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Background: Macroscopic T wave alternans (macro-TWA) often heralds the onset of Torsades de Pointes in patients with QT prolongation. However, the mechanisms underlying macro-TWA remain unclear. We examined the cellular and ionic basis for macro-TWA in rabbits with left ventricular hypertrophy (LVH). Methods: The renovascular hypertension model was used to induce LVH in rabbits. Action potentials were simultaneously recorded from epicardium and endocardium together with a transmural ECG and isometric contractility in arterially perfused left ventricular wedges. Late sodium current (I Na-L ) was recorded in single-isolated left ventricular myocytes with the whole cell patch-clamp technique. Results: Macro-TWA and accompanied mechanical alternans occurred spontaneously in 8 of 33 LVH rabbits ( P Na-L enhancer ATX-II at 1 to 3 nM in additional 7. Macro-TWA and mechanical alternans occurred discordantly, that is, that longer QT interval and larger T wave were associated with weaker isometric contvractility. Alternating early afterdepolarizations in the endocardium caused macro-TWA in 12 of 15 LVH rabbits and, therefore, early afterdepolarization-dependent R-from-T extrasystoles and Torsades de Pointes always originated from the beats with longer QT and larger T wave during macro-TWA. I Na-L density was significantly larger in LVH myocytes than that of control myocytes. Macro-TWA, mechanical alternans, R-from-T extrasystoles, and Torsades de Pointes were all abolished by I Na-L blocker ranolazine or mexiletine. Conclusions: LVH enhances I Na-L density and promotes alternating early afterdepolarizations in the left ventricular endocardium that manifest as macro-TWA with discordant mechanical alternans. I Na-L blockade abolishes macro-TWA, mechanical alternans, early afterdepolarization-dependent R-from-T extrasystoles, and Torsades de Pointes.

Background: Shock index-based risk indices predicting in-hospital mortality for ST-elevation myocardial infarction (STEMI) patients have been recently described, debate continues about their accuracy, especially compared with classic scoring system. Thus, we aim to evaluate the predictive value of shock index-based risk indices in STEMI patients and compared with thrombolysis in myocardial infarction (TIMI) risk score.Method: Consecutive 5063 STEMI patients were divided into 2 groups: non-survivor (392, 7.7%) and survivor (4671, 92.3%). Predictive performance of shock index-based risk indices and TIMI risk score were assessed by C-statistic, Hosmer-Lemeshow test, Nagelkerke-R2, brier scores, integrated discrimination improvement(IDI) and net reclassification improvement(NRI). Odd ratios (OR) and corresponding 95% confidence intervals of bipartite shock index-based risk indices were estimate by generalized linear mixed model.Results: The area under the curves (AUC) of shock index-based risk indices were smaller, whereas the sensitivity and specificity of age shock index (age SI) (0.73, 0.69) and age modified shock index (age MSI) (0.70, 0.73) were comparable to TIMI risk score (0.73, 0.77). The Hosmer-Lemeshow P values and the Nagelkerke-R2 of shock index-based risk indices were lower, whereas the brier scores were comparable with TIMI risk score. In-hospital mortality was increasing with the SI based risk indices, when the cut-off value were set, in-hospital mortality in the patients with larger shock index-based risk indices were relatively higher. The prognostic performance of shock index (SI, C-statistic: z=7.944, PConclusions: Shock index-based risk indices do not have a significant advantage over TIMI risk score. Age SI and age MSI, with comparable sensitivity, were valuable prognostic tools to identify STEMI patients at high risk of in-hospital death.Trial registration: [NCT02641262] [29 December, 2015].

Background Renal denervation (RDN) targeting the sympathetic nerves in the renal arterial adventitia as a treatment of resistant hypertension can cause endothelial injury and vascular wall injury. This study aims to evaluate the risk of atherosclerosis induced by RDN in renal arteries. Methods A total of 15 minipigs were randomly assigned to 3 groups: (1) control group, (2) sham group, and (3) RDN group (n = 5 per group). All pigs were fed a high-fat diet (HFD) for 6 months after appropriate treatment. The degree of intimal thickening of renal artery and the conversion of endothelin 1 (ET-1) receptors were evaluated by histological staining. Western blot was used to assess the expression of nitric oxide (NO) synthesis signaling pathway, ET-1 and its receptors, NADPH oxidase 2 (NOX2) and 4-hydroxynonenal (4-HNE) proteins, and the activation of NF-kappa B (NF-κB). Results The histological staining results suggested that compared to the sham treatment, RDN led to significant intimal thickening and significantly promoted the production of endothelin B receptor (ETBR) in vascular smooth muscle cells (VSMCs). Western blotting analysis indicated that RDN significantly suppressed the expression of AMPK/Akt/eNOS signaling pathway proteins, and decreased the production of NO, and increased the expression of endothelin system proteins including endothelin-1 (ET-1), endothelin converting enzyme 1 (ECE1), endothelin A receptor (ETAR) and ETBR; and upregulated the expression of NOX2 and 4-HNE proteins and enhanced the activation of NF-kappa B (NF-κB) when compared with the sham treatment (all p p > 0.05). Conclusions RDN aggravated endothelial endocrine dysfunction and intimal thickening, and increased the risk of atherosclerosis in renal arteries of HFD-fed pigs.

