Decreased circulating lipoprotein-associated phospholipase A2 levels are associated with coronary plaque regression in patients with acute coronary syndrome

Objective

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a vascular-specific inflammatory enzyme, of which increases are associated with cardiovascular events. However, the relationship between circulating Lp-PLA2 levels and coronary plaque volume has not been clarified in patients with acute coronary syndrome (ACS).

Methods

We studied 40 patients with ACS (age, 61.4 ± 8.0 years; male, 87.5%; statin use, 45.0%) who had undergone successful percutaneous coronary intervention (PCI). Plaque volume (PV) in non-culprit sites of PCI lesions was precisely determined using grayscale intravascular ultrasound (IVUS) at onset and at six months later. We then analyzed associations among PV, lipid profiles and Lp-PLA2 levels.

Results

Circulating Lp-PLA2 levels and PV significantly decreased between baseline and six months of follow-up (458.6 ± 166.7 IU/L vs. 378.4 ± 158.5 IU/L, p < 0.001 and 82.2 ± 34.8 mm³ vs. 77.3 ± 33.1 mm³, p < 0.001, respectively). The % change in PV positively and significantly correlated with % change in LDL-C and in the LDL-C/HDL-C ratio (r = 0.444, p = 0.004 and r = 0.462, p = 0.003, respectively). Furthermore, % changes in Lp-PLA2 and in PV correlated even more closely (r = 0.496, p = 0.001). The absolute change in PV also significantly correlated with the change in Lp-PLA2 levels (r = 0.404, p = 0.009).

Conclusions

Circulating Lp-PLA2 levels are associated with changes in coronary plaque determined by IVUS in patients with ACS.     

Qualitative score of systemic arteriosclerosis by vascular ultrasonography as a predictor of coronary artery disease in type 2 diabetes

Objective

Patients with type 2 diabetes mellitus (T2DM) are at risk of polyvascular comorbidities and poor prognosis. Non-invasive techniques for early prediction of coronary artery disease (CAD) are desirable to prevent cardiovascular events in these patients. The aim of the present study was to investigate the association between CAD and systemic arteriosclerosis by qualitative vascular ultrasonography.

Methods

The study subjects were 102 consecutive outpatients with T2DM [males/females = 60/42, age: mean ± SD 67 ± 9 (range, 40–85) years] evaluated by vascular ultrasonography for arteriosclerosis in the abdominal aorta, carotid, renal, and common iliac arteries. The total number of detected arteriosclerotic vascular lesions in the four arteries was determined. CAD was diagnosed by two cardiologists using either stress electrocardiography, myocardial scintigraphy, multi-detector row computed tomography or coronary angiography.

Results

Multiple arteriosclerotic vascular lesions (>1) were detected in 64 (63%) patients. The total systemic vascular score was significantly higher in patients with CAD than those without (average score 2.7 versus 1.0, p < 0.0001). None of the CAD patients had a total score of 0. Age- and sex-adjusted multiple logistic regression analysis identified total score of ≥2 as the only predictor of CAD (p < 0.001). The sensitivity, specificity, positive and negative predictive values for total systemic vascular score in the prediction of CAD were 98%, 77%, 83%, and 97%, respectively, which were better than those for carotid mean and maximum intima-media thickness.

Conclusion

Non-invasive qualitative evaluation of systemic arteriosclerosis by the total systemic vascular score is potentially useful for the early prediction of CAD in T2DM patients.     

ABCA1 impacts athero-thrombotic risk and 10-year survival in a contemporary secondary prevention setting

Objectives

We prospectively investigated the effects of ATP-binding cassette protein-1 (ABCA1) variants on long-term clinical outcome in patients with coronary artery disease (CAD).

Background

ABCA1 is implicated in the etiology of atherothrombosis and may offer a target to reduce cardiovascular risk. However, the impact of ABCA1 on recurrent cardiovascular disease in a secondary prevention setting is as of yet unknown.

