Importance The appropriate follow-up surveillance strategy for patients with acute coronary syndrome (ACS) who have undergone percutaneous coronary intervention (PCI) remains unknown. Objective To assess clinical outcomes in patients with and without ACS who have undergone high-risk PCI according to a follow-up strategy of routine stress testing at 12 months after PCI vs standard care alone. Design, Setting, and Participants The POST-PCI (Pragmatic Trial Comparing Symptom-Oriented vs Routine Stress Testing in High-Risk Patients Undergoing Percutaneous Coronary Intervention) trial was a randomized clinical trial that compared follow-up strategies of routine functional testing vs standard care alone 12 months after high-risk PCI. Patients were categorized as presenting with or without ACS. Patients were enrolled in the trial from November 2017 through September 2019, and patients were randomized from 11 sites in South Korea; data analysis was performed in 2022. Intervention Patients categorized as presenting with or without ACS were randomized to either a routine functional testing or standard care alone follow-up strategy 12 months after high-risk PCI. Main Outcomes and Measures The primary outcome was a composite of death from any cause, myocardial infarction, or hospitalization for unstable angina at 2 years following randomization. Kaplan-Meier event rates through 2 years and Cox model hazard ratios (HRs) were generated, and interactions were tested. Results Of 1706 included patients, 350 patients (20.5%) were female, and the mean (SD) patient age was 64.7 (10.3) years. In total, 526 patients (30.8%) presented with ACS. Compared with those without ACS, patients with ACS had a 55% greater risk of the primary outcome (HR, 1.55; 95% CI, 1.03-2.33; P = .03) due to higher event rates in the first year. The 2-year incidences of the primary outcome were similar between strategies of routine functional testing or standard care alone in patients with ACS (functional testing: 16 of 251 [6.6%]; standard care: 23 of 275 [8.5%]; HR, 0.76; 95% CI, 0.40-1.44; P = .39) and in patients without ACS (functional testing: 30 of 598 [5.1%]; standard care: 28 of 582 [4.9%]; HR, 1.04; 95% CI, 0.62-1.74; P = .88) ( P for interaction for ACS = .45). Although a landmark analysis suggested that the rates of invasive angiography and repeat revascularization were higher after 1 year in the routine functional testing group, the formal interactions between ACS status and either invasive angiography or repeat revascularization were not significant. Conclusion and Relevance Despite being at higher risk for adverse clinical events in the first year after PCI than patients without ACS, patients with ACS who had undergone high-risk PCI did not derive incremental benefit from routine surveillance stress testing at 12 months compared with standard care alone during follow-up. Trial Registration ClinicalTrials.gov Identifier: NCT03217877

BACKGROUND AND AIMS:The Apo B/A1 ratio is a major factor that predicts future cardiovascular outcomes. However, it is unclear whether the apolipoprotein B (Apo B)/apolipoprotein A1 (Apo A1) is a better predictor of future outcome than the total cholesterol (TC)/HDL-C ratio or lipoprotein (a) (Lp (a)) after the percutaneous coronary intervention (PCI). Therefore, we performed this study to evaluate the impact of the Apo B/A1 ratio on the patients who achieved LDL-C below 70 mg/dL one year after PCI.METHODS:We included 448 PCI patients whose LDL-C levels were below 70 mg/dL at follow-up. The Apo B/A1 ratio, TC/HDL-C ratio, and Lp (a) levels were measured at the time of PCI and follow-up, and decreases in these parameters between baseline and follow-up were assessed as potential markers to predict major cardiovascular adverse events (MACEs).RESULTS:During a median follow-up period of 38.0 months, 115 MACEs were recorded. The tertile with the lowest decrease in the Apo B/A1 ratio (≤ 0.146) showed a lower MACE survival rate compared to the other tertiles. There were no differences in MACE survival rates for the TC/HDL-C ratio or Lp (a) levels.CONCLUSIONS:The Apo B/A1 ratio had better predictive accuracy for clinical outcomes compared to the TC/HDL-C ratio and Lp (a) level. A lower decrease in the Apo B/A1 ratio may be a residual risk factor for MACEs in patients who have reached LDL-C levels below 70 mg/dL after PCI.

