Glucagon-like Peptide-1 analogues and delipidation of coronary atheroma in statin-treated type 2 diabetic patients with coronary artery disease: The prespecified sub-analysis of the OPTIMAL randomized clinical trial.

Background and aims: Randomized clinical trials have demonstrated the ability of glucagon-like peptide-1 analogues (GLP-1RAs) to reduce atherosclerotic cardiovascular disease events in patients with type 2 diabetes (T2D). How GLP-1RAs modulate diabetic atherosclerosis remains to be determined yet. Methods: The OPTIMAL study was a prospective randomized controlled study to compare the efficacy of 48-week continuous glucose monitoring- and HbA1c-guided glycemic control on near infrared spectroscopty (NIRS)/intravascular ultrasound (IVUS)-derived plaque measures in 94 statin-treated patients with T2D (jRCT1052180152, UMIN000036721). Of these, 78 patients with evaluable serial NIRS/IVUS images were analyzed to compare plaque measures between those treated with (n = 16) and without GLP-1RAs (n = 72). Results: All patients received a statin, and on-treatment LDL-C levels were similar between the groups (66.9 ± 11.6 vs. 68.1 ± 23.2 mg/dL, p = 0.84). Patients receiving GLP-1RAs demonstrated a greater reduction of HbA1c [-1.0 (-1.4 to -0.5) vs. -0.4 (-0.6 to -0.2)%, p = 0.02] and were less likely to demonstrate a glucose level >180 mg/dL [-7.5 (-14.9 to -0.1) vs. 1.1 (-2.0 - 4.2)%, p = 0.04], accompanied by a significant decrease in remnant cholesterol levels [-3.8 (-6.3 to -1.3) vs. -0.1 (-0.8 - 1.1)mg/dL, p = 0.008]. On NIRS/IVUS imaging analysis, the change in percent atheroma volume did not differ between the groups (-0.9 ± 0.25 vs. -0.2 ± 0.2%, p = 0.23). However, GLP-1RA treated patients demonstrated a greater frequency of maxLCBI4mm regression (85.6 ± 0.1 vs. 42.0 ± 0.6%, p = 0.01). Multivariate analysis demonstrated that the GLP-1RA use was independently associated with maxLCBI4mm regression (odds ratio = 4.41, 95%CI = 1.19-16.30, p = 0.02). Conclusions: In statin-treated patients with T2D and CAD, GLP-1RAs produced favourable changes in lipidic plaque materials, consistent with its stabilization.

Successful healing of aneurysmal false lumen using a second-generation drug-eluting stent in spontaneous coronary artery dissection: a case report.

BACKGROUND: According to 2023 ESC Guideline, conservative medical management is generally recommended for the treatment of spontaneous coronary artery dissection (SCAD) except for patients with signs of ongoing myocardial ischemia. However, in some cases, invasive treatment (coronary artery bypass graft surgery or percutaneous coronary intervention (PCI)) is performed because of the progression of aneurysm in SCAD. Although there is no established strategy for the management of coronary aneurysm in SCAD, we report a case of successful healing of aneurysmal false lumen (AFL) using a second-generation drug-eluting stent (DES) in SCAD. CASE PRESENTATION: A 44-year-old woman without any cardiovascular risk factors was transferred to our hospital due to inferior myocardial infarction. Coronary angiography (CAG) showed multiple SCADs in the coronary artery. We performed PCI to the distal right coronary artery (RCA) because the RCA showed severe stenosis (99%) with bradycardia. Six days after the first PCI, SCAD relapsed in the mid left anterior descending artery (LAD). Furthermore, AFL was observed by intravascular ultrasound imaging. To avoid enlargement of the AFL and progression of the dissection toward the proximal site of the LAD, we performed PCI to the mid LAD to seal the entry tear of the dissection using a second-generation DES. CAG revealed that the AFL in the mid LAD completely diminished at 1 year after PCI. CONCLUSIONS: The implantation of a second-generation DES might be one of therapeutic options for sealing AFL in SCAD patients.

The effect of continuous glucose monitoring-guided glycemic control on progression of coronary atherosclerosis in type 2 diabetic patients with coronary artery disease: The OPTIMAL randomized clinical trial.