Methods

We studied cause-specific 10-year mortality and quantitative coronary angiography data from the Regression GRowth Evaluation Statin Study (REGRESS), comprising 884 male CAD patients genotyped for promoter variants encompassing a proximal regulatory region (rs2422493, rs1800976, rs2740483 and rs1800977). Kaplan–Meier, proportional hazards and haplotype analyses were used to ascertain single-variant and multi-marker effects on absolute risk and extent of CAD.

Results

Protection from 10-year vascular death could be attributed to the rs2422493 genotype (available in 639 patients) T allele with absolute risk decreasing stepwise from 12.2% to 8.6% to 4.7% per each added allele copy, HR 0.64, p = 0.03 and HR 0.53, p = 0.04 in the TGCC haplotype context. The TGCC (p = 0.04) and TCCT (p = 0.003) haplotypes exhibited less extensive CAD.

Conclusions

On a background of contemporary secondary prevention, variation in the ABCA1 promoter influences 10-year risk of vascular death and angiographic extent of CAD in men. These insights contribute to identification of patients sharing a specific prognosis, understanding of its etiological basis and development of strategies of risk reduction in CAD.     

LDL cholesterol as a novel risk factor for contrast-induced acute kidney injury in patients undergoing percutaneous coronary intervention

Background: Low density lipoprotein cholesterol (LDL-C) is associated with endothelial dysfunction, inflammation and increased vasoconstriction, which are involved in the development of contrast-induced acute kidney injury (CI-AKI). However, whether LDL-C is an independent risk factor of CI-AKI in patients undergoing percutaneous coronary intervention (PCI) is unknown. Methods: We prospectively enrolled 3236 consecutive patients undergoing PCI between January 2010 and September 2012. Multivariate logistic regression analysis was used to determine whether LDL-C is an independent risk factor of CI-AKI. CI-AKI was defined as an absolute increase in serum creatinine of ≥0.5 mg/dL or ≥25% over the baseline value within 48–72 h after contrast exposure. Results: CI-AKI was observed in 338 patients (10.4%). Patients with CI-AKI had a significantly higher rate of in hospital mortality (4.4% vs. 0.5%, p < 0.001), and significantly higher rates of other in hospital complications compared with those without CI-AKI. The LDL-C quartiles were as follows: Q1 (<2.04 mmol/L), Q2 (2.04–2.61 mmol/L), Q3 (2.61–3.21 mmol/L) and Q4 (>3.21 mmol/L). Patients with high baseline LDL-C levels were more likely to develop CI-AKI and composite end points including all-cause mortality, renal replacement therapy, non-fatal myocardial infarction, acute heart failure, target vessel revascularization or cerebrovascular accident during the observation period of hospitalization (8.9%, 9.9%, 10.5%, 12.6%, p = 0.001, and 5.0%, 5.2%, 6.1%, 8.1%, respectively; p = 0.007). Univariate logistic analysis showed that LDL-C levels (increment 1 mmol/L) were significantly associated with CI-AKI (odds ratio = 1.25, 95% confidence interval (CI), 1.11–1.39, p < 0.001). Furthermore, LDL-C remained a significant risk factor of CI-AKI (odds ratio = 1.23, 95% CI, 1.04–1.45, p = 0.014), even after adjusting for potential confounding risk factors. Conclusions: Measurement of plasma LDL-C concentrations in patients undergoing PCI may be helpful to identify those who are at risk of CI-AKI and poor in hospital outcomes.     

Increase in epicardial fat volume is associated with greater coronary artery calcification progression in subjects at intermediate risk by coronary calcium score: a serial study using non-contrast cardiac CT

Objective

Epicardial fat volume (EFV) is related to calcified coronary plaques. However, it is unknown whether baseline EFV or changes in EFV affect the progression of coronary artery calcification over time.

Methods

We identified 375 consecutive asymptomatic subjects with an intermediate risk of developing coronary artery disease, who underwent serial non-contrast CT at least 3–5 years apart. Subjects were divided into tertiles of CCS progression (% increase) between the 2 scans. Subjects from the upper tertile (High Progressors) were matched by age and gender to 81 subjects from the lower tertile (Low Progressors). All subjects underwent serial measurements of CCS and EFV. Relationships between EFV and CCS progression, and change in plaque number were examined.