Background:The clinical efficacy and safety of second-generation drug-eluting stents in complex percutaneous coronary interventions (PCIs) are not well established.Objectives:The clinical influence of the lesion complexity after PCI with zotarolimus-eluting stents (ZES) was evaluated.Methods:From a prospective multicenter observational study, a total of 926 patients that underwent successful PCIs with ZES were included. Complex PCIs were defined as patients with ≥3 lesions treated, 3 vessels treated, severe calcified lesions, bifurcated lesions with 2 stents implanted, left main disease, chronic total occlusion lesions, and/or diffuse long (total stent length ≥60 mm) lesions and were compared to the noncomplex group. The primary outcome was incidence of target lesion failures at 2 years, defined as a composite of cardiac death, target lesion-myocardial infarctions, and target lesion revascularization.Results:The patients were divided into complex PCI (n = 249) and noncomplex (n = 677) groups. In the complex PCI group, the 2-year risk of a target lesion failure was not significantly higher than in the noncomplex PCI group (4.8% vs 3.7%; adjusted hazard ratio: 1.373; 95% confidence interval: 0.689-2.738; P = 0.367). The same trend was observed for all composites of the clinical outcomes. Older age and advanced chronic kidney disease were independent predictors for the primary outcome.Conclusions:Up to 2 years after a ZES implantation, the clinical outcomes did not differ according to lesion complexity.

Hypertension has been associated with atherosclerosis and cardiovascular disease. Carotid intima media thickness is increased in hypertensive patients. But, the correlation between carotid intima media thickness and antihypertensive agents is still uncertain. Therefore, we investigated carotid intima media thickness based on types of antihypertensive agents. 1809 patients were enrolled in this study and it showed that 1079 hypertensive patients had thicker carotid intima media thickness than non‐hypertensive patients, with carotid intima media thicknesses of (0.72 ± 17 mm vs 0.64 ± 15 mm, P < .001), (0.31 ± 0.07 mm vs 0.30 ± 0.06 mm, P < .001), and (0.41 ± 0.13 mm vs 0.35 ± 0.12 mm, P < .001). Additionally, hypertensive patients on beta‐blockers also had thicker carotid intima media thickness than the non‐beta‐blocker group, with carotid intima media thicknesses of (0.74 ± 0.18 mm vs 0.71 ± 0.16 mm, P = .018), (0.33 ± 0.09 mm vs 0.31 ± 0.07 mm, P = .029), and (0.43 ± 0.13 mm vs 0.40 ± 0.13 mm, P = .035). Multivariate analysis showed that carotid intima thickness was only correlated with beta‐blockers (odds ratio = 2.489, confidence interval = 1.183‐5.239, P = .016); however, this study showed that beta‐blocker could be associated with increased carotid wall thickness as well.

Objective: Salt-taste threshold can influence salt appetite, and is thought to be another marker of sodium intake. Many studies mentioned the relationship between sodium intake and blood pressure. The aim of this study was to evaluate the relationship the salt-taste threshold and urinary sodium excretion between normotension and hypertension. Design and Method: We enrolled 172 patients (mean age 52 yrs, male 85 (49.4 %)), who was visited our clinic for further evaluation of high blood pressure. Hypertension was diagnosed as day time systolic/diastolic BP > 135/85mmHg by ambulatory BP monitoring. We compared the salt taste threshold assessed by graded solutions of saline and 24-hour urinary sodium excretion. Results: The salt-taste threshold was not significant between normotensive (51 patients (29.7%), mean age 53 years) and hypertensive patients (121 patients (70.3%), mean age 51 years)(6.6 ± 1.1 vs. 6.7 ± 1.2, respectively). The 24-hour urinary sodium excretion of hypertensive patients was significant higher than normontensive patients (143.8 ± 63.8 mg vs 120.0 ± 61.4 mg, respectively, P < 0.05). Also, the ration of urinary sodium-potassium was significantly higher in the hypertensive patients. However, there is no relationship between the salt-taste threshold and 24-hour urinary sodium excretion in the both groups. Conclusions: The salt-taste threshold might be not related to blood pressure status as well as urinary sodium excretion.

Summary Aim It is still unclear which layer (intima or media) is mainly involved in increased carotid intima‐media thickness ( CIMT ) by aging and also unclear regarding CIMT value suggesting high cardiovascular risk, although 75th percentile value of CIMT is known as a high risk in asymptomatic adults. We sought to find the changes of carotid intima thickness ( CIT ) and carotid media thickness ( CMT ) by aging and the 75th percentile value of CIMT in asymptomatic Korean adults. Method This is an observational cohort study. Carotid ultrasound findings (n=2204 from 12 hospitals) were prospectively collected. The carotid images were sent to Korea Research Institute of Standards and Science for analysis using specialized software which can measure intima and media wall also. Results Mean age was 58.1±13.5 years old (52% of men). Pearson's correlation coefficient between age and right CIMT ( r =.489, P <.001) and right CMT ( r =.482, P <.001) was higher than that between age and right CIT ( r =.284, P <.001). Mean right CIMT in male and female was 0.696±0.163 and 0.686±0.167 mm ( P =.180), and the 75 percentile value was 0.778 and 0.771 mm, respectively. Mean right CIT was 0.311±0.069 and 0.303±0.064 mm ( P =.009), and mean right CMT was 0.391±0.124 and 0.388±0.131 mm ( P =.694) in male and female, respectively. Left carotid ultrasound findings showed similar to the right one. Conclusion An increased CIMT by aging was mainly due to increased CMT rather than CIT in asymptomatic adults. The 75th percentile values of right CIMT were 0.778 and 0.771 mm in asymptomatic Korean male and female adults, respectively.