BACKGROUND: Continuous glucose monitoring (CGM) improves glycemic fluctuation and reduces hypoglycemic risk. Whether CGM-guided glycemic control favorably modulates coronary atherosclerosis in patients with type 2 diabetes (T2DM) remains unknown. METHODS: The OPTIMAL trial was a prospective, randomized, single-center trial in which 94 T2DM patients with CAD were randomized to CGM- or HbA1c-guided glycemic control for 48 weeks (jRCT1052180152). The primary endpoint was the nominal change in total atheroma volume (TAV) measured by serial IVUS. The secondary efficacy measure was the nominal change in maxLCBI4mm on near-infrared spectroscopy imaging. RESULTS: Among the 94 randomized patients, 82 had evaluable images at 48 weeks. Compared to HbA1c-guided glycemic control, CGM-guided control achieved a greater reduction in %coefficient of variation [-0.1 % (-1.8 to 1.6) vs. -3.3 % (-5.1 to -1.5), p = 0.01] and a greater increase in the duration with glucose between 70 and 180 mg/dL [-1.5 % (-6.0 to 2.9) vs. 6.7 % (1.9 to 11.5), p = 0.02]. TAV increased by 0.11 ± 1.9 mm3 in the HbA1c-guided group and decreased by -3.29 ± 2.00 mm3 in the CGM-guided group [difference = -3.4 mm3 (95%CI: -8.9 to 2.0 mm3), p = 0.22]. MaxLCBI4mm, increased by 90.1 ± 25.6 in the HbA1c-guided group and by 50.6 ± 25.6 in the CGM-guided group (difference = -45.6 (95%CI: -118.1 to 26.7) p = 0.21]. A post-hoc exploratory analysis showed a greater regression of maxLCBI4mm in the CGM-guided group [difference = 20.4 % (95%CI:1.3 to 39.5 %), p = 0.03]. CONCLUSIONS: CGM-guided control for 48 weeks did not slow disease progression in T2DM patients with CAD. A greater regression of lipidic plaque under CGM-guided glycemic control in the post-hoc analysis requires further investigation.

Calcified plaque harboring lipidic materials associates with no-reflow phenomenon after PCI in stable CAD.

Calcified atheroma has been viewed conventionally as stable lesion which less likely increases no-reflow phenomenon. Given that lipidic materials triggers the formation of calcification, lipidic materials could exist within calcified lesion, which may cause no-reflow phenomenon after PCI. The REASSURE-NIRS registry (NCT04864171) employed near-infrared spectroscopy and intravascular ultrasound imaging to evaluate maximum 4-mm lipid-core burden index (maxLCBI4mm) at target lesions containing small (maximum calcification arc < 180°: n = 272) and large calcification (maximum calcification arc ≥ 180°: n = 189) in stable CAD patients. The associations of maxLCBI4mm with corrected TIMI frame count (CTFC) and no-reflow phenomenon after PCI were analyzed in patients with target lesions containing small and large calcification, respectively. No-reflow phenomenon occurred in 8.0% of study population. Receiver-operating characteristics curve analyses revealed that optimal cut-off values of maxLCBI4mm for predicting no-reflow phenomenon were 585 at small calcification (AUC = 0.72, p < 0.001) and 679 at large calcification (AUC = 0.76, p = 0.001). Target lesions containing small calcification with maxLCBI4mm ≥ 585 more likely exhibited a greater CTFC (p < 0.001). In those with large calcification, 55.6% of them had maxLCBI4mm ≥ 400 [vs. 56.2% (small calcification), p = 0.82]. Furthermore, a higher CTFC (p < 0.001) was observed in association with maxLCBI4mm ≥ 679 at large calcification. On multivariable analysis, maxLCBI4mm at large calcification still independently predicted no-reflow phenomenon (OR = 1.60, 95%CI = 1.32-1.94, p < 0.001). MaxLCBI4mm at target lesions exhibiting large calcification elevated a risk of no-reflow phenomenon after PCI. Calcified plaque containing lipidic materials is not necessarily stable lesion, but could be active and high-risk one causing no-reflow phenomenon.

Characterization of plaque phenotypes exhibiting an elevated pericoronary adipose tissue attenuation: insights from the REASSURE-NIRS registry.

