Drug-coated balloon angioplasty for coronary stenotic lesions in a paediatric patient after Kawasaki disease.

Percutaneous coronary intervention for stenosis of coronary artery after Kawasaki disease presents various challenges. The diameters of reference vessels and femoral artery in children are smaller, and the morphological changes are different from adults. Herein, we describe our successful experience with a severe coronary artery stenosis at the proximal portion of left anterior descending treated with drug-coated balloon dilation.

Analysis of MicroRNAs Associated With Carotid Atherosclerotic Plaque Rupture With Thrombosis.

Atherosclerosis is a progressive vascular wall inflammatory disease, and the rupture of atherosclerotic vulnerable plaques is the leading cause of morbidity and mortality worldwide. This study intended to explore the potential mechanisms behind plaque rupture and thrombosis in ApoE knockout mice. The spontaneous plaque rupture models were established, and left carotid artery tissues at different time points (1-, 2-, 4-, 6-, 8-, 12-, and 16-week post-surgery) were collected. By the extent of plaque rupture, plaque was defined as (1) control groups, (2) atherosclerotic plaque group, and (3) plaque rupture group. Macrophage (CD68), MMP-8, and MMP-13 activities were measured by immunofluorescence. Cytokines and inflammatory markers were measured by ELISA. The left carotid artery sample tissue was collected to evaluate the miRNAs expression level by miRNA-microarray. Bioinformatic analyses were conducted at three levels: (2) vs. (1), (3) vs. (2), and again in seven time series analysis. The plaque rupture with thrombus and intraplaque hemorrhage results peaked at 8 weeks and decreased thereafter. Similar trends were seen in the number of plaque macrophages and lipids, the expression of matrix metalloproteinase, and the atherosclerotic and plasma cytokine levels. MiRNA-microarray showed that miR-322-5p and miR-206-3p were specifically upregulated in the atherosclerotic plaque group compared with those in the control group. Meanwhile, miR-466h-5p was specifically upregulated in the plaque rupture group compared with the atherosclerotic plaque group. The highest incidence of plaque rupture and thrombosis occurred at 8 weeks post-surgery. miR-322-5p and miR-206-3p may be associated with the formation of atherosclerotic plaques. miR-466h-5p may promote atherosclerotic plaque rupture via apoptosis-related pathways.

Sulindac-derived retinoid X receptor-α modulator attenuates atherosclerotic plaque progression and destabilization in ApoE-/- mice.

BACKGROUND AND PURPOSE: Atherosclerosis is a chronic inflammatory disease, and retinoid X receptor-α (RXRα) is an intriguing anti-atherosclerosis target. This study investigated whether and how an RXRα modulator, K-80003, derived from a non-steroidal anti-inflammatory drug attenuates atherosclerotic plaque progression and destabilization. EXPERIMENTAL APPROACH: Our previously established ApoE-/- mouse model of carotid vulnerable plaque progression was treated with K-80003 or vehicle for 4 or 8 weeks. Samples of carotid arteries and serum were collected to determine atherosclerotic lesion size, histological features, expression of related proteins, and lipid profiles. In vitro studies were carried out in 7-ketocholesterol (7-KC)-stimulated macrophages treated with or without K-80003. KEY RESULTS: K-80003 significantly reduced lesion size, plaque rupture, macrophage infiltration, and inflammatory cytokine levels. Plaque macrophages positive for nuclear p65 (RelA) NF-κB subunit were markedly reduced after K-80003 treatment. Also, K-80003 treatment inhibited 7-KC-induced p65 nuclear translocation, IκBα degradation, and transcription of NF-κB target genes. In addition, K-80003 inhibited NF-κB pathway mainly through the reduction of p62/sequestosome 1 (SQSTM1), probably due to promotion of autophagic flux by K-80003. Mechanistically, cytoplasmic localization of RXRα was associated with decreased autophagic flux. Increasing cytoplasmic RXRα expression by overexpression of RXRα/385 mutant decreased autophagic flux in RAW264.7 cells. Finally, K-80003 strongly inhibited 7-KC-induced RXRα cytoplasmic translocation. CONCLUSIONS AND IMPLICATIONS: K-80003 suppressed atherosclerotic plaque progression and destabilization by promoting macrophage autophagic flux and consequently inhibited the p62/SQSTM1-mediated NF-κB proinflammatory pathway. Thus, targeting RXRα-mediated autophagy-inflammation axis by its noncanonical modulator may represent a promising strategy to treat atherosclerosis.