Few simple and effective tools are available for determining the prognosis of 30-day survivors after acute myocardial infarction. We aimed to assess whether the simple age, creatinine, and ejection fraction (ACEF) score could predict 1-year mortality of 12,000 post-myocardial infarction 30-day survivors who underwent percutaneous coronary intervention. The ACEF score was computed as follows: (age/ejection fraction)+1, if the serum creatinine was >2 mg/dl. Accuracy was defined through receiver-operating characteristics analysis and area under the curve (AUC) evaluation. Twelve risk factors were selected and ranked according to their AUC value. Age, ejection fraction, and serum creatinine levels indicated the best AUC value. The ACEF score was significantly higher in the nonsurvivors (1.95±0.82 vs 1.28±0.50; p<0.001) and was an independent predictor of 1-year mortality (adjusted hazard ratio 2.26; p<0.001). The best accuracy was achieved by a prediction model including 12 risk factors (AUC=0.80), but this did not significantly differ compared with the AUC (0.79) of the ACEF score (p=ns). Adjusted hazard ratios for 1-year mortality were 1 (reference), 3.11 (p<0.001), and 10.38 (p<0.001) for the ACEFLOW (ACEF score<1.0), ACEFMID (ACEF score 1.0 to 1.39), and ACEFHIGH (ACEF score≥1.4) groups, respectively. The ACEF score may be a novel valid model to stratify the 1-year mortality risk in 30-day survivors who underwent percutaneous coronary intervention after acute myocardial infarction.

The increased proliferation and migration of vascular smooth muscle cells (VSMC) are key process in the development of atherosclerosis lesions. Platelet-derived growth factor (PDGF) initiates a multitude of biological effects that contribute to VSMC proliferation and migration. Apamin, a component of bee venom, has been known to block the Ca(2+)-activated K(+) channels. However, the effects of apamin in the regulation PDGF-BB-induced VSMC proliferation and migration has not been identified. In this study, we investigate the inhibitory effect of apamin on PDGF-BB-induced VSMC proliferation and migration. Apamin suppressed the PDGF-BB-induced VSMC proliferation and migration with no apparent cytotoxic effect. In accordance with these findings, apamin induced the arrest of cell cycle progression at G0/G1 phase. Apamin also decreased the expressions of G0/G1 specific regulatory proteins including proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin-dependent kinases (CDK) 4, cyclin E and CDK2, as well as increased the expression of p21(Cip1) in PDGF-BB-induced VSMC. Moreover, apamin inhibited PDGF-BB-induced phosphorylation of Akt and Erk1/2. These results suggest that apamin plays an important role in prevention of vascular proliferation and migration through the G0/G1 cell cycle arrest by PDGF signaling pathway. Thus, apamin may be a promising candidate for the therapy of atherosclerosis.

Background— Procedural and clinical outcomes still remain unfavorable for patients with long coronary lesions who undergo percutaneous coronary intervention. The current study, therefore, evaluated 2 innovative drug-eluting stents for the management of long-lesion coronary artery disease. Methods and Results— This randomized, multicenter, prospective trial, called the Long Drug-Eluting Stent (LONG-DES) V trial, compared the biodegradable polymer–based biolimus A9–eluting stent (BES) and the durable polymer–based platinum chromium everolimus-eluting stent (PtCr-EES) in 500 patients with long (≥25 mm) coronary lesions. The primary end point of the trial was in-segment late luminal loss at the 9-month angiographic follow-up. The BES and PtCr-EES groups had similar baseline characteristics, with a slightly shorter lesion length in the BES group versus the PtCr-EES group (29.24±12.17 versus 32.27±13.84 mm; P =0.016). In-segment late luminal loss was comparable between the 2 groups at the 9-month angiographic follow-up (BES, 0.14±0.38 versus PtCr-EES, 0.11±0.37 mm; difference, 0.031; 95% confidence interval, −0.053 to 0.091; P =0.03 for a noninferiority margin of 0.11, P =0.45 for superiority), as was in-stent late luminal loss (0.20±0.41 versus 0.24±0.38 mm; P =0.29). The incidence of in-segment (6.1% versus 4.9%; P =0.63) and in-stent (3.7% versus 4.9%; P =0.59) binary restenosis was also similar between the groups. There was no significant between-group difference in the rate of composite outcome of death, myocardial infarction, and target vessel revascularization (41, 16.7% in BES versus 42, 16.5% in PtCr-EES; P =0.94). Conclusions— BES and PtCr-EES implantation showed analogous angiographic and clinical outcomes for patients with de novo long coronary lesions. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01186120.