Inflammation has been considered to promote atheroma instability. Coronary computed tomography angiography (CCTA) visualizes pericoronary adipose tissue (PCAT) attenuation, which reflects coronary artery inflammation. While PCAT attenuation has been reported to predict future coronary events, plaque phenotypes exhibiting high PCAT attenuation remains to be fully elucidated. The current study aims to characterize coronary atheroma with a greater vascular inflammation. We retrospectively analyzed culprit lesions in 69 CAD patients receiving PCI from the REASSURE-NIRS registry (NCT04864171). Culprit lesions were evaluated by both CCTA and near-infrared spectroscopy/intravascular ultrasound (NIRS/IVUS) imaging prior to PCI. PCAT attenuation at proximal RCA (PCATRCA) and NIRS/IVUS-derived plaque measures were compared in patients with PCATRCA attenuation ≥ and < -78.3 HU (median). Lesions with PCATRCA attenuation ≥ -78.3 HU exhibited a greater frequency of maxLCBI4mm ≥ 400 (66% vs. 26%, p < 0.01), plaque burden ≥ 70% (94% vs. 74%, p = 0.02) and spotty calcification (49% vs. 6%, p < 0.01). Whereas positive remodeling (63% vs. 41%, p = 0.07) did not differ between two groups. On multivariable analysis, maxLCBI4mm ≥ 400 (OR = 4.07; 95%CI 1.12-14.74, p = 0.03), plaque burden ≥ 70% (OR = 7.87; 95%CI 1.01-61.26, p = 0.04), and spotty calcification (OR = 14.33; 95%CI 2.37-86.73, p < 0.01) independently predicted high PCATRCA attenuation. Of note, while the presence of only one plaque feature did not necessarily elevate PCATRCA attenuation (p = 0.22), lesions harboring two or more features were significantly associated with higher PCATRCA attenuation. More vulnerable plaque phenotypes were observed in patients with high PCATRCA attenuation. Our findings suggest PCATRCA attenuation as the presence of profound disease substrate, which potentially benefits from anti-inflammatory agents.

Sex Differences in the Density of Lipidic Plaque Materials: Insights From the REASSURE-NIRS MultiCenter Registry.

BACKGROUND: Intravascular imaging has shown better response of coronary atheroma to statin-mediated lowering of low-density lipoprotein cholesterol in women. However, its detailed mechanism remains to be determined yet. Modifiability of coronary atheroma under lipid-lowering therapies is partly driven by lipidic plaque component. Given a smaller plaque volume in women, lipidic plaque features including their density may differ between sex. Therefore, the current study sought to characterize sex-related differences in the density of lipidic plaque. METHODS: We analyzed 1429 coronary lesions (culprit/nonculprit lesions=825/604) in 758 coronary artery disease patients (men/women=608/150) from the REASSURE-NIRS multicenter registry (Revelation of Pathophysiological Phenotypes of Vulnerable Lipid-Rich Plaque on Near-Infrared Spectroscopy). Total atheroma volume at 4-mm segment, maximum 4-mm-lipid-core burden index, and lipid plaque density index (=maximum 4-mm-lipid-core burden index/total atheroma volume at 4-mm segment) on near-infrared spectroscopy/intravascular ultrasound imaging at culprit and nonculprit lesions were compared in men and women. RESULTS: Statin and high-intensity statin were used in 72.4 (P=0.81) and 22.9% (P=0.32) of study subjects, respectively. Women exhibited a smaller adjusted total atheroma volume at 4-mm segment (culprit lesions: 50.3±0.4 versus 54.2±0.3mm3, P<0.001, nonculprit lesions: 31.5±3.0 versus 44.4±2.1mm3, P<0.001), whereas their adjusted maximum 4-mm-lipid-core burden index did not differ between sex (culprit lesions: 544.7±29.9 versus 501.7±19.1, P=0.11, nonculprit lesions: 288.8±26.7 versus 272.7±18.9, P=0.51). Furthermore, a greater adjusted lipid plaque density index was observed in women (culprit lesions: 18.2±0.9 versus 9.8±0.6, P<0.001, nonculprit lesions: 23.0±2.0 versus 7.8±1.4, P<0.001). These adjustments of total atheroma volume at 4-mm segment, maximum 4-mm-lipid-core burden index, and lipid plaque density index included age, body mass index, hypertension, dyslipidemia, diabetes, smoking, a history of myocardial infarction and chronic kidney disease, low-density lipoprotein cholesterol level, statin and ezetimibe use, vessel volume, and hospital unit. The aforementioned plaque features consistently existed in both acute coronary syndrome and stable coronary artery disease subjects. CONCLUSIONS: Women harbored greater condensed lipidic plaque features, accompanied by smaller atheroma volume. These observations indicate potentially better modifiable disease in women, which underscores the need to intensify their lipid-lowering therapies for further improving their outcomes. REGISTRATION: URL: https://www. CLINICALTRIALS: gov/; Unique identifier: NCT04864171.

