Background Ventricle preexcitation through accessory pathway changes QRS initial vector, and manifests as delta wave on electrocardiogram (ECG). However, QRS terminal vector can also be affected. Methods A total of 158 patients who had single accessory pathway (AP) with antegrade conduction capacity were included and divided into two groups according to the ECG with or without delta wave. Note that 150 patients had delta wave (overt AP group) on ECG; classical preexcitation syndrome was diagnosed before radiofrequency ablation. Eight patients had no delta wave on ECG (unapparent AP group); preexcitation was induced by transesophageal atrial pacing. ECGs and intracardiac electrogram (IEGM) before and after ablation and during atrioventricular reentrant tachycardia were analyzed. Results (1) In the overt AP group: QRS terminal vector amplitude and polarity changes were observed in all the 150 patients, and were related to AP location and delta wave polarity. (2) In the unapparent AP group: QRS terminal vector changes were found in two out of eight patients, and the initial activation of ventricle myocardium via AP on IEGM was almost simultaneous with the onset of QRS complex on ECG. Conclusions It is not only the QRS initial vector, but also the QRS terminal vector that can be changed by the antegrade accessory pathway conduction in patients with preexcitation syndrome. The change of QRS terminal vector is valuable for the diagnosis of atypical preexcitation.

Mitochondrial transfer RNA (tRNA) mutation with high-salt stimulation can cause high blood pressure. However, the underlying mechanisms remain unclear. In the present study, we examined the potential molecular mechanisms of cardiac damage caused by mitochondrial tRNA mutation with high-salt stimulation in spontaneously hypertensive rats (SHR). Unanesthetized, 44-wk-old, male, SHR were divided into four groups: SHR, SHR with high-salt stimulation for 8 wk (SHR + NaCl), SHR carrying tRNA mutations (SHR + M), and SHR + M with high-salt stimulation for 8 wk (SHR + M + NaCl). Healthy Wistar-Kyoto (WKY) rats were used as controls. Left ventricular mass and interventricular septum were highest in the SHR + M + NaCl group ( P < 0.05), while ejection fraction was lowest in the SHR + M + NaCl group ( P < 0.05). Hematoxylin and eosin staining showed myocardial cell hypertrophy with interstitial fibrosis and localized inflammatory cell infiltration, in the hypertensive groups, particularly in the SHR + M + NaCl group. Electron microscopy showed different degrees of mitochondrial cavitation in heart tissue of the hypertensive groups, which was highest in the SHR + M + NaCl group. In hypertensive animals, levels of reactive oxygen species were highest in the SHR + M + NaCl group ( P < 0.05). Expression of the voltage-dependent anion channel (VDAC) and the apoptosis regulator Bax were highest in the SHR + M + NaCl group ( P < 0.05), which also showed evidence of VDAC and Bax colocalization ( P < 0.05). Overall, these data suggest that mitochondrial tRNA mutation with high-salt stimulation can aggravate cardiac damage, potentially because of increased expression and interaction between Bax and VDAC and increased reactive oxygen species formation and initiation of apoptosis.

We aimed to study the effect of allitridum (All) on the transient outward potassium current (Ito) of ventricular myocytes of spontaneously hypertensive rats (SHR). Totally 30 male SHRs were randomly divided into three groups: low-dose All group (7.5 mg·kg(-1)), high-dose All group (15.0 mg·kg(-1)) and normal saline group. The other 10 sex and age matched Wistar-kyoto rats (WKY) were also taken as control group (WKY group). All animals received i.p. administration for 8 weeks. The dual enzymatic method was used to separate single ventricular myocyte from animals. Patch-clamp technique was used to record Ito and analyze the effect of All on the current. It was shown that the left ventricular hypertrophy of SHR was reversed significantly by All. Furthermore, the density of Ito was recovered in both high and low dose All groups. The peak current densities of Ito were enhanced from 18.23±3.64 to 25.17±2.86 pA/pF (P<0.01) and 36.47±5.42 pA/pF (P<0.01) at +50 mV by All 7.5 mg·kg(-1) and 15.0 mg·kg(-1), respectively, which was not significantly different with WKY group. The effect was associated with positive shift of the steady-state, close-state inactivation, and shortened recovery from inactivation of Ito. It is concluded that All decreases the remodeling of Ito of ventricular hypertrophic myocytes of SHR.

The electrocardiogram (ECG) has broad applications in clinical diagnosis and prognosis of cardiovascular disease. Many researchers have contributed to its progressive development. To commemorate those pioneers, and to better study and promote the use of ECG, we reviewed and present here a systematic introduction about the history, hotspots, and trends of ECG. In the historical part, information including the invention, improvement, and extensive applications of ECG, such as in long QT syndrome (LQTS), angina, and myocardial infarction (MI), are chronologically presented. New technologies and applications from the 1990s are also introduced. In the second part, we use the bibliometric analysis method to analyze the hotspots in the field of ECG-related research. By using total citations and year-specific total citations as our main criteria, four key hotspots in ECG-related research were identified from 11 articles, including atrial fibrillation, LQTS, angina and MI, and heart rate variability. Recent studies in those four areas are also reported. In the final part, we discuss the future trends concerning ECG-related research. The authors believe that improvement of the ECG instrumentation, big data mining for ECG, and the accuracy of diagnosis and application will be areas of continuous concern.