Background: This study aims to compare whether 2 different routes of renal denervation (RDN) from the intima and adventitia of the renal artery can reduce renal fibrosis in a pig model of hypertension induced by a high-fat diet and to explore possible molecular mechanisms. Methods: Twenty-four Bama miniature pigs were randomly divided into a control group (normal diet, n = 6) or a hypertension model group (high-fat diet, n = 18). The model group was randomly divided into the intima-RDN group (n = 6), the adventitia-RDN group (n = 6), or the renal arteriography-only group (sham group, n = 6). All animals were fed separately. The model group was fed a high-fat diet after the operation, and the control group was fed conventionally for 6 months. After 6 months, renal artery angiography was performed again to observe the condition of the renal arteries, after which all animals were euthanized. The blood pressure and blood biochemical results of each group were evaluated 6 months after the operation; kidney tissue morphology and collagen fiber content were examined by hematoxylin-eosin staining and Masson staining; superoxide dismutase activity and the malondialdehyde content of kidney tissue were assessed by a biochemical enzyme method; the protein expression level of transforming growth factor-β 1 (TGF-β1), α-smooth muscle actin (α-SMA), and Smad3 was assessed by Western blot, and electron microscopy was used to examine changes in the kidney microstructure. Results: After 6 months of a high-fat diet, the blood lipid levels of the model group were significantly higher compared to baseline and to that of the control group during the same period (all showed p < 0.05); the blood lipid levels of the control group did not change significantly from baseline (p > 0.05). The degree of glomerular damage caused by hyperlipidemia in the intima-RDN group and the adventitia-RDN group was significantly lower than that of the sham and control groups, and the renal fibrosis area percentage was also significantly lower (p < 0.05). Electron microscopy showed that both the intima-RDN group and the adventitia-RDN group had a more even distribution of chromosomes and less mitochondrial swelling compared with the sham group. Conclusion: RDN from the adventitia of the renal artery and RDN from the intima of the renal artery have the similar advantages of delaying high-fat-induced renal fibrosis. The antifibrotic effect of RDN may be related to inhibition of the TGF-β1/Smad3 pathway.

ObjectivesTo assess differences in reperfusion treatment and outcomes between secondary and tertiary hospitals in predominantly rural central China.DesignMulticentre, prospective and observational study.SettingSixty-six (50 secondary and 16 tertiary) hospitals in Henan province, central China.ParticipantsPatients with ST elevation myocardial infarction (STEMI) within 30 days of symptom onset during 2016–2018.Primary outcome measuresIn-hospital mortality, and in-hospital death or treatment withdrawal.ResultsAmong 5063 patients of STEMI, 2553 were treated at secondary hospitals. Reperfusion (82.0% vs 73.0%, pConclusionsWith fibrinolytic therapy as the main reperfusion strategy, the reperfusion rate was higher in secondary hospitals, whereas in-hospital outcomes were similar compared with tertiary hospitals. Public awareness, capacity of primary and secondary care institutes to treat STEMI, and establishment of deeper cooperation among different-level healthcare institutes need to further improve.Trial registration numberNCT02641262.

On surface electrocardiographic (ECGs), it is difficult to differentiate IA retrospective analysis was performed on adults with ECGs consisting of one of the four following manifestations: J waves associated with hypothermia and early repolarization, and pseudo J waves associated with right bundle branch block (RBBB) and non-specific intraventricular conduction delay (NS-IVCD). All ECGs were assessed individually and the maximum and minimum discrete QRS deflections on 12-lead tracings, defined as "QRSA total of 60 patients consisting of 15 patients in each arm were included in the study. ΔQRS was significantly larger in the hypothermia and early repolarization groups, compared to RBBB and NS-IVCD (p .0001), with the following mean ∆QRS: hypothermia 54.3 ± 13.7 ms, early repolarization pattern 47.3 ± 15.3 ms, RBBB 19.3 ± 6.5 ms, and NS-IVCD 16.0 ± 6.6 ms.∆QRS may serve as a reliable ECG parameter for distinguishing I

