Radiomics-based discrimination of coronary chronic total occlusion and subtotal occlusion on coronary computed tomography angiography.

OBJECTIVES: Differentiating chronic total occlusion (CTO) from subtotal occlusion (SO) is often difficult to make from coronary computed tomography angiography (CCTA). We developed a CCTA-based radiomics model to differentiate CTO and SO. METHODS: A total of 66 patients with SO underwent CCTA before invasive angiography and were matched to 66 patients with CTO. Comprehensive imaging analysis was conducted for all lesioned vessels, involving the automatic identification of the lumen within the occluded segment and extraction of 1,904 radiomics features. Radiomics models were then constructed to assess the discriminative value of these features in distinguishing CTO from SO. External validation of the model was performed using data from another medical center. RESULTS: Compared to SO patients, CTO patients had more blunt stumps (internal: 53/66 (80.3%) vs. 39/66 (59.1%); external: 36/50 (72.0%) vs. 20/50 (40.0%), both p < 0.01), longer lesion length (internal: median length 15.4 mm[IQR: 10.4-22.3 mm] vs. 8.7 mm[IQR: 4.9-12.6 mm]; external:11.8 mm[IQR: 6.1-23.4 mm] vs. 6.2 mm[IQR: 3.5-9.1 mm]; both p < 0.001). Sixteen unique radiomics features were identified after the least absolute shrinkage and selection operator regression. When added to the combined model including imaging features, radiomics features provided increased value for distinguishing CTO from SO (AUC, internal: 0.772 vs. 0.846; p = 0.023; external: 0.718 vs. 0.781, p = 0.146). CONCLUSIONS: The occluded segment vessels of CTO and SO have different radiomics signatures. The combined application of radiomics features and imaging features based on CCTA extraction can enhance diagnostic confidence.

PU.1 inhibition does not attenuate cardiac function deterioration or fibrosis in a murine model of myocardial infarction.

Activated cardiac fibroblasts are involved in both reparative wound healing and maladaptive cardiac fibrosis after myocardial infarction (MI). Recent evidence suggests that PU.1 inhibition can enable reprogramming of profibrotic fibroblasts to quiescent fibroblasts, leading to attenuation of pathologic fibrosis in several fibrosis models. The role of PU.1 in acute MI has not been tested. We designed a randomized, blinded study to evaluate whether DB1976, a PU.1 inhibitor, attenuates cardiac function deterioration and fibrosis in a murine model of MI. A total of 44 Ai9 periostin-Cre transgenic mice were subjected to 60 min of coronary occlusion followed by reperfusion. At 7 days after MI, 37 mice were randomly assigned to control (vehicle) or DB1976 treatment and followed for 2 weeks. Left ventricular ejection fraction (EF), assessed by echocardiography, did not differ between the two groups before or after treatment (final EF, 33.3 ± 1.0% in control group and 31.2 ± 1.3% in DB1976 group). Subgroup analysis of female and male mice showed the same results. There were no differences in cardiac scar (trichrome stain) and fibrosis (interstitial/perivascular collagen; picrosirius stain) between groups. Results from the per-protocol dataset (including mice with pre-treatment EF < 35% only) were consistent with the full dataset. In conclusion, this randomized, blinded study demonstrates that DB1976, a PU.1 inhibitor, does not attenuate cardiac functional deterioration or cardiac fibrosis in a mouse model of MI caused by coronary occlusion/reperfusion.

ST-segment resolution as a marker for severe myocardial fibrosis in ST-segment elevation myocardial infarction.

OBJECTIVE: To investigate the relationship between ST-segment resolution (STR) and myocardial scar thickness after percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI). METHODS: Forty-two STEMI patients with single-branch coronary artery stenosis or occlusion were enrolled. ST-segment elevations were measured at emergency admission and at 24 h after PCI. Late gadolinium-enhanced cardiac magnetic resonance imaging (CMR-LGE) was performed 7 days after PCI to evaluate myocardial scars. Statistical analyses were performed to assess the utility of STR to predict the development of transmural (> 75%) or non-transmural (< 75%) myocardial scars, according to previous study. RESULTS: The sensitivity and specificity of STR for predicting transmural scars were 96% and 88%, respectively, at an STR cut-off value of 40.15%. The area under the curve was 0.925. Multivariate logistic proportional hazards regression analysis disclosed that patients with STR < 40.15% had a 170.90-fold higher probability of developing transmural scars compared with patients with STR ≥ 40.15%. Pearson correlation and linear regression analyses showed STR percentage was significantly associated with myocardial scar thickness and size. CONCLUSION: STR < 40.15% at 24 h after PCI may provide meaningful diagnostic information regarding the extent of myocardial scarification in STEMI patients.

