When not to use strophanthin? Contraindications

Strophanthin is a cardiac glycoside, the use of which requires knowledge of specific contraindications. If you are interested in learning when its use may be inadvisable or associated with risks, below you will find a structured list of situations in which special caution should be exercised or therapy should be completely avoided. The information is based on current clinical data.

When should strophanthin not be used? – Absolute contraindications

Strophanthin should never be used in the following cases:

Hypersensitivity to ouabain

Allergic reactions can be rapid and dangerous. However, since ouabain is also an endogenous substance, such reactions are extremely rare and are essentially limited to the presence of autoimmune disorders.

Atrioventricular block of the second or third degree (without a pacemaker)

Strophanthin can exacerbate conduction disturbances in the heart. Atrioventricular block of the second or third degree without a pacemaker is a contraindication to its use due to its effects on the cardiac conduction system. As a cardiac glycoside, strophanthin can slow conduction through the atrioventricular node and prolong the refractory period. In the presence of an existing advanced block, administration of strophanthin may lead to a complete interruption of conduction between the atria and ventricles, potentially resulting in cardiac arrest. Without a pacemaker to take over rhythm control in such a scenario, the risk of severe complications, including sudden cardiac arrest, is too high.

Obstructive hypertrophic cardiomyopathy (HCM)

Increasing myocardial contractility is undesirable in this condition. Obstructive hypertrophic cardiomyopathy is characterized by excessive thickening of the heart muscle, particularly in the interventricular septum. This hypertrophy leads to narrowing of the left ventricular outflow tract, making blood flow more difficult. In this situation, further enhancement of myocardial contraction by drugs such as strophanthin is undesirable, as it may exacerbate the obstruction and worsen symptoms. A stronger contraction can cause the hypertrophied septum to move even closer to the anterior leaflet of the mitral valve, increasing the pressure gradient in the outflow tract and potentially leading to worsening hemodynamics and clinical symptoms.

Sick sinus syndrome (without a pacemaker)

Strophanthin may exacerbate bradycardia and cause additional complications. Sick sinus syndrome is characterized by dysfunction of the heart’s natural pacemaker, leading to bradycardia and other rhythm disturbances. As a cardiac glycoside, strophanthin has negative chronotropic properties, meaning it can further slow the heart rate. In patients with sick sinus syndrome who do not have a pacemaker, administration of strophanthin can significantly worsen existing bradycardia. This, in turn, may lead to serious complications such as syncope, dizziness, organ hypoxia, and, in extreme cases, even cardiac arrest. Therefore, the use of strophanthin in such patients without pacemaker support is contraindicated due to the high risk of clinical deterioration.

Relative contraindications to the use of strophanthin

In certain cases, the use of strophanthin may be considered, but it requires great caution and close monitoring. These include:

Atrial fibrillation with a rapid ventricular response

Atrial fibrillation with a rapid ventricular response is a relative contraindication to the use of strophanthin for several reasons. Firstly, strophanthin may initially increase conduction through the atrioventricular node, which can paradoxically accelerate the ventricular rate before its slowing effect takes hold. This can lead to a dangerous increase in heart rate shortly after administration. Secondly, atrial fibrillation is associated with an increased risk of life-threatening ventricular arrhythmias, and strophanthin may further elevate this risk due to its proarrhythmic properties.Additionally, patients with atrial fibrillation often have electrolyte imbalances that can potentiate the toxic effects of strophanthin. In this scenario, other methods of heart rate control, such as beta-blockers or calcium channel antagonists, are generally preferred due to their safer profile. If strophanthin is used in a patient with atrial fibrillation and rapid ventricular response, extremely cautious dosing and strict monitoring are necessary. Special attention should be given to heart rate, ECG changes, and electrolyte levels.Before initiating therapy with strophanthin, it is important to consider alternative rhythm control strategies and correct any existing electrolyte imbalances. In some cases, concurrent use of other antiarrhythmic drugs or electrical cardioversion may be required as alternative approaches. The decision to use strophanthin in this setting should always be made on an individual basis, taking into account the patient’s overall condition, comorbidities, and the risk-benefit balance.