The left ventricular (LV) systolic function in patients with ST elevation myocardial infarction (STEMI) has been well known as prognostic factor. Still, decrease of LV systolic function remains due to stunned myocardium even though early revascularization preserves LV systolic function in patients with acute STEMI. There is a possible association between LV remodeling following acute MI and high Sensitivity C-reactive protein (hs-CRP). In this study, we investigated whether hs-CRP is a predictor for improvement of ejection fraction in patients with acute STEMI with successful reperfusion and preserved LV systolic function.

An infectious burden has been suggested to be associated with atherosclerosis in humans, based on the shared and underlying inflammatory responses during infection and atherosclerosis. However, the efficacy of anti-atherogenic drugs is yet to be tested against atherosclerosis in a scenario involving an infectious burden. We have examined alpha-lipoic acid (ALA) for anti-atherogenic effects in a hypercholesterolemic diet-induced atherosclerotic mouse model with inflammatory stimulation. C57BL/6 mice were fed with a hypercholesterolemic diet for 12 weeks to induce atherosclerosis. Lipopolysaccharide was intraperitoneally injected for the 1st week of study to simulate underlying infectious burden during development of atherosclerosis. ALA treatment alleviated atherosclerotic pathologies and reduced serum cholesterol and inflammatory cytokines. Consistently, atherosclerotic markers were improved by ALA treatment. In addition, ALA attenuated the proliferation and migration of vascular smooth muscle cells upon platelet-derived growth factor stimulation through the targeting of the Ras-MEK1/2-ERK1/2 pathway. This study demonstrates the efficacy of ALA on atherosclerosis with immunological complication, by showing that ALA modulates multiple pathogenic aspects of atherosclerosis induced by a hypercholesterolemic diet with inflammatory stimulation consisting of hypercholesterolemia, inflammation and VSMC activation.

The objective of the present study was to assess global and regional left ventricular diastolic function in SLE patients when compared to healthy individuals using echocardiography. A total of 104 SLE patients (mean age: 43.7 years, female: 96) were enrolled and matched to 104 control subjects on

The development of atherosclerotic lesions is mainly due to macrophage death. The oxidative stresses of monocytes/macrophages play a vital role in the initiation and amplification of atherosclerosis. Apamin, a component of bee venom, exerts an anti-inflammatory effect, and selectively inhibits the Ca(2+)-activated K(+) channels. The mechanisms involved in the inhibition of macrophage apoptosis have been fully elucidated. We induced oxidized low-density lipoprotein (oxLDL) in THP-1-derived macrophage and studied the effect of apamin on intercellular lipid levels, mitochondria-related apoptotic pathway and numbers of apoptotic cells. Oil-red O staining indicates that the inhibition of apamin in the condition significantly prevents intracellular lipid deposition. Treatment with apamin significantly decreased the apoptotic macrophages by decreasing the expression of pro-apoptotic genes Bax, caspase-3 and PARP protein levels, as well as through increasing expression of anti-apoptotic genes Bcl-2 and Bcl-xL protein levels in the absence and presence of oxLDL. In vivo, with apamin treatment reduced apoptotic cells death by TUNEL staining. These results indicate that apamin plays an important role in monocyte/macrophage apoptotic processing, which may provide a potential drug for preventing atherosclerosis.