Autopsy Cardiac Troponin I Plasma Levels Can Be Elevated in Myocardial Infarction Type 3: A Proposal to Modify the Definition of Myocardial Infarction Type 3.

AIMS: The definition of myocardial infarction (MI) type 3 does not include the possible elevation of postmortem biomarkers if measured at autopsy. We determined postmortem cardiac troponin I (cTnI) levels in plasma samples obtained at autopsy in patients who died from MI type 3 to determine whether cTnI plasma levels may be elevated. METHODS AND RESULTS: Using a chemiluminescent microparticle immunoassay system, we determined postmortem cTnI plasma levels at autopsy performed within 24 hours of death in every decedent who died from MI type 3, confirmed by an autopsy. Over 2 years, autopsy confirmed 52 decedents who died from MI type 3 due to coronary atherosclerotic disease. The age range and mean age were 40 to 78 and 60.6 years, respectively, 38 (73%) men and 14 (27%) women. Ten percent of the decedents exhibited postmortem cTnI plasma levels that were within the normal reference levels (0.01-0.30 ng/mL). Ninety percent of the decedents exhibited elevated cTnI plasma levels at autopsy, which ranged from 0.31 to greater than 4400 ng/mL. Sixty-nine percent of our decedents showed severe/significant (75%-100%) luminal occlusion in 2 or 3 major coronary arteries. CONCLUSIONS: If cTnI plasma levels are measured in autopsy blood samples after sudden and unexpected death due to MI type 3, highly elevated cTnI plasma levels may be detected. We propose that the current MI type 3 definition be slightly modified to include the possible elevation of cTnI plasma levels if measured at autopsy in the immediate postmortem period.

Citric Acid Cycle Metabolites Predict Infarct Size in Pigs Submitted to Transient Coronary Artery Occlusion and Treated with Succinate Dehydrogenase Inhibitors or Remote Ischemic Perconditioning.

Succinate dehydrogenase (SDH) inhibition with malonate during reperfusion reduced myocardial infarction in animals, whereas its endogenous substrate, succinate, is detected in plasma from STEMI patients. We investigated whether protection by SDH inhibition is additive to that of remote ischemic perconditioning (RIC) in pigs submitted to transient coronary artery occlusion, and whether protective maneuvers influence plasma levels of citric acid cycle metabolites. Forty pigs were submitted to 40 min coronary occlusion and reperfusion, and allocated to four groups (controls, sodium malonate 10 mmol/L, RIC, and malonate + RIC). Plasma was obtained from femoral and great cardiac veins and analyzed by LC-MS/MS. Malonate, RIC, and malonate + RIC reduced infarct size (24.67 ± 5.98, 25.29 ± 3.92 and 29.83 ± 4.62% vs. 46.47 ± 4.49% in controls, p < 0.05), but no additive effects were detected. Enhanced concentrations of succinate, fumarate, malate and citrate were observed in controls during initial reperfusion in the great cardiac vein, and most were reduced by cardioprotective maneuvers. Concentrations of succinate, fumarate, and malate significantly correlated with infarct size. In conclusion, despite the combination of SDH inhibition during reperfusion and RIC did not result in additive protection, plasma concentrations of selected citric acid cycle metabolites are attenuated by protective maneuvers, correlate with irreversible injury, and might become a prognosis tool in STEMI patients.

Relationship of a thinned medial layer to the attenuated contractile response in atherosclerotic coronary arteries.