Deep Learning-based Post Hoc CT Denoising for the Coronary Perivascular Fat Attenuation Index.

RATIONALE AND OBJECTIVES: Coronary inflammation related to high-risk hemorrhagic plaques can be captured by the perivascular fat attenuation index (FAI) using coronary computed tomography angiography (CCTA). Since the FAI is susceptible to image noise, we believe deep learning (DL)-based post hoc noise reduction can improve diagnostic capability. We aimed to assess the diagnostic performance of the FAI in DL-based denoised high-fidelity CCTA images compared with coronary plaque magnetic resonance imaging (MRI) delivered high-intensity hemorrhagic plaques (HIPs). MATERIALS AND METHODS: We retrospectively reviewed 43 patients who underwent CCTA and coronary plaque MRI. We generated high-fidelity CCTA images by denoising the standard CCTA images using a residual dense network that supervised the denoising task by averaging three cardiac phases with nonrigid registration. We measured the FAIs as the mean CT value of all voxels (range of -190 to -30 HU) located within a radial distance from the outer proximal right coronary artery wall. The diagnostic reference standard was defined as HIPs (high-risk hemorrhagic plaques) using MRI. The diagnostic performance of the FAI in the original and denoised images was assessed using receiver operating characteristic curves. RESULTS: Of 43 patients, 13 had HIPs. The denoised CCTA improved the area under the curve (0.89 [95% confidence interval (CI) 0.78-0.99]) of the FAI compared with that in the original image (0.77 [95% CI, 0.62-0.91], p = 0.008). The optimal cutoff value for predicting HIPs in denoised CCTA was -69 HU with 0.85 (11/13) sensitivity, 0.79 (25/30) specificity, and 0.80 (36/43) accuracy. CONCLUSION: DL-based denoised high-fidelity CCTA improved the AUC and specificity of the FAI for predicting HIPs.

The Residual Lipid-Rich Coronary Atheroma Behind the Implanted Newer-Generation Drug-Eluting Stent and Future Stent-Related Event Risks.

BACKGROUND: Lipid-rich plaque is an important substrate that causes future coronary events. However, the clinical implications of underlying plaque characteristics in coronary lesions after newer-generation drug-eluting stent (DES) implantation remain unknown. METHODS: The current study analyzed 445 target lesions after newer-generation DES implantation in 416 patients with coronary artery disease (CAD) (chronic coronary syndrome/acute coronary syndrome = 264/181) from the REASSURE-NIRS multicentre registry. Near-infrared spectroscopy (NIRS) imaging was used to evaluate maximum lipid core burden index after stent implantation in target lesions (residual maxLCBI4mm). The primary and secondary outcomes were 3-year lesion-oriented clinical outcomes (LOCO): cardiac death, nonfatal target-lesion-related myocardial infarction (MI), or ischemia-driven target-lesion revascularization (ID-TLR) and patient-oriented clinical outcomes (POCO): all-cause death, nonfatal MI, or ID unplanned revascularization. Outcomes were compared by residual maxLCBI4mm tertile. RESULTS: Median residual maxLCBI4mm was 183; 16% of lesions had residual maxLCBI4mm > 400. Higher residual maxLCBI4mm was not associated with a greater likelihood of LOCO or POCO during the observational period (LOCO, log-rank P = 0.76; POCO, log-rank P = 0.84). Mixed-effects logistic regression demonstrated that residual maxLCBI4mm does not predict LOCO (odds ratio [OR], 1.000; 95% confidence interval [CI], 0.997-1.003; P = 0.95). There was no significant relationship between residual maxLCBI4mm and POCO (OR, 1.001; 95% CI, 0.999-1.002; P = 0.30). CONCLUSIONS: Residual maxLCBI4mm is not associated with LOCO or POCO in patients with CAD after newer-generation DES implantation. Our findings suggest that NIRS-derived underlying lipid-rich plaque is not associated with the risk of stent-related events and patient-based outcomes in patients with CAD who have received newer-generation DESs.

