In the last three decades, great achievements have been made in the field of cardiovascular medicine. The rapid development of new drugs, the invention of novel devices and techniques, all of these, have significantly decreased the mortality and morbidity from cardiovascular disease. Mortality and morbidity rates fell by at least 50% from about 1980 to 2000. However, are we winning the war against cardiovascular disease?

Objective: Percutaneous coronary intervention (PCI) triggers an acute inflammatory response, while sirolimus is known to have anti-inflammatory properties; the inflammatory system response to PCI after sirolimus-eluting stent placement remains unclear. The purpose of this study is to determine the changes in high sensitive C-reactive protein (hs-CRP) and apelin after PCI procedure and drug-eluting stent implantation in patients with and without reduced left ventricular systolic function. Methods: Forty-eight consecutive patients undergoing PCI at the Beijing Anzhen Hospital between July and September 2006 were recruited. Sirolimus-eluting stents were employed in all patients. Blood samples were drawn immediately before and 24 h after the procedure. Plasma hs-CRP and apelin levels were determined by enzyme immunoassay. Results: Paired t-test revealed a significant increase in both hs-CRP and apelin post-procedure (P=0.006 and P<0.0001, respectively). Patients with reduced left ventricular ejection fraction (LVEF) had significantly lower baseline apelin levels compared to those with normal ventricular function [(46.8±10.8) vs. (72.0±8.4) pg/ml, P<0.001]. However, apelin increased to a level similar to the level of those with normal left ventricular systolic function 24 h after the PCI procedure [(86.7±11.6) vs. (85.1±6.1) pg/ml, P=0.72]. Conclusions: hs-CRP and apelin levels increased after PCI and sirolimus-eluting stent implantation. Patients with impaired left ventricular systolic function had significantly lower baseline apelin levels, which increased significantly after PCI.

Objective: Although drug-eluting stent (DES) implantation is the primary treatment modality for bare-metal stent (BMS) in-stent restenosis (ISR), little is known about the efficacy and safety profile of DES in the treatment of DES-ISR. The goal of this study was to compare the clinical outcomes following DES treatment for BMS-ISR and DES-ISR. Methods: Rates of major adverse cardiac events (MACE) were compared in 97 consecutive patients who underwent DES implantation for the treatment of ISR (56 BMS-ISR and 41 DES-ISR) from January 2004 to December 2008. Results: Baseline clinical and procedural characteristics were comparable, except that the DES used in the BMS-ISR group was longer and had a larger diameter. The length of follow-up was (28.60±1.96) and (20.34±1.54) months for the BMS-ISR and DES-ISR groups, respectively. One patient (1.8%) experienced non-cardiac mortality and one (1.8%) had target-vessel revascularization (TVR) in the BMS-ISR group. In the DES-ISR group, three patients (7.3%) died of sudden death with a documented acute ST-segment elevation myocardial infarction, and three suffered TVR (7.3%). Kaplan-Meier analysis indicated that cumulative survival probability and MACE-free probability were both significantly lower for the DES-ISR group (log rank test P=0.047 and P=0.005, respectively). In Cox regression analysis, DES-ISR remained an independent predictor for future MACE occurrence after adjustment for other factors (compared with BMS-ISR, risk ratio (RR)=8.743, 95% confidence interval (CI) 1.54–49.54, P=0.014). Switching to a different type of DES to treat DES-ISR did not improve the prognosis. Conclusion: DES-ISR patients had a poorer prognosis than BMS-ISR patients after DES therapy.

Renal artery stenosis (RAS) with a bifurcation lesion is a challenge for interventional therapy. The aim of this study is to summarize our experience in RAS with a bifurcation lesion. Five patients with RAS involving bifurcation lesion are described. In cases 1 to 3, a single-stent strategy was first adopted. However, these three patients were converted to a two-stent strategy for bailout stent implantation in the side branches. In cases 4 and 5, a simultaneous kissing stent technique was performed. Angiography showed that the reference vascular diameter of the main branch was much larger than those of the side branches. Although obvious residual stenosis existed in cases 1 to 3 after stent implantation, no obvious residual stenosis was seen in cases 4 and 5. Renal artery duplex sonography was performed in cases 1 through 5 at 6, 7, 7, 8, and 6 months, respectively, after the procedures. No evidence of restenosis or occlusion was seen. In conclusion, stent implantation with the simultaneous kissing stent technique may result in more simple and more satisfactory immediate angiographic results.