This study examined the current changes of human ether-a-go-go-related gene (hERG) mutation derived from a LQT2 Chinese family with a highly penetrating phenotype. Mutation was identified and site-directed mutagenesis was performed to induce the mutation in wild-type (WT) hERG. WT hERG and mutated V535M were cloned and transiently expressed in HEK293 cells. At the 48th and 72nd h after transfection, membrane currents were recorded using whole cell patch-clamp procedures. An A>G transition at 1605 resulting in replacement of V535M was identified. Compared to WT, V535M mutation significantly decreased tail currents of hERG. At test potential of −40 mV after depolarizing at +50 mV, tail current densities were 83.35±7.06 pA/pF in WT and 50.38±7.74 pA/pF in V535M respectively (n=20, P<0.01). Gating kinetics of hERG revealed that V 1/2 of steady-state inactivation shifted to negative potential in the mutant (V 1/2,V535M: −61.81±1.7 mV vs. V 1/2, WT: −43.1±0.71 mV). The time constant of recovery from inactivation was markedly prolonged in the mutant compared to WT among test potentials. V535M hERG mutation demonstrated markedly decreased tail current densities, which suggests that V535M is a new loss-of-function mutation of hERG channel responsible for LQT2.

PURPOSE:Experimental and epidemiological studies suggest that omega-3 fatty acids have an antiarrhythmic effect. However, evidence from randomized controlled trials (RCTs) for prevention of sudden cardiac death (SCD) remains controversial. This study sought to evaluate the efficacy of omega-3 fatty acids for secondary prevention of SCD in patients with cardiovascular disease (CVD) in the era of guidelines-based therapy.METHODS:We conducted a PubMed/EMBASE/CENTRAL search for RCTs evaluating omega-3 fatty acids for CVD secondary prevention with at least 6 months follow-up and with data on SCD. Primary outcome was SCD. Secondary outcomes were cardiovascular mortality and all-cause mortality.RESULTS:Ten randomized controlled trials were identified evaluating a total of 33,429 patients with CVD. In patients with guidelines-adjusted therapy, omega-3 fatty acids did not reduce the risk ratio (RR) of SCD (RR:0.96; 95% CI: 0.84-1.10). In patients with non- guidelines-adjusted therapy, omega-3 fatty acids reduced the RR of SCD (RR: 0.64; 95% CI: 0.51-0.80). Overall, RR for cardiac death and all-cause mortality were 0.81 (95% CI: 0.69-0.95) and 0.89 (95% CI: 0.79-1.01), respectively.CONCLUSIONS:In the era of guidelines-adjusted treatment for CVD secondary prevention, omega-3 fatty acids do not appear to reduce SCD.

OBJECTIVE:To investigate the impact of cyclosporine A (CsA) on atrial expression change of L-type calcium channel alpha1c subunit in a canine model of atrial fibrillation (AF).METHODS:AF was induced by rapid atrial pacing (400 beats/min) for 8 weeks in adult male dogs and placebo (n = 6) or CsA (5 mg x kg(-1) x d(-1), n = 6) were orally administered to these animals. Sham operated animals served as normal controls (n = 6). The atrial electrophysiological parameters including P wave duration, atrial effective refractory period (AERP) were recorded and analyzed at baseline and 8 weeks later. Animals were scarified at 8 weeks post final electrophysiological examinations and atrial expressions of L-type calcium channel alpha1c subunit were determined by Western blot.RESULTS:Compared to sham group, the P wave duration was significantly prolonged while AERP was significantly decreased in AF and CsA groups (all P < 0.05). AERP was significantly longer in CsA group than that in AF group (P < 0.05). L-type calcium channel alpha1c subunit expression was significantly downregulated in AF group compared to sham group (P < 0.05) and CsA significantly attenuated this downregulation (P < 0.01 vs. AF group).CONCLUSION:CsA could attenuate the downregulation of the L-type calcium channel alpha1c subunit expression and improve the atrial electrophysiological remodeling in this canine model of AF.

由中国人民解放军总医院老年心血管病研究所、<中华老年多器官疾病杂志>和英文版<老年心脏病学杂志>承办的第八届长城国际老年心脏病学论坛于2009年10月11日在北京国际会议中心成功举办.

OBJECTIVE:To investigate whether the PJ interval in the patients with pre-excitation syndrome can be shortened by pathway conduction, and to explore the clinical implications of the prolonged PJ interval.METHODS:143 patients with single pathway, who experienced successful radiofrequency (RF) ablation, were divided into two groups: Group A (n = 132) with normal atrioventricular and ventricular conduction (sub-divided into 10 subsets further according to the location of the pathway) and Group B (n = 11) with first degree atrioventricular block or with bundle branch block. The ECG images with and without pathway conduction were analyzed.RESULTS:(1) The PJ interval in the patients with right posterior pathway or with right septal pathway was shortened significantly after the RF [(226 +/- 18) ms vs (236 +/- 19) ms and (221 +/- 18) ms vs (238 +/- 31) ms respectively, both P < 0.05 ]; (2) The PJ interval in Group B was shortened to different extents. The PJ interval values in 4 patients with first degree atrioventricular block were shortened, but still beyond normal extent. The PJ interval values in 4 patients with bundle branch block were shortened to normal extent.CONCLUSION:If the pre-excitation syndrome patients have normal atrioventricular conduction the PJ interval is normal or the PJ interval may be shortened. If the patients have prolonged atrioventricular conduction, the PJ interval may be shortened by the pathway prograde conduction. PJ interval prolongation indicates atrioventricular conduction delay or ventricular conduction block, but bundle branch block cannot be excluded when the PJ interval is normal.