Prognostic value of Toll-like receptor 4 on human monocyte subsets combined with computed tomography-adapted Leaman score assessing coronary artery disease.

BACKGROUND: Upregulation of Toll-like receptor 4 (TLR-4) is associated with coronary plaque vulnerability assessed by coronary computed tomography angiography (CCTA). Computed tomography-adapted Leaman score (CT-LeSc) is an independent long-term predictor of cardiac events. The relationship between the TLR-4 expression of CD14 ++ CD16 + monocytes and future cardiac events is unknown. We investigated this relationship using CT-LeSc in patients with coronary artery disease (CAD). METHODS: We analyzed 61 patients with CAD who underwent CCTA. Three monocyte subsets (CD14 ++ CD16 - , CD14 ++ CD16 + , and CD14 + CD16 + ) and the expression of TLR-4 were measured by flow cytometry. We divided the patients into two groups according to the best cutoff value of the TLR-4 expression on CD14 + CD16 + which could predict future cardiac events. RESULTS: CT-LeSc was significantly greater in the high TLR-4 group than the low TLR-4 group [9.61 (6.70-13.67) vs. 6.34 (4.27-9.09), P  < 0.01]. The expression of TLR-4 on CD14 ++ CD16 + monocytes was significantly correlated with CT-LeSc ( R2  = 0.13, P  < 0.01). The expression of TLR-4 on CD14 ++ CD16 + monocytes was significantly higher in patients who had future cardiac events than in those who did not [6.8 (4.5-9.1) % vs. 4.2 (2.4-7.6) %, P  = 0.04]. High TLR-4 expression on CD14 ++ CD16 + monocytes was an independent predictor for future cardiac events ( P  = 0.01). CONCLUSION: An increase in the TLR-4 expression on CD14 ++ CD16 + monocytes is related to the development of future cardiac events.

Prognostic Value of Human Peripheral Monocyte Subsets for Future Coronary Events in Patients Without Significant Coronary Artery Stenosis.

BACKGROUND: Monocytes in human peripheral blood are heterogeneous and can be divided into 2 groups, inflammatory and pro-inflammatory, according to the differential expression of CD14 and CD16. Pro-inflammatory monocytes (CD14+CD16+) seem to contribute to the development of coronary artery disease. This study aimed to investigate the involvement of specific human peripheral monocyte subsets in the development of future coronary events.Methods and Results:We enrolled 271 patients who were suspected to have either stable angina pectoris or silent myocardial ischemia and underwent coronary angiography (CAG). Two monocyte subsets (CD14+CD16-and CD14+CD16+) were measured by flow cytometry. Patients who did not undergo coronary artery revascularization at initial CAG were followed as the medical therapy group, which included 136 patients among whom 15 had future coronary events. The frequency of CD14+CD16+monocytes was significantly higher in patients who had future coronary events than in those who did not (P<0.01). Furthermore, the frequencies of CD14+CD16+monocyte were not significantly different between patients who had future coronary events and those who underwent coronary revascularization at initial CAG (P<0.33). Multivariate analysis revealed that the frequency of CD14+CD16+monocytes was an independent predictor for future coronary events (P<0.01). CONCLUSIONS: An increase in the abundance of human peripheral pro-inflammatory monocytes is related to the development of future coronary events.

Association of Toll-Like Receptor 4 on Human Monocyte Subsets and Vulnerability Characteristics of Coronary Plaque as Assessed by 64-Slice Multidetector Computed Tomography.

