A Comparison of Intravascular Imaging Modalities for Detection of Stent Struts in Acute Coronary Syndrome.

BACKGROUND: We used optical coherence tomography (OCT) and intravascular ultrasound (IVUS) to assess the struts of implanted stents in patients with acute coronary syndrome (ACS). METHODS: A totle of 10,756 stent struts were analyzed with OCT in 42 patients of ACS. Of them, both of IVUS and OCT imaging were performed in 33 patients. Appearance of stent struts was classified as well apposed, buried, malapposed, and nondetectable, and the number of stent struts were counted by OCT and IVUS was compared. RESULTS: Most of stent struts were well apposed (78.1%, 8,407/10,756). However, malapposed struts were 5.6% (607/10,756), and 14.1% (1,514/10,756) of stent struts were buried by thrombus. The nondetectable struts were 2.11% (228/10,756) in ACS. 94.7% (216/228) of nondetectable stent struts were associated with red thrombus, and plaque prolapse was in 5.3% (12/228). The number of stent struts counted by OCT were larger than that of IVUS. The mean number of stent struts at the proximal and distal stent edges were 24 ± 6.57 in OCT, the stent struts IVUS counted were 20 ± 4.18 (P < 0.0001). Although the frequency of malapposed struts were similar 4.6% (376/8,248) in OCT versus 4.8% (369/7,674) in IVUS (P = 0.788). Stent struts were often buried by thrombus in ACS 15.2% (1,252/8,248) in OCT versus 9.7% (747/7,674) in IVUS; P = 0.006. The nondetectable struts were fewer in IVUS than OCT 0.2% (16/7,674) in IVUS versus 2.2% (187/8,248) in OCT; P < 0.0001. CONCLUSION: Stent struts are frequently buried and nondetectable due to thrombi burden in ACS patients. Adequate thrombus removal and proper selection of the imaging device is warranted in ACS.

Gap junction remodelling by chronic pressure overload is related to the increased susceptibility to atrial fibrillation in rat heart.

AIMS: Left atrial (LA) fibrosis caused by various pathological stimuli is a common finding. However, the difference of atrial remodelling via haemodynamic change in diverse cardiomyopathy has not been elucidated. METHODS AND RESULTS: Male Sprague-Dawley rats (6-8 weeks, n = 180) were randomly assigned to three groups and corresponding sham control groups: (i) ischaemic cardiomyopathy, (ii) left ventricular hypertrophy (LVH), and (iii) dilated cardiomyopathy. At 12 weeks after operation, atrial fibrillation (AF) inducibility and duration were assessed by in vivo burst transoesophageal pacing. Using the Langendorff apparatus, left ventricular (LV) function and pressure were measured. The expression of connexin-43 (Cx43) and alpha-smooth muscle actin (α-SMA) in atrial tissues was assessed by quantitative real-time polymerase chain reaction and immunohistochemical staining. Fibrosis was analysed by Masson's trichrome staining. Compared with controls, the LA weight/heart weight ratio was increased in the LVH group alone, and was significantly correlated with AF duration (P < 0.001, R = 0.388). Atrial fibrillation inducibility and duration were higher and longer only in the LVH group (P = 0.002, 0.079, respectively), and isolated LV diastolic dysfunction and elevated LV pressure were observed. Although α-SMA expression and fibrosis were increased in all three cardiomyopathy models, down-regulation of Cx43 expression in the LA was observed in the LVH group alone. CONCLUSION: Chronic pressure overload in the absence of LV systolic dysfunction resulted in LA hypertrophy and increased susceptibility to AF, which might be related to conduction abnormality via decreased expression and lateral distribution of Cx43 as well as interstitial fibrosis.

Plaque Vulnerability as Assessed by Radiofrequency Intravascular Ultrasound in Patients with Valvular Calcification.