MicroRNAs (miRNAs) play essential roles in the regulation and pathophysiology of various types of human diseases including atherosclerosis. Increasing numbers of miRNAs have been identified to be important regulators in the progression of atherosclerosis by regulating gene expression. However, functional miRNAs and the underlying mechanisms involved in atherosclerosis need fully elucidation. In the present study, the function of miRNA let-7b was investigated in human aortic endothelial cells (HAECs). The results showed that downregulation of let-7b in the high-fat diet mice and HAECs was inversely correlated with the expression level of HAS-2. upregulation of let-7b significantly reduced apoptosis of HAECs. The results also revealed that HAS-2 was a target gene of let-7b and HAS-2 reduction reversed the antiapoptotic effect of let-7b through regulation of the P13K/Akt pathway. These results together suggest the potential of regulating the let-7b expression and endothelial apoptosis against development and progression of atherosclerosis.

Background Cardiovascular disease including ST elevation myocardial infarction (STEMI) is increasing and the leading cause of death in China. There has been limited data available to characterize STEMI management and outcomes in rural areas of China. The Henan STEMI Registry is a regional STEMI project with the objectives to timely obtain real-world knowledge about STEMI patients in secondary and tertiary hospitals and to provide a platform for care quality improvement efforts in predominantly rural central China. Methods The Henan STEMI Registry is a multicentre, prospective and observational study for STEMI patients. The registry includes 66 participating hospitals (50 secondary hospitals; 16 tertiary hospitals) that cover 15 prefectures and one city direct-controlled by the province in Henan province. Patients were consecutively enrolled with a primary diagnosis of STEMI within 30 days of symptom onset. Clinical treatments, outcomes and cost are collected by local investigators and captured electronically, with a standardized set of variables and standard definitions, and rigorous data quality control. Post-discharge patient follow-up to 1 year is planned. As of August 2018, the Henan STEMI Registry has enrolled 5479 patients of STEMI. Discussion The Henan STEMI Registry represents the largest Chinese regional platform for clinical research and care quality improvement for STEMI. The board inclusion of secondary hospitals in Henan province will allow for the exploration of STEMI in predominantly rural central China. Trial registration [NCT02641262] [29 December, 2015].

The aim of this study was to explore the long‐term clinical results of Renal denervation (RDN) from the adventitia of the renal artery plus unilateral laparoscopic adrenalectomy to treat patients with resistant hypertension caused by unilateral aldosterone‐producing adenoma (APA). Sixty patients with resistant hypertension caused by APA who were treated at Henan Provincial People's Hospital from December 2016 to March 2018 were selected and randomly assigned to undergo RDN from the adventitia of the renal artery plus adrenalectomy (RDN group, n = 30) or adrenalectomy alone (control group, n = 30). Office blood pressure (BP), antihypertensive medication usage and other laboratory characteristics were followed every 6 months through 36 months. Follow‐up data were available at 36 months for 23 of 30 subjects in the RDN group and for 21 of 30 subjects who were in the control group. At 36 months postprocedure, the reduction in the RDN group was 42.2 ± 21.6 mmHg and that in the control group was 29.8 ± 13.5 mmHg (p = .029 between the groups). During the follow‐up to 36 months postprocedure, no patients in either the RDN group or the control group died due to surgical complications, and the RDN group had no procedural complications, including renal artery dissection, perforation, and renal artery stenosis. There was no change in the mean eGFR of the two groups, and no serious adverse events were reported. In conclusion, RDN from the adventitia of the renal artery plus unilateral laparoscopic adrenalectomy resulted in sustained lowering of BP at 3 years in a selected population of subjects with resistant hypertension caused by unilateral APA without serious safety concerns.