Coronary arteries with advanced atherosclerosis do not necessarily have greater contractile responses than those with early atherosclerosis. This study aimed to clarify the relationship between thickness of the medial layer and the contractile response to acetylcholine (ACh) in coronary artery using optical coherence tomography (OCT). The OCT and the vasomotor response to ACh in the left anterior descending coronary artery were assessed in 32 patients with previous myocardial infarction. The intimal and medial layer areas were measured by planimetric analysis of the OCT images. The coronary contractile response to ACh had a positive linear relationship with medial area (r = 0.61, P < 0.001). In contrast, the relationship between the coronary contractile response to ACh and intimal area was described by an inverted U-shaped curve that was fitted to a quadratic regression model (R2 = 0.35, P = 0.002, y-axis, contraction; x-axis, intimal area). The contractile response increased as the intimal layer thickened up to the inflection point; thereafter, the contractile response declined. The relationship between medial area and intimal area was also described by an inverted U-shaped curve that was fitted to a quadratic regression model (R2 = 0.41, P < 0.01, y-axis, medial area; x-axis, intimal area). The medial area increased as the intimal area thickened up to the inflection point; thereafter, the medial area thinned. In conclusion, the thinned medial layer was associated with the attenuated contractile response in a coronary artery with greater atherosclerosis.NEW & NOTEWORTHY This is the first clinical study to show the relationship between the contractile response and the thickness of medial smooth muscle layer in coronary artery of patients with previous myocardial infarction using OCT. The contractile response to acetylcholine was attenuated, and medial layer area was thinned in coronary artery with greater atherosclerosis compared with those in coronary artery with mild or moderate atherosclerosis. The coronary contractile response was positively correlated with thickness of the medial layer in coronary arteries with either mild or greater atherosclerosis. Thus, coronary arteries with advanced atherosclerosis do not necessarily have greater contractile responses than those with early atherosclerosis, which could be related to the thinned medial layer.

T2 and T2∗ mapping in ex situ porcine myocardium: myocardial intravariability, temporal stability and the effects of complete coronary occlusion.

Diagnosis of ischaemia-related sudden cardiac death in the absence of microscopic and macroscopic ischaemic lesions remains a challenge for medical examiners. Medical imaging techniques increasingly provide support in post-mortem examinations by detecting and documenting internal findings prior to autopsy. Previous studies have characterised MR relaxation times to investigate post-mortem signs of myocardial infarction in forensic cohorts. In this prospective study based on an ex situ porcine heart model, we report fundamental findings related to intramyocardial variability and temporal stability of T2 as well as the effects of permanent coronary occlusion on T2 and T2∗ relaxation in post-mortem myocardium. The ex situ porcine hearts included in this study (n= 19) were examined in two groups (Ss, n= 11 and Si, n= 8). All magnetic resonance imaging (MRI) examinations were performed ex situ, at room temperature and at 3 T. In the Ss group, T2 mapping was performed on slaughterhouse porcine hearts at different post-mortem intervals (PMI) between 7 and 26 h. Regarding the intramyocardial variability, no statistically significant differences in T2 were observed between myocardial segments (p= 0.167). Assessment of temporal stability indicated a weak negative correlation (r=- 0.21) between myocardial T2 and PMI. In the Si group, animals underwent ethanol-induced complete occlusion of the left anterior descending artery. T2 and T2∗ mapping were performed within 3 h of death. Differences between the expected ischaemic and remote regions were statistically significant for T2 (p= 0.007), however not for T2∗ (p= 0.062). Our results provide important information for future assessment of the diagnostic potential of quantitative MRI in the post-mortem detection of early acute myocardial infarction.

Two females with coronary artery occlusion caused by presumed Kawasaki disease would have delivered without recognition of ischaemic heart disease.

We report two females with coronary artery occlusion caused by presumed Kawasaki disease that delivered children without any special treatment. After a 58-year-old female had ventricular tachycardia, a giant coronary artery aneurysm with calcification at the bifurcation of the left coronary artery and segmental stenosis of the right coronary artery were pointed out by CT angiography. She had an episode of sepsis when 3 years old. Further, she remembered chest pain during sleep after that episode. She had delivered twice without any complication during her 20s. Her diagnosis was undiagnosed coronary artery lesions caused by presumed Kawasaki disease and a previous myocardial infarction, and she underwent radiofrequency catheter ablation and implantable cardioverter defibrillator implantation. The other 48-year-old female was accidentally discovered to have coronary artery calcification on CT, while experiencing pneumonia. Her CT angiograms revealed a right coronary artery occlusion and coronary artery calcification at segments 1, 6, and 11. She had a history of "scarlet fever" before 12 months. Premature ventricular contractions were detected, while delivering her first child when 31 years old. However, she was not diagnosed as ischaemic heart disease and delivered twice by a vaginal delivery without any complication. Current guidelines recommend systemic anti-coagulation and anti-platelet therapy for all patients with giant aneurysms resulting from Kawasaki disease in childhood. The two women reported here were fortunate not to have had complications during pregnancy and delivery despite their severe coronary artery aneurysms, which were unrecognised clinically until later in life. They were lucky cases.

