Diagnosis of myocardial viability by fluorodeoxyglucose distribution at the border zone of a low uptake region.

PURPOSE: In cardiac 2-[F-18]fluoro-2-deoxy-D-glucose (FDG)-positron emission tomography (PET) examination, interpretation of myocardial viability in the low uptake region (LUR) has been difficult without additional perfusion imaging. We evaluated distribution patterns of FDG at the border zone of the LUR in the cardiac FDG-PET and established a novel parameter for diagnosing myocardial viability and for discriminating the LUR of normal variants. MATERIALS AND METHODS: Cardiac FDG-PET was performed in patients with a myocardial ischemic event (n = 22) and in healthy volunteers (n = 22). Whether the myocardium was not a viable myocardium (not-VM) or an ischemic but viable myocardium (isch-VM) was defined by an echocardiogram under a low dose of dobutamine infusion as the gold standard. FDG images were displayed as gray scaled-bull's eye mappings. FDG-plot profiles for LUR (= true ischemic region in the patients or normal variant region in healthy subjects) were calculated. Maximal values of FDG change at the LUR border zone (a steepness index; S(max) scale/pixel) were compared among not-VM, isch-VM, and normal myocardium. RESULTS: S(max) was significantly higher for n-VM compared to those with isch-VM or normal myocardium (ANOVA). A cut-off value of 0.30 in Smax demonstrated 100% sensitivity and 83% specificity for diagnosing n-VM and isch-VM. S(max) less than 0.23 discriminated LUR in normal myocardium from the LUR in patients with both n-VM and isch-VM with a 94% sensitivity and a 93% specificity. CONCLUSION: S(max) of the LUR in cardiac FDG-PET is a simple and useful parameter to diagnose n-VM and isch-VM, as well as to discriminate thr LUR of normal variants.

Activator of G protein signaling 8 (AGS8) is required for hypoxia-induced apoptosis of cardiomyocytes: role of G betagamma and connexin 43 (CX43).

Ischemic injury of the heart is associated with activation of multiple signal transduction systems including the heterotrimeric G-protein system. Here, we report a role of the ischemia-inducible regulator of G betagamma subunit, AGS8, in survival of cardiomyocytes under hypoxia. Cultured rat neonatal cardiomyocytes (NCM) were exposed to hypoxia or hypoxia/reoxygenation following transfection of AGS8siRNA or pcDNA::AGS8. Hypoxia-induced apoptosis of NCM was completely blocked by AGS8siRNA, whereas overexpression of AGS8 increased apoptosis. AGS8 formed complexes with G-proteins and channel protein connexin 43 (CX43), which regulates the permeability of small molecules under hypoxic stress. AGS8 initiated CX43 phosphorylation in a G betagamma-dependent manner by providing a scaffold composed of G betagamma and CX43. AGS8siRNA blocked internalization of CX43 following exposure of NCM to repetitive hypoxia; however it did not influence epidermal growth factor-mediated internalization of CX43. The decreased dye flux through CX43 that occurred with hypoxic stress was also prevented by AGS8siRNA. Interestingly, the G betagamma inhibitor Gallein mimicked the effect of AGS8 knockdown on both the CX43 internalization and the changes in cell permeability elicited by hypoxic stress. These data indicate that AGS8 is required for hypoxia-induced apoptosis of NCM, and that AGS8-G betagamma signal input increased the sensitivity of cells to hypoxic stress by influencing CX43 regulation and associated cell permeability. Under hypoxic stress, this unrecognized response program plays a critical role in the fate of NCM.

Development of cardiac dysfunction induced by repetitive transient myocardial ischemia is inhibited by edaravone in conscious rats.