BACKGROUND: Although Toll-like receptor 4 (TLR-4) is involved in monocyte activation in patients with accelerated forms of atherosclerosis, the relationship between the expression of TLR-4 on circulating monocytes and coronary plaque vulnerability has not previously been evaluated. We investigated this relationship using 64-slice multidetector computed tomography (MDCT) in patients with stable angina pectoris (SAP).Methods and Results:We enrolled 65 patients with SAP who underwent MDCT. Three monocyte subsets (CD14++CD16-, CD14++CD16+, and CD14+CD16+) and expression of TLR-4 were measured by flow cytometry. Intracoronary plaques were assessed by 64-slice MDCT. We defined vulnerability of intracoronary plaques according to the presence of positive remodeling (remodeling index >1.05) and/or low CT attenuation (<35 HU). The circulating CD14++CD16+monocytes more frequently expressed TLR-4 than CD14++CD16-and CD14+CD16+monocytes (P<0.001). The relative proportion of the expression of TLR-4 on CD14++CD16+monocytes was significantly greater in patients with vulnerable plaque compared with those without (10.4 [4.1-14.5] % vs. 4.5 [2.8-7.8] %, P=0.012). In addition, the relative proportion of TLR-4 expression on CD14++CD16+monocytes positively correlated with the remodeling index (r=0.28, P=0.025) and negatively correlated with CT attenuation value (r=-0.31, P=0.013). CONCLUSIONS: Upregulation of TLR-4 on CD14++CD16+monocytes might be associated with coronary plaque vulnerability in patients with SAP.

Resistance to Thyroid Hormone Complicated with Type 2 Diabetes and Cardiomyopathy in a Patient with a TRß Mutation.

Resistance to thyroid hormone (RTH) is a genetic disorder characterized by reduced tissue responsiveness to thyroid hormone. We herein describe a 60-year old man who presented with the clinical features of cardiomyopathy, diabetes mellitus and elevated thyroid hormones with unsuppressed thyroid stimulating hormone. A genetic analysis of thyroid hormone receptor (TR) revealed a missense mutation (A268D) in the TRß gene. Clinical manifestations of RTH may be variable due to different tissue distributions of TR subtypes and different actions of mutant receptors. The current case demonstrates that patients with a TRß mutation may have impaired his glucose metabolism and a reduced cardiac function, although patients appear clinically euthyroid.

Inflammatory Biomarkers in Peripheral Artery Disease: Diagnosis, Prognosis, and Therapeutic Challenges.

Peripheral artery disease (PAD) is an inflammatory disease caused by atherosclerosis. It has been demonstrated that PAD is related to chronic inflammation. While conventional risk factors lead to the pathogenesis and progression of PAD, the role of novel inflammatory biomarkers in relation to PAD is being increasingly recognized. The novel biomarkers for PAD may allow for earlier screening and detection, suppression of disease progression, and development of new therapeutic approaches. In this review, inflammatory biomarkers that should be contributory to diagnosis, prognosis, and avenues for therapeutic challenges in PAD are summarized.

Circulating CD14++CD16+ Monocyte Subsets as a Surrogate Marker of the Therapeutic Effect of Corticosteroid Therapy in Patients With Cardiac Sarcoidosis.

BACKGROUND: We aimed to evaluate whether specific monocyte subsets could serve as surrogate markers of disease activity in cardiac sarcoidosis (CS) evaluated by 18F-fluoro-2-deoxyglucose positron emission tomography (18F-FDG PET). METHODS AND RESULTS: We studied 28 patients with CS (8 men; mean age: 61±9 years) diagnosed according to consensus criteria. We divided the patients into 2 groups: known CS receiving corticosteroid therapy (Rx(+); n=13) and new-onset CS (Rx(-); n=15), and analyzed 3 distinct monocyte subsets (CD14+CD16-, CD14++CD16+, and CD14+ -CD16+). Monocyte subsets were also analyzed in 10 Rx(-) patients before and 12 weeks after starting corticosteroid therapy. Inflammatory activity was quantified by 18F-FDG PET using the coefficient of variation (COV) of the standardized uptake value (SUV). The proportion of CD14++CD16+ monocytes in Rx(+) patients (10.8 [0.2-23.5] %) was significantly lower than in Rx(-) patients (23.0 [11.5-38.4] %, P=0.001). After corticosteroid therapy, the COV of the SUV was significantly improved from 0.32 [0.14-0.62] to 0.17 [0.04-0.43] (P=0.017). The proportion of CD14++16+ monocytes showed a significant decrease from 22.2 [8.8-38.4] % to 8.4 [1.8-16.8] % (P=0.001). The decrease in the proportion of CD14++16+ monocytes significantly correlated with the decrease in the COV of the SUV (r=0.495, P=0.027). CONCLUSIONS: CD14++16+ monocytes are a possible surrogate marker of the therapeutic effect of corticosteroid therapy in CS.