Comparison of cardiac MRI with PET for assessment of myocardial viability in patients with coronary chronic total occlusion.

AIM: To compare cardiac magnetic resonance imaging (MRI) and positron-emission tomography (PET) assessment of myocardial viability in patients with coronary chronic total occlusion (CTO). MATERIALS AND METHODS: Eighty patients with coronary CTO underwent cardiac MRI and PET. Cardiac MRI images were analysed using a 17-segment model, and late gadolinium enhancement (LGE) and wall motion were scored. PET was used to classify myocardial viability via myocardial perfusion and 18F-fluorodeoxyglucose, digital superscript uptake. RESULTS: With PET as the reference standard, the sensitivity of cardiac MRI in detecting myocardial viability was 95.3%, specificity was 87.5%, positive predictive value was 96.8%, negative predictive value was 84.2%, and accuracy was 93.8% on a per patient basis. The receiver operator characteristic curve was used to analyse the performance of cardiac MRI in the detection of myocardial viability on a per-patient basis and the area under the curve was 0.910 (95% confidence interval 0.805 to 1). Cardiac MRI had the highest sensitivity and specificity for differentiating viable and non-viable myocardium as defined by PET when the cut-off value of LGE was 50%. The motion consistency and correlation of cardiac MRI and PET were analysed and kappa was 0.788 (r=0.825; p<0.001). CONCLUSION: Compared with PET, cardiac MRI assessment of myocardial viability in patients with coronary CTO has high sensitivity, specificity, and accuracy. Therefore, cardiac MRI can be used as an important method for evaluating myocardial viability in coronary CTO patients.

Triggering of Acute Coronary Occlusion by Episodes of Vigorous Physical Exertion.

BACKGROUND: There is increasing recognition that heavy exertion can occasionally trigger an acute myocardial infarction (MI), although some uncertainties exist regarding the link. The primary aim of this study was to compare the relative risk (RR) of MI following vigorous exertion between those with confirmed coronary occlusion and those with a non-occluded culprit artery on acute angiography. Secondary aims were to determine if the risk of coronary occlusion is modified by the type of exercise (dynamic or isometric resistance), the frequency of regular exertion or whether the exertion was emotionally charged. METHODS: Seven hundred sixty-two (762) participants with MI (410 with coronary occlusion TIMI 0,1), and 352 (46%) with a non-occluded culprit artery (TIMI 2,3) completed a questionnaire within 4days of admission, detailing episodes of physical exertion in the 28hours prior to symptom onset and the usual frequency of such exertion. Exertion exposures within 1hour prior to symptom onset were compared to subjects' usual yearly exposure, with case-crossover methodology. RESULTS: The RR of symptom onset following heavy physical exertion level ≥6 (exertion scale 1-8), was higher in those with TIMI 0,1 compared to those with TIMI 2,3 flow (RR 6.30, 95% CI 4.70-8.50 vs 3.93, 2.89-5.30). The increased risk of coronary occlusion following vigorous exertion was observed following both dynamic exertion and isometric resistance, and did not differ between exertion types. The highest risk of coronary occlusion following exertion was observed in those who were sedentary (regular vigorous exertion <1day weekly) (RR=77, 95% CI 46-132), whereas in those who frequently perform regular vigorous physical exertion (>4days weekly), the RR of symptom onset during exertion was significantly lower, RR 2.3 (95% CI 1.5-3.6). There was no significant difference in relative risk based on whether the exertion was reported as emotionally charged. CONCLUSIONS: The relative risk that heavy exertion will trigger a non-fatal MI with an occluded artery is greater than for a non-occluded culprit artery. Both dynamic and isometric exertion increase the relative risk of event, while exposure to regular vigorous exertion reduces the relative risk.

Microvascular Dysfunction Related to Progressive Left Ventricular Remodeling due to Chronic Occlusion of the Left Anterior Descending Artery in an Adult Porcine Heart.