Elevated Lipoprotein(a) as a potential residual risk factor associated with lipid-rich coronary atheroma in patients with type 2 diabetes and coronary artery disease on statin treatment: Insights from the REASSURE-NIRS registry.

BACKGROUND AND AIMS: The residual risk of atherosclerotic cardiovascular disease (ASCVD) in patients with diabetes on statin therapy warrants identification of other pro-atherogenic drivers. Lipoprotein(a) [Lp(a)] promotes the formation of necrotic cores within vessel walls. Given that patients with diabetes have an Lp(a)-associated ASCVD risk, Lp(a) might lead to plaque vulnerability in patients with diabetes on statin therapy. METHODS: We analyzed target lesions that underwent PCI in 312 patients with coronary artery disease (CAD) on statin treatment from the REASSURE-NIRS registry (NCT04864171). Maximum 4-mm lipid-core-burden index (maxLCBI4mm) in target lesions was measured with near-infrared spectroscopy (NIRS) imaging. The relationship between Lp(a) levels and maxLCBI4mm was investigated in patients with and without diabetes. RESULTS: High-intensity statin use (p = 0.49) and on-treatment low-density lipoprotein cholesterol (LDL-C) (p = 0.32) and Lp(a) levels (p = 0.09) were comparable between patients with and without diabetes. Lp(a) levels were significantly associated with maxLCBI4mm in patients with diabetes (p = 0.01) but not in patients without diabetes (p = 0.96). Multivariate analysis showed that LDL-C levels (p = 0.03) predict maxLCBI4mm in patients without diabetes, but not Lp(a) levels (p = 0.91). Both LDL-C (p = 0.01) and Lp(a) (p = 0.04) levels were independent predictors of maxLCBI4mm in patients with diabetes. Even in patients with diabetes achieving LDL-C <1.8 mmol/L (70 mg/dL), Lp(a) levels remained associated with maxLCBI4mm (p = 0.04). CONCLUSIONS: A significant relationship between Lp(a) and maxLCBI4mm exists in patients with diabetes and CAD on statin treatment, even with LDL-C <1.8 mmol/L (70 mg/dL). Lp(a) might be associated with more vulnerable coronary atheroma in patients with diabetes despite receiving statin therapy.

Mid-Right Coronary Artery Spasm Diagnosed by an Ergometrine Provocation Test Through a Saphenous Vein Graft.

Although coronary artery spasm is a cause of acute coronary syndrome (ACS), demonstration of its possible cause in patients with a history of coronary artery bypass grafting remains challenging. We report a case of ACS that successfully provoked coronary artery spasm by pharmacological testing through a saphenous vein graft. (Level of Difficulty: Beginner.).

The association between the extent of lipidic burden and delta-fractional flow reserve: analysis from coronary physiological and near-infrared spectroscopic measures.

BACKGROUND: Vulnerable plaque features including lipidic plaque have been shown to affect fractional flow reserve (FFR). Given that formation and propagation of lipid plaque is accompanied by endothelial dysfunction which impairs vascular tone, the degree of lipidic burden may affect vasoreactivity during hyperemia, potentially leading to reduced FFR. Our aim is to elucidate the relationship of the extent of lipidic plaque burden with coronary physiological vasoreactivity measure. METHODS: We analyzed 89 subjects requeuing PCI due to angiographically intermediate coronary stenosis with FFR ≤0.80. Near-infrared spectroscopy (NIRS) and intravascular ultrasound were used to evaluate lipid-core burden index (LCBI) and atheroma volume at both target lesion (maxLCBI4mm; maximum value of LCBI within any 4 mm segments) and entire target vessel (LCBIvessel: LCBI within entire vessel). In addition to FFR, delta-FFR was measured by difference of distal coronary artery pressure/aortic pressure (Pd/Pa) between baseline and hyperemic state. RESULTS: The averaged FFR and delta-FFR was 0.74 (0.69-0.77), and 0.17±0.05, respectively. On target lesion-based analysis, maxLCBI4mm was negatively correlated to FFR (ρ=-0.213, P=0.040), and it was positively correlated to delta-FFR (ρ=0.313, P=0.002). Furthermore, target vessel-based analysis demonstrated similar relationship of LCBIvessel with FFR (ρ=-0.302, P=0.003) and delta-FFR (ρ=0.369, P<0.001). Even after adjusting clinical characteristics and lesion/vessel features, delta-FFR (by 0.10 increase) was independently associated with maxLCBI4mm (ß=57.2, P=0.027) and LCBIvessel (ß=24.8, P=0.007) by mixed linear model analyses. CONCLUSIONS: A greater amount of lipidic plaque burden at not only "target lesion" alone but "entire target vessel" was associated with a greater delta-FFR. The accumulation of lipidic plaque materials at both local site and entire vessel may impair hyperemia-induced vasoreactivity, which causes a reduced FFR.