Myocardial Damage Detected by Two-Dimensional Speckle-Tracking Echocardiography in Patients with Extracardiac Sarcoidosis: Comparison with Magnetic Resonance Imaging.

BACKGROUND: The aim of this study was to determine whether two-dimensional speckle-tracking echocardiography can identify the myocardial damage detected by delayed enhancement (DE) magnetic resonance imaging via the differences in myocardial deformation in patients with extracardiac sarcoidosis who showed no structural and functional abnormalities in the heart. METHODS: Forty-five patients with biopsy-proven extracardiac sarcoidosis were analyzed retrospectively. Patients with abnormal electrocardiographic and echocardiographic findings, including ventricular arrhythmias, heart block, regional wall motion abnormalities, valvular heart disease, and cardiomyopathy, were excluded. Ten age-matched healthy control subjects were recruited as a control group. Comprehensive echocardiography and DE magnetic resonance imaging were performed, and circumferential, longitudinal, and radial strain were consecutively assessed using two-dimensional speckle-tracking echocardiographic software in a 16-segment model of the left ventricle in accordance to the presence (DE+) or absence (DE-) of DE. RESULTS: Among the 45 patients, 36 segments in 13 patients showed DE. DE+ segments had lower peak circumferential strain than DE- and control segments (-14 ± 5% vs -28 ± 7% vs -30 ± 7%, P < .0001). Peak longitudinal strain in DE+ segments was significantly decreased compared with control segments (-19 ± 4% vs -23 ± 5%, P = .005). However, peak radial strain was similar among the three groups: 41 ± 17% in DE+ segments, 45 ± 23% in DE- segments, and 46 ± 18% in control segments (P = .50). CONCLUSIONS: Circumferential and longitudinal strain via two-dimensional speckle-tracking echocardiography can identify the myocardial damage detected by DE magnetic resonance imaging in patients with extracardiac sarcoidosis.

Impact of low signal intensity assessed by cine magnetic resonance imaging on detection of poorly viable myocardium in patients with prior myocardial infarction.

Late gadolinium enhancement magnetic resonance imaging (LGE-MRI) has been established as a modality to detect myocardial infarction (MI). However, the use of gadolinium contrast is limited in patients with advanced renal dysfunction. Although the signal intensity (SI) of infarct area assessed by cine MRI is low in some patients with prior MI, the prevalence and clinical significance of low SI has not been evaluated. The aim of this study was to evaluate how low SI assessed by cine MRI may relate to the myocardial viability in patients with prior MI. Fifty patients with prior MI underwent both cine MRI and LGE-MRI. The left ventricle was divided into 17 segments. The presence of low SI and the wall motion score (WMS) of each segment were assessed by cine MRI. The transmural extent of infarction was evaluated by LGE-MRI. LGE was detected in 329 of all 850 segments (39%). The low SI assessed by cine MRI was detected in 105 of 329 segments with LGE (32%). All segments with low SI had LGE. Of all 329 segments with LGE, the segments with low SI showed greater transmural extent of infarction (78 [72 - 84] % versus 53 [38 - 72] %, P < 0.01), thinner wall (4.0[3.1 - 4.8] mm versus 6.5 [5.2 - 8.1] mm, P < 0.01), and higher WMS (4.0 [4.0 - 4.0] versus 2.0 [2.0 - 3.0], P < 0.01). The low SI assessed by cine MRI may be effective for detecting poorly viable myocardium in patients with prior MI.

MicroRNAs and cardiovascular diseases.