Xuezhikang ameliorates contrast media-induced nephropathy in rats via suppression of oxidative stress, inflammatory responses and apoptosis.

BACKGROUND: The aim of this study was to assess the preventive effect of xuezhikang (XZK) to replace atorvastatin on the contrast media-induced acute kidney injury (CI-AKI). METHODS: The male Sprague-Dawley rats were divided into five groups: group 1 (sham), injected with normal saline; group 2 (XZK), treated with XZK; group 3 contrast media (CM), injected with CM; group 4 (CM + ATO), injected with CM + pretreatment with atorvastatin; group 5 (CM + XZK), injected with CM + pretreatment with XZK. Twenty-four hours after injection with normal saline or CM, the blood sample and the kidneys were collected for the measurement of biochemical parameters, oxidative stress markers, nitric oxide production, inflammatory parameters, as well as renal histopathology and apoptosis detection. RESULTS: Our results indicated that XZK restored the renal function by reducing serum blood urea nitrogen (BUN) and serum creatinine (Scr), depressing renal malondialdehyde (MDA), increasing renal NO production, decreasing TNF-ɑ and IL-6 expression, attenuating renal pathological changes and inhibiting the apoptosis of renal tubular cells. CONCLUSION: XZK's therapeutic effect is similar, or even better than atorvastatin at the same effectual dose in some parts.

Orphan nuclear receptor Nur77 Inhibits Oxidized LDL-induced differentiation of RAW264.7 murine macrophage cell line into dendritic like cells.

BACKGROUND: Nur77 is an orphan nuclear receptor expressed in human atheroma. In vascular cells in vitro, Nur77 expression is induced by pro-inflammatory factors, such as oxidized LDL (oxLDL). METHODS: We analyze the role of Nur77 in the oxLDL-induced differentiation of macrophages into dendritic cells (DC). The murine RAW264.7 macrophage cell line was stably transfected with expression plasmids encoding either GFP or GFP fusions with either full-length Nur77 (GFP-Nur77), Nur77 lacking the DNA binding domain (GFP-Nur77-ΔDBD) or Nur77 lacking the transactivation domain (GFP-Nur77-ΔTAD). RESULTS: GFP-Nur77 overexpression significantly suppressed the effect of oxLDL treatment on DC morphologic changes, expression of DC maturation markers, endocytic activity, allogeneic activation of T cell proliferation, and the activity and secretion of pro-inflammatory cytokines. Analysis of GFP-Nur77-ΔTAD and GFP-Nur77-ΔDBD indicated that the Nur77 DNA binding and transactivation domains were both required for this effect. GFP-Nur77-ΔDBD consistently had the opposite effect to GFP-Nur77, increasing DC-type differentiation in all assays. Interestingly, GFP-Nur77-ΔDBD protein was cytosolic, whereas GFP-Nur77 and GFP-Nur77-ΔTAD were both nuclear. CONCLUSIONS: These data show that GFP-Nur77 inhibited differentiation of oxLDL-treated macrophages into DC. The effects of Nur77 on the macrophage phenotype may involve changes in its subcellular distribution.

Atorvastatin improves plaque stability in ApoE-knockout mice by regulating chemokines and chemokine receptors.

