Tachycardiomyopathy

Introduction to tachycardia cardiomyopathy Long-term chronic tachycardia or sustained rapid cardiac pacing can cause cardiac expansion and cardiac insufficiency and other similar dilated cardiomyopathy. As long as tachycardia is controlled, cardiac morphology and cardiac function can partially or completely return to normal. This cardiomyopathy caused by tachycardia is called tachycardiomyopathy (TCM). basic knowledge Sickness ratio: 0.05% Susceptible people: no special people Mode of infection: non-infectious Complications: Cardiogenic shock Infective endocarditis Arrhythmias Chronic cardiac insufficiency

Causes of tachycardia cardiomyopathy

The disease can be induced by a variety of persistent or recurrent tachyarrhythmias, such as atrial tachycardia, borderline tachycardia, ventricular tachycardia, atrial fibrillation and atrial flutter. Not sure.

Atrial fibrillation (40%):

Atrial fibrillation (AF) is the most common persistent arrhythmia. With the increasing incidence of atrial fibrillation, the number of people over the age of 75 can reach 10%. The frequency of atrial excitement during atrial fibrillation is 300-600 beats/min. The heartbeat frequency is often fast and irregular. Sometimes it can reach 100-160 beats/min. It is not only much faster than normal people's heartbeat, but also is not neat, the atrium is lost. Effective shrinkage function.

Ventricular tachycardia (35%):

Ventricular tachycardia (VT) is a rapid arrhythmia of bundle branches, myocardial conduction fibers, and ventricular muscles that occur below the His bundle bifurcation. Wellens defines it as: frequency over 100 beats/min, 3 consecutive Or more than 3 spontaneous ventricular depolarization activities, including monomorphic non-sustained and persistent ventricular tachycardia and polymorphic ventricular tachycardia, if induced by cardiac electrical stimulation in cardiac electrophysiological examination For ventricular tachycardia, it must be 6 or more rapid ventricular beats (frequency > 100 beats / min). Ventricular tachycardia can originate in the left ventricle and right ventricle. The frequency of persistent episodes often exceeds 100 beats/min, and the hemodynamic state may worsen. It may become atrial flutter and ventricular fibrillation, leading to cardiac origin. Sudden death requires active treatment.

Pathogenesis

Pathogenesis

Its pathogenesis is not well understood and may be related to the following factors:

(1) myocardial high-energy phosphate depletion: myocardial creatinine, phosphate creatinine and adenosine triphosphate reserve depletion.

(2) sympathetic and renin-angiotensin-aldosterone system activation, renin, angiotensin II, aldosterone, norepinephrine, adrenaline and vasopressin increased, can induce cardiac hypertrophy, before and after the heart The load increases, affecting the heart's cardiac output.

(3) The decrease in -receptor sensitivity of cardiomyocytes and the down-regulation of -receptor density.

(4) Abnormal calcium ion transport in sarcoplasmic reticulum of cardiomyocytes, decreased activity of Ca2+-ATPase and sarcoplasmic reticulum Ca2+-ATP transferase, and decreased content and stability of Ryanodin receptor in sarcoplasmic reticulum.

(5) Myocardial ischemia and changes in blood flow distribution in the myocardium.

Tachycardia is associated with low activity of Na+-K+-ATPase. It is also suggested that the development of tachycardia is associated with increased apoptosis of cells, and that P53 and its related genes are involved in cell death. Regulation of death.