Coronary artery diseases (CAD) and heart failure have high mortality rate in the world, although much progress has been made in this field in last two decades. There is still a clinical need for a novel diagnostic approach and a therapeutic strategy to decrease the incidence of CAD. MicroRNAs (miRNAs) are highly conserved noncoding small RNA molecules that regulate a large fraction of the genome by binding to complementary messenger RNA sequences, resulting in posttranscriptional gene silencing. Recent studies have shown that specific miRNAs are involved in whole stage of atherosclerosis, from endothelium dysfunction to plaque rupture. These findings suggest that miRNAs are potential biomarkers in early diagnosis and therapeutic targets in CAD. In the present review, we highlight the role of miRNAs in every stage of atherosclerosis, and discuss the prospects of miRNAs in the near future.

Two-dimensional speckle tracking echocardiography for the prediction of reversible myocardial dysfunction after acute myocardial infarction: comparison with magnetic resonance imaging.

BACKGROUND: We aimed to determine the predictive value of longitudinal, circumferential, and radial strains by two-dimensional speckle tracking echocardiography (2DSTE) for improvement in cardiac function after acute myocardial infarction (AMI) compared with that of contrast-enhanced cardiac magnetic resonance imaging (ceMRI). METHODS: In 35 patients with first-time AMI, myocardial viability was assessed to predict recovery of function at follow-up (7 ± 2 months), prospectively. For each left ventricular segment, each peak strains were determined using 2DSTE, and the relative extent of hyperenhancement was assessed using ceMRI. RESULTS: Of 176 segments with impaired function early after AMI, 99 segments showed regional recovery. Compared with segments showing functional improvement, those that failed to recover had lower peak radial (20 ± 16% vs. 32 ± 21%; P < 0.001), circumferential (-10 ± 5% vs. -20 ± 6%; P < 0.001), and longitudinal (-10 ± 5% vs. -14 ± 5%; P < 0.001) strain and a greater extent of hyperenhancement (71 ± 22% vs. 27 ± 20%; P < 0.001). Among strain parameters, circumferential strain yielded greater area under the curve (AUC; 0.899) than radial and longitudinal strain (0.682 and 0.718, respectively). The predictive value of circumferential strain (sensitivity 81.0%, specificity 79.6%, at a cutoff value of -14.3%) could be comparable to that of hyperenhancement (sensitivity 86.2%, specificity 83.9%, AUC 0.921, at a cutoff value of 47%) (P = 0.439). CONCLUSION: Circumferential strain can identify reversible myocardial dysfunction after AMI with a diagnostic ability comparable to that of ceMRI.

Comparison of vascular response between everolimus-eluting stent and bare metal stent implantation in ST-segment elevation myocardial infarction assessed by optical coherence tomography.

AIMS: The long-term safety of second-generation everolimus-eluting stents (EESs) in ST-segment elevation myocardial infarction (STEMI) remains unclear. The aim of this study was to evaluate the late vascular response after stent implantation in STEMI between EES and bare-metal stent (BMS) by using optical coherence tomography (OCT). METHODS AND RESULTS: A prospective OCT examination was performed in 102 patients at 10 months after stent implantation for treatment of STEMI. A total of 1253 frames with 12 772 struts in 61 EESs and 776 frames with 8594 struts in 41 BMSs were analysed. There were no significant differences in the percentage of uncovered struts (2.1 ± 2.8 vs. 1.7 ± 2.7%, P = 0.422) and malapposed struts (0.7 ± 1.3 vs. 0.6 ± 1.2%, P = 0.756) between EES and BMS. The frequency of intra-stent thrombus was comparable between the two stents (13 vs. 10%, P = 0.758). The mean neointimal thickness was smaller in EES compared with BMS (104 ± 39 vs. 388 ± 148 µm, P < 0.001). In-segment binary restenosis and target lesion revascularization was less often seen in EES compared with BMS (3 vs. 17%, P = 0.028 and 2 vs. 12%, P = 0.037, respectively). CONCLUSION: When compared with BMS, EES showed a lower rate of stent restenosis, similar frequency of neointimal coverage, stent malapposition, and intra-stent thrombus at 10 months after stent implantation in STEMI. Our results suggest the safety and effectiveness of EES in primary percutaneous coronary intervention for STEMI patients.