Objective: The aim of this study is to investigate if dual-source computed tomography (DSCT) could guide the percutaneous coronary intervention (PCI) of chronic total occlusion (CTO). Methods: We enrolled patients who were confirmed to have at least one native coronary artery CTO by DSCT before they underwent selective PCI in the period from December 2007 to October 2008. A CTO was defined as an obstruction of a native coronary artery with no luminal continuity. The CT-guided PCI procedure involved placing CT and fluoroscopic images side-by-side on the screen. DSCT images were analyzed for location, segment, plaque characteristics, calcification, and proximal lumen diameter of the CTO before PCI. The guidewire was advanced and manipulated under CT guidance. The PCI was carried out and the results were compared. Results: Seventy-four CTOs were assessed. PCI was successful in 57 cases of CTOs (77.0%). According to the results, CTOs were divided into two groups: successful-PCI and failed-PCI. All coronary artery paths of CTOs were clearly recognized by DSCT. In the successful-PCI group, soft plaques were detected much more often than those in the failed-PCI group, but fibrous and calcified plaques were seen more often in the failed-PCI group. Calcification severity in CTO segments showed a significant difference between the groups (P=0.014). Calcified plaques were detected in 20 (35.1%) lesions in the successful-PCI group. More than 70% of the failures were calcified plaques, of which there were two arc-calcified and one circular-calcified lesions. Occlusions were longer in the failed-PCI group than those in the successful-PCI group [(38.8±25.0) vs. (18.0±15.3) mm, respectively, P<0.01]. Fewer guidewires were used in the successful-PCI group compared with the failed-PCI group (1.7±1.0 vs. 2.5±0.9, respectively, P<0.01). The logistic regression analysis indicated that predictors of recanalization of CTOs included occlusion length (P=0.0035, risk ratio (RR)=0.93) and calcification severity (P=0.05, RR=0.27). Multi-linear trends analysis showed that the factors affecting procedural time were CTO location (P=0.0141) and occlusion length (P=0.0035). Conclusions: DSCT could delineate the path of CTOs and characterize plaques. The outcomes of PCI were related to thrombolysis in myocardial infarction (TIMI) flow grade, CTO characteristics, severity of calcified plaques, and the length of occlusive segments. Occlusion length and calcification severity were independent predictors of CTOs. Occlusion length and CTO segments could also help to estimate the duration of interventional procedures.

Objective: This study aims to determine the mechanisms underlying restenosis and ischemia-reperfusion injury of the myocardium after percutaneous coronary intervention (PCI). Methods: The present study examined serial changes (5 min, 30 min, 2 h, 6 h, and 24 h after PCI) in circulating P-selectin, plasminogen activator inhibitor-1 (PAI-1), magnesium (Mg), and creatine kinase-myocardial band fraction (CK-MB) levels, which may be associated with restenosis and myocardial injury in patients undergoing PCI. The occurrence rates of major adverse cardiovascular events were collected over a six-month follow-up. Results: PCI induced an early elevation of P-selectin, which correlated positively with the inflation pressure used in the PCI procedure. PCI also caused a significant and sustained decrease in serum Mg in PCI patients, without an effect on PAI-1. An increase in CK-MB was observed in PCI patients, although values were within normal reference range. In addition, elevated P-selectin and decreased Mg measured shortly after the coronary angioplasty procedure were associated with recurrent treatment and heart failure, respectively. Conclusions: Our study demonstrates that PCI induces temporal changes of P-selectin, Mg, and CK-MB, which may be involved in restenosis and ischemia-reperfusion injury. These findings highlight the need for using antiplatelet therapy and Mg to reduce the risks associated with PCI.