Ventricular tachycardia (VT)

Ventricular tachycardia is a significant relative contraindication to the use of strophanthin for several key reasons. First and foremost, strophanthin can exacerbate existing cardiac rhythm disturbances, including ventricular tachycardia, due to its proarrhythmic properties. This drug increases the automaticity of myocardial cells, which, in the presence of ventricular tachycardia, can intensify the arrhythmia or trigger more dangerous forms, such as ventricular fibrillation.Moreover, strophanthin can enhance myocardial excitability, which is particularly hazardous in ventricular tachycardia as it may lead to rhythm destabilization. In such cases, the priority is to terminate the tachycardia and stabilize the heart rhythm using other methods, such as electrical cardioversion or antiarrhythmic medications with proven efficacy in treating ventricular arrhythmias.The use of strophanthin in patients with ventricular tachycardia may also mask symptoms of myocardial ischemia, which often underlies this arrhythmia, thereby complicating accurate diagnosis and treatment. Additionally, ventricular tachycardia frequently occurs in the context of severe cardiac conditions such as myocardial infarction or advanced heart failure, where strophanthin use poses an even greater risk.If an inotropic agent is necessary for a patient with ventricular tachycardia, alternative therapeutic options with a lower proarrhythmic potential should be considered. Should the use of strophanthin be deemed necessary, very close monitoring is required, including continuous ECG surveillance and readiness for immediate intervention in case of worsening arrhythmia.

Ventricular extrasystoles (VES)

Ventricular extrasystoles (ventricular premature beats) are a relative contraindication to the use of strophanthin for several important reasons. Firstly, as a cardiac glycoside, strophanthin can increase myocardial excitability, potentially exacerbating existing ventricular extrasystoles. This, in turn, may elevate the risk of developing more complex and dangerous ventricular arrhythmias, such as ventricular tachycardia or even ventricular fibrillation.Additionally, strophanthin can lower the excitability threshold of myocardial cells, which, in combination with existing extrasystoles, may create conditions favorable for the **R-on-T** phenomenon. This occurs when an extra beat coincides with the repolarization phase of the previous contraction, significantly increasing the risk of life-threatening arrhythmias.In patients with frequent or complex ventricular extrasystoles, the use of strophanthin requires special caution and strict monitoring. Regular ECG recordings and Holter monitoring are necessary to assess the drug's impact on the frequency and complexity of extrasystoles. It is also crucial to identify and treat potential underlying causes of extrasystoles before initiating strophanthin therapy, such as electrolyte imbalances, myocardial ischemia, or hyperthyroidism.In some cases, concurrent use of antiarrhythmic medications or alternative treatment options may be necessary. The decision to use strophanthin in patients with ventricular extrasystoles should always be made on an individual basis, considering the patient's overall condition, comorbidities, and the balance of potential benefits versus risks. If extrasystoles worsen after initiating therapy, dose reduction or drug discontinuation may be required.

Strophanthin has proarrhythmic potential. In some patients, instead of stabilizing the heart rhythm, it may worsen arrhythmias.

Electrolyte imbalances

• Hypokalemia (low potassium levels)
• Hypercalcemia (elevated calcium levels)
• Hypomagnesemia (magnesium deficiency)

Irregular electrolyte levels increase the toxicity of cardiac glycosides and the risk of arrhythmias.