Occlusion of a major coronary artery induces myocardial infarction (MI), leading to left ventricle (LV) remodeling due to progressive microvasculature dysfunction. Irreversible impairment in microvascular function has been suggested to extend from the infarcted region into the infarct-border or remote regions, depending on the time to revascularization. Our aim was to determine whether the occlusion of a major coronary artery induces microvascular dysfunction in the adjacent area perfused by intact coronary arteries using a porcine model for chronic total occlusion of the left anterior descending artery (LAD). MI was induced via an ameroid constrictor ring around the LAD in adult Göttingen pigs (Sus scrofa domesticus, n = 5). Age-matched normal pigs were treated as controls (n = 3). Cardiac magnetic resonance showed reduced systolic regional wall motion in the left circumflex (LCx) and right coronary artery (RCA) territories, with a progressively worsening motion in the infarction-adjacent area over an eight-week period. On 13N-ammonia positron emission tomography (PET), myocardial blood flow (MBF) during hyperemia was significantly greater in the LCx and RCA territories (particularly in the infarction-adjacent area) compared to that in the LAD territory at four weeks after infarct induction. Subsequently, the flow significantly decreased, approaching that in the LAD territory at eight weeks after infarct induction. Fluoroscopy-guided pressure-wire studies showed significantly higher microvascular resistance in the LCx area at eight weeks compared to that in controls. Electron microscopy showed endothelium swelling and microvasculature disruption in areas adjacent to the LCx and RCA territories. Anterior MI caused coronary microvascular dysfunction in the adjacent area, associated with a reduced MBF and regional wall motion.

Impact of subintimal plaque modification procedures on health status after unsuccessful chronic total occlusion angioplasty.

OBJECTIVES: We sought to determine the impact of subintimal plaque modification (SPM) on early health status following unsuccessful chronic total occlusion (CTO) PCI. BACKGROUND: Intentionally dilating the subintimal space during unsuccessful CTO PCI to facilitate flow through dissection planes and improve success of repeat PCI attempts is a technique used by some hybrid operators, and may improve health status by restoring distal vessel flow despite unsuccessful CTO PCI. METHODS: We studied 138 patients who underwent unsuccessful CTO PCI in a 12-center CTO PCI registry. Safety was assessed by comparing in-hospital outcomes of patients undergoing unsuccessful CTO PCI with and without SPM. The association between SPM and health status was quantified using the Seattle Angina Questionnaire Summary Score (SAQ SS), and the association between SPM and SAQ SS was determined using multivariable regression. RESULTS: SPM was performed in 59 patients (42.8%). Complication rates were similar comparing those with and without SPM. At 1-month, patients treated with SPM had larger increases in SAQ SS compared to patients who were not (28.3 ± 21.7 vs. 16.8 ±20.2, P = 0.012), and SPM was associated with an adjusted mean 10.5 point (95% CI 1.4-19.7, P = 0.02) greater SAQ SS improvement through 30 days. CONCLUSION: SPM was performed in almost half of unsuccessful CTO PCIs and was not associated with increased procedural complications. SPM was independently associated with better patient-reported health status at 30 days. Further studies are needed to assess the necessity of subsequent PCI in patients with significant health status improvements after SPM.

Epicardial collateral channel for retrograded recanalization of chronic total occlusion percutaneous coronary intervention: Predictors of failure and procedural outcome.

OBJECTIVES: This study set out to identify significant lesion features of chronic total occlusion (CTO) that predict successful retrograde recanalization via epicardial collateral channels (CCs). BACKGROUND: Epicardial CCs remain essential in retrograde percutaneous coronary intervention (PCI) of CTO. However, the unpredictability of success and occurrence of complications limit the application of epicardial CCs for retrograde PCI technique for CTO. METHODS: 103 retro-recanalization cases were analyzed using epicardial CCs with successful recanalization as an end point. Clinical and angiography data were collected. RESULTS: The total success rate was 76.3%. Independent predictors associated with technical success included CCs tortuosity, side branch at CCs tortuosity, inadequate CCs Size and inadequate CCs exit location. Assigning a score of one for each variable, four levels of difficulty were obtained and formed the EPI-CTO score (Epicardial CTO). This score had significant predictive value for the likelihood of successful recanalization (AUC: 0.94, 95%CI: 0.89-0.98). Coronary and CCs perforation occurred in 6 and 10 cases respectively. Four cases including two coronary and two CCs perforations had tamponade that needed pericardiocentesis. CONCLUSIONS: Using epicardial CCs for retrograde approach of CTO PCI is effective. Complication rate was acceptable. We found four independent predictors relative to procedure success.

Short-term and long-term clinical outcomes of rotational atherectomy in resistant chronic total occlusion.