Background Coronary artery disease (CAD) and atrial fibrillation (AF) frequently coexist in clinical practice, making it challenging for the treating physician to choose anticoagulation and antiplatelet therapies. The aim of this study was to investigate antithrombotic strategies and assess related adverse outcomes in stable coronary artery disease (SCAD) and acute coronary syndrome (ACS) patients with AF when the CHA2DS2-VASc score was ≥2. Methods We performed a retrospective study and collected data from a computer-based patient record management system in Zhengzhou University People’s Hospital in China. In total, 2978 patients with a hospital discharge diagnosis of CAD and concomitant AF who met the inclusion criteria were enrolled from January 1, 2012 to December 31, 2016, and data from 2050 patients were finally analysed. The χ2 test was used to compare the incidences of clinical endpoints between the SCAD+AF group and the ACS + AF group. Multivariable Cox regression analysis was performed to identify independent predictive factors of adverse outcomes in both groups. Results Oral anticoagulant (OAC) monotherapy was the most common antithrombotic therapy in SCAD+AF patients (49.55%), while double antiplatelet therapy (DAPT) was the most common treatment in ACS + AF patients (54.19%) at discharge. OAC monotherapy significantly increased and the use of single antiplatelet therapy (SAPT) decreased during follow-up (34 ± 13 months) when compared to their use at discharge in the SCAD+AF group (all p p p p p Conclusions In this study, the proportion of anticoagulant-antiplatelet combined therapy was low in ACS + AF patients with high stroke risk. In clinical practice, the awareness of anticoagulation needs to be strengthened regarding patients with CAD and AF.

Background This study aims to evaluate the effects and safety of laparoscopic-based perivascular renal sympathetic nerve denervation (RDN) in a porcine model fed a high-fat diet. Method Thirty-six high-fat diet-fed Bama minipigs were randomly divided into an RDN group (n = 18), in which minipigs received laparoscopic-based perivascular RDN, and a sham group (n = 18). All pigs were fed the high-fat diet after the operation to establish a model of obesity-induced hypertension. Bama pigs in the RDN and sham groups were killed at 3 time points [2 days after RDN (n = 6), day 90 (n = 6) and day 180 (n = 6)]. Result The systolic blood pressure (SBP) and noradrenaline (NE) concentration in the kidney tissue were significantly lower in the RDN group than in the sham group at 2 days (113.83 ± 3.26 mmHg vs 129.67 ± 3.32 mmHg, P = 0.011, and 112.02 ± 17.34 ng/g vs 268.48 ± 20.61 ng/g, P P = 0.001, respectively) and 180 days (129.33 ± 2.87 mmHg vs 168.57 ± 2.86 mmHg, P P P = 0.037, and 76.83 ± 2.75 mmHg vs 86.33 ± 2.22 mmHg P = 0.021, respectively). Based on the pathological evaluation, the renal sympathetic nerve fascicles were successfully disrupted by radiofrequency energy after laparoscopic-based perivascular RDN, but the intima was intact. Tyrosine hydroxylase (TH) expression was decreased, while the expression of the S100 protein was increased in treated renal arteries after RDN. Conclusions Laparoscopic-based perivascular RDN prevented the occurrence and development of hypertension, and thus it may be an efficient and safe method for controlling blood pressure in an experimental model.

Additional file 1: Supplement Table 1. Warfarin duration and Levels of INR in patients at discharge.

Additional file 2: Supplement Table 2. The incidences of thromboembolism and bleeding events in patients prescribed warfarin or NOAC during follow-up.

To investigate the effect of miR-181a targeting XIAP gene on the apoptosis of cardiomyocytes induced by hypoxia/reoxygenation (H/R) and its mechanism. The primary cultured cardiomyocytes were treated with hypoxia for 3 hours and reoxygenation for 4 hours to construct H/R cell model. The expression of miR-181a and XIAP messenger RNA in cardiomyocytes was detected by reverse-transcription polymerase chain reaction, and the expression of XIAP protein in cardiomyocytes was detected by Western blot analysis. H/R cardiomyocytes with low expression of miR-181a and overexpression of XIAP were constructed, and the effects of low expression of miR-181a and upregulation of XIAP on cardiomyocyte apoptosis were detected by flow cytometry. A dual luciferase reporter assay was used to detect the target relationship between miR-181a and XIAP. Further, H/R myocardial cells with low XIAP expression were constructed to observe the effect of downregulation of XIAP expression on apoptosis of myocardial cells with low expression of microarray-181a. The expression of apoptosis-related proteins Bax and Bcl-2 in myocardial cells was detected by Western blot analysis. After H/R treatment, the expression of microRNAs-181a was high but that of XIAP was low. The apoptosis of cardiomyocytes could be inhibited by both the low expression of miR-181a and the upregulation of XIAP. The results of dual luciferase reporter gene showed that XIAP was a potential target gene for miR-181a. The inhibitory effect of low expression of miR-181a on myocardial apoptosis could be reversed and the inhibitory effect of low expression of miR-181a on Bax protein expression and the promotion of Bcl-2 protein expression could be reversed by the downregulation of XIAP. MiR-181a can inhibit the apoptosis of hypoxic-reoxygenated cardiomyocytes by targeting XIAP to downregulate Bax and upregulate Bcl expression.