Results

At baseline, there was no difference in EFV, and EFV indexed to body surface area (EFVi) between the groups. At follow-up, EFV, EFVi and percent increase in EFVi-change were higher in High Progressors than Low Progressors (EFV, 102 ± 38 cm³ vs. 90 ± 35 cm³, p = 0.03; EFVi, 50 ± 16 cm³/m² vs. 46 ± 15 cm³/m², p = 0.03; percent increase in EFVi-change, 15 ± 22% vs. 7 ± 20%, p = 0.02). On multivariate analysis, after adjusting for conventional risk factors, EFVi increase ≥ 15% [odds ratio (OR) 2.3, p < 0.05], log (baseline CCS) [OR 0.3, p < 0.0001] and scan interval time [p = 0.003, OR 1.0] were predictive of being a High Progressor. EFVi increase ≥ 15% (β = 3.0, p = 0.02) and hypertension (β = 3.1, p = 0.01) were independent predictors of number of new calcified plaques on follow-up.

Conclusion

Increase in EFV is associated with greater progression of coronary artery calcification in intermediate-risk subjects.     

Serum cystatin C is associated with early stage coronary atherosclerotic plaque morphology on multidetector computed tomography

Objective

Cystatin C, a novel marker of kidney function, has been reported to be a predictor of adverse cardiovascular outcomes in patients without established chronic kidney disease. However, the relationship between serum cystatin C concentrations and early stage coronary atherosclerotic plaque morphology among patients with preserved kidney function has not been fully evaluated.

Methods and results

405 outpatients with early coronary artery disease with estimated glomerular filtration rate (eGFR) ≥60 ml/min/1.73 m² and <50% stenosis on 64-slice CT coronary angiography were enrolled. Subjects were categorized into quartiles by serum cystatin C (quartile I: ≤0.88 mg/L – quartile IV: ≥1.16 mg/L). Plaques in coronary segments were categorized as calcified or noncalcified. Multiple linear regression analysis revealed that lower eGFR, higher age, increasing numbers of noncalcified and calcified plaques, lower high-density lipoprotein cholesterol, and female gender were statistically significant predictors of increased cystatin C concentrations. The risk for presence of noncalcified plaques increased significantly with increasing quartiles of cystatin C. Compared with those in the lowest quartile, patients in each subsequent quartile were at steadily increased risk of having noncalcified plaque (quartile IV: OR 5.6; 95% CI 2.3–13.9, p-value <0.001). Both number of segments with calcified plaque and Agatston score were highly correlated with cystatin C concentrations (both p < 0.001), but when adjusted for segments with noncalcified plaque and other risk factors, calcified plaque segments were no longer independently predictive.

Conclusion

Higher serum cystatin C concentrations were correlated with early stage coronary atherosclerotic plaques among patients without established chronic kidney dysfunction. Noncalcified plaques increased with serum cystatin C concentrations, an association independent of eGFR and other cardiovascular risk factors.     

Early intensive statin treatment for six months improves long-term clinical outcomes in patients with acute coronary syndrome (Extended-ESTABLISH trial): A follow-up study

Background

The ESTABLISH trial found using volumetric intravascular ultrasound that atorvastatin therapy started early and continued for 6 months significantly reduced plaque volume in patients with acute coronary syndrome (ACS). However, the benefits of early statin administration on long-term outcomes remain unclear. We therefore examined whether the early initiation of statin in patients with ACS improves long-term prognosis.

Methods and results

The Extended-ESTABLISH trial included 180 patients with ACS who underwent emergency percutaneous coronary intervention (PCI). These patients were randomized here to groups given either early intensive lipid-lowering therapy (n = 90; atorvastatin 20 mg/day) or standard care (control, n = 90) within 48 h of events. Baseline characteristics between the two groups did not significantly differ at the time of ACS onset. Six months after PCI, all patients were treated with statins to achieve an LDL-C value of <100 mg/dL. We compared the first occurrence of major adverse cardiac and cerebrovascular events (MACCE). Prognostic data were fully documented during the entire follow-up period (mean, 1538 ± 707 days). Cumulative event-free survival was significantly higher in the atorvastatin, than in the control group (p = 0.041; log-rank test). Furthermore, by adjusting for validated prognosticators, early statin administration was identified as a good predictor of MACCE (HR 0.46, 95%CI 0.23–0.86; p = 0.015).