Objective: To investigate the effect of enalapril on plasma homocysteine (Hcy) levels and the association of methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism with the changes of Hcy levels in response to enalapril among patients with essential hypertension. Methods: A total of 130 patients with mild-to-moderate essential hypertension were enrolled and enalapril was orally administered at a dose of 10 mg/d for eight weeks. Plasma Hcy levels were measured by denaturing high-performance liquid chromatography (DHPLC) at baseline and after eight weeks of treatment. Genotyping of MTHFR C677T polymorphism was performed by TaqMan probe technique. Results: Compared with baseline, plasma Hcy levels did not change significantly after eight weeks (P=0.81). Stratified by baseline Hcy levels, a significant increase in plasma Hcy levels (P=0.02) among those with Hcy <10 μmol/L was observed, in contrast to no significant changes in plasma Hcy levels (P=0.54) among those with Hcy ≥10 μmol/L. No significant association was observed between MTHFR C677T polymorphism and changes in Hcy levels in response to enalapril. Conclusions: Enalapril may cause an increase in plasma Hcy levels among the hypertensives with low baseline Hcy levels. There was no significant association between MTHFR C677T genotypes and changes in Hcy levels in response to enalapril among subjects with essential hypertension.

Objective: Uric acid (UA) is considered to be a powerful predictor of cardiovascular risk and hyperuricemia might be involved in the metabolic syndrome (MS). This study aims to investigate the relation between UA levels and aortic root dilatation. Methods: A total of 348 hypertensive patients [age (67.5±9.8) years] with or without MS were included in the study. The aortic root diameters at the aortic annulus, the sinuses of Valsalva, the sinotubular junction, and the proximal part of the ascending aorta were measured using a two-dimensional (2D) echocardiography. Serum UA levels were also measured for all patients. Results: A high UA level is independently associated with aortic root diameters at the sinuses of Valsalva (P=0.001) and the proximal ascending aorta (P<0.0001) in the hypertensive patients without MS. In contrast, aortic root diameters were not significantly related to UA levels in the hypertensive patients with MS. Furthermore, increased UA levels were associated with an increased risk for aortic root dilatation in the patients without MS (sex-adjusted hazard ratio 1.75, 95% confidence intervals (CI) 1.27–2.41), but not in those with MS. Conclusions: This study demonstrated an independent relationship between the aortic root dimensions and increased levels of serum UA in the hypertensive patients without MS. Further understanding of the mechanisms underlying these associations may allow a clearer interpretation of the potential value of specific urate-lowering treatment on cardiovascular disease.

Objective: Atherosclerotic plaques and neovascularization play an important role in the course of coronary atherosclerosis. This study evaluated the effect of recombinant endostatin on experimental atherosclerotic plaques and neovascularization in rabbits. Methods: Eighteen healthy male rabbits were divided into three groups: control group, atherosclerotic model group, and recombinant endostatin treated group. The atherosclerotic model was established via a high-cholesterol diet after balloon catheter injury. The subject weights, serum total cholesterol, creatine kinase-myocardial band fraction (CKMB), and matrix metalloproteinase-2 (MMP-2) were measured. Six weeks after treatment, the aortic roots were taken for pathological assay. The thickness ratio of the intima to media was measured by hematoxylin and eosin (HE) staining, and the number of neovessels was measured by immunohistochemistry via monoclonal antibody CD31 staining. Results: The weight, plasma total cholesterol, and CKMB were not significantly different between the atherosclerotic model group and the recombinant endostatin treated group, but much higher than those of the control group (P<0.05). The thickness ratio of the intima to media in the recombinant endostatin treated group was distinctly less than that in the atherosclerotic model group (P<0.05). The number of neovessels decreased dramatically (P<0.05) and the content of MMP-2 decreased slightly without statistical difference (P>0.05) in the recombinant endostatin treated group, compared to the atherosclerotic model group. Conclusions: Recombinant endostatin is able to inhibit the growth of neovascularization in the atherosclerotic plaque and the development of plaque.

Mesenchymal stem cell (MSC) transplantation has shown a therapeutic potential to repair the ischemic and infracted myocardium, but the effects are limited by the apoptosis and loss of donor cells in host cardiac microenvironment. The aim of this study is to explore the cytoprotection of heat shock protein 90 (Hsp90) against hypoxia and serum deprivation-induced apoptosis and the possible mechanisms in rat MSCs. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was assessed by Hoechst 33258 nuclear staining and flow cytometric analysis with annexin V/PI staining. The gene expression of Toll-like receptor-4 (TLR-4) and V-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (ErbB2) was detected by real-time polymerase chain reaction (PCR). The protein levels of cleaved caspase-3, Bcl-2, Bcl-xL, Bax, total-ERK, phospho-ERK, total-Akt, phospho-Akt, and Hsp90 were detected by Western blot. The production of nitric oxide was measured by spectrophotometric assay. Hsp90 improves MSC viability and protects MSCs against apoptosis induced by serum deprivation and hypoxia. The protective role of Hsp90 not only elevates Bcl-2/Bax and Bcl-xL/Bax expression and attenuates cleaved caspase-3 expression via down-regulating membrane TLR-4 and ErbB2 receptors and then activating their downstream PI3K/Akt and ERK1/2 pathways, but also enhances the paracrine effect of MSCs. These findings demonstrated a novel and effective treatment strategy against MSC apoptosis in cell transplantation.