OBJECTIVES: To evaluate the short- and long-term clinical outcomes of RA in CTO coronary intervention. BACKGROUND: The application of rotational atherectomy (RA) may improve the success rate of percutaneous recanalization of chronic total occlusion (CTO) with heavy calcification. METHODS: From January 2011 to September 2014, we enrolled 285 patients with CTO who underwent successful percutaneous coronary intervention (PCI). Resistant CTO lesions were defined as those with heavy calcifications as well as those that no devices are able to pass after guide wire crossing. RESULTS: All patients with resistant CTO lesions (n = 26) were successfully treated by RA without major complications, except 1 patient complicated with coronary perforation and treated by surgery successfully (success rate: RA group vs non-RA group: 96.2%, vs 89.5%, P = 0.038). Compared to the non-RA group, the patients in the RA group were older (P = 0.028), had higher J-CTO scores (P = 0.001), and needed longer stents (P = 0.001). All patients were followed up for a mean period of 3.4 ± 2.3 years, and the 1-year and long-term clinical outcomes of the RA group were excellent and comparable with those not receiving RA in multivariate analysis adjusted for multiple variables. CONCLUSION: The treatment of RA is safe and feasible for resistant CTO lesions with heavy calcification. The short- and long-term clinical outcomes of the treatment of RA were excellent and comparable with those not needing RA for CTO PCI.

Outcomes after drug-coated balloon treatment for patients with calcified coronary lesions.

OBJECTIVES: To investigate the efficacy of drug-coated balloon (DCB) for calcified coronary lesions. BACKGROUND: Calcified coronary lesions is associated with poor clinical outcomes after revascularization. Recently, DCB is emerging as an alternative strategy for de novo coronary lesions. However, reports describing the efficacy of DCB for calcified coronary lesions are limited. METHODS: A total of 81 patients (96 lesions) who electively underwent DCB treatment for de novo coronary lesions were enrolled: 46 patients (55 lesions) in the calcified group and 35 patients (41 lesions) in the non-calcified group. Angiographic follow-up data and clinical outcomes after the procedure were evaluated. RESULTS: The diameter of the DCB used was 2.5 ± 0.5 mm. No bail-out stenting was observed after DCB treatment. Rotational atherectomy was used in 82% of lesions in the calcified group. Follow-up angiography (median, 6.5 months after intervention) was performed for 59 patients (30 in the calcified group and 29 in the non-calcified group). Late lumen loss and rates of restenosis were comparable between the groups (0.03 mm in the calcified group vs -0.18 mm in the non-calcified group, P = 0.093 and 13.9% vs 3.03%, P = 0.095, respectively). The survival rates for target lesion revascularization free survival and major adverse cardiac events at 2 years were comparable between the groups (85.3% vs 93.4%, P = 0.64 and 81.4% vs 88.5%, P = 0.57, respectively). CONCLUSION: Calcified coronary lesions might dilute the effect of DCB. However, clinical outcomes in the calcified group were similar to those in the non-calcified group.

Relationship of Autophagy and Apoptosis with Total Occlusion of Coronary Arteries.

BACKGROUND The primary aim of this study was to evaluate the level of autophagy and apoptosis enzymes in patients with coronary artery disease (CAD). Furthermore, we investigated the role of autophagy and apoptosis in the progression of coronary collateral and coronary total occlusion (TO). MATERIAL AND METHODS We enrolled 115 patients in this prospective, observational, controlled study, who were categorized into 3 groups as follows: group 1, patients with chronic TO (n=49); group 2, patients with acute TO such as myocardial infarction (n=36); and group 3, healthy control patients (n=30). We used the enzyme-linked immunosorbent assay (ELISA) kit for autophagy-related protein 5 (ATG5) and apoptosis (M30) in the plasma for these 3 groups. RESULTS Autophagy levels significantly varied among the groups (13.7±5.3 ng/mL, 11.7±3.4 ng/mL, and 7.5±3, respectively; P<0.001). In addition, apoptosis levels significantly varied among the groups (78.6±33.4 ng/mL, 64.9±30.6 ng/mL, and 47.6±18.2, respectively; P<0.001). The subgroup analysis revealed significant positive correlations between the autophagy level and the Rentrop score in contrast to apoptosis in group 1 (r=0.463; P<0.001). CONCLUSIONS This study determined that autophagy and apoptosis levels were higher in patients with CAD than in healthy controls. In contrast to the serum apoptosis level, serum autophagy levels demonstrated a significant positive correlation with the Rentrop score. Hence, an elevated autophagy level might be a potential activator and marker of the process by which the body protects