Long-term outcome after deferral of revascularization in patients with intermediate coronary stenosis and gray-zone fractional flow reserve.

BACKGROUND: A strategy of deferred percutaneous coronary intervention for coronary stenosis with fractional flow reserve (FFR) 0.75-0.80, termed the gray zone, remains a matter of debate. The aim of this study was to assess the safety of deferring revascularization for patients with FFR 0.75-0.80 compared with those with FFR >0.80. METHODS AND RESULTS: We assessed 3-year clinical outcome in 150 patients with angiographically intermediate stenosis who had revascularization deferred on the basis of FFR ≥ 0.75 (FFR 0.75-0.80, n=56; FFR >0.80, n=94). Target vessel failure (TVF), defined as a composite of cardiac death, target vessel-related myocardial infarction (MI), and ischemia-driven target vessel revascularization (TVR) was evaluated during follow-up. Cardiac death was observed in 1 patient with FFR 0.75-0.80. There was no target vessel-related MI in either group. The incidence of ischemia-driven TVR was higher in patients with FFR 0.75-0.80 than in those with FFR >0.80 (14% vs. 3%, P=0.020). TVF-free survival was significantly worse for the patients with FFR 0.75-0.80 than those with FFR >0.80 (hazard ratio, 5.2; 95% confidence intervals: 1.4-19.5; P=0.015). CONCLUSIONS: Patients with FFR 0.75-0.80 were at higher risk of TVF mainly due to TVR than those with FFR >0.80.

Impact of eicosapentaenoic acid treatment on the fibrous cap thickness in patients with coronary atherosclerotic plaque: an optical coherence tomography study.

AIM: Previous clinical trials have demonstrated the effectiveness of eicosapentaenoic acid (EPA) in preventing cardiovascular events. The aim of the present study was to investigate the effects of EPA treatment on the accumulation of coronary atherosclerotic plaque using optical coherence tomography (OCT). METHODS: A total of 46 acute coronary syndrome (ACS) patients without dyslipidemia were divided into two groups: those who received 1,800 mg/day of EPA (n = 15) or the control group (n = 31). Serial OCT examinations were performed at baseline and after eight months of follow-up. The target for the OCT analysis was non-culprit plaque with a percent diameter of stenosis of 30% to 70% in non-culprit vessels of ACS. RESULTS: Between the baseline and follow-up visits, the serum EPA levels increased (50 ± 26 mg/dL to 200 ± 41 mg/dL, p ＜ 0.001) in the EPA group, although they did not change in the control group. According to the OCT analysis, the lipid arc did not change in the EPA group (131 ± 52 degrees to 126 ± 54 degrees, p = 0.106) or the control group (137 ± 50 degrees to 138 ± 50 degrees, p=0.603). In contrast, the fibrous cap thickness significantly increased in both the EPA group (169 ± 70 µm to 201 ± 49 µm, p ＜ 0.001) and the control group (164 ± 63 µm to 174 ± 72 µm, p=0.018); however, the relative change in the fibrous cap thickness was significantly greater in the EPA group than in the control group (131 ± 35% vs. 106 ± 15%, p = 0.001). CONCLUSIONS: In the present study, the administration of EPA for eight months significantly increased the fibrous cap thickness in patients with coronary atherosclerotic plaque.

Improvement of cardiac function by increasing stimulus strength during left ventricular pacing in cardiac resynchronization therapy.