Objective: To investigate the relationship between morning hypertension (MH) and T-peak to T-end interval (Tp-e interval) in patients with suspected coronary heart disease. Methods: Patients with typical symptoms of coronary heart disease were examined by ambulatory blood monitoring, electrocardiogram, echocardiography, and coronary angiography, and were assigned to two groups on the basis of blood pressure: an MH group and a morning normotension (MN) group. The following data were collected and compared: basic characteristic, Tp-e interval, corrected QT (QTc) interval, echocardiography parameters, and Gensini score of the two groups. Results: Three hundred fifty-eight patients, with a mean age of 64 years (54.1% men), were divided into the MH group (n=170) and the MN group (n=188). Tp-e interval (84.52±14.77 ms vs. 65.19±19.03 ms, P2 vs. 105.63±17.10 g/m2, Pr=0.678, Pr=0.404, Pr=0.513, Pr=0.646, P Conclusion: Tp-e interval is correlated with morning systolic blood pressure and diastolic blood pressure in patients with coronary heart disease. More research on how the Tp-e interval changes after control of MH is necessary.

The mechanisms of vascular endothelial growth factor 165 (VEGF165) on electrical properties of cardiomyocytes have not been fully elucidated. The aim of this study is to test the hypothesis that VEGF165, an angiogenesis-initiating factor, affects L-type calcium currents (ICa,L) and cell membrane potential in cardiac myocytes by acting on VEGF type-2 receptors (VEGFR2). ICa,L and action potentials (AP) were recorded by the whole-cell patch clamp method in isolated guinea-pig ventricular myocytes treated with different concentrations of VEGF165 proteins. Using a VEGFR2 inhibitor, we also tested the receptor of VEGF165 in cardiomyocytes. We found that VEGF165 increased ICa,L in a concentration-dependent manner. SU5416, a VEGFR2 inhibitor, almost completely eliminated VEGF165-induced ICa,L increase. VEGF165 had no significant influence on action potential 90 (APD90) and other properties of AP. We conclude that in guinea-pig ventricular myocytes, ICa,L can be increased by VEGF165 in a concentration-dependent manner through binding to VEGFR2 without causing any significant alteration to action potential duration. Results of this study may further expound the safety of VEGF165 when used in the intervention of heart diseases.

Myocardial ischemia-reperfusion (I/R) injury, a major contributor to morbidity and mortality, represents a combination of intrinsic cellular response to ischemia and the extrinsic acute inflammatory response. In the present study, microarray analysis of GSE67308 and GSE50885 identified differentially expressed GPR30 and upstream regulatory miR-2861 and miR-5115 in myocardial I/R. Furthermore, GPR30 was confirmed as a common target gene of miR-2861 and miR-5115, and miR-2861 and miR-5115 inhibited GPR30 expression. Poor expression of GPR30 was identified in the myocardial I/R injury mouse model. Overexpressed GPR30 led to alleviated the pathological conditions, diminished myocardial infarct size and apoptosis of myocardial tissue in mice. Moreover, miR-2861 and miR-5115 were found to be highly expressed in the myocardial I/R injury mouse model and to subsequently accelerate the disease progression. Notably, PR30 curtailed the development of myocardial I/R injury through activation of the mTOR signaling pathway. The key findings suggested that miR-2861 and miR-5115 blocked the activation of the GPR30/mTOR signaling pathway by targeting GPR30, thereby accelerating myocardial I/R injury in mice.

Comparison of mean endothelium-independent vasodilation rate changes at different concentrations of all pigs was as follows. (DOC 15 kb)

Additional file 1. Full list of hospitals in the Henan STEMI registry

Background Resistant hypertension and renal sympathetic hyperactivity are closely linked, and catheter-based renal denervation (RDN) is regarded as a new treatment strategy. However, the acute changes in vascular morphology and relaxation function have yet to be evaluated, and these may be important for the efficacy and safety of the procedure. In this study, we explored these questions by conventional temperature-controlled cardiac radiofrequency catheter-based RDN in a pig model. Methods Six mini-pigs were randomly divided into the renal denervation (RDN) group (n = 3) and the Sham-RDN group (n = 3). Animals in the RDN group underwent unilateral radiofrequency ablation, and those in the Sham-RDN group underwent the same procedure except for the ablation. The pigs were examined by angiography pre- and post-RDN and were euthanized immediately thereafter. Renal arteries were processed for histological and molecular biology analyses as well as for in vitro vascular tension testing. Results Compared with the Sham-RDN group, the RDN caused vascular intima and media injury, renal nerve vacuolization, mild collagen fiber hyperplasia and elastic fiber cleavage (all p