The feasibility and limitation of coronary computed tomographic angiography imaging to identify coronary lipid-rich atheroma in vivo: Findings from near-infrared spectroscopy analysis.

BACKGROUND: Coronary computed tomography angiography (CCTA) non-invasively visualizes lipid-rich plaque. However, this ability is not fully validated in vivo. The current study aimed to elucidate the association of CCTA features with near-infrared spectroscopy-derived lipidic plaque measure in patients with coronary artery disease. METHODS: 95 coronary lesions (culprit/non-culprit = 51/44) in 35 CAD subjects were evaluated by CCTA and NIRS imaging. CT density, positive remodeling, spotty calcification, napkin-ring sign and NIRS-derived maximum 4-mm lipid-core burden index (maxLCBI4mm) were analyzed by two independent physicians. The association of CCTA-derived plaque features with maxLCBI4mm ≥ 400 was evaluated. RESULTS: The median CT density and maxLCBI4mm were 57.7 Hounsfield units (HU) and 304, respectively. CT density (r = -0.75, p < 0.001) and remodeling index (RI) (r = 0.58, p < 0.001) were significantly associated with maxLCBI4mm, respectively. Although napkin-ring sign (p < 0.001) showed higher prevalence of maxLCBI4mm ≥ 400 than those without it, spotty calcification did not (p = 0.13). On multivariable analysis, CT density [odds ratio (OR) = 0.95, 95% confidence interval (CI) = 0.93-0.97; p < 0.001] and positive remodeling [OR = 7.71, 95%CI = 1.37-43.41, p = 0.02] independently predicted maxLCBI4mm ≥ 400. Receiver operating characteristic curve analysis demonstrated CT density <32.9 HU (AUC = 0.92, sensitivity = 85.7%, specificity = 91.7%) and RI ≥ 1.08 (AUC = 0.83, sensitivity = 74.3%, specificity = 85.0%) as optimal cut-off values of maxLCBI4mm ≥ 400. Of note, only 52.6% at lesions with one of these plaque features exhibited maxLCBI4mm ≥ 400, whereas the frequency of maxLCBI4mm ≥ 400 was highest at those with both features (88.5%, p < 0.001 for trend). CONCLUSIONS: CT density <32.9 HU and RI ≥ 1.08 were associated with lipid-rich plaque on NIRS imaging. Our findings underscore the synergistic value of CT density and positive remodeling to detect lipid-rich plaque by CCTA.

COVID-19 pandemic is associated with mechanical complications in patients with ST-elevation myocardial infarction.

OBJECTIVE: Although there are regional reports that the COVID-19 pandemic is associated with a reduction in acute myocardial infarction presentations and primary percutaneous coronary intervention (PCI) procedures, little is known about the impact of the COVID-19 pandemic on mechanical complications resulting from ST-segment elevation myocardial infarction (STEMI) and mortality. METHODS: This single-centre retrospective cohort study analysed presentations, incidence of mechanical complications, and mortality in patients with STEMI before and after a state of emergency was declared due to the COVID-19 pandemic by the Japanese government on 7 April 2020. RESULTS: We analysed 359 patients with STEMI hospitalised before the declaration and 63 patients hospitalised after the declaration. The proportion of patients with late presentation was significantly higher after the declaration than before (25.4% vs 14.2%, p=0.03). The incidence of late presentation was significantly higher during the COVID-19 pandemic than before (incidence rate ratio (IRR), 2.41; 95% CI, 1.37 to 4.05; p=0.001, even after adjusting for month (IRR, 2.61; 95% CI, 1.33 to 5.13; p<0.01). Primary PCI was performed significantly less often after the declaration than before (68.3% vs 82.5%, p=0.009). The mechanical complication resulting from STEMI occurred in 13 of 359 (3.6%) patients before the declaration and 9 of 63 (14.3%) patients after the declaration (p<0.001). However, the incidence of in-hospital death (before, 6.2% vs after, 6.4%, p=0.95) was comparable. CONCLUSIONS: Following the COVID-19 pandemic, an increased incidence of mechanical complications resulting from STEMI was observed. Instructing people to stay at home, without effectively educating them to immediately seek medical attention when suffering symptoms of a heart attack, may worsen outcomes in patients with STEMI.