Conclusions

In-hospital initiation of statin therapy immediately after ACS conferred long-term benefits and 6 months of intensive lipid-lowering therapy improved long-term clinical outcomes after PCI in patients with ACS.     

Correlation of TIMI risk score with angiographic extent and severity of coronary artery disease in non-ST-elevation acute coronary syndromes

Aim of study

To determine whether the TIMI risk score correlates with the angiographic extent and severity of coronary artery disease in patients with non-ST-elevation acute coronary syndrome undergoing cardiac catheterization.

Patients and method

We conducted a retrospective review of 239 medical records of patients who underwent coronary angiography secondary to non-ST-elevation acute coronary syndrome between 2002 and 2006. Patients were classified into three groups according to TIMI risk score: TIMI scores 0 to 2 (group 1: n = 121), 3 to 4 (group 2: n = 100), and 5 to 7 (group 3: n = 18). We compared the coronary angiography findings of the three groups.

Results

Patients of group 1 had a greater likelihood of normal or non significant CAD than patients of group 2 (36.3 % vs 13 %, P < 0.001) and than patients of group 3 (36.3 % vs 0 %, P = 0.002). One-vessel disease was found more often in patients with TIMI score 0 to 2 than in patients with TIMI score 5 to 7 (28.9 % vs 0 %; P = 0.01), and in patients with TIMI score 3 to 4 than in those with score 5 to 7 (35 % vs 0 %, P = 0.006). However, 1-vessel disease was found in patients of group 1 as often as in patients of group 2. The frequency of two-vessel disease was similar whatever the level of TIMI score was low, intermediate or high. Three-vessel or left main disease was more likely found in patients of group 3 than in patients of group 2 (66.7 % vs 26 %; P = 0.01), and than patients of group 1 (66.7 % vs 13.2 %; P < 0.001). Chronic coronary occlusions and coronary calcifications were also more likely found in patients with TIMI score 5 to 7.

Conclusion

In patients with non-ST-elevation acute coronary syndrome undergoing cardiac catheterization, the TIMI risk score correlated with the extent and severity of coronary artery disease.     

Long-term outcomes of women with coronary artery disease following complete coronary revascularization

Background

Although coronary artery disease (CAD) is less prevalent in women than in men, early mortality rate is higher in women with CAD than in men with CAD following coronary revascularization. In terms of the long-term outcomes after coronary revascularization, limited data are available. Especially, in the Japanese CAD population, no data about sex-related differences in long-term outcomes after coronary revascularization exist. The aim of this study was to compare long-term outcomes between men and women following complete revascularization in Japanese patients with CAD.

Methods

We collected data from 1836 consecutive patients who underwent complete revascularization by percutaneous coronary interventions and/or bypass surgeries. All-cause and cardiac mortality and the incidence of stroke were compared between men and women. In addition to the univariate analysis, a multivariate Cox regression was carried out in order to adjust for differences in baseline characteristics.

Results

There were 274 female patients (14.9%). They were older, had greater total cholesterol levels, and were more likely to have multivessel disease than men. During follow-up [mean (SD), 11.4 (2.9) years], 412 patients died (including 131 patients who died of cardiac causes), and 130 had a stroke. In the multivariate analysis, female patients did not have a significant risk for all-cause mortality (hazard ratio [HR], 1.01; p = 0.993), cardiac mortality (HR, 1.41; p = 0.256), or stroke (HR, 0.71; p = 0.309).

Conclusions

In the present study involving CAD patients who underwent complete revascularization, we showed that, although women were older and had more unfavorable risk profiles, they did not have a greater risk of long-term all-cause mortality, cardiac mortality, or stroke incidence, compared to men.     

Relationship of coronary artery plaque composition to coronary artery stenosis severity: results from the prospective multicenter ACCURACY trial

Objectives

The purpose of this study was to determine the relationship of coronary artery plaque composition as detected by coronary computed tomographic angiography (CCTA) to luminal diameter stenosis severity quantified by quantitative coronary angiography (QCA) in individuals without known coronary artery disease (CAD) presenting with stable chest pain syndrome.