It is well documented that statins protect atherosclerotic patients from inflammatory changes and plaque instability in coronary arteries. However, the underlying mechanisms are not fully understood. Using a previously established mouse model for vulnerable atherosclerotic plaque, we investigated the effect of atorvastatin (10 mg/kg/day) on plaque morphology. Atorvastatin did not lower plasma total cholesterol levels or affect plaque progression at this dosage; however, vulnerable plaque numbers were significantly reduced in the atorvastatin-treated group compared to control. Detailed examinations revealed that atorvastatin significantly decreased macrophage infiltration and subendothelial lipid deposition, reduced intimal collagen content, and elevated collagenase activity and expression of matrix metalloproteinases (MMPs). Because vascular inflammation is largely driven by changes in monocyte/macrophage numbers in the vessel wall, we speculated that the anti-inflammatory effect of atorvastatin may partially result from decreased monocyte recruitment to the endothelium. Further experiments showed that atorvastatin downregulated expression of the chemokines monocyte chemoattractant protein (MCP)-1, chemokine (C-X3-C motif) ligand 1 (CX3CL1) and their receptors CCR2 and, CX3CR1, which are mainly responsible for monocyte recruitment. In addition, levels of the plasma inflammatory markers C-reactive protein (CRP) and tumor necrosis factor (TNF)-α were also significantly decrease in atorvastatin-treated mice. Collectively, our results demonstrate that atorvastatin can improve plaque stability in mice independent of plasma cholesterol levels. Given the profound inhibition of macrophage infiltration into atherosclerotic plaques, we propose that statins may partly exert protective effects by modulating levels of chemokines and their receptors. These findings elucidate yet another atheroprotective mechanism of statins.

Atorvastatin suppresses oxidized LDL-induced dendritic cell-like differentiation of RAW264.7 cells regulated by the p38 MAPK pathway.

Dendritic cells (DCs) are the most potent professional antigen-presenting cells and are involved in the initiation and progression of atherosclerosis. Recent data suggest that mature macrophages differentiate into dendritic-like cells when exposed to oxidized low-density lipoprotein (oxLDL). The purpose of the present study was to determine the effect of atorvastatin on the differentiation of macrophages to DCs and the molecular mechanisms of this transition. Mouse macrophage-like RAW264.7 cell was differentiated into a dendritic-like phenotype by incubation with oxLDL in the absence or presence of atorvastatin. The results showed that atorvastatin suppressed DC-like morphologic changes in vitro as assessed by decreased expression of DC maturation markers (CD83, CD11c, CD86, major histocompatibility complex class II, and CD1d). Atorvastatin also inhibited other oxLDL-induced functional changes including endocytic activity, ability to induce T cell proliferation, and cytokine secretion. Western blot analysis showed that oxLDL treatment of RAW264.7 cells induced phosphorylation of p38 mitogen-activated protein kinase (MAPK). However, blocking p38 MAPK with SB203580 significantly downregulated the expression of DC maturation markers, accompanied by decreased cytokine secretion. The findings of the present work demonstrate that that atorvastatin suppresses the oxLDL-induced DC-like differentiation of RAW264.7 cells by inactivating the p38 MAPK signaling pathway.

Endogenous renovascular hypertension combined with low shear stress induces plaque rupture in apolipoprotein E-deficient mice.

OBJECTIVE: The development of a murine model of spontaneous atherosclerotic plaque rupture with luminal thrombus. METHODS AND RESULTS: Combined partial ligation of the left renal artery and left common carotid artery in 8-week-old apolipoprotein E-deficient mice induced endogenous renovascular hypertension and local low oscillatory shear stress in the left common carotid artery. After 8 weeks, a fresh left common carotid artery lumen thrombus associated with severe plaque burden was found in 50% (10/20) of the mice. Histological analyses indicated that all left common carotid artery lesions had vulnerable features, and 50% (5/10) of the mice showed plaque rupture with a lumen thrombus. Multiple layers with layering discontinuity and intraplaque hemorrhages were found in 80% (8/10) of the mice. Further experiments showed that both increased blood pressure, and angiotensin-II contributed to plaque progression and vulnerability. Decreased intimal collagen associated with increased collagenase activity and matrix metalloproteinase expression also resulted in plaque disruption. CONCLUSIONS: We demonstrate a murine model of spontaneous plaque rupture with a high incidence of luminal thrombus. The model not only nicely recapitulates the pathophysiological processes of human plaque rupture but it is also simple, fast, and highly efficient to generate.