Background Vascular endothelial growth factor ( VEGF ) exerts a number of beneficial effects on ischemic myocardium via its angiogenic properties. However, little is known about whether VEGF has a direct effect on the electrical properties of cardiomyocytes. In the present study, we investigated the effects of different concentrations of VEGF on delayed rectifier potassium currents ( I K ) in guinea pig ventricular myocytes and their effects on action potential ( AP ) parameters. Methods and Results I K and AP were recorded by the whole‐cell patch clamp method in ventricular myocytes. Cells were superfused with control solution or solution containing VEGF at different concentrations for 10 minutes before recording. Some ventricular myocytes were pretreated with a phosphatidylinositol 3‐kinase inhibitor for 1 hour before the addition of VEGF . We found that VEGF inhibited the slowly activating delayed rectifier potassium current ( I K s ) in a concentration‐dependent manner (18.13±1.04 versus 12.73±0.34, n=5, P =0.001; 12.73±0.34 versus 9.05±1.20, n=5, P =0.036) and prolonged AP duration (894.5±36.92 versus 746.3±33.71, n=5, P =0.021). Wortmannin, a phosphatidylinositol 3‐kinase inhibitor, eliminated these VEGF ‐induced effects. VEGF had no significant effect on the rapidly activating delayed rectifier potassium current ( I K r ), resting membrane potential, AP amplitude, or maximal velocity of depolarization. Conclusions VEGF inhibited I K s in a concentration‐dependent manner through a phosphatidylinositol 3‐kinase–mediated signaling pathway, leading to AP prolongation. The results indicate a promising therapeutic potential of VEGF in prevention of ventricular tachyarrhythmias under conditions of high sympathetic activity and ischemia.

Background The QT interval, an index of ventricular repolarization, is rate dependent. Exaggerated rate dependence of repolarization is arrhythmogenic. Whether there are differences in rate-dependent repolarization among different heart chambers is unknown. Objective The purpose of this study was to test our hypothesis that heterogeneous distribution in late sodium current (INa-L) is responsible for interregional differences in rate adaptation of repolarization. Methods Action potential duration (APD), QT intervals, and their rate adaptation were studied in isolated arterially perfused ventricular and atrial wedge preparations. APD and INa-L were recorded in isolated rabbit myocytes using the microelectrode and the whole-cell patch clamp technique, respectively. Results There were distinct interregional differences in repolarization and its rate adaptations among different cardiac chambers: the left ventricle exhibited the longest QT and APD with the greatest rate dependence, followed by the right ventricle, whereas the atria had the shortest APD without significant rate dependence. Interestingly, INa-L densities distributed heterogeneously and matched to interregional APDs and rate dependences as follows: left ventricle > right ventricle > left/right atria. Both dofetilide (an IKr blocker) and anemone toxin (a specific INa-L enhancer) amplified QT/APD rate adaptation preferentially in the left ventricle and therefore exacerbated interregional dispersion of repolarization. On the other hand, the atria exhibited blunted responses to both QT-prolonging agents. Mexiletine with an INa-L blockade effect blunted QT/APD rate adaptation preferentially in the ventricles and significantly reduced bradycardia-dependent interregional dispersion of repolarization. Conclusion Our results demonstrate that heterogeneous distribution of INa-L contributes importantly to the interregional heterogeneity of repolarization in response to rate changes and APD/QT-prolonging agents.

To compare and analyze the effect and the safety of the paclitaxel-eluting stents and paclitaxel-eluting balloon in the treatment for in-stent rest enosis. 120 cases, who had been undergone percutaneous coronary intervention (PCI) in the Department of Cardiology of Henan Provincial People's Hospital from January 2012 to January 2014 were selected. All the patients were randomly treated with paclitaxel-eluting balloon or paclitaxel-eluting stents. The former were divided into different groups that named group A and the later group B. All the selected patients signed the informed consent on interventional therapy and be given anti-platelet drugs before operating. At the same time, they had routine examination, like chest X-ray, ultrasound, biochemical detection, Myocardial injury markers. (1) The two groups had no significant difference in the general information (P0.05); (2) The success rate in the two groups reached 100% and (3) All the patients were visited in the 9th, 12th and 24th month to see if any of them was dead. The reexamination results in the 9th month showed that both drug-eluting balloon and drug-eluting stents were safe and effective in treating coronary artery in-stent restenosis. In addition, drug-eluting balloon was more effective than drug-eluting stents to prevent from the in-stent restenosis.