Atherosclerosis is a multifactorial and progressive disease in which the inflammatory reaction and inflammation‐related factors play important roles at all stages. Modulation of NF‐κB and Sp1 expression may be important targets for the prevention and treatment of atherosclerotic vascular disease. To develop a novel therapeutic approach in atherosclerosis, we examined the simultaneous suppression of the transcription factors NF‐κB and Sp1 which regulate inflammation. We employed chimeric decoy oligodeoxynucleotide (ODN) containing the consensus of NF‐κB and Sp1‐binding sites to suppress these transcription factors simultaneously and to test chimeric decoy for anti‐atherogenic effects in an atherogenic diet‐induced atherosclerotic mouse model with inflammatory stimulation. C57BL/6 mice were fed with an atherogenic diet (15% fat, 1.25% cholesterol and 0.5% cholic acid) for 12 weeks to induce atherosclerosis; lipopolysaccharide (LPS, 2 mg/kg) was intraperitoneally injected in the first week of study to simulate underlying infectious burden during development of atherosclerosis. Decoy ODNs were injected into tail vein at 2, 4, 6, 8, 10 and 12 weeks after only three LPS injections in mice fed the atherogenic diet. Chimeric decoy ODN alleviated atherosclerotic changes and reduced serum cholesterol and inflammatory cytokines. In accordance with these results, the expressions of atherosclerotic markers were inhibited by chimeric decoy ODN. Chimeric decoy ODN modulates multiple pathogenic aspects of an atherogenic diet‐induced atherosclerosis with inflammatory stimulation: hypercholesterolaemia and inflammation. Therefore, this study demonstrates the efficacy of chimeric decoy ODN on atherosclerosis with immunological complication.

AIM:Atherosclerosis is influenced by multiple environmental factors that involve a complex interaction between blood components and the arterial wall and is characterized by inflammatory reactions. Melittin has been used in treatment of various chronic inflammatory diseases. We investigated the effects of melittin regulated atherosclerotic changes in an animal model of atherosclerosis.METHODS:Atherosclerotic mice were induced by intraperitoneal (i.p) injection of lipopolysaccharide (LPS, 2 mg/kg) three times a week and an atherogenic diet for 12 weeks.RESULTS:Melittin (0.1 mg/kg) treatment was administered with i.p injection. Melittin treatment showed that total cholesterol and triglyceride levels decreased in atherosclerotic mice however, high-density lipoprotein cholesterol (HDL-C) levels were higher in atherosclerotic mice treated with melittin than in atherosclerotic mice. H&E staining showed that heart and descending aorta were significantly recovered by melittin, compared to atherosclerotic mice. In addition, melittin decreased the expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, fibronectin and transforming growth factor (TGF)-β1 in atherosclerotic mice. In vitro, melittin decreased LPS-induced THP-1 cells-derived macrophages TNF-α and IL-1β expression levels and nuclear factor (NF)-κB signal pathway.CONCLUSIONS:These results demonstrate that melittin has an anti-atherogenic effect by suppression of pro-inflammatory cytokines and adhesion molecules.

Atherosclerosis is a chronic inflammatory process occurring in the walls of arteries, in large part due to the accumulation of inflammatory cells. This study was conducted to determine the effect of nuclear factor (NF)-κB decoy oligodeoxynucleotide (ODN) in an atherosclerosis animal model. The mice received i.p. injections of lipopolysaccharide (LPS, 2 mg/kg) three times a week to induce atherosclerotic change, and fed an atherogenic diet for 12 weeks. NF-κB decoy ODN (0.4 mg/kg) was injected into the tail vein. Treatment with NF-κB decoy ODN decreased pro-inflammatory cytokines, tumour necrosis factor (TNF)-α and interleukin (IL)-1β and inflammatory markers, vascular adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1, in the LPS/Fat-induced mice. In addition, the expression of proteins related to fibrosis, transforming growth factor (TGF)-β1 and fibronectin were markedly decreased in the mice treated with NF-κB decoy ODN compared with the LPS/Fat-induced mice without decoy ODN treatment. These data suggest that NF-κB decoy ODN may exert an inhibitory effect on the expression levels of pro-inflammatory cytokines and cell adhesion molecules in atherosclerotic mice.

BACKGROUND:The myocardial bridge (MB) is an intramural segment of coronary artery that is covered with myocardial tissue. The current diagnostic methods are coronary angiography, intravascular ultrasound and intracoronary Doppler, which are all invasive modalities. In this study, multidetector computed tomography (MDCT) was used to detect and evaluate the anatomical properties of the MB.METHODS AND RESULTS:The 607 patients with suspected or known coronary artery disease underwent 64-slice MDCT. MB was diagnosed when an intramural segment of coronary artery was visualized on axial and multiplanar reconstruction images. The prevalence, length, myocardial thickness, and location were evaluated. Of the 607 patients, 39 (6.42%) had a MB. In 20 patients (52.6%), the MB was located in the mid left anterior descending artery. The length of tunneled artery was a mean 16.3 mm, from 6.9 mm to 30 mm, and the maximum thickness of the myocardial tissue was between 0.5 mm and 3.9 mm, with a mean of 1.8 mm. The length of the MB correlated significantly with thickness (P=0.049).CONCLUSIONS:The incidence of MB and its anatomical properties can be evaluated with MDCT, which might be a useful and noninvasive method of detecting this variant. (Circ J 2010; 74: 137 - 141).