BACKGROUND: Cardiac valvular calcification is associated with the overall coronary plaque burden and considered an independent cardiovascular risk and prognostic factor. The purpose of this study was to evaluate the relationship between the presence of valvular calcification and plaque morphology and/or vulnerability. METHODS: Transthoracic echocardiography was used to assess valvular calcification in 280 patients with coronary artery disease who underwent radiofrequency intravascular ultrasound (Virtual Histology IVUS, VH-IVUS). A propensity score-matched cohort of 192 patients (n = 96 in each group) was analyzed. Thin-capped fibroatheroma (TCFA) was defined as a necrotic core (NC) >10% of the plaque area with a plaque burden >40% and NC in contact with the lumen for ≥3 image slices. A remodeling index (lesion/reference vessel area) >1.05 was considered to be positive. RESULTS: Patients were divided into two groups: any calcification in at least one valve (152 patients) vs. no detectable valvular calcification (128 patients). Groups were similar in terms of age, risk factors, clinical diagnosis, and angiographic analysis after propensity score-matched analysis. Gray-scale IVUS analysis showed that the vessel size, plaque burden, minimal lumen area, and remodeling index were similar. By VH-IVUS, % NC and % dense calcium (DC) were greater in patients with valvular calcification (p = 0.024, and p = 0.016, respectively). However, only % DC was higher at the maximal NC site by propensity score-matched analysis (p = 0.029). The frequency of VH-TCFA occurrence was higher depending on the complexity (p = 0.0064) and severity (p = 0.013) of valvular calcification. CONCLUSIONS: There is a significant relationship between valvular calcifications and VH-IVUS assessment of TCFAs. Valvular calcification indicates a greater atherosclerosis disease complexity (increased calcification of the coronary plaque) and vulnerable coronary plaques (higher incidence of VH-TCFA).

Multimodality Intravascular Imaging Assessment of Plaque Erosion versus Plaque Rupture in Patients with Acute Coronary Syndrome.

BACKGROUND AND OBJECTIVES: We assessed plaque erosion of culprit lesions in patients with acute coronary syndrome in real world practice. SUBJECTS AND METHODS: Culprit lesion plaque rupture or plaque erosion was diagnosed with optical coherence tomography (OCT). Intravascular ultrasound (IVUS) was used to determine arterial remodeling. Positive remodeling was defined as a remodeling index (lesion/reference EEM [external elastic membrane area) >1.05. RESULTS: A total of 90 patients who had plaque rupture showing fibrous-cap discontinuity and ruptured cavity were enrolled. 36 patients showed definite OCT-plaque erosion, while 7 patients had probable OCT-plaque erosion. Overall, 26% (11/43) of definite/probable plaque erosion had non-ST elevation myocardial infarction (NSTEMI) while 35% (15/43) had ST elevation myocardial infarction (STEMI). Conversely, 14.5% (13/90) of plaque rupture had NSTEMI while 71% (64/90) had STEMI (p<0.0001). Among plaque erosion, white thrombus was seen in 55.8% (24/43) of patients and red thrombus in 27.9% (12/43) of patients. Compared to plaque erosion, plaque rupture more often showed positive remodeling (p=0.003) with a larger necrotic core area examined by virtual histology (VH)-IVUS, while negative remodeling was prominent in plaque erosion. Overall, 65% 28/43 of plaque erosions were located in the proximal 30 mm of a culprit vessel-similar to plaque ruptures (72%, 65/90, p=0.29). CONCLUSION: Although most of plaque erosions show nearly normal coronary angiogram, modest plaque burden with negative remodeling and an uncommon fibroatheroma might be the nature of plaque erosion. Multimodality intravascular imaging with OCT and VH-IVUS showed fundamentally different pathoanatomic substrates underlying plaque rupture and erosion.

Frequency and evolution of thin-capped fibroatheromas in left main coronary artery as assessed by serial virtual histology intravascular ultrasound analysis.

BACKGROUND: The objective of the current study was to assess thin-capped fibroatheroma (TCFA) of the left main coronary artery (LMCA) and its changes after statin therapy. METHODS: We assessed the frequency and distribution of virtual histology intravascular ultrasound (VH-IVUS) thin-capped fibroatheroma (VH-TCFA) in the LMCA in 500 patients. Serial VH-IVUS examinations were available in 50 patients at 12-month follow-up. RESULTS: The incidence of LM-TCFA was 8.8% (44/500). IVUS LMCA length was longer in patients with VH-TCFA vs without VH-TCFA. Reference external elastic membrane (EEM) area was similar, but reference lumen area and minimal lumen area were smaller in LMCA with VH-TCFA vs without VH-TCFA (P<.001). LMCA with VH-TCFA had a higher plaque burden (P<.001), a larger necrotic core area (P<.001), and more dense calcium (P<.001) at the maximum necrotic core (NC) site vs LMCA without VH-TCFA. In patients with an LMCA length greater than the median, 62% were located in the distal half of the LMCA. After 12 months of statin therapy, only 44.4% (4/9) of VH-TCFA had evolved to a non- VH-TCFA phenotype and 3 new VH-TCFA had appeared. CONCLUSION: VH-TCFAs are clustered in the distal half of the LMCA with infrequent positive remodeling. It might persist despite the usual dose of statin therapy. Further study should confirm the changes in large vessels like the LMCA.