Premature beat, also known as premature contraction or extrasystole, is an early ectopic heartbeat. It can be classified into four types based on the origin: sinus, atrial, atrioventricular junctional, and ventricular. Among these, ventricular premature beats are the most common, followed by atrial, while sinus premature beats are rare. Premature beats are a common type of ectopic rhythm. They can occur on the basis of sinus or ectopic rhythms (such as atrial fibrillation). They may be occasional or frequent, and can occur irregularly or regularly after every or several normal beats, forming bigeminy or coupled premature beats.

bubble_chart Etiology

Premature beats can occur in normal individuals. However, patients with cardiac neurosis Guanneng or organic heart disease are more prone to them. Emotional agitation, nervous tension, fatigue, indigestion, excessive smoking, alcohol consumption, or drinking strong tea can all trigger episodes, or they may occur without obvious triggers. The toxic effects of substances such as Rehmannia, barium compounds, quinidine, sympathomimetic drugs, chloroform, cyclopropane anesthetics, as well as potassium deficiency, and cardiac surgery or catheterization can also induce them. Coronary heart disease, advanced stage mitral valve disease, heart disease, myocarditis, hyperthyroid heart disease, and mitral valve prolapse are often associated with a higher incidence of premature beats.

bubble_chart Pathogenesis

It can be generated through various means:

1. Abnormal impulse formation due to abnormal automaticity (1) Under certain conditions, such as when a sinus impulse reaches an ectopic pacemaker site, the Weidenbach phenomenon causes a decrease in the threshold potential and changes in the slope of diastolic depolarization, leading to premature beats. (2) Pathological changes in the atrial, ventricular, or Purkinje fiber cell membranes alter the permeability to different ions, converting fast-response fibers into slow-response fibers. This accelerates diastolic automatic depolarization, enhances automaticity, and results in premature beats.
2. Reentry phenomenon—circus movement reentry or focal microreentry. If the reentry pathway is the same, the morphology of the premature beats will be consistent; if the conduction velocity during reentry is uniform, the coupling interval between the premature beat and the preceding beat will be fixed.
3. Parasystole.
4. Triggered activity.

bubble_chart Clinical Manifestations

Premature beats may be asymptomatic or may cause palpitations or a sensation of a skipped heartbeat. Frequent premature beats can lead to symptoms such as lack of strength and dizziness (due to reduced cardiac output), and in patients with pre-existing heart disease, they may trigger or worsen colicky pain or heart failure. Auscultation may reveal an irregular heart rhythm with a prolonged compensatory pause following the premature beat. The first heart sound of a premature beat is often accentuated, while the second heart sound is usually diminished or absent. When premature beats occur in bigeminy or trigeminy, a long pause can be heard after every two or three heartbeats. If a premature beat is interpolated between two regular beats, it may present as three consecutive heartbeats. Palpation of the pulse may reveal a missing intermittent pulse.

bubble_chart Auxiliary Examination

The electrocardiogram (ECG) has diagnostic significance for premature beats. Atrial premature beats are characterized by an early QRS complex preceded by an abnormal P wave, followed by an incomplete compensatory pause, with the QRS morphology usually consistent with the normal QRS complex. Junctional premature beats exhibit an early QRS complex identical to the normal QRS, without a preceding P wave, and have a complete compensatory pause. Ventricular premature beats show an early, wide, and abnormally shaped QRS complex with a complete compensatory pause. A 24-hour Holter monitor can record the frequency, pattern, and treatment response of premature beats in detail. For suspected myocarditis, cardiac enzyme tests may be performed. Echocardiography can detect cardiomyopathy and some cases of coronary artery disease. Patients on long-term diuretics or suspected of digitalis toxicity should have blood electrolyte levels measured, and blood digitalis concentration checked if necessary.

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The common ECG feature of premature beats is one or more P-QRS complexes occurring earlier than the basic rhythm.

1. Atrial premature beats show an early P wave with a morphology different from the basic rhythm's P wave and a P-R interval >0.12s. The QRS complex is usually similar to the sinus rhythm, but may occasionally be slightly widened or deformed, accompanied by corresponding ST and T wave changes—termed aberrant ventricular conduction, which needs differentiation from ventricular premature beats. In atrial premature beats with aberrant conduction, an early deformed P' wave can be seen before the abnormal QRS complex. The early deformed P' wave may also not be followed by a corresponding QRS complex, termed blocked atrial premature beats, which should be differentiated from sinus arrhythmia or sinus arrest. Identifying a deformed early P' wave on the ST segment or T wave of the preceding beat confirms a blocked atrial premature beat. Atrial premature impulses often invade the sinoatrial node, causing its early depolarization, after which the sinoatrial node resumes its original cycle, resulting in an incomplete compensatory pause. Rarely, a complete compensatory pause may follow an atrial premature beat.
2. Atrioventricular junctional premature beats, apart from occurring early, share ECG features similar to atrioventricular junctional escape beats. If the premature impulse invades the sinoatrial node, it results in an incomplete compensatory pause; if it does not interfere with the sinoatrial node's spontaneous depolarization, a complete compensatory pause occurs.
3. Ventricular premature beats feature an early, abnormally shaped QRS complex, usually with a duration >0.12s, a T wave opposing the QRS main wave direction, ST segment displacement with the T wave, and no preceding P wave. Ventricular premature beats originating near the bundle branches may not show QRS widening. Most ventricular premature beats are followed by a complete compensatory pause. When the basic rhythm is slow, ventricular premature beats may occur between two sinus beats, forming interpolated ventricular premature beats. Rarely, retrograde P' waves from ventricular premature beats may appear on the ST segment.