Background

While CCTA has been previously evaluated for its ability to detect and exclude coronary artery stenosis, CCTA also permits assessment of other important plaque characteristics, including plaque composition. Identification of the relationship between plaque composition by CCTA and plaque severity by invasive angiography may provide valuable insight into the pathophysiology of coronary artery plaque.

Methods

Patients enrolled in the ACCURACY trial, a 16-site multicenter study of patients with stable chest pain syndrome but without known CAD undergoing both CCTA and invasive coronary angiography (ICA), comprised the study population. CCTAs were scored on a per-segment basis for plaque composition and graded as non-calcified (>70% non-calcified), calcified (>70% calcified) or “mixed” (30–70% non-calcified or calcified) by concordance of ≥2 of 3 readers. CCTAs were also scored on a per-patient basis, and individuals were categorized as possessing primarily non-calcified plaques, primarily calcified plaques or primarily mixed plaques. Quantitative coronary angiography (QCA) was performed in all patients, used as the reference standard for stenosis severity, and interpreted blinded to patient characteristics and CCTA results.

Results

230 subjects comprised the study population (59.1% male, 57 ± 10 years). QCA was performed in all subjects following CCTA (mean inter-test interval 5.9 ± 4.3 days), and demonstrated obstructive CAD in 24.8% and 13.9% at the 50% and 70% stenosis severity threshold, respectively. On a per-segment based analysis, obstruction by QCA at both the 50% and 70% stenoses thresholds was more often for mixed composition plaques by CCTA (69.1% and 67.9%, respectively), as compared to non-calcified plaques (24.7% and 28.6%, respectively) and calcified plaques (6.1% and 3.6%, respectively) [p < 0.01 for comparisons]. On a per-patient basis, patients with mixed plaque or mixtures of plaque types more often exhibited obstructive coronary stenosis by QCA at the 50% level (39/96; 40.6%) compared to those with primarily non-calcified (12/43; 27.9%) or primarily calcified (4/29; 13.8%) plaques [p = 0.02].

Conclusions

In this multicenter trial of chest pain patients without known CAD, QCA-confirmed obstructive coronary stenosis was associated with mixed plaque composition by CCTA at both the per-segment and the per-patient levels. Coronary artery segments exhibiting calcified plaque were rarely associated with obstructive coronary stenosis.     

Prognostic impact of interventional approach in non-ST segment elevation acute coronary syndrome in very elderly patients

Introduction and objectives

In moderate or high risk non-ST segment elevation acute coronary syndrome, clinical practice guidelines recommend a coronary angiography with intent to revascularize. However, evidence to support this recommendation in very elderly patients is poor.

Methods

All patients over 85 years old admitted to our hospital between 2004 and 2009 with a diagnosis of non-ST segment elevation acute coronary syndrome were retrospectively included. Using a propensity score, patients undergoing the interventional approach and those undergoing conservative management were matched and compared for survival and survival without ischemic events.

Results

We included 228 consecutive patients with a mean age of 88 years (range: 85 to 101). Those in the interventional approach group (n = 100) were younger, with a higher proportion of males and less comorbidity, less cognitive impairment and lower troponin I levels compared with patients in the conservative management group (n = 128). We matched 63 patients from the interventional approach group and 63 from the conservative management group using propensity score.In the matched patients, the interventional approach group exhibited better survival (log rank 4.24; P = .039) and better survival free of ischemic events (log rank 8.63; P = .003) at the 3-year follow-up. In the whole population, adjusted for propensity score quintiles, the interventional approach group had lower mortality (hazard ratio 0.52; 95% confidence interval: 0.32-0.85) and a better survival free of ischemic events (hazard ratio 0.48; 95% confidence interval: 0.32-0.74).