Cardiac resynchronization therapy (CRT) is an established therapy in patients with severe heart failure due to left ventricular (LV) dyssynchrony. Increasing stimulus strength (SS) of LV pacing could capture an enlarged myocardial area and provide rapid electrical conduction. The aim of the present study was to investigate whether increasing SS of LV pacing improves LV mechanical dyssynchrony and cardiac function in patients treated with CRT.We enrolled 26 patients with CRT and changed the SS of LV pacing: 2.5 V (standard SS) and 5 V (high SS). Electrocardiography and echocardiography were performed to assess QRS duration, LV mechanical dyssynchrony, and cardiac function under each condition.The QRS duration (138.6 ± 21.4 ms versus 126.8 ± 23.1 ms, P < 0.001), septal-posterior wall motion delay (126.5 ± 42.7 ms versus 111.4 ± 55.3 ms, P = 0.012), standard deviation of time from QRS (69.6 ± 21.8 ms versus 55.6 ± 19.4 ms, P < 0.001), LV ejection fraction (29.4 ± 10.6% versus 33.4 ± 11.6%, P = 0.005), and LV stroke volume (50.7 ± 15.5 mL versus 63.8 ± 18.3 mL, P < 0.001) improved significantly in high SS compared with standard SS.Increasing SS of LV pacing in CRT improves LV mechanical dyssynchrony and cardiac function. The capture of an enlarged myocardial area by increasing SS of LV pacing might offer an acute hemodynamic benefit to patients treated with CRT.

Association between hyperglycemia at admission and microvascular obstruction in patients with ST-segment elevation myocardial infarction.

BACKGROUND: Blood glucose level at admission in ST-segment elevation myocardial infarction (STEMI) is a predictor of heart failure and mortality. A previous study showed the association between hyperglycemia and microvascular dysfunction using myocardial contrast echocardiography. Late gadolinium enhancement (LGE) cardiovascular magnetic resonance imaging (CMR) can demonstrate microvascular obstruction (MVO) as the area with hypointense core within LGE. This study was performed to investigate the association between hyperglycemia at admission and MVO using CMR in patients with STEMI. METHODS: Ninety-three patients with first STEMI who were treated by percutaneous coronary intervention (PCI) were included. CMR was performed within 7 days after PCI. Venous blood was collected routinely immediately after admission for plasma glucose determination before intravenous injection of some medications. Samples were analyzed in the hospital's central laboratory. We performed LGE-CMR to assess the presence of MVO. RESULTS: MVO was found in 34 (37%) of all 93 patients; their glucose level at admission was significantly higher than that of patients who did not exhibit MVO [204 (153-267)mg/dl vs. 157 (127-200)mg/dl, p=0.002]. There were no differences in glycosylated hemoglobin and incidence of diabetes mellitus between the two groups. A multivariable logistic regression analysis showed that glucose level at admission was an independent predictor of MVO (odds ratio, 1.014; 95% confidence interval, 1.004 to 1.023; p=0.006). The glucose level at admission 190mg/dl was the best threshold value for identifying MVO. The occurrence of MVO was significantly higher in the patients with glucose level at admission ≧190mg/dl compared with the patients with glucose level <190mg/dl [18 (53%) vs. 16 (27%), p=0.023]. CONCLUSIONS: Hyperglycemia at admission in STEMI patients who were treated by PCI was associated with the presence of MVO assessed by LGE-CMR.

Effect of atorvastatin therapy on fibrous cap thickness in coronary atherosclerotic plaque as assessed by optical coherence tomography: the EASY-FIT study.

BACKGROUND: The detailed mechanism of plaque stabilization by statin therapy is not fully understood. OBJECTIVES: The aim of this study was to assess the effect of lipid-lowering therapy with 20 mg/day of atorvastatin versus 5 mg/day of atorvastatin on fibrous cap thickness in coronary atherosclerotic plaques by using optical coherence tomography (OCT). METHODS: Seventy patients with unstable angina pectoris and untreated dyslipidemia were randomized to either 20 mg/day or 5 mg/day of atorvastatin therapy. OCT was performed to assess intermediate nonculprit lesions at baseline and 12-month follow-up. RESULTS: Serum low-density lipoprotein cholesterol level was significantly lower during therapy with 20 mg/day compared with 5 mg/day of atorvastatin (69 mg/dl vs. 78 mg/dl; p = 0.039). The increase in fibrous cap thickness was significantly greater with 20 mg/day compared with 5 mg/day of atorvastatin (69% vs. 17%; p < 0.001). The increase in fibrous cap thickness correlated with the decrease in serum levels of low-density lipoprotein cholesterol (R = -0.450; p < 0.001), malondialdehyde-modified low-density lipoprotein (R = -0.283; p = 0.029), high-sensitivity C-reactive protein (R = -0.276; p = 0.033), and matrix metalloproteinase-9 (R = -0.502; p < 0.001), and the decrease in grade of OCT-derived macrophages (R = -0.415; p = 0.003). CONCLUSIONS: Atorvastatin therapy at 20 mg/day provided a greater increase in fibrous cap thickness in coronary plaques compared with 5 mg/day of atorvastatin. The increase of fibrous cap was associated with the decrease in serum atherogenic lipoproteins and inflammatory biomarkers during atorvastatin therapy. (Effect of Atorvastatin Therapy on Fibrous Cap Thickness in Coronary Atherosclerotic Plaque as Assessed by Optical Coherence Tomography: The EASY-FIT Study; NCT00700037).