In this study, we examined the protective effects of Danshen both on endothelial progenitor cells (EPCs) in patients with hypercholesterolemia and on in-vitro EPCs of healthy volunteers. In the clinical study, we randomly divided 24 subjects with hypercholesterolemia into two groups (the control group and the Danshen-treated group). At the end of two weeks of treatment, the EPC cellular functions of both groups were tested. The results indicated that, compared to the control group, EPCs in the Danshen-treated group showed significantly better cellular functions, which was manifested in the cloning number, the proliferation capacity, the number of EPC adhesions, and cell migration. In the subsequent in-vitro experiments, EPCs were treated with vehicle, oxidized low-density lipoprotein (Ox-LDL, 100 μg/ml), or Ox-LDL (100 μg/ml) plus different concentrations of Danshen (Danshensu 2, 10, or 50 μg/ml, respectively) for 24 h. The results showed that Danshen treatments can prevent the detrimental effects of Ox-LDL on EPC cellular functions measured by proliferation capacity (0.24±0.08, 0.37±0.11, 0.30±0.04 vs. 0.13±0.02, P<0.05, P<0.01, and P<0.01, respectively), and adhesion ability (63.00±11.60, 70.00±10.80, 85.50±11.41 vs. 40.50±6.85, all P<0.01). Compared to the group treated with Ox-LDL alone, Danshen treatment significantly decreased the lipid peroxidation end product malondialdehyde (MDA) [(4.34±0.54), (3.98±0.47), (3.46±0.31) vs. (5.57±0.64) nmol/ml, all P<0.01], increased the production of superoxide dismutase (SOD) [(29.74±0.71), (31.09±0.83), (30.41±0.65) vs. (14.76±3.99) U/ml, all P<0.01], and lowered the expression of interleukin-6 (IL-6) [(24.62±7.69), (27.04±3.14), (33.38±18.86) vs. (230.67±33.53) pg/ml, all P<0.01] and tumor necrosis factor-α (TNF-α) [(41.72±6.10), (17.02±6.82), (3.73±2.26) vs. (228.71±41.53) pg/ml, all P<0.01] in Ox-LDL treated EPCs. These results suggest that Danshen may exert a protective effect through its antioxidant and anti-inflammatory features.

It is a challenge to confirm chronic mesenteric ischemia (CMI) as a cause of gastrointestinal (GI) symptoms such as postprandial epigastric bloating, anorexia, and debilitating weight loss. Endovascular intervention for CMI has been gaining popularity because of the high morbidity associated with surgical revascularization. However, in EVI for superior mesenteric artery (SMA) occlusion, the transfemoral approach is limited by difficulty in coaxial alignment of the guiding catheter, which leads to insufficient back-up support. Herein, we report on a 58-year-old male patient with chronic total occlusion of the SMA, which was successfully revascularized by endovascular intervention via the left radial artery. Transradial endovascular therapy may be another treatment option for the treatment of CMI.

Dr. Gruntzig et al. (1979) successfully completed the world鈥檚 first percutaneous coronary intervention (PCI), a percutaneous transluminal coronary angioplasty (PTCA), in 1977. The first reported PTCA in China was in 1984. With the development of PCI techniques, while more and more patients have benefited, there are ongoing challenges as well.

Over the last five decades, pacemaker therapy has undergone remarkable technological advances with increasing sophistication of pacemaker features. However, device longevity has remained one of the major issues in pacemaker design ever since the first endocardial pacing lead implantation in 1958. In addition to various hardware design to enhance device longevity, software-based solutions to minimize pacing energy and yet with good safety margin have also been developed. Together with desire and need of fully automatic pacing system in increasingly busy pacemaker clinic, several manufacturers have introduced different automatic threshold management algorithm. This article summarizes the current state-of-the-art management in pacing threshold in the modern pacemakers.