Background Although atrial fibrillation ( AF ) is the most common abnormal heart rhythm and its prevalence continues to rise, there is a marked paucity of effective and safe antiarrhythmic drugs for AF . This study was done to test whether combined use of dofetilide and mexiletine exhibits not only a synergistic effect on AF suppression but also a safer profile in drug‐induced ventricular proarrhythmias. Methods and Results The effects of dofetilide plus mexiletine on atrial effective refractory period ( ERP ), AF inducibility, QT , and QT ‐related ventricular arrhythmias were studied using the isolated arterially perfused rabbit atrial and ventricular wedge preparations. Dofetilide or mexiletine alone mildly to moderately prolonged atrial ERP , but their combined use produced a markedly rate‐dependent increase in atrial ERP . Dofetilide (3 nmol/L) plus mexiletine (10 μmol/L) increased the ERP by 28.2% from 72.2±5.7 to 92.8±5.9 ms (n=9, P P AF inducibility. On the other hand, dofetilide at 10 nmol/L produced marked QT and T p‐e prolongation, steeper QT ‐ BCL and T p‐e ‐ BCL slopes, and induced early afterdepolarizations and torsade de pointes in the ventricular wedges. Mexiletine at 10 μmol/L reduced dofetilide‐induced QT and T p‐e prolongation, QT ‐ BCL and T p‐e ‐ BCL slopes, and abolished early afterdepolarizations and torsade de pointes. Conclusions In rabbits, combined use of dofetilide and mexiletine not only synergistically increases atrial ERP and effectively suppresses AF inducibility, but also markedly reduces QT liability and torsade de pointes risk posed by dofetilide alone.

Objective Diabetes substantially increases the risk of cardiovascular disease (CAD) and is associated with an increased risk of CAD mortality. The purpose of this study was to investigate the differences in coronary artery plaque, coronary artery calcification (CAC) measured in outpatients with and without type 2 diabetes, and the occurrence rate of a major adverse cardiac event (MACE) throughout follow-up with the same patients. Methods Five hundred eighty-eight outpatients with suspected CAD comprising 208 diabetic and 380 non-diabetic patients were enrolled in this study. Coronary artery plaque and CAC scores were detected and measured by dual-source computed tomography. The major MACE during the follow-up period (4.0–20 months) was recorded and its relationship to type 2 diabetes and CAC was investigated. Results The diabetes group had higher CAC scores in the left anterior descending, left circumflex, and right coronary arteries and total CAC burden than the group without diabetes. The diabetes group had more diseased coronary segments and more obstructed vessels than the non-diabetes group. Logistic regression analysis demonstrated that diabetes is positively associated with mixed coronary plaque and non-calcified plaque. All patients in the diabetes group and all patients with higher CACs in both groups had a higher incidence rate of MACEs. Conclusion Patients with type 2 diabetes have a higher prevalence of obstructive CAD, higher CAC scores, and a higher incidence rate of MACEs than those without diabetes. Diabetes and higher CAC scores were the important predictors of the occurrence of MACEs throughout follow-up with patients.

The safety and efficacy of rivaroxaban in the periprocedural anticoagulation for patients undergoing catheter ablation of atrial fibrillation is not well established. We sought to systematically review this evidence using data from multiple studies. A thorough literature search was conducted in MEDLINE, EMABSE, Web of knowledge, clinicaltrials.gov, and the Cochrane library up to November 2014. Studies of at least 100 patients in rivaroxaban and warfarin groups were included. Nine observational studies were identified enrolling a total of 4,334 patients (1,210 treated with rivaroxaban and 3,124 with warfarin). The primary outcomes were thromboembolic events and major bleeding. The fixed-effects model meta-analysis was performed and risk ratios (RRs) were calculated. No significant differences were found between patients treated with rivaroxaban and warfarin with regard to thromboembolic events (0.25% rivaroxaban vs. 0.29% warfarin; RR: 0.61; 95%CI: 0.21-1.76; P=0.36) and major bleeding (1.03% rivaroxaban vs. 1.83% warfarin; RR: 0.51; 95%CI: 0.26-1.00; P=0.05). This meta-analysis suggests that patients treated with rivaroxaban have a similar incidence of thromboembolic events and major bleeding compared to warfarin. Signals were seen favoring rivaroxaban; however, considering low events rates, more high-quality studies are necessary to thoroughly compare the two strategies.