Pharmacoinvasive therapy for ST elevation myocardial infarction in China: a pilot study.

Most patients with acute ST-elevation myocardial infarction (STEMI) cannot receive timely primary percutaneous coronary intervention (PCI) because of lack of facilities or delays in patient transfer or catheterization team mobilization. In these patients, early routine post-thrombolysis PCI might be a reasonable, useful strategy. This study investigated feasibility and safety of early PCI after successful half-dose alteplase reperfusion in a Chinese population. Patients with STEMI received half-dose alteplase if expected time delay to PCI was ≥90 min. Patients who reached clinical criteria of successful thrombolysis reperfusion were recommended to undergo diagnostic angiography within 3-24 h after thrombolysis. Patients with residual stenosis ≥70% in the infarct-related artery underwent PCI, regardless of flow or patency status. Epicardial arterial flow was assessed using thrombolysis in myocardial infarction (TIMI) flow grade and TIMI frame count (CTFC). Myocardial perfusion was assessed using myocardial blush grade (MBG) and TIMI myocardial perfusion frame count (TMPFC). Forty-nine patients were enrolled and underwent diagnostic angiography 3-11.3 h (median 6.5 h) after thrombolysis. Forty-six patients underwent PCI. No procedure-related complications occurred, except two patients who had no reflow after PCI. Twenty-two (47.8%) patients had TIMI grade 3 flow before PCI and 33 (71.7%) after PCI. CTFC was significantly improved after PCI (48.5 ± 32.1 vs. 37.9 ± 25.6, P = 0.01). MBG and TMPFC exhibited a similar improving trend after PCI, and the best myocardial perfusion tended to be achieved 3-12 h after lysis. During the 30-day follow-up, there were two deaths. The composite end point of death, cardiogenic shock, heart failure, reinfarction, and recurrent ischemia occurred in four patients. TIMI minor bleeding occurred in four patients. No TIMI major bleeding and stroke occurred. Early routine PCI after half-dose alteplase thrombolysis in Chinese population appears feasible. A larger clinical trial should be designed to further elucidate its efficacy and safety. Early PCI after thrombolysis in STEMI: The EARLY-PCI pilot feasibility study, ChiCTR-TNC-11001363.

Factors affecting thrombolysis in myocardial infarction myocardial perfusion frame count: insights of myocardial tissue-level reperfusion from a novel index for assessing myocardial perfusion.

BACKGROUND: Myocardial tissue-level perfusion failure is associated with adverse outcomes following ST-elevation myocardial infarction (STEMI) despite successful epicardial recanalization. We have developed a new quantitative index-thrombolysis in myocardial infarction (TIMI) myocardial perfusion frame count (TMPFC)--for assessing myocardial tissue level perfusion. However, factors affecting this novel index of myocardial perfusion are currently unknown. METHODS: A total of 255 consecutive STEMI patients undergoing primary angioplasty were enrolled. Myocardial tissue level perfusion was assessed by TMPFC, which measures the filling and clearance of contrast in the myocardium using cine-angiographic frame counting. We differentiate three groups with two cut off values for TMPFC: a TMPFC of 90 frames was the upper boundary of the 95% confidence interval (CI) for the TMPFC observed in normal arteries, and a TMPFC of 130 was the 75th percentile of TMPFC. RESULTS: STEMI patients with TMPFC > 130 frames (68 patients, 26.7%) had higher clinical and angiographic risk factor profiles as well as a higher 30-day MACE rate compared with those with TMPFC ≤ 90 frames and those with TMPFC > 90 and ≤ 130 frames. Multivariable analysis identified that the independent predictors of TMPFC > 130 frames were age ≥ 75 years (OR 2.08, 95%CI 1.21 to 3.58, P = 0.007), diabetes (OR 1.37, 95%CI 1.01 to 1.86, P = 0.042), Killip class ≥ 2 (OR 1.52, 95%CI 1.05 to 2.21, P = 0.027), and prolonged pain-to-balloon time (OR 1.73, 95%CI 1.07 to 2.79, P = 0.013). TMPFC > 130 frames was identified as the strongest independent predictor of 30-day major adverse cardiac event (MACE) (OR 2.77, 95%CI 1.21 to 6.31, P = 0.008), along with age ≥ 75 years (OR 2.19, 95%CI 1.11 to 4.33, P = 0.016), female gender (OR 1.67, 95%CI 1.03 to 2.70, P = 0.038), and Killip class ≥ 2 (OR 1.83, 95%CI 1.07 to 3.14, P = 0.021). CONCLUSIONS: STEMI patients with poor myocardial perfusion assessed by TMPFC had higher risk factor profiles. Advanced age, diabetes, higher Killip class, and longer ischemia time were independent predictors of impaired TMPFC after primary percutaneous coronary intervention. These results emphasize that particular attention should be paid on myocardial microvascular reperfusion in STEMI patients with these risk factors.

