glycosides, severe bradycardia and a slowdown in the conduction of excitation in the heart may develop.
Beta blockers may potentiate withdrawal hypertension following discontinuation of clonidine, so beta blockers should be discontinued gradually, several days before tapering clonidine.
Prescribing insulin or other oral hypoglycemic agents, especially during physical activity, can lead to increased hypoglycemia and the manifestation of its symptoms (increased sweating, rapid pulse, tremor). In case of diabetes mellitus, dose adjustment of insulin and/or hypoglycemic drugs is necessary.
Potassium-sparing diuretics (eg, furosemide, hydrochlorothiazide) may cause arrhythmias caused by hypokalemia.
When used concomitantly with Sotahexal, the use of higher doses of beta-agonists such as salbutamol, terbutaline and isoprenaline may be required.

Overdose

Symptoms: decreased blood pressure, bradycardia, bronchospasm, hypoglycemia, loss of consciousness, generalized seizures, ventricular tachycardia; in severe cases – symptoms of cardiogenic shock, asystole.
Treatment: gastric lavage, hemodialysis, administration of activated carbon. Symptomatic therapy: atropine – 1-2 times intravenously; glucagon – first in the form of a short IV infusion at a dose of 0.2 mg/kg body weight, then at a dose of 0.5 mg/kg body weight IV infusion over 12 hours.

Storage conditions

In a place protected from light, at a temperature not exceeding 25 °C.

Shelf life

Shelf life: 5 years.

Manufacturer

Salutas Pharma GmbH, Germany