1. In the present study, we investigated the effects of treatment with the hydroxyl radical scavenger 3-methyl-1-phenyl-2-pyrazolin-5-one (edaravone) on myocardial dysfunction induced by transient but frequent ischaemia in conscious rats. 2. Conscious male Wistar rats were subjected to repetitive ischaemia (RI; 40 s ischaemia every 20 min for 72 h). After the ninth episode of RI, edaravone (1 mg/kg, i.v., at each ischaemic event) or vehicle control (acetate buffer solution, i.v.) was administered. Dilation of the left ventricle (LV) after the eighth RI (fractional area change; %FAC(initial)) and after the final RI (%FAC(final)) was determined by comparing measurements (12 MHz echocardiogram) at these time-points with baseline LV area prior to RI. 3. In controls, %FAC(final) was correlated with %FAC(initial) (r = 0.98; P < 0.0001), making %FAC(initial) a predictor of %FAC(final). Edaravone treatment shifted the %FAC(initial)­%FAC(final) relationship downward (P < 0.0001), indicating that edaravone inhibited progression of LV dilation. In addition, %FAC(final) was correlated with myocardial generation of reactive oxygen species (ROS) in control samples (r = 0.88, P = 0.008), although both %FAC(final) and ROS were suppressed by edaravone treatment (P = 0.016). 4. We conclude that repetitive transient ischaemia in conscious rats induced development of cardiac dysfunction and that this phenomenon was inhibited by edaravone. We speculate that edaravone is a potential therapeutic agent that may interfere with the progression of cardiac dysfunction in high-risk patients with RI.

C-reactive protein predicts non-target lesion revascularization and cardiac events following percutaneous coronary intervention in patients with angina pectoris.

BACKGROUND: C-reactive protein (CRP) plays a pivotal role in the pathogenesis of atherosclerosis progression. We hypothesized that CRP might be related to progression of non-target lesion and prognosis in patients with angina pectoris. METHODS AND RESULTS: We enrolled 111 patients with angina pectoris treated with coronary stenting. CRP was measured before coronary stenting. Patients were grouped according to the CRP value, high CRP group (n=56, ≥ 0.12 mg/dl) and low CRP group (n=55, <0.12 mg/dl). Kaplan-Meier analysis showed that non-target lesion revascularization (TLR) free survival was significantly lower in the high CRP group than in the low CRP group (log-rank, p=0.004). Moreover, cardiac event (death, myocardial infarction, TLR, and non-TLR) free survival was also significantly lower in the high CRP group than in the low CRP group (p=0.004). By univariate and multivariate analysis, CRP was the only independent predictor of non-TLR (odds ratio, 1.26; p<0.001 [95% confidence interval (CI) 0.98-1.64]). Also, CRP was a predictor of the cardiac events (odds ratio, 1.32; p=0.04 [95% CI 1.02-1.72]). CONCLUSIONS: CRP was a predictor of non-TLR and cardiac events following stenting in patients with angina pectoris.

Quantitative measurement of mitral valve coaptation in functional mitral regurgitation: In vivo experimental study by real-time three-dimensional echocardiography.

BACKGROUND: The degree of mitral valve (MV) coaptation should be an important parameter in the assessment of functional mitral regurgitation (MR). This study aimed to quantify the degree of MV coaptation in experimental models of functional MR caused by acute left ventricular (LV) pressure overload, using real-time three-dimensional (3D) echocardiography. METHODS AND RESULTS: Using canine models, LV pressure overload was induced by staged ascending aortic banding. Echocardiographic examinations were performed before and during the aortic banding. By using a novel software system for 3D quantification (REALVIEW®), the annulus and leaflet were traced manually both at the onset of MV closure and at the maximum MV closure. The coaptation index was calculated by the following formula: [(3D tenting surface area at the onset of MV closure-3D tenting surface area at the maximum MV closure)/3D tenting surface area at the onset of MV closure] x 100. MR area gradually increased with the decrease in coaptation index during progressively exacerbated aortic banding. MR area was significantly correlated with the coaptation index. A coaptation index < 12 had a high sensitivity and specificity in the presence of significant MR. CONCLUSIONS: The degree of MV coaptation can be quantified using 3D echocardiography. The coaptation index should be a useful parameter in the assessment of functional MR.

C-Reactive protein predicts severity, progression, and prognosis of asymptomatic aortic valve stenosis.