Gender differences in epicardial and tissue-level reperfusion in patients undergoing primary angioplasty for acute myocardial infarction.

OBJECTIVE: The impact of gender on clinical course after ST-elevation myocardial infarction (STEMI) is not fully understood. We prospectively investigated whether there are gender-related differences in epicardial and myocardial tissue-level perfusion, both of which represent important prognostic determinants in STEMI patients undergoing primary percutaneous coronary intervention (PPCI). METHODS: A total of 594 consecutive non-selected STEMI patients undergoing PPCI were prospectively enrolled. Primary end-point of the study was post-procedural epicardial and myocardial perfusion. Secondary end-points were the 30-day and 6-month composite occurrence of major adverse cardiac events (MACE). RESULTS: Women with STEMI had higher risk factor profiles than men. Although PPCI achieved equal rates of successful epicardial reperfusion, women tended to have impaired microvascular reperfusion as reflected by lower rates of normal TIMI myocardial perfusion grade (P=0.007) and complete ST-segment resolution (P=0.079). After adjustment for the risk profiles, multivariable analysis showed that gender itself was not an independent predictor of impaired microvascular reperfusion. Both female gender and impaired myocardial reperfusion were independent predictors of 30-day MACE, whereas gender lost its prognostic significance for 6-month MACE. Multivariable analysis restricted to female patients identified incomplete ST-segment resolution as the strongest determinant of 30-day MACE. CONCLUSION: The differences in microvascular reperfusion after PPCI between women and men are attributed to higher risk profiles in women. Both female gender and impaired myocardial reperfusion were independent predictors of 30-day outcomes after PPCI, emphasizing the importance of successful microvascular reperfusion in the women with STEMI.

Efficacy of coronary angioplasty on long-term outcome in elderly Chinese patients with ST elevated myocardial infarction.

The benefit and efficacy of interventional coronary therapies in elderly patients is still a controversial subject, especially in parts of the world where traditional and conservative medicine is still mainstream. In China, the benefit of intervention is still questionable, hence, this study investigated the prognostic significance of coronary angioplasty on outcomes of elderly patients presenting with ST-segment elevated myocardial infarction (STEMI). The study cohort comprised of 270 elderly (age >or= 75 years) patients who had confirmed STEMI. Some 116 patients underwent coronary angioplasty (called CA group) and their prognoses and survival over the short- and long-term periods (up to 80 months) were compared to 154 comparable patients who received a noninvasive, more conservative medical therapy (non-CA group). The subsequent Kaplan-Meier survival curves and statistical analyses were used to ascertain any difference between the groups. There was no significant differences between the two groups in terms of their clinical presentation, clinical risk, cardiac features, medications and medical procedures, except that the peak creatine kinase was significantly higher in the CA group. The success rate of interventional percutaneous coronary intervention observed in the CA group was 92.4% and during the hospitalization period, there were fewer deaths in the CA group (11 vs. 61 in the non-CA group). Furthermore, after 1-year and up to 7 years postsurgery, the CA group had a significant survival when compared to the non-CA cohort. Analysis of the longer-term data, using multivariate Cox regression analysis after 80 months indicated a hazard ratio of mortality for patients in CA group to be 0.283 (95% CI: 0.140-0.534, P < 0.001). Also, multivariate logistic regression analysis identified conservative treatment, chronic renal failure, cardiac arrhythmia, chronic lung disease and left ventricular ejection fraction, as predictors of higher long-term mortality in elderly patients with STEMI. In conclusion, this study clearly indicates that elderly Chinese patients with STEMI who undergo coronary angioplasty benefit and have a better survival rates in both the short- and long-term.