In vivo imaging of vulnerable plaque with intravascular modalities: its advantages and limitations.

In vivo imaging of plaque instability has been considered to have a great potential to predict future coronary events and evaluate the stabilization effect of novel anti-atherosclerotic medical therapies. Currently, there are several intravascular imaging modalities which enable to visualize plaque components associated with its vulnerability. These include virtual histology intravascular ultrasound (VH-IVUS), integrated backscatter IVUS (IB-IVUS), optical coherence tomography (OCT), near-infrared spectroscopy and coronary angioscopy. Recent studies have shown that these tools are applicable for risk stratification of cardiovascular events as well as drug efficacy assessment. However, several limitation exists in each modality. The current review paper will outline advantages and limitation of VH-IVUS, IB-IVUS, OCT, NIRS and coronary angioscopy imaging.

[IMPACT OF MEMBRANOUS URETHRAL LENGTH IN DE NOVO STRESS URINARY INCONTINENCE FOLLOWING HOLMIUM LASER ENUCLEATION OF THE PROSTATE].

(Purpose) Holmium laser enucleation of the prostate (HoLEP) is widely performed in recent years; however, difficulties of surgical techniques and high frequency of postoperative stress urinary incontinence (SUI) remain as significant problems. We determined the predictive factors for de novo SUI after HoLEP. (Patients and methods) A total of 303 patients with benign prostatic hyperplasia who underwent HoLEP were retrospectively evaluated between July 2013 and April 2019. Of these, 109 patients underwent MRI preoperatively. Patients who were unable to answer the questionnaire regarding their SUI because of dementia, those who presented with SUI preoperatively, and those with placed Foley catheter at the time of MRI were excluded. Hence, a total of 83 patients were eligible for the present study. We recorded the MRI findings and clinical variables, including membranous urethral length (MUL), transitional zone (TZ) volume, serum prostate-specific antigen levels, operative time, and presence or absence of SUI. The predictive factors for de novo SUI were determined using multivariable logistic regression analysis. (Results)De novo SUI occurred in 19 (22.9%) patients but disappeared in 16 (84.2%) patients at a mean duration of 14 weeks. The mean MUL was 17.2 mm. Univariate analysis showed that MRI TZ volume >40 mL, MUL ≤17 mm, operative time >100 min, and enucleation time >50 min were associated with de novo SUI. In multivariable logistic regression analysis, MUL ≤17 mm (odds ratio [OR], 23.81; 95% confidence interval [CI], 4.34-447.19; P < 0.0001) and operative time >100 min (OR, 3.91; 95% CI, 1.20-14.01; P = 0.023) were significantly associated with de novo SUI. (Conclusions) Although de novo SUI occurred occasionally after HoLEP, most of them improved in about 3 months. The MRI measurement of MUL was shown to be a practical tool for predicting de novo SUI after HoLEP.

Delayed cardiac tamponade 8 months after pulmonary vein isolation.

We herein report the case of a 55 year-old male who underwent pulmonary vein isolation (PVI) for paroxysmal atrial fibrillation. From 8 months after PVI, exertional dyspnea rapidly appeared. When he was referred to our hospital, massive pericardial effusion was observed by transthoracic echography. The pericardiocentesis revealed bloody pericardial effusion, and improved symptoms. Although aortic dissection, autoimmune disease, infection, metastatic pericardial tumor, primary pericardial tumor, and malignant neoplasm were considered as differential diagnosis, the cause of pericardial effusion failed to be found. From these findings, the cause of hemorrhagic pericardial effusion was considered delayed cardiac tamponade induced by PVI performed 8 months earlier. .