BACKGROUND: C-Reactive protein (CRP) has been shown to play a pivotal role in the pathogenesis of atherosclerosis progression. The aim of this study was to assess whether CRP predicts severity, progression, and prognosis of aortic valve stenosis (AS). METHODS: One hundred and thirty-five patients with asymptomatic AS were studied. Patients were diagnosed as mild (n = 18, aortic valve area [AVA] > or =1.5 cm(2)), moderate (n = 57, AVA 1.0-1.49 cm(2)), or severe AS (n = 60, AVA <1.0 cm(2)) by Doppler echocardiography. Patients with serial (baseline and at 1 year) echocardiographic examination (n = 47) were grouped as either slow (n = 22, DeltaAVA <-0.15 cm(2)/y) or rapid progression group (n = 25, DeltaAVA > or =-0.15 cm(2)/y). In addition, long-term prognosis was compared between patients with low CRP (n = 68, CRP <0.15 mg/dL) and those with high CRP (n = 67, CRP > or =0.15 mg/dL). RESULTS: Baseline CRP was significantly higher in patients with severe AS than in those with mild or moderate AS (mild AS 0.17 +/- 0.43, moderate AS 0.22 +/- 0.28, severe AS 0.53 +/- 0.66 mg/dL, P = .001). By multivariate logistic regression analysis, CRP was an independent predictor of severe AS (odds ratio 3.51, P = .015). Similarly, CRP was significantly higher in the rapid progression group than in the slow progression group (0.56 +/- 0.76 vs 0.19 +/- 0.25 mg/dL, P = .004). Furthermore, long-term survival was significantly lower in the high CRP group than in the low CRP group (log rank: P < .001). CONCLUSION: C-Reactive protein predicts severity, progression, and prognosis in patients with asymptomatic AS.

Mechanism of increasing systolic coronary flow velocity in patients with aortic regurgitation.

BACKGROUND AND AIM OF THE STUDY: The mechanism of increasing systolic coronary flow velocity of the epicardial coronary artery in patients with aortic regurgitation (AR) has not been well investigated. Thus, an evaluation was made of the flow velocity pattern of the epicardial coronary artery in these patients. METHODS: In 12 patients with AR, epicardial coronary flow velocity was monitored using Doppler guidewire, and diameter changes of the epicardial coronary artery using intravascular ultrasound (IVUS). RESULTS: The systolic coronary vascular resistance in AR patients was significantly less than that in controls (1.8 +/- 0.9 versus 3.3 +/- 0.7 mmHg/ml/min; p <0.01). Likewise, area and diameter changes of the epicardial coronary artery during the cardiac cycle in AR patients were significantly less than those in controls (102 +/- 1% versus 106 +/- 4%; p <0.01; and 102 +/- 1% versus 106 +/- 4%; p = 0.03). CONCLUSION: In patients with AR, the increase in systolic coronary flow velocity of the epicardial coronary artery during the systolic phase was considered to result from a major coronary perfusion of blood into the intramyocardial vessels (which showed a decreased resistance), rather than it being stored in the epicardial coronary artery.

Local release of catecholamines from the hearts of patients with tako-tsubo-like left ventricular dysfunction.

BACKGROUND: The precise mechanism of tako-tsubo-like left ventricular (LV) dysfunction remains unclear, although recent studies have shown that activation of sympathetic tone might be involved. However, local release of catecholamines from cardiac sympathetic efferent neurons in patients with tako-tsubo-like LV dysfunction remains poorly understood. The purpose of this study was to investigate evidence of local release of catecholamines from the hearts of patients with tako-tsubo-like LV dysfunction. METHODS AND RESULTS: Five consecutive patients with tako-tsubo-like LV dysfunction were studied. After confirming LV apical ballooning and a normal coronary angiogram, sampling of blood for the measurement of plasma catecholamine levels was performed at the aortic root (Ao) and coronary sinus (CS). In all 5 cases, increased local release of norepinephrine from the heart was documented (597, 4,238, 2,121, 486, 371 pg/ml at the Ao; 836, 5,719, 3,386, 658, 472 pg/ml at the CS, respectively). CONCLUSIONS: Increased cardiac catecholamines might cause the transient LV apical ballooning in patients with tako-tsubo-like LV dysfunction.

Three-dimensional quantitation of mitral valve coaptation by a novel software system with transthoracic real-time three-dimensional echocardiography.

We investigated the degree of mitral valve coaptation with a custom quantitation software system using transthoracic three-dimensional (3D) echocardiography. With real-time 3D echocardiography, we obtained transthoracic volumetric images in 20 healthy subjects and 20 patients with dilated cardiomyopathy. With our novel software system, the surface area of mitral valve tenting in the onset of mitral leaflet closure [O] and the timing of maximum closure of mitral leaflet [M] were reconstructed for quantitative measurement. The coaptation index was calculated by the following formula: [(3D tenting surface area in O-3D tenting surface area in M)/3D tenting surface area in O]. The coaptation index in patients with dilated cardiomyopathy was significantly smaller than that in healthy subjects (11% +/- 4.1% vs. 18% +/- 8.0%, P = .004). The custom quantitation software system with 3D echocardiography allowed us to assess the degree of mitral valve coaptation.