Incremental value of coronary flow velocity reserve, measured by transthoracic echocardiography, compared with computed tomography angiography alone, for detecting flow-limiting coronary stenoses.

BACKGROUND: Computed tomographic (CT) angiography provides high sensitivity for the detection of coronary stenosis, while its specificity is relatively low. The aim of this study was to determine the incremental value of coronary flow velocity reserve (CFVR) by transthoracic echocardiography when used with CT angiography for detecting stenosis of the major coronary arteries compared with invasive quantitative coronary angiography. METHODS: Sixty patients who underwent CFVR measurement before coronary angiography were retrospectively selected, and the cutoff value of CFVR to predict diameter stenosis > 70% was determined using receiver operating characteristic curve analysis. Second, CFVR measurement and CT angiography were prospectively performed in 50 patients who were scheduled to undergo coronary angiography. CT angiography using a 64-detector row scanner and CFVR measurement in the proximal to middle portions of the three major coronary arteries by transthoracic echocardiography were performed on the same day, <48 hours before invasive angiography. RESULTS: The cutoff values of CFVR were determined to be 2.0 for the left anterior descending coronary artery and 2.1 for the circumflex and right coronary arteries. Using these determined cutoff values, the sensitivity, specificity, and positive and negative predictive value of CFVR to identify diameter stenosis ≥ 70% stenosis on invasive quantitative coronary angiography were determined to be 84%, 87%, 66%, and 95%, respectively, and those of CT angiography were 91%, 80%, 58%, and 97%, respectively, in the prospective study with 50 patients. The combination of ≥70% stenosis on CT angiography and impaired CFVR was 94% specific for ≥70% stenosis, while the presence of <70% stenosis on CT angiography and preserved CFVR was 100% specific for the exclusion of ≥70% stenosis on invasive quantitative coronary angiography. CONCLUSIONS: When the results of CT angiography and CFVR are concordant, the combination is highly accurate in the detection and exclusion of coronary stenosis. CFVR measurement in addition to CT angiography could be helpful in identifying false-positive CT angiographic results.

Assessment of cardiac sarcoidosis with advanced imaging modalities.

Sarcoidosis is a chronic systemic disease of unknown etiology that is characterized by the presence of noncaseating epithelioid granulomas, usually in multiple organs. Several studies have shown that sarcoidosis might be the result of an exaggerated granulomatous reaction after exposure to unidentified antigens in genetically susceptible individuals. Cardiac involvement may occur and lead to an adverse outcome: the heart mechanics will be affected and that causes ventricular failure, and the cardiac electrical system will be disrupted and lead to third degree atrioventricular block, malignant ventricular tachycardia, and sudden cardiac death. Thus, early diagnosis and treatment of this potentially devastating disease is critically important. However, sensitive and accurate imaging modalities have not been established. Recent studies have demonstrated the promising potential of cardiac magnetic resonance imaging (MRI) and (18)F-fluoro-2-deoxyglucose positron emission tomography ((18)F-FDG PET) in the diagnosis and assessment of cardiac sarcoidosis (CS). In this review, we discuss the epidemiology, etiology, histological findings, and clinical features of sarcoidosis. We also introduce advanced imaging including (18)F-FDG PET and cardiac MRI as more reliable diagnostic modalities for CS.