Conclusions

Nearly all the very elderly patients admitted with non-ST segment elevation acute coronary syndrome were of moderate or high risk. In these patients, the interventional approach was associated with overall better survival and better survival free of ischemic events.Full English text available fromwww.revespcardiol.org     

阻塞性睡眠呼吸暂停对冠状动脉粥样硬化斑块的影响

目的 探讨阻塞性睡眠呼吸暂停(OSAS)对冠状动脉粥样硬化斑块的影响.方法 126例老年冠心病(CAD)患者根据多导睡眠仪监测结果,分为OSAS合并CAD组(62例)、无OSAS组(64例).所有患者常规清晨空腹卧位取静脉血测定测定胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、血常规白细胞计数、中性粒细胞分类及血清(hs-CRP)水平.根据冠状动脉造影术、64层螺旋CT检查结果记录OSAS合并CAD组、无OSAS组冠状动脉病变、Gensini评分及粥样硬化斑块情况.结果 CAD合并OSAS组TC、TG、LDL-C分别为(5.76+0.85)mmol/L、(3.37±0.97)mmol/L、(3.65±0.58)mmol/L,HDL-C为(1.06±0.20)mmol/L,无OSAS组TC、TG、LDL-C分别为(4.26±0.78)mmol/L、(1.72±0.54)mmol/L、(2.91±0.58)mmol/L,HDL-C为(1.13±0.14)mmol/L,CAD合并OSAS组TC、TG、LDL-C均高于无OSAS组(t值分别为2.959、3.556、2.165,P<0.05),HDL-C低于无OSAS组(t=2.545,P<0.05);OSAS合并CAD组患者血白细胞数、中性粒细胞百分比及hs-CRP水平较无OSAS组明显增高(P<0.05);OSAS合并CAD组冠状动脉多支病变发生率为51%,Gensini积分为(23.6±20.7)分,冠状动脉软斑块为(67.6+9.7)个,无OSAS组分别为30%,(18.9±19.4)分,(39.3±9.4)个,两组比较差异有统计学意义(t值分别为5.39,2.048,19.001,P<0.05).结论 OSAS和冠状动脉粥样硬化性心脏病密切相关,促进冠状动脉粥样硬化斑块的形成.     

The association between circulating endothelial progenitor cells and coronary collateral formation

Aim

We investigated the relationship between coronary collateral formation and circulating endothelial progenitor cells (EPC) in patients undergoing coronary angiography.

Methods and results

Circulating CD133⁺/34⁺ and CD34⁺/KDR⁺ EPCs were determined in 68 patients (normal coronary vessels in 24 patients and coronary artery disease (CAD) in 44 patients) (age: 58.7 ± 10.1, 64.7% male). Circulating EPCs were higher among patients with normal coronary vessels compared to patients with CAD for CD133⁺/34⁺ (p < 0.05) and CD34⁺/KDR⁺ cells (p < 0.05). The number of EPCs were significantly greater in patients with good coronary collateral formation (p < 0.05). EPC count was independent predictor for coronary collateral formation after adjustment for other cardiovascular risk factors and extent of CAD (p = 0.037).

Conclusion

In patients with severe coronary stenosis, those with increased circulating EPCs had better collateral formation compared to those with lower EPC counts. Our findings implicate that in addition to presence of critical stenosis, intact response of bone marrow is necessary for collateral formation in CAD.     

Long-term prognostic implication of coronary plaque characterization as detected by 64-multidetector computed tomography in Egyptian population

Objectives

We aimed to determine the role of multi-detector computed tomography (MDCT) in prognosis of patients with known or suspected coronary artery disease (CAD) by applying plaque characterization and whether obstructive versus non-obstructive plaque volume is a predictor of future cardiac events.