TIMI myocardial perfusion frame count: a new method to assess myocardial perfusion and its predictive value for short-term prognosis.

OBJECTIVES: We sought to develop a new quantitative method to evaluate the degree of myocardial perfusion. BACKGROUND: Currently available methods for assessing myocardial perfusion, both TIMI myocardial perfusion grading (TMPG) and myocardial blush grading (MBG), are subjective. METHODS: TIMI Myocardial Perfusion Frame Count (TMPFC), an objective method that measures the filling and clearance of contrast in the myocardium using cine-angiographic frame-counting, was developed to quantify myocardial perfusion. Myocardial perfusion of 45 normal coronary arteries in 15 patients, and 137 culprit arteries in 137 patients immediately after primary angioplasty, was successfully assessed with TMPFC. RESULTS: The mean TMPFC in the normal arteries was 83.47 +/- 17.96 frames (95% CI: 78.07 frames

Comparison of epicardial and myocardial perfusions after primary coronary angioplasty for ST-elevation myocardial infarction in patients under and over 75 years of age.

BACKGROUND AND AIMS: Patients aged ≥75 years compose a high-risk subgroup for acute myocardial infarction (AMI). It is unknown whether myocardial perfusion in these patients is decreased compared with younger ones after primary percutaneous coronary intervention (PPCI), which may contribute to their worse prognosis. We compared epicardial and myocardial perfusions as well as short-term outcomes between elderly and younger patients undergoing PPCI. METHODS: A total of 547 consecutive PPCI patients were prospectively enrolled; of these, 106 were elderly (≥75 yrs). Epicardial perfusion was evaluated by the Thrombolysis in Myocardial Infarction (TIMI) flow grade and corrected TIMI frame count (CTFC), and myocardial perfusion was evaluated by the TIMI myocardial perfusion grade (TMPG) and ST-segment resolution (STR). RESULTS: Despite comparable epicardial perfusion pre- and post-PPCI, elderly patients had impaired myocardial perfusion after PPCI, as measured by reduced TMPG (35.9% vs 14.5%, p=0.001) and absent STR (18.9% vs 9.8%, p=0.009). After adjusting for clinical and angiographic risk profiles, multivariate analysis showed that age ≥75 years remained independently associated with reduced TMPG or absent STR. In the whole population, multivariate analysis revealed that both age ≥75 years and absent STR were independently associated with 3-month major adverse cardiac events (MACE). In the elderly subgroup, multivariate analysis identified absent STR as the strongest determinant of 3-month MACE. CONCLUSIONS: Age is associated with impaired myocardial perfusion, but not epicardial perfusion, after PPCI for AMI. To further improve the outcome of elderly AMI patients, efforts should be aimed at improving myocardial perfusion beyond epicardial recanalization.

[Prognostic value of plasma brain natriuretic peptide and C-reactive protein in patients with acute coronary syndromes underwent percutaneous coronary intervention].