To survey the association of serum free triiodothyronine (FT3) level with coronary artery calcification and major adverse cardiac events (MACE) in outpatients with suspected coronary artery disease (CAD).A total of 577 outpatients with suspected CAD, who underwent dual-source computed tomography and FT3 detection were included, patients were followed up for 8-29 months for the major adverse cardiac events (death, MI, PCI, CABG). These patients were divided into low FT3 (3.5 pmol/L, n = 126) and normal FT3 ( ≥ 3.5 pmol/L, n = 451) group based on the FT3 level, and divided into CACS100 (n = 235) and CACS ≤ 100 (n = 342) group based on the coronary artery calcium score (CACS). Related factors to CACS and MACE were analyzed using logistic regression (stepwise) analysis.CACS (146.7 (55.8, 599.1) vs. 34.8 (0, 261.9), P0.001) and MACE (7.9% (10/126) vs. 2.0% (9/451) , P = 0.003) were significantly higher in the low FT3 group than in normal FT3 group. Logistic regression analysis demonstrated that the FT3 levels are inversely associated with the CACS (OR = 0.442, 95%CI = 0.317-0.618, P0.001). Kaplan-Meier analysis displayed that patients with low FT3 levels had a lower cumulative survival rate than patients with normal FT3 levels (P = 0.005), and patients with CACS100 also had a lower cumulative survival rate than patients with CACS ≤ 100(P0.001).FT3 levels are associated with coronary artery calcification scores and the incidence rate of MACE in patients with suspected coronary artery disease. A low FT3 level is considered as an important risk factor of high calcification scores and MACE.

Considerable evidence suggests that thyroid dysfunction, especially hypothyroidism, may lead to coronary artery disease (CAD). The aim of this study is to investigate the effect of low serum levels of free triiodothyronine (FT3) on coronary artery calcification in outpatients with suspected CAD and the occurrence rate of major adverse cardiac events (MACE) in these patients.A total of 588 outpatients with suspected CAD were enrolled in this study. The patients' blood samples were assayed for FT3, free thyroxine, thyroid stimulating hormone and serum lipids. On the basis of FT3 levels, these patients were divided into low FT3 (FT33.5 pmol/l; n=127) and normal FT3 (≥3.5 pmol/l; n=461) groups. Coronary artery calcification scores (CACS) were measured using dual-source computed tomography. The occurrence of MACE was recorded during the follow-up period (8-29 months) and their relationship with FT3 levels was investigated.Patients with low FT3 levels had higher CACS (337.52±339.36 vs. 194.89±347.29, P0.001) and a higher incidence of MACE (7.9 vs. 2.2%, P=0.002) compared with those with normal FT3 levels (≥3.5 pmol/l). Logistic regression analysis showed that the FT3 levels are inversely associated with CACS (odds ratio=0.463, 95% confidence interval=0.282-0.761, P=0.002) and patients with CACS greater than 100 have lower FT3 levels than those with lower CACS (P0.001). Kaplan-Meier analysis showed that patients with low FT3 levels have a higher incidence of MACE.FT3 levels were inversely associated with CACS and the incidence of MACE in patients with suspected CAD. A low FT3 level was an important predictor of the occurrence of MACE.

ObjectivesThis study aimed to survey the adherence to smoking cessation and assess the influence of persistent smoking on the prognosis in male patients after drug-eluting stent (DES) implantation.MethodsThe smoking status at the time of the index procedure and at follow-up was surveyed in 656 male patients undergoing successful percutaneous coronary intervention (PCI) with DES in our center. These patients were divided into three groups, based on their smoking status: nonsmokers (n=226), quitters (n=283), and persistent smokers (n=147). Major adverse cardiac and cerebrovascular events (MACCE) during the follow-up period were carefully recorded and their relationship with smoking status was investigated for 24–41 months.ResultsAmong 656 patients who were followed up for 27.24±6.33 (7–40) months, 430 of them were smokers (65.5%) at the index procedure. A total of 147 patients (22.4%) who continued to smoke, accounted for 34.2% of smokers at the time of PCI. Persistent smokers and quitters were more likely to be young (p

BackgroundAbnormal thyroid hormone metabolism influences the occurrence and progress of coronary heart disease (CHD). The aim of the present study was to analyze the severity of coronary artery lesions and the prognosis of thyroid dysfunction patients admitted for coronary angiography (CAG).MethodsFrom July 2011 to July 2012, 605 consecutive patients with suspected coronary heart disease admitted for CAG were selected. The patients were divided into three groups, based on their thyroid function prior to CAG: euthyroid group (n=455 patients), low T3 syndrome group (n=96 patients), and hypothyroidism group (n=54 patients). All patients underwent CAG. Then the severity of coronary artery lesions was assessed by Gensini scores. All patients were followed up for major adverse cardiac events.ResultsThe prevalence of CHD in low T3 syndrome group and hypothyroidism group was significantly higher than that in the euthyroid group (p