Experimental studies have shown that after atrial or ventricular rapid pacing for 24h, hemodynamic changes (blood pressure and cardiac output decreased); continued pacing, ventricular filling pressure and pulmonary artery pressure can be increased, and reached at 1 week The typical peak platform, while cardiac output, ejection fraction and ventricular volume continue to deteriorate, develops into end-stage heart failure after 3 to 5 weeks, producing hemodynamics and neurohormonal changes similar to human cardiac insufficiency, but The lesion was basically reversible. Within 48 hours after termination of rapid pacing, the right atrial pressure, mean arterial pressure and cardiac index were significantly improved. The left ventricular ejection fraction improved most within 24 hours, after 1 to 2 weeks. Basically normal, completely normal after 4 weeks, all hemodynamic indicators can be restored within 4 weeks, but the end-systolic and end-diastolic volume does not return to normal until 12 weeks. This cardiac dysfunction is characterized by left ventricular systole Ventricular wall tension and cardiac filling pressure increased significantly, left and right ventricular systolic function and cardiac output decreased severely, accompanied by a significant increase in plasma atrial natriuretic peptide and catecholamines and renin-vessels Activation of the angiotensin-aldosterone system, however, is the improvement in cardiac function as a result of rapid arrhythmia control or an improvement in heart disease itself.

Some scholars have conducted a series of studies on patients with chronic atrial fibrillation with rapid ventricular rate before and after cardioversion, including atrial, ventricular systolic function and metabolic exercise tests. The results show that early atrial function recovery (1 day to 1 week) Left ventricular ejection fraction and peak oxygen consumption were not associated with late (1 month), suggesting that improvement in late cardiac function may be associated with reversal of cardiomyopathy caused by rapid atrial fibrillation and not related to atrial function recovery. In addition, heart rate Accelerating indirect data leading to cardiac insufficiency is derived from a clinical trial of beta-blockers in the treatment of chronic heart failure, in which beta-blockers significantly slow down heart rate while hemodynamics and Symptoms of heart failure have also improved.

2. Pathology

There is no change in heart weight. At the cellular level, myocardial cells and extracellular matrix remodeling are observed. The extracellular matrix structure and myocardial cell basement membrane-muscle fiber membrane interface are separated. Extracellular matrix disorder can damage myocardial cell alignment and pressure coupling. With transmission and opening of capillaries, cardiomyocytes can disappear, elongate, muscle fiber disorders and sarcomere disappear.

Tachycardia cardiomyopathy prevention

1. Prevention of incentives

Once diagnosed, patients are often highly nervous, anxious, depressed, seriously concerned, frequently seek medical treatment, and urgently require medication to control arrhythmia. The complete neglect of the cause and the prevention of the cause, often caused the shackles to take the lead, and put the cart before the horse. Common causes: smoking, alcoholism, overwork, nervousness, agitation, overeating, indigestion, colds and fever, excessive intake of salt, low blood potassium, low blood magnesium. The patient can combine the actual situation of the previous disease, sum up the experience, avoid the incentive, and is simpler, safer and more effective than simply taking the drug.

2. Stabilizing emotions

Maintain a calm and stable mood, relax and not be overly nervous. Especially stressful emotions in mental factors are easy to induce arrhythmia. Therefore, patients should be treated with a peaceful attitude, avoiding overjoy, sorrow, and anger, regardless of minor matters. If you are in trouble, you can comfort yourself, not watching nervous TV, ball games, etc.

Complications of tachycardia cardiomyopathy Complications cardiogenic shock infective endocarditis arrhythmia chronic cardiac insufficiency

Complications such as cardiac insufficiency and cardiogenic shock can be found. The disease usually has symptoms caused by ventricular tachycardia, such as palpitations, chest tightness, syncope, etc., severe cases can lead to cardiac insufficiency, cardiogenic shock or death. Some patients also had no significant hemodynamic changes. Arrhythmia, heart failure, embolism, infective endocarditis and sudden death. Embolism occurs in patients with myocardial fibrosis and decreased contractility, with atrial fibrillation, prolonged or diuretic.

Symptoms of tachycardia cardiomyopathy Common symptoms Chest tightness arrhythmia tachycardia palpitations Heart failure to the first high blood pressure heart expansion heartbeat very disordered shock shock

TCM can occur in a variety of tachyarrhythmias, including supraventricular tachycardia such as atrial tachycardia, atrial flutter, atrial fibrillation, atrioventricular node and atrioventricular reentry tachycardia, which can occur in The age and frequency of tachycardia attacks affect the occurrence of this disease at any age, as well as normal and abnormal hearts.

