Sudden sleep death

Introduction J wave syndrome is the culprit of sudden death from sleep, and J wave has an intrinsic connection with sudden death. J wave syndrome is a general term for various clinical syndromes related to J wave, including premature repolarization syndrome, unexpected sudden death syndrome, Brugada syndrome, and idiopathic ventricular fibrillation. Brugada syndrome is a primary cardiac disease caused by abnormal ion channel genes. It is a high-risk group with sudden cardiac death and has a serious prognosis. The disease was first proposed by the Spanish scholars Brugada P and Brugada J in 1992. In 1996, Miyazaki et al. named the disease Brugada syndrome. Brugada syndrome is more common in men. Brugada syndrome needs to be identified in a timely manner in clinical work to intervene as early as possible. Patients with symptoms such as electrocardiogram are also normal, can do induction tests, can also do electrophysiological examination to confirm the diagnosis. Once the diagnosis is established, immediate implantation of ICD is the only effective way to prevent sudden death.

Cause

First, the genetic mechanism

Brugada syndrome is an autosomal dominant hereditary disease. It is suggested that gene mutations encoding sodium current, transient outward potassium current (Ito), ATP-dependent potassium current, and calcium-sodium exchange current ion channel may be the molecular biological basis of Brugada syndrome.

In 1998, Chen et al. first confirmed that the -subunit mutation encoding the cardiac sodium channel gene (SCN5A) is one of the genetic basis of Brugada syndrome. In the early stage of ventricular repolarization, due to the SCN5A gene mutation, the inward sodium current (INa) decreased and Ito increased significantly. The potential difference between Ito and the intima was significantly increased, resulting in the elevation of J point and the elevation of ST segment. high. Since the epicardial Ito current of the right ventricle is superior to the Ito current of the left ventricular epicardium, the electrocardiographic performance is also characteristically located in the right chest lead of V1-V3. 2-phase reentry is the electrophysiological cause of VT and VF in Brugada syndrome, which is related to the increase of cross-wall overlap and the trigger mechanism of premature activity. When the ion flux and potential difference between the inner and outer membranes of a certain part of the ventricle are significantly increased, it can cause the 2-phase reentry of adjacent parts, thereby inducing VT and VF.

Second, ECG changes and mechanisms to induce rapid arrhythmia

The cause of ST-segment elevation and induced ventricular tachycardia/ventricular fibrillation in Brugada syndrome is unclear. During the formation of right ventricular epicardial action potential, transient outward current seems to indicate the relevant mechanism. Cell electrophysiological studies have shown that the endocardial and epicardial action potentials (AP) are distinctly different, that is, the epicardial action potential repolarization process is characterized by a special and significant "spike-round shape", which is at least It is related to three kinds of ion currents, namely sodium ion inward potential (INa), transient outward current (Ito) and L-type calcium ion current (ICa), and there is no Ito in the epicardium and no endocardium. The action potential I phase is notched, which is reflected in the J wave and J point elevation of the electrocardiogram, while the action potential roundness of the outer membrane cell disappears, and the action potential time course is shortened, causing the endocardial to form a transmural current toward the epicardium. Reflected on the ECG is the ST segment elevation. Because the right ventricular wall is thinner, the right ventricular epicardial AP has a more pronounced effect on the electrocardiogram than the left ventricle, so the ST segment changes often occur in the V1 and V2 leads. As mentioned above, the AP repolarization condition is determined by a variety of ions. The changes in these ion currents can cause potential differences in different parts of the myocardium, causing significant re-repolarization of the repolarization and local re-excitation. This re-excitation in the repolarization process is generated. The mechanism or trigger of a rapid arrhythmia.

The excitation or inhibition of autonomic nerves also has an effect on the ST segment depression. For example, after the receptor is excited, the L-type LCa ion flux increases, and the epicardial AP rounds recover, which is close to the endocardial time limit, and the difference between the inner and outer membrane action potentials becomes smaller. Therefore, the ST segment is decreased, and the action of the beta blocker is reversed, so that the ST segment is elevated, and the excitation and inhibition of the alpha receptor have similar effects. Another scholars have suggested that late-potential and surface electrocardiographic studies suggest that there is a conduction delay in the anterior wall and septal area of the right ventricular outflow tract. This delay is more pronounced when the vagus nerve is excited, which may be easy for patients with Brugada syndrome to appear at night. Quiver related.

an examination

Related inspection

Electrocardiogram CT scan

Detailed medical history and family history are the key to diagnosis. Unexplained syncope, syncope, a history of sudden death, and a history of familial cardiac death are important clues to diagnosis. Brugada syndrome can be diagnosed if the patient has a typical type I ECG change and one of the following clinical manifestations, and excludes other factors that cause ECG abnormalities:

1 recorded ventricular fibrillation.

2 Self-terminating polymorphic ventricular tachycardia.

3 family history of sudden death.

For type II and III electrocardiograms, the drug challenge test is positive, and the above clinical manifestations can be used to diagnose Brugada syndrome. If there is no clinical symptom above, only the characteristic ECG changes can not be diagnosed as Brugada syndrome, which can only be called the special-type Brugada-like ECG changes.

Differential diagnosis

"Brugada syndrome-like electrocardiographic changes" can be caused by the following conditions and should be identified in the clinic.

(1) Acute anterior wall myocardial infarction.

(2) Right or left bundle branch block.

(3) left ventricular hypertrophy.

(4) Right ventricular infarction.

(5) left ventricular ventricular aneurysm.

(6) Aortic dissection aneurysm.

(7) Acute pulmonary embolism.

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