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Atrial and ventricular premature beats can be classified into two types based on their relationship with the basic rhythm, using ventricular premature beats as an example:

1. Coupled type: All premature beats have a fixed interval from the preceding QRS complex, which is the more common type.
2. Parasystolic type: The premature beats are not coupled to the preceding QRS complexes, but there is a fixed interval between premature beats, with the longest and shortest intervals being integer multiples of each other, often accompanied by ventricular fusion beats.

Premature beats without a fixed coupling interval to the preceding beat may form ventricular fusion beats when occurring late and coinciding with a sinus impulse (e.g., the 6th beat in lead II).

Experimental studies have shown that the above patterns can be altered due to subthreshold potentials generated by slow decremental conduction of sinus or ectopic impulses in protected zones of entrance block, affecting the spontaneous depolarization of parasystolic impulses, causing them to occur earlier, later, or be completely suppressed. This phenomenon is termed electrotonic modulated parasystole.

Atrial or ventricular premature beats are sometimes generated by more than two ectopic pacemakers. The electrocardiogram shows two or more types of premature beats with different morphologies and unequal coupling intervals, which are called multifocal premature beats. Two or three consecutive premature beats or more are called consecutive beats and short bursts of tachycardia, respectively.

bubble_chart Diagnosis

1. Medical history and symptoms: Due to varying patient sensitivity, there may be no obvious discomfort or only palpitations, precordial discomfort, or a sensation of skipped heartbeats. Inquiring about a history of hypertension, coronary heart disease, cardiomyopathy, or rheumatic heart disease helps identify the cause of premature beats and guide treatment. Pay attention to recent histories of common cold, fever, or diarrhea, which may aid in determining whether acute viral myocarditis is present. The use of digitalis, antiarrhythmic drugs, and diuretics may sometimes induce premature beats.
2. Physical examination findings: In addition to the positive signs of the underlying heart disease, auscultation may reveal an early heartbeat within a regular rhythm, followed by a longer pause (compensatory pause). The first heart sound of the premature beat is enhanced, while the second heart sound is weakened, and may be accompanied by a weakened or absent pulse for that beat.

bubble_chart Treatment Measures

The treatment principles should be determined by considering the presence or absence of organic heart disease, whether it affects cardiac output, and the potential for developing severe arrhythmias.

Most premature beats without underlying organic heart disease do not require special treatment. For symptomatic patients, alleviating anxiety is advisable. Premature beats induced by excessive tension, emotional agitation, or exercise may be treated with sedatives and β-blockers.

For frequent episodes, significant symptoms, or cases associated with organic heart disease, it is essential to promptly identify the disease cause and triggers of the premature beats and provide corresponding treatment. At the same time, the potential lethal risks should be accurately recognized, with active treatment of the disease cause and symptomatic management.

In addition to treating the disease cause, antiarrhythmic drugs may be selected. For atrial and atrioventricular junctional premature beats, drugs acting on the atria and atrioventricular junction (Class Ia, Ic, II, and IV) are often chosen, whereas for ventricular premature beats, Class I and III drugs acting on the ventricles are preferred (refer to the drug classification above and also to Chapter 7, "Introduction to Clinical Pharmacology"). Ventricular premature beats with potential lethal risks often require urgent intravenous administration, with Class Ib drugs as the first choice. In the initial stage of acute myocardial infarction, intravenous lidocaine is still commonly the first-line treatment. Post-myocardial infarction, β-blockers are often used if there are no contraindications. For patients with primary or secondary QT prolongation syndrome, Class I drugs are contraindicated. For primary cases, β-blockers, phenytoin, or carbamazepine may be used. For secondary cases, the disease cause should be addressed, and treatment with isoproterenol or atrial/ventricular pacing is advisable.

Recent research (CAST 1989) suggests that antiarrhythmic drugs may increase the risk of mortality. Even in patients with heart disease, controlling ventricular premature beats has not been proven to reduce sudden death rates (except for β-blockers post-myocardial infarction). Therefore, the benefits and risks of antiarrhythmic drugs should be carefully weighed. In China, a large multicenter trial with long-term follow-up in non-myocardial infarction arrhythmia patients (mainly premature beats) showed that propafenone and moricizine were effective for supraventricular arrhythmias, while propafenone, moricizine, and mexiletine were effective for ventricular arrhythmias, without serious cardiac events observed. However, close follow-up monitoring of efficacy and potential adverse effects is still necessary during treatment, especially for patients with cardiac dysfunction.