OBJECTIVE: To evaluate the prognostic value of plasma brain natriuretic peptide (BNP) and C-reactive protein (CRP) in patients with acute coronary syndromes (ACS) underwent percutaneous coronary intervention (PCI). METHODS: Patients with ACS underwent PCI in our hospital from December 2004 to September 2005 were included in this study. Plasma BNP (n = 189) and CRP (n = 141) were measured at a median of (34.2 +/- 16.3) hours from symptom onset, total mortality and the risk for major adverse cardiac events (MACE, including death, recurrent MI, recurrent angina, heart failure, readmission for any reason) at 30 days and at 3 months was analyzed. RESULTS: Patients were divided into 4 groups according to their BNP levels (BNP 100 ng/L to 300 ng/L to 600 ng/L) and the 3-month mortality was 0%, 1.4%, 7.7%, 48.3% and 3-month incidence of MACE was 7.9%, 17.1%, 57.7%, 79.3% respectively. Multivariate logistic regression analyses showed that the plasma BNP level predicted 30-day (r = 0.8515, P < 0.01) and 3-month (r = 0.9201, P < 0.01) mortality and 30-day (r = 0.7066, P < 0.01) and 3-month (r = 0.7090, P < 0.01) incidence of MACE independent of other known prognostic factors such as age, gender, family heredity, hypercholesterolemia diabetes, hypertension, smoking and LVEF. Patients were divided into 3 groups according to their CRP levels (CRP 8.0 mg/L to 32.0 mg/L) and 3-month mortality was 2.7%, 7.7% and 28.6% and 3-month incidence of MACE was 28.4%, 41.0% and 60.7% respectively. CRP predicted 30-day (r = 0.5882, P = 0.0044) and 3-month (r = 0.5235, P = 0.0038) mortality independent of traditional risk factors, and predicted 30-day (r = 0.2705, P = 0.0380) and 3-month (r = 0.2290, P = 0.0429) incidence of MACE after adjustment for patient age. CRP lost its predictive value after BNP was introduced into the model, while BNP was still an independent predictor for mortality and incidence of MACE at 30 days and 3 months in ACS patients underwent PCI. CONCLUSION: Both plasma BNP and CRP are good predictors for early mortality and MACE incidence in ACS patients underwent PCI.

[The clinical value of sixteen-detector row computed tomography angiography for the assessment of coronary artery bypass graft].

OBJECTIVE: The aim of this study was to evaluate the value of sixteen-detector row computed tomography angiography (CTA) for the assessment of coronary artery bypass graft (CABG). METHODS: Sixty-two consecutive patients undergoing coronary artery bypass grafting were recruited. Among them, 6 patients were excluded from the study due to unfavorable control of heart rate. A total of 56 patients with 152 coronary artery bypass grafts (internal mammary artery, n = 48; saphenous venous grafts, n = 104) were examined by computed tomography angiography (CTA) with sixteen-detector row CT and by conventional invasive coronary angiography (CAG). All CT procedures were performed with retrospective electrocardiogram gating method. The patients' mean heart rate was 58 +/- 6 beats/minute. 120 ml of Visipaque 320 were continuously injected with the rate of 4.0 ml/sec during the procedure. The patency and the stenosis of coronary artery bypass grafts were evaluated by two experienced readers. RESULTS: All the coronary artery bypass grafts were visualized by CTA, and all the proximal bypass anastomoses and 71% of the distal bypass anastomoses were also visualized by CTA. Furthermore, 29 occlusions and 13 significant stenoses of coronary artery bypass grafts were detected by CTA. The comparison of the results between CTA and CAG showed that among all the 42 occluded and stenosed coronary artery bypass grafts detected by CTA, 34 were confirmed by CAG; among all the 110 normal coronary artery bypass grafts detected by CTA, 108 were confirmed by CAG. There were 8 false positive and 2 false negative findings, resulting in a sensitivity of 94%, a specificity of 95%, a positive predictive value of 86%, and a negative predictive value of 99%. CONCLUSION: Sixteen-detector row CTA technology may provide a reliable visualization and higher diagnostic accuracy of coronary artery bypass grafts lesions. This technique can be used as a noninvasive procedure for the diagnosis of suspected coronary artery bypass grafts dysfunction.