Persistent epicardial adipose tissue accumulation is associated with coronary plaque vulnerability and future acute coronary syndrome in non-obese subjects with coronary artery disease

Objective. Epicardial adipose tissue (EAT) is recognized as a novel risk factor for coronary artery disease (CAD), and its contribution is thought to be stronger in non-obese patients than in obese patients. However, the prognostic impact of the progression of EAT accumulation after comprehensive management for atherosclerotic risk factors remains unclear. This study aimed to investigate whether an increase of the EAT volume during follow-up predicts future acute coronary syndrome (ACS) events in non-obese CAD patients. Methods. This study consisted of 517 non-obese CAD patients (368 men; age, 66 ± 10 years) who underwent serial multidetector computed tomography (MDCT) examinations to evaluate coronary atherosclerosis progression. The MDCT examination was used to assess the severity of stenosis, plaque characteristics, and EAT volume. All patients received comprehensive management to reduce CAD risk factors after the first MDCT examination. The MDCT examination was repeated at 6–24 months, and patients were followed-up for more than 1 year or until the occurrence of ACS events. Results. Of 517 patients, 159 (31%) patients were classified into increase of EAT volume during follow-up, 91 (18%) into decrease of EAT volume during follow-up, and 267 (51%) patients into constant of EAT volume during follow-up. The prevalence of obstructive plaques and MDCT-derived vulnerable features of coronary plaques were significantly elevated in patients with increase of EAT volume during follow-up. In contrast, no significant changes were observed in the other 2 groups. During the follow-up period of 4.1 ± 1.8 years (median 4.4 years) after the second MDCT examination, ACS occurred in 43 (8.3%) patients. Multivariate Cox regression analysis showed that the presence of low-attenuation plaque (hazard ratio [HR]; 1.78, p = 0.04) and napkin-ring sign (HR; 3.74, p < 0.001) at second MDCT examination, and changes of EAT volume per 10 ml (HR; 1.34, p = 0.004) were associated with future ACS events. Conclusion. Patients with increase of EAT volume during follow-up despite comprehensive management for CAD risks had an increased prevalence of obstructive plaques and plaques with high-risk features, which could be associated with unfavorable ACS outcomes in non-obese CAD patients.     

Patients with non-obstructive coronary artery disease admitted with acute myocardial infarction carry a better outcome compared to those with obstructive coronary artery disease

Background

The characterization of patients who have acute myocardial infarction (AMI) and insignificant coronary stenosis is unclear.

Long-term outcomes following coronary drug-eluting- and bare-metal-stent implantation

Background

Although drug-eluting stents (DES) reduce restenosis rates relative to bare-metal stents (BMS), recent reports have indicated that the use of DES may be associated with an increased risk of stent thrombosis. Our study focused on the effect of stent type on clinical outcomes in a “real world” setting.

Methods

889 patients undergoing percutaneous coronary intervention (PCI) with either DES (Cypher or Taxus; n = 490) or BMS (n = 399) were enrolled in a prospective single center registry. The outcome analysis covered a period of up to 3.2 years (mean 2.7 years ± 0.5 years) and was based on 65 deaths, 27 myocardial infarctions, 76 clinically driven target lesion revascularizations (TLR), and 15 angiographically confirmed cases of definite stent thrombosis and was adjusted for differences in baseline characteristics.

Results

In total 1277 stents (613 BMS and 664 DES) were implanted in 1215 lesions. Despite a significantly different unadjusted death rate (10.1% and 5.1% in BMS and DES patients, respectively; p < 0.05), the patient groups did not differ significantly in the risk of myocardial infarction during 2.7 years of follow-up. After adjustment for differences in baseline characteristics between groups, the difference in the cumulative incidence of death did not remain statistically significant (p = 0.22). Target lesion revascularizations occurred significantly less frequently in patients with DES compared to individuals after BMS implantation (5.9% and 11.8% in patients with DES and BMS, respectively; p < 0.05). The rate of angiographically confirmed stent thrombosis was 2.1% in patients with DES and 1.1% in BMS patients (p = 0.31).There was a significantly lower unadjusted event rate (including deaths, myocardial infarction, target lesion revascularization, and stent thrombosis) in patients with drug-eluting stents than in those with bare-metal stents (16.4% and 25.8%, respectively), with 9.4 fewer such events per 100 patients (unadjusted hazard ratio [HR], 0.64; 95% confidence interval [CI], 0.46 to 0.87). After adjustment, the relative risk for all outcome events in patients with drug-eluting stents was 0.79 (95% CI, 0.67 to 0.95). However, the adjusted relative risk for death and myocardial infarction did not differ significantly between groups (adjusted relative risk in patients with drug-eluting stents 0.94 (95% CI, 0.77 to 1.37)).

