Arrhythmic risk stratification in ischemic,non-ischemic and hypertrophic cardiomyopathy:A two-step multifactorial,electrophysiology study inclusive approach

Annual arrhythmic sudden cardiac death ranges from 0.6%to 4%in ischemic cardiomyopathy(ICM),1%to 2%in non-ischemic cardiomyopathy(NICM),and 1%in hypertrophic cardiomyopathy(HCM).Towards a more effective arrhythmic risk stratification(ARS)we hereby present a two-step ARS with the usage of seven non-invasive risk factors:Late potentials presence(≥2/3 positive criteria),premature ventricular contractions(≥30/h),non-sustained ventricular tachycardia(≥1episode/24 h),abnormal heart rate turbulence(onset≥0%and slope≤2.5 ms)and reduced deceleration capacity(≤4.5 ms),abnormal T wave alternans(≥65μV),decreased heart rate variability(SDNN<70ms),and prolonged QT_(c)interval(>440 ms in males and>450 ms in females)which reflect the arrhythmogenic mechanisms for the selection of the intermediate arrhythmic risk patients in the first step.In the second step,these intermediate-risk patients undergo a programmed ventricular stimulation(PVS)for the detection of inducible,truly high-risk ICM and NICM patients,who will benefit from an implantable cardioverter defibrillator.For HCM patients,we also suggest the incorporation of the PVS either for the low HCM Risk-score patients or for the patients with one traditional risk factor in order to improve the inadequate sensitivity of the former and the low specificity of the latter.

Arrhythmic syncope: From diagnosis to management

Syncope is a concerning symptom that affects a large proportion of patients.It can be related to a heterogeneous group of pathologies ranging from trivial causes to diseases with a high risk of sudden death.However,benign causes are the most frequent,and identifying high-risk patients with potentially severe etiologies is crucial to establish an accurate diagnosis,initiate effective therapy,and alter the prognosis.The term cardiac syncope refers to those episodes where the cause of the cerebral hypoperfusion is directly related to a cardiac disorder,while arrhythmic syncope is cardiac syncope specifically due to rhythm disorders.Indeed,arrhythmias are the most common cause of cardiac syncope.Both bradyarrhythmia and tachyarrhythmia can cause a sudden decrease in cardiac output and produce syncope.In this review,we summarized the main guidelines in the management of patients with syncope of presumed arrhythmic origin.Therefore,we presented a thorough approach to syncope work-up through different tests depending on the clinical characteristics of the patients,risk stratification,and the management of syncope in different scenarios such as structural heart disease and channelopathies.

Reverse dedifferentiation of atrial cardiomyocytes after restoration of sinus rhythm from atrial fibrillation in goats

Objective Chronic atrial fibrillation （AF） results in dedifferentiation of atrial cardiomyocytes that plays an important role in the perpetuation of AF. In this study, we aimed to investigate the changes oftitin and a-smooth muscle actin （α-SMA） after long time of AF reversal. Methods Twenty-four goats were randomized into four groups： （1） sinus rhythm （SR）, （2） 3 months AF （3-too AF）, （3） 3 months SR after 3 months AF （3-mo post AF）, （4） 6 months SR after 3-mo AF （6-mo post AF）, with 6 in each group. By pacing on the anterior bottom of left atria appendage （LAA）, we established a goat model of chronic AF. Atria effective refractory period （AERP） was measured with electrophysiological methods. Ultra-structure was studied with echocardiography, light and electron microscopy. Titin and α-SMA protein expressions were determined by Western blot. Results The animals underwent high rate pacing on LAA for a mean of 42.23± 21.70 days before presenting AF. Electrophysiological analysis revealed that AERP completely resumed in 3-mo post AF goats. Echocardiography displayed that the size of left atrium resumed almost in 6-too post AF goats （P〈 0.01）. Pathological and electron microscopic examination revealed the disorder of myofibrils, augmentation of intercellular space, myolysis, accumulation of glycogen, and numerous bigger mitochondria among atrial cardiomyocytes in 3-mo AF goats. They recovered mostly in 6-mo post AF goats. Western blot showed that the band density oftitin significantly reduced in 3-mo AF goats compared to SR ones [1826 ± 319 vs 5012±854, P 〈 0.01]. In 3- and 6-mo post AF goats, titin increased gradually and it reversed completely in 6-mo post AF goats （3841 ± 601 and 4523 ±833 respectively, P 〈 0.01）. Conversely, the band density ofa-SMAwas significantly higher in 3-mo AF goats （5324 ± 948） than in SR ones （1619 ±271, P 〈 0.01）. In 3- and 6-mo post-AF goats, α-SMA decreased gradually, and it recovered mostly in 6- mo post AF goats （4437 ± 792 and 2205 ± 540 respectively, P〈 0.01,）. Conclusions These data indicate that the reversal of dedifferentiation of atrial cardiomyocyts is a very slow process, and it is definitely essential for normal cardiac function .

THE ELECTROPHYSIOLOGIC EFFECTS OF ENDOTHELIN A PATCH CLAMP STUDY IN GUINEA PIG VENTRICULAR MYOCYTES

To study the electrophysiologic effects of endothelin-1 (ET-1), we used patch clamp and glass microelectrode techniques to investigate the effects of ET-1 on cardiac L-Ica, Ik and Ik2 in guinea pig ventricular myocytes. The prolongation of APD50, was induced and EADs was triggered by 50 nM ET-1 perfusion. L-lea and Ik were enhanced by various ET-1 concentration from 1 to 50 nM with dose-dependence. Their steady-state activations of L-Iea and Ik shifted left with ET-1 concentration increments. ET-1 elicited a kind of GTP- dependent inward rectifier K current having a mean conductance of 82.36±1.27 pS. The open time and close time ( both interburst intervals and burst durations ) abbreviated with ET-1 concentration increase. The results suggested that EADs -ET evoked was ascribed to the prolongation on the plateau level, which resulted from L-Ica inhancement. The ET- evoked inward rectifier K+ current should be further studied.