Relationship between coronary remodeling and plaque characterization in patients without clinical evidence of coronary artery disease.

AIMS: The objectives of this study were: (1) to evaluate the relationship between coronary arterial remodeling assessed by intravascular ultrasound (IVUS) and plaque morphology assessed by histological examination in patients without clinical evidence of coronary artery disease and (2) to compare plaque morphology between histological examination and optical coherence tomography (OCT). METHODS: Coronary segments (n=98) were harvested from the heart of 34 patients who died without clinical evidence of coronary artery disease. The segments with remodeling were assessed by IVUS and compared with corresponding OCT and histological images. RESULTS: The fibrofatty plaque area was larger in lesions with expansive remodeling (ER) than in lesions with intermediate/constrictive remodeling (IR/CR) (p<0.01). Incidence of lipid containing plaque with the thickness of the fibrous cap smaller than 200 microm tended to be higher in ER than in IR/CR (34% versus 13%, p=0.10). OCT assessment of lipid containing plaque with thinner fibrous cap was achieved with 92% sensitivity and 75% specificity. CONCLUSIONS: The fibrofatty plaque area was larger in lesions with ER than IR/CR even in patients without clinical evidence of coronary artery disease. The current capabilities of OCT are well suited for evaluation of lipid containing plaques with thinner fibrous cap.

Histological characteristics of plaque with ultrasonic attenuation: a comparison between intravascular ultrasound and histology.

OBJECTIVES: Intermediate echogenic plaque without acoustic shadow on intravascular ultrasound (IVUS) imaging has been recognized as fibrous plaque. Such echogenic plaque with ultrasonic attenuation may have higher risk for distal flow disturbance (slow flow/no-reflow) during percutaneous coronary intervention. However, histological evaluation of plaque with ultrasonic attenuation has not been performed. This study evaluated the histological characteristics of plaque with ultrasonic attenuation assessed by IVUS. METHODS: By using IVUS, 36 samples of human cadaveric coronary arterial echogenic plaque (percentage plaque area > 40%) without calcium were selected, and classified into the attenuation group; plaque with ultrasonic attenuation, and the non-attenuation group; plaque without attenuation. These plaques were classified for fibrous, fibrofatty, calcium, and necrotic core areas by histological examination. RESULTS: True fibrous plaque was found in 91.7% of the non-attenuation group, but only 68.0% of the attenuation group (p < 0.01) . On the other hand, the percentage fibrofatty and necrotic core plaque areas in the attenuation group were significant larger than those in the non-attenuation group (fibrofatty: 16.3 +/- 13.8% vs. 2.7 +/- 3.1%, p < 0.01; necrotic core: 13.0 +/- 19.4% vs. 3.9 +/- 8.0%, p = 0.03). CONCLUSIONS. Plaque with ultrasonic attenuation contains more fibrofatty tissue and necrotic core compared to fibrous plaque without attenuation.

The relationship between coronary plaque characteristics and small embolic particles during coronary stent implantation.

OBJECTIVES: We investigated the relationship between coronary plaque components and small embolic particles during stenting and examined the influence on the coronary microcirculation. BACKGROUND: In vivo tissue characterization of atherosclerotic plaques was introduced by the Virtual Histology intravascular ultrasound (VH-IVUS) system (Volcano Therapeutics, Inc., Rancho Cordova, California). METHODS: The study consisted of 44 patients who underwent elective coronary stenting. Plaque characteristics were identified with VH-IVUS, and small embolic particles liberated during stenting were detected as high-intensity transient signals (HITS) with a Doppler guidewire. Coronary flow velocity reserve (CFVR) was also measured before and after stenting. RESULTS: Patients were divided into the tertiles according to the HITS counts: the lowest, HITS <5 (n = 16); the middle, 5 to 12 (n = 15); and the highest, >12 (n = 13). Dense calcium and necrotic core area identified with VH-IVUS were significantly larger in the highest tertile (lowest vs. middle vs. highest; dense calcium: 0.2 +/- 0.3 mm2 vs. 0.3 +/- 0.6 mm2 vs. 0.8 +/- 0.7 mm2, p = 0.007; necrotic core: 0.5 +/- 0.4 mm2 vs. 0.9 +/- 0.9 mm2 vs. 1.8 +/- 1.0 mm2, p < 0.001, respectively). Multivariate logistic regression analysis revealed only necrotic core area was an independent predictor of high HITS counts (odds ratio 4.41, p = 0.045). Furthermore, there was a significant negative correlation between the HITS count and CFVR after stenting (r = -0.35, p = 0.017). CONCLUSIONS: The necrotic core component identified with VH-IVUS is related to liberation of small embolic particles during coronary stenting, which results in the poorer recovery of CFVR.