Conclusions

In this real-world population, the beneficial effect of first generation DES in reducing the need for new revascularization compared with BMS extends to more than 2.5 years without evidence of a worse safety profile. The minor risk of stent thrombosis and myocardial infarction within this period after implantation of DES seems unlikely to outweigh the benefit of these stents.     

Recurrence of angina pectoris after percutaneous coronary intervention is reduced by statins in Japanese patients

Background

Statins have been reported to reduce cardiovascular events in patients with coronary artery disease (CAD). Percutaneous coronary intervention (PCI) is commonly used to relieve ischemic symptoms in patients with CAD. However, there is little information on the effect of statins on cardiovascular events after PCI, even in the era of coronary stent implantation.

Methods

A total of 1019 patients with acute or chronic CAD and modest total cholesterol levels (180–240 mg/dl) were enrolled and randomly assigned to treatment with or without statins. We evaluated the effect of any available statin on the incidence of cardiovascular events after PCI. The primary endpoint was a composite of cardiovascular death, nonfatal acute myocardial infarction (MI), recurrent angina pectoris requiring emergency rehospitalization (rAP), heart failure, and stroke.

Results

Indications for PCI were stable angina in 54%, ST-elevation MI in 41% and non-ST-elevation MI/unstable angina pectoris in 5%. After 2 years of statin treatment, low-density lipoprotein cholesterol (LDL-C) decreased from 133 to 96 mg/dl. Stents were implanted in 84% of all cases. The primary endpoint event rate was 9.5% in the statin group and 14.7% in the non-statin group (p = 0.0292). Of all primary endpoint events, only rAP was significantly suppressed by statins (p = 0.0027). In rAP patients, coronary angiography revealed that statins suppressed restenosis but not new lesions.

Conclusions

For Japanese CAD patients treated with PCI and stent implantation, statin therapy reduced the incidence of recurrent cardiovascular events, particularly rAP. Discretionary statin treatment to achieve LDL-C levels <100 mg/dl effectively reduced restenosis causing rAP.     

Helicobacter pylori seropositivity is not associated with inflammatory parameters, lipid concentrations and degree of coronary artery disease

Regnström J, Jovinge S, Båvenholm P, Ericssond C-G, de Faire U, Hamsten A, Hellenius M-L, Nilsson J, Tornvall P (Karolinska Hospital and Danderyd Hospital, Stockholm, Sweden). Helicobacter pylori seropositivity is not associated with inflammatory parameters, lipid concentrations and coronary artery disease. J Intern Med 1998; 243 : 109–13.

Objectives

To determine the prevalence of chronic infection with Helicobacter pylori (HP) in patients with established coronary artery disease (CAD) and in healthy controls. Furthermore, to investigate whether HP infection is associated with inflammatory parameters, lipid concentrations and degree and progression of CAD.

Design

A case–control study combined with a prospective angiographic study.

Setting

Stockholm Metropolitan Area, Sweden.

Patients and methods

A material consisting of 92 young men aged 40.9 ± 3.2 (mean ± SD) years, with previous myocardial infarction and documented coronary atherosclerosis, and 95 healthy sex-matched controls, aged 43.2 ± 3.0 (mean ± SD) years, with similar socio-economic status and ethnic background was analysed for the prevalence of HP seropositivity, plasma concentrations of the inflammatory parameters fibrinogen, tumour necrosis factor alpha and orosomucoid, and serum concentrations of lipids. The impact of HP seropositivity on degree and progression of CAD, as assessed by quantitative coronary angiography, was also determined.

Results

The study population of mainly Scandinavian origin had a low prevalence of HP seropositivity in comparison with previously published European populations. No significant increase in HP seropositivity was found in patients compared with controls (42.2 vs. 32.6%). Furthermore, HP infection was not associated with increased levels of inflammatory parameters, lipid concentrations or with degree of angiographically determined CAD at baseline, or progression of CAD and clinical events over 5 years.

Conclusions

HP infection is not associated with inflammatory parameters and lipid concentrations and could not be confirmed as a risk factor for CAD.