RESUMO
AIM:To observe the effect of thyroxine on the expression of T-type calcium channels Cav3. 1, Cav3. 2 and Cav3. 3 in rat myocardium, and to explore the possible biological mechanism between the changes of the ex-pression of T-type calcium channels and the arrhythmia in hyperthyroid heart disease. METHODS:Healthy SD rats (n=20) were randomly divided into normal control group (n=10) and hyperthyroid heart disease group (n=10). The animal model was established by intraperitoneal injection of levothyroxine for 35 d. The contents of T3 and T4 in serum, the heart-to-body weight ratio, the diameter of cardiac myocytes and electrocardiograph were measured to evaluate hyperthyroid heart disease. Moreover, the mRNA and protein expression levels of T-type calcium channels in the myocardium were measured by RT-PCR, immunohistochemistry and Western blot. RESULTS:After intraperitoneal injection of levothyroxine for 35 d, compared with the normal control group, the serum contents of T3 and T4, the heart-to-body weight ratio and the diameter of cardiac myocytes were significantly increased in hyperthyroid heart disease group (P<0.05), and arrhythmia occurred in hyperthyroid heart disease group. By immunohistochemistry and Western blot, the protein expression of Cav3. 1 in-creased significantly (P<0.05), while the protein expression of Cav3.2 decreased significantly (P<0.01). However, no change of the Cav3. 3 protein was observed. The results of RT-PCR were the same as immunohistochemistry and Western blot. CONCLUSION:Thyroxine promotes the expression of Cav3. 1 in the myocardium but inhibits the expression of Cav3. 2 at mRNA and protein levels, which might be involved in arrhythmia in hyperthyroid heart disease.
RESUMO
Congenital long QT syndrome ( LQTS) is a cardiac ion channel dysfunction, leading to prolonged myocardial repolarization time. It is characterized by the typical ECG QT interval prolongation and torsades de pointes. It shows clinical recurrence of cardiogenic syncope and even lead to sudden death. Molecular genetic studies have revealed a total of 12 forms of congenital LQTS caused by mutations in genes of the potassium, sodium and calcium channels or membrane adapter located on chromosomes 3, 4, 7, 11, 12, 17, 20 and 21. This review summarized the studies of the pathogenesis of LQTS and gene-related treatments.
RESUMO
Early repolarization syndrome,Brugada syndrome and Brugada syndrome variant(including sudden cardiac death associated with a prominent J waves in the inferior leads and ventricular fibrillation associated with a prominent J waves and ST segment elevation in the inferior leads)are identical in terms of their ionic and cytological mechanism and may be referred to an Ito-mediated J-wave syndrome.The only difference among these clinical entities is the difference in Ito densities and associated J wave sizes.Ito densities and wave sizes play a key role in arrhythmogenesis.In the leads V1～V3,the J wave and ST segment elevation are the signs that indicate a high risk of sudden cardiac death,i.e.,the Brugada syndrome.In contrast,the J wave and ST segment elevation in V4～V6 is generally considered to be benign,i.e.,the early repolarization syndrome.In other words,J wave that involve the right ventricle are arrhythmogenic;those that involve the left ventricular anterolateral regions are generally benign.Prominent J waves and ST segment elevation involve the left ventricular inferior wall may serve as an important diagnostic sign to detect high risk individuals with a history of unexplained syncope in the condition of sudden cardiac death.