Edaravone preserves coronary microvascular endothelial function after ischemia/reperfusion on the beating canine heart in vivo.

We examined whether edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger, exerts its protective effect on coronary microvessels after ischemia/reperfusion (I/R) in vivo. Ninety-minute coronary occlusion followed by reperfusion was performed in 16 open-chest dogs with and without edaravone administration. Coronary small artery (> or = 100 microm in size) and arteriolar (< 100 microm) vasodilation, in the presence of endothelium-dependent (acetylcholine) or -independent (papaverine) vasodilators, was directly observed using intravital microscopy before and after I/R. I/R impaired microvascular vasodilation in response to acetylcholine, whereas administration of edaravone preserved the response in microvessels of both sizes, but to a greater extent in the coronary small arteries. No significant changes were noted with papaverine administration. In the edaravone group, the fluorescent intensity from reactive oxygen species (ROS) was lower, whereas nitric oxide (NO) intensity was higher relative to controls in the microvessels of the ischemic area. In conclusion, edaravone preserves coronary microvascular endothelial function after I/R in vivo. These effects, which were NO-mediated, were attributed to the ROS scavenging properties of edaravone.

Rapid progression of mild to moderate aortic stenosis in patients older than 80 years.

OBJECTIVE: The purpose of this study was to evaluate the rate of progression of mild and moderate aortic stenosis in patients aged 80 years and older. METHODS: In all, 41 patients with mild and moderate aortic stenosis were included and divided into two groups by age: 19 patients aged 80 years and older (mean 84 +/- 4 years), and 21 patients younger than 80 years (mean 66 +/- 6 years). RESULTS: The rate of degression of aortic valve area was more rapid in the 80 years and older age group than that in the younger than 80 years age group (-0.05 +/- 0.06 and -0.10 +/- 0.08 cm2/y, P = .014). Univariate and multivariate analysis of the rate of degression of aortic valve area were performed, and age was the only independent predictor of the rate of degression of aortic valve area. CONCLUSION: Progression of mild and moderate aortic stenosis in patients aged 80 years and older was more rapid than that in those aged younger than 80 years.

Assessment of the histological characteristics of coronary arterial plaque with severe calcification.

BACKGROUND: Several studies have shown that rotational atherectomy (RA) is associated with higher rates of the slow-flow phenomenon and that ablated particles may be the possible cause. Intravascular ultrasound (IVUS) has an intrinsic limitation in assessing plaque morphology behind the calcification because of acoustic shadowing. Therefore, the purpose of this study was to investigate plaque characteristics behind severe calcification by histological examination. METHODS AND RESULTS: One hundred eight coronary arterial segments from 40 human cadavers (24 males, 16 females, mean age 74+/-7 years) were examined. Serial images of IVUS were obtained and 18 severe calcified lesions were collected. Experienced observers quantitatively analyzed the lesions by computerized planimetry for fibrous, fibrofatty, calcification, and necrotic tissue area. Histologically, 15 of 18 severely calcified lesions (83%) had an extensive necrotic tissue containing large numbers of cholesterol crystals and microcalcifications; 16 of same 18 severely calcified lesions (89%) had fibrofatty tissue as well as calcification. The necrotic tissue occupied 14+/-13% and fibrofatty tissue occupied 13+/-11% of severely calcified lesions. CONCLUSION: Necrotic core and fibrofatty tissue components "hidden" behind calcification might cause emboli-induced thrombus formation and distal flow disturbance during RA.

Novel rat model of ischemic cardiomyopathy induced by repetitive myocardial ischemia/reperfusion injury while conscious.

