Drug-induced cardiomyopathy

Introduction to drug-induced cardiomyopathy Drug-induced cardiomyopathy refers to a patient who is treated with certain drugs. Due to the toxic effects of the drug on the myocardium, myocardial damage is caused by myocardial damage and/or cardiac enlargement. Broadly speaking, any heart disease caused by direct or indirect myocardial toxicity, whether due to the influence of drugs on myocardial electrophysiology, abnormalities of myocardial depolarization and repolarization or various arrhythmias, or contraction of the myocardium Cardiac inflammation caused by the toxic effects of drugs, which is induced or aggravated, or caused by allergies to certain drugs, can be called drug-induced cardiomyopathy. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: arrhythmia heart failure infective endocarditis

Cause of drug-induced cardiomyopathy

Use of anti-tumor drugs (30%):

Drug-induced heart disease is commonly used in the use of anti-tumor drugs, some psychotropic drugs (such as antidepressants), drugs for the treatment of cardiovascular diseases and anti-parasitic drugs, most of the severe cases of drug-induced heart disease clinically manifested as expansion The characteristics of cardiomyopathy can eventually lead to fatal heart failure, such as doxorubicin cardiomyopathy. A few patients have clinical features similar to restrictive cardiomyopathy; some drugs such as catecholamines can cause thickening of ventricular muscles. It is like hypertrophic cardiomyopathy. In addition, certain poisons such as cocaine may cause cardiomyopathy due to its direct myocardial toxicity.

Direct toxicity (10%):

The drug has a direct toxic effect on the myocardium, leading to inflammation, degeneration, necrosis and interstitial edema of the cardiomyocytes. It can be fibrotic at a certain stage, and its toxic effect is often closely related to the dose of the drug and the length of the drug. Anti-tumor drugs such as doxorubicin, daunorubicin, cyclophosphamide (CTX), fluorouracil (5-Fu); antiparasitic drugs such as imidin, chloroquine, expectorant, etc.; some cardiovascular Drugs, such as verapamil, quinidine, procainamide and sympathomimetic; some Chinese medicines, such as tripterygium, etc., with doxorubicin cardiomyopathy as an example, the direct myocardial damage can be specific Histopathological ultrastructural changes were confirmed, which showed myofibril loss and cytoplasmic vacuolization, and severe cell necrosis.

Metabolic abnormalities (10%):

Some drugs can inhibit oxidative phosphorylation of cardiomyocytes, leading to mitochondrial damage, such as certain antiparasitic drugs (Imidin, etc.), a recent study by Jeyseelan (1997), the antitumor drug doxorubicin and soft red Mycomycin can rapidly sensitize and inactivate myocardial cell membrane ribonucleic acid (RNA), block the formation of ATP, block the expression of myocardial specific genes, and inhibit myofibrillar proteins and proteins that supply cardiomyocytes (such as ADP/). Transcription of the nuclear gene code of ATP-converting enzyme, phosphofructokinase isoenzyme), degeneration and necrosis of cardiac myofibrils due to intracellular ATP storage depletion and loss of energy.

Electrolyte disturbance (10%):

If long-term use of diuretic drugs can cause severe hypokalemia and hypomagnesemia, long-term application of aminoglycoside antibiotics can also cause hypokalemia crisis leading to myocardial lesions.

Inhibition of myocardial contractility leads to decreased myocardial contractility and increased ventricular stress, mainly in antidepressants, especially tricyclic antidepressants, and secondly, certain antiarrhythmic drugs, especially beta blockers and Calcium ion antagonists also have significant inhibitory effects on the myocardium.

Effects on myocardial electrophysiological properties (10%):

The electrophysiology of the myocardium is interfered by the action of the drug, which may be manifested as changes in myocardial depolarization and repolarization, or increased myocardial stress, such as doxorubicin, tricyclic antidepressants, digitalis overdose, and certain antiarrhythmias. Drugs, which can prolong myocardial action potential (including non-cardiovascular drugs such as tricyclic antidepressants) may have potential arrhythmogenic effects, especially when the drug is improperly combined with hypokalemia, low magnesium blood When the disease.

Drug interactions (10%):

When considering the toxic effects of drugs on the heart, the combination of multiple drugs should lead to sufficient attention. The combination of two (or more) drugs can be combined by cardiotoxicity, or one drug can affect another. The metabolism and excretion of a drug, or increase its bioavailability, thereby increasing the toxicity of the drug to the heart. For example, when the combination of digitalis and quinidine is used, the latter can increase the blood concentration of digitalis by one time, such as carelessness. It is easy to cause digitalis poisoning.

Drug-induced cardiomyopathy prevention

1. For patients with allergic constitution, especially those who are allergic to drugs in the past, should choose medication carefully.

2. In the case of suspected disease, the immediate cessation of sensitizing drugs is the key to treatment, otherwise it can cause irreversible consequences in a short period of time.

Drug-induced cardiomyopathy Complications, arrhythmia, heart failure, infective endocarditis, sudden death

Common complications of drug-induced cardiomyopathy include arrhythmia, heart failure, embolism, infective endocarditis, and sudden death.