The disease usually has symptoms caused by ventricular tachycardia, such as palpitations, chest tightness, syncope, etc., severe cases can lead to cardiac insufficiency, cardiogenic shock or death, and some patients have no obvious hemodynamic changes.

The clinical manifestations of TCM are very broad. The original normal heart is well tolerated by chronic tachycardia and can be asymptomatic. However, the original organic heart disease is prone to symptoms, early treatment, and persistent rapid heart rate. The time of occurrence of the disease may vary from a few weeks to 20 years after the discovery of tachycardia. The time and extent of cardiac function recovery after arrhythmia control or termination may be complete, partial or unrecoverable. Because the degree of myocardial damage is related to the time of tachycardia and the condition of the underlying heart disease, clinical studies have found that left ventricular function is greatly improved 1 month after the termination of tachycardia, but the recovery process is slower. The maximum recovery after 6-8 months, the difference in high energy phosphate depletion time may be the reason for the inconsistent recovery time of left ventricular function; the development process and treatment of primary disease will also affect the recovery of cardiac function.

Examination of tachycardia cardiomyopathy

Electrocardiogram

Have the corresponding tachycardia performance, left ventricular hypertrophy and ST-T abnormalities.

2. Echocardiography

Similar to the performance of dilated cardiomyopathy, such as heart enlargement, decreased heart function.

3. Inspection related to differential diagnosis

For example, thyroid function is excluded to exclude hyperthyroidism. For patients with risk factors for coronary heart disease, coronary angiography is required to exclude coronary heart disease. Ventricular angiography showed a narrowing of the ventricular cavity in hypertrophic cardiomyopathy, and hypertrophic myocardium protruded into the ventricular cavity. In the examination of dilated cardiomyopathy, the X-ray shows a slight enlargement of the heart, and some of the endocardial calcification shadows are visible.

Diagnosis and diagnosis of tachycardia cardiomyopathy

diagnosis

1. Diagnosis basis

There are no specific diagnostic indicators, medical history and clinical features are still the only way to diagnose this disease. Chronic tachycardia attacks more than 10% to 15% of the total time, and may also lead to TCM. Typical cases are seen in recurrent rooms. Sexual tachycardia, atrial flutter or ventricular tachycardia, patients with organic heart disease or heart failure should also be suspected of having chronic atrial fibrillation or recurrent supraventricular or ventricular tachycardia Participation, should not be considered that arrhythmia is only secondary to heart disease, in fact there is a vicious circle between cardiac insufficiency and arrhythmia.

Diagnosis of tachycardia cardiomyopathy:

Left ventricular function is normal before 1 ventricular tachycardia occurs;

2 progressive damage to left ventricular function after frequent or persistent ventricular tachycardia, and other factors leading to cardiac dysfunction may be excluded;

Left ventricular function improved after 3 ventricular tachycardia was cured or controlled. However, left ventricular function was not improved after partial ventricular tachycardia was controlled. The possibility of tachycardia cardiomyopathy could not be ruled out because tachycardia was induced. Myocardial damage may also progress to an irreversible stage.

2. Clinical classification

Given that TCM can occur in both normal and diseased hearts, Fenelon et al. recommend splitting them into two types:

1 simple tachycardiomyopathy (pure tachycardiomyopathy): in addition to tachycardia, the heart has no other abnormalities, tachycardia is a cause of heart enlargement and cardiac function throughout the course of the disease;

2 impure tachycatdiomyopathy: the presence of lesions other than tachycardia in the heart and/or other factors other than tachycardia leading to deterioration of cardiac function.

Simple type is well tolerated by long-term tachycardia. It usually takes several years or longer to develop from tachycardia to tachycardia. The symptoms appear later, and the impure type is from tachycardia. The process of tachycardia is short, and the tachycardia of these patients is prone to symptoms, from the first tachycardia to tachycardia cardiomyopathy. Different patients need different time, from weeks to 20 years. Not waiting.

Differential diagnosis

Attention should be paid to the identification of arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy and the like.

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