BACKGROUND: A rodent model of ischemic cardiomyopathy (ICM) induced by repetitive brief ischemia/reperfusion (I/R) injury while conscious has not been previously established. METHODS AND RESULTS: A newly developed coronary occluder was implanted in male Wistar rats. A repetitive I/R protocol (20 s, 2 min, followed by main 30 min--ischemia, every 48 h, for 4 weeks) was introduced while the animals were conscious. The I/R protocol did not induce transmural scar formation but induced (1) residual myocytes with scattered infiltration of fibrosis (Masson trichrome stain), (2) coronary hypoperfusion ((201)Tl-Cl autoradiogram), (3) reduced coronary microvascular volume fraction (microCT), and (4) gradually progressive left ventricular (LV) dilation (echocardiography). These parameters of ICM showed interindividual variation; however, the percent increase in LV diastolic area on day 3 was significantly correlated with LV dilation (r=0.91, p<0.0001), fibrosis (r=0.77, p=0.0034), and reduction in microvessels (r=0.67, p=0.040) at week 4. The LV dilatory response on day 3 also correlated with inducible nitric oxide synthase expression (immunohistochemistry, day 3) in the LV (r=0.92, p=0.028). CONCLUSIONS: A novel rat model of ICM induced by repetitive I/R while conscious showed interindividual variation in the severity of ICM in the advanced stage, but this was predictable non-invasively (by LV dilatory response) during the initial stage of repetitive I/R.

Measurement of the thickness of the fibrous cap by optical coherence tomography.

BACKGROUND: Identification of the fibrous cap is important because its thickness is a major determinant of plaque vulnerability in lipid-rich plaque. Thus, a high-resolution imaging technique may be a promising method for the identification of the fibrous cap within lipid-rich plaque. The purpose of this study was to investigate the feasibility of using optical coherence tomography (OCT) to measure the thickness of the fibrous cap within lipid-rich plaque. METHODS AND RESULTS: We examined 35 lipid-rich plaques from 102 coronary arterial segments of 38 human cadavers (22 men and 16 women; mean ages, 74 +/- 7 years). Optical coherence tomography and corresponding histological images were digitized for measurement of the thickness of fibrous cap, and the results between OCT and histological examination were compared. There was good correlation of the thickness of the fibrous cap between OCT and histological examination (y = 0.97x + 28.49; r = 0.90; P < .001). A Bland-Altman test showed good agreement of the thickness of the fibrous cap between OCT and histological examination (mean difference, -24 +/- 44 microm). CONCLUSIONS: Optical coherence tomography provides an accurate representation of the thickness of the fibrous cap and may prove useful in assessing plaque vulnerability in lipid-rich plaque.

Rate of progression of valvular aortic stenosis in patients undergoing dialysis.

BACKGROUND: In patients undergoing dialysis, aortic valve calcification and aortic stenosis are frequently found. However, the rate of progression of aortic stenosis is still unclear. METHODS: In all, 55 consecutive patients undergoing dialysis were followed up by echocardiography for a period of 12 months. Patients were divided into two groups: noncalcification (no or mildly calcified aortic valve) and calcification (moderate or heavily calcified aortic valve). RESULTS: The rate of progression of maximum aortic jet velocity and degression of aortic valve area were more rapid in calcification group than in noncalcification group (0.37 +/- 0.36 m/s and 0.17 +/- 0.29 m/s, P = .027; 0.17 +/- 0.15 cm2 and 0.04 +/- 0.07 cm2, P < .001, respectively). CONCLUSIONS: The degree of aortic stenosis progressed more rapidly in patients undergoing dialysis with aortic valve calcification than without aortic valve calcification.

Assessment of coronary arterial thrombus by optical coherence tomography.

We analyzed optical coherence tomographic (OCT) characteristics of different types of coronary thrombi that had been confirmed at postmortem histologic examination. We examined 108 coronary arterial segments of 40 consecutive human cadavers. OCT images of red and white thrombi were obtained and the intensity property of these thrombi was analyzed. Red and white thrombi were found in 16 (17%) and 19 (18%) of the 108 arterial segments, respectively. Red thrombi were identified as high-backscattering protrusions inside the lumen of the artery, with signal-free shadowing in the OCT image. White thrombi were identified as low-backscattering projections in the OCT image. There were no significant differences in peak intensity of OCT signal between red and white thrombi (130+/-18 vs 145+/-34, p=0.12). However, the 1/2 attenuation width of the signal intensity curve, which was defined as the distance from peak intensity to its 1/2 intensity, was significantly different between red and white thrombi (324+/-50 vs 183+/- 42 microm, p<0.0001). A cut-off value of 250 microm in the 1/2 width of signal intensity attenuation can differentiate white from red thrombi with a sensitivity of 90% and specificity of 88%. We present the first detailed description of the characteristics of different types of coronary thrombi in OCT images. Optical coherence tomography may allow us not only to estimate plaque morphology but also to distinguish red from white thrombi.