Symptoms of drug-induced cardiomyopathy Common symptoms First hypertensive myocardial hibernation phenomenon edema hypotension calcium ion influx block ventricular fibrillation death shock

Antineoplastic agent

(1) Daunorubicin: This drug can increase the production of oxygen free radicals, interfere with mitochondrial energy metabolism, and promote the direct damage of myocardial cells caused by calcium ion overload in cardiomyocytes, which can reduce myocardial contractility and even cause heart failure. If combined with other anti-tumor drugs, it can increase toxicity. Therefore, it is generally considered that the dosage should be <550mg/m2. Daunorubicin can cause various arrhythmias, including ventricular and supraventricular arrhythmia, and even Sudden ventricular fibrillation, it must be pointed out that the drug's effect on myocardial damage can sometimes last for several years or even more than 10 years, should be noted.

(2) Doxorubicin: This drug can increase the mitochondrial acetylation of cardiomyocyte cytochrome C and increase oxygen consumption; doxorubicin can also cause intracellular calcium overload, causing direct damage to the myocardium; The consumption of triphosphate adenosine increases, the myocardial energy is depleted, causing cardiac insufficiency. The cardiac manifestation of this drug can be expressed as: a variety of arrhythmias appear in intravenous drip or intravenous drip, and can also appear like dilated cardiomyopathy. Clinical manifestations.

(3) cyclophosphamide: can cause coronary artery endothelial damage and myocardial cell damage, interstitial can produce edema, the drug damage to the myocardium occurs more than 2 weeks after administration, most of them are reversible changes, a few can cause secondary cardiac disease.

(4) Paclitaxel: can cause bradycardia and weakened myocardial contractility, but most of them have no obvious clinical symptoms and are mostly transient.

2. Antipsychotic and antidepressants

(1) antipsychotic drugs: can cause hypotension, individual sensitive people can cause persistent hypotension or even shock, phenothiazine drugs have a special inhibitory effect on the central nervous system, and also have alpha receptor blockade In addition, there are reports of sudden death in chlorpromazine treatment, which may be caused by lowering the concentration of catecholamine in the myocardium, causing the decrease of myocardial contractility and causing ventricular fibrillation. It may also be related to irreversible shock, excessive central nervous system depression, and electrocardiogram may have T wave is low, U wave appears, QT interval is extended and ST segment is depressed, and various arrhythmias, including ventricular premature contraction, atrioventricular block and QT interval prolonged polymorphic ventricular tachycardia ( Torsional ventricular tachycardia).

(2) Tricyclic antidepressants: Cardiovascular adverse reactions include inhibition of myocardium, orthostatic hypotension, sinus tachycardia, atrioventricular block, etc., because this class of drugs can inhibit cytochrome P450 When combined with other drugs, it may affect the metabolism of other drugs or aggravate the cardiovascular response.

3. Antiarrhythmic drugs Various antiarrhythmic drugs have different degrees of negative inotropic effects, especially for patients with existing heart disease. In addition, antiarrhythmic drugs may cause arrhythmia, improper application or even Can induce fatal arrhythmia.

4. -blockers can inhibit the cardiac -receptor, as confirmed by MDC, CIBIS) on the basis of conventional heart failure treatment, appropriate and rational use of -blockers such as bisoprolol, carvedil Lol, metoprolol, etc. can not only reduce the hospitalization rate, but also reduce the mortality rate.

5. Calcium ion antagonists These drugs have a certain negative inotropic effect on the myocardium by inhibiting the influx of calcium ions, so it may aggravate cardiac insufficiency, especially non-dihydropyridines such as verapamil, and dihydropyridines. In particular, short-acting dihydropyridines such as nifedipine can increase heart rate, and reflex causes sympathetic excitation. On the contrary, verapamil can cause bradycardia and increase the blood concentration of digitalis.

6. Other non-steroidal anti-inflammatory analgesics can inhibit the synthesis of prostaglandins by inhibiting cyclooxygenase, causing water and sodium retention, especially for patients with heart disease. In addition, anesthetics such as halothane It has a certain inhibitory effect on the myocardium.

Mainly based on the use of certain drugs such as the above anti-tumor drugs, anti-psychotic or anti-depressant drugs without evidence of heart disease, arrhythmia after the drug, heart enlargement, signs of cardiac insufficiency, can not be diagnosed with other heart disease interpreters The disease.

Examination of drug-induced cardiomyopathy

1. Hematological examination The increase of serum enzymes contributes to the diagnosis of myocardial infarction caused by drugs and myocarditis.

2. Blood immunological examination, if positive change, has diagnostic significance for drug allergy.

3. Determination of blood concentration can help diagnose certain drug overdose or poisoning.

5. Electrocardiogram examination may indicate myocardial damage or drug-induced arrhythmia in drug-induced heart disease.

6 echocardiography is helpful for drug-induced pericardial disease, cardiomyopathy and cardiac function judgment.

7. Radionuclide cardiac imaging is helpful for drug-induced myocardial changes and cardiac function judgment.

8 cardiac catheterization, endomyocardial biopsy has a certain value for the diagnosis of drug-induced cardiomyopathy, myocarditis.

Diagnosis and identification of drug-induced cardiomyopathy

It is necessary to rule out the illusion that other factors than drugs may cause, such as the possibility of excluding the disease caused by the patient's original disease, especially the heart disease itself, but also to understand the type, method, dosage, etc. of the drug, and try to Find the pathogenic drugs in the drug. The drug-induced cardiovascular disease may be accompanied by the damage of other system organs. Pay attention to the relevant aspects and provide clues for differential diagnosis.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.