Other medical conditions that constitute contraindications

Certain chronic diseases or acute conditions may compromise the safety of strophanthin therapy:

Hypothyroidism

It alters drug metabolism and affects its pharmacokinetics. Hypothyroidism influences the metabolism and pharmacokinetics of strophanthin for several reasons. Firstly, thyroid hormones play a key role in regulating systemic metabolism, including liver function, which is crucial for the metabolism of many drugs. In hypothyroidism, slowed hepatic metabolism can lead to a prolonged half-life of strophanthin in the body, increasing the risk of accumulation and toxicity.Secondly, hypothyroidism affects kidney function, which may alter drug excretion. Additionally, reduced metabolic activity in the body can influence tissue sensitivity to strophanthin, potentially enhancing its pharmacological effects. These changes in the pharmacokinetics and pharmacodynamics of strophanthin in patients with hypothyroidism require special caution when using the drug and may necessitate dose adjustments.

Acute phase of myocardial infarction

Increased risk of arrhythmias and hemodynamic instability. In the acute phase of myocardial infarction, the use of strophanthin is contraindicated due to the heightened risk of arrhythmias and hemodynamic instability. During this period, the heart is particularly susceptible to arrhythmogenic stimuli, and the damaged myocardium may respond unpredictably to inotropic drugs.By increasing myocardial contractility, strophanthin can excessively strain the infarcted area, potentially expanding the zone of myocardial damage. Additionally, it may exacerbate existing arrhythmias or induce new ones, which is especially dangerous in the context of a recent infarction. Hemodynamic instability caused by acute ischemia can be further aggravated by strophanthin, increasing the risk of cardiogenic shock or other severe complications.

Advanced renal failure

Accumulation of the drug and increased risk of toxic effects. Advanced renal failure is a significant relative contraindication to the use of strophanthin due to its impact on the drug’s pharmacokinetics. Under normal conditions, strophanthin is largely excreted by the kidneys. However, in cases of advanced renal failure, the body’s ability to eliminate the drug is significantly impaired. This leads to the accumulation of strophanthin in the body, increasing the risk of reaching toxic concentrations.Drug accumulation can enhance its adverse effects, including severe cardiac arrhythmias. Additionally, renal failure is often associated with electrolyte imbalances, which can further increase myocardial sensitivity to cardiac glycosides. As a result, the use of strophanthin in patients with advanced renal failure requires extreme caution, close monitoring of serum drug levels and kidney function, and frequent dose adjustments.In some cases, a significant dose reduction or complete avoidance of strophanthin may be necessary in patients with severe renal impairment. Alternatively, other medications with a lower risk of accumulation or those metabolized via different pathways may be considered. It is also important to recognize that patients with renal failure often have coexisting conditions that further complicate strophanthin use and increase the likelihood of adverse effects. Therefore, the decision to use this drug should always be made on an individual basis, following a thorough assessment of the potential benefits and risks for each patient.

Considerations for the clinical use of strophanthin

• Strophanthin acts faster than digoxin – the therapeutic effect appears approximately 10 minutes after intravenous administration.
• Studies have shown an improvement in exercise tolerance in patients with heart failure.
• Dosage should be tailored individually.

Regular monitoring should include:

• Electrolyte levels (K⁺, Mg²⁺, Ca²⁺)
• Kidney function (creatinine, GFR)
• ECG parameters.

How does strophanthin differ from digoxin?

• It is administered intravenously (but also orally), which allows for a faster achievement of the therapeutic effect.
• As an endogenous substance, it may be better tolerated by the body.
• It does not accumulate to the same extent as digoxin, which reduces the risk of adverse effects.
• It may have a more beneficial effect on cardiac performance in certain patient populations.

Summary – When to avoid strophanthin and what to be cautious about

Do not use strophanthin if:

• you have second- or third-degree heart block without a pacemaker,
• you suffer from obstructive hypertrophic cardiomyopathy,
• you have sick sinus syndrome,
• you are allergic to the active substance or any components of the preparation.

Use caution if:

• you have cardiac arrhythmias,
• you have electrolyte imbalances,
• you suffer from hypothyroidism or renal failure.

Strophanthin can be effective and helpful – but only when used wisely and in accordance with medical knowledge. If you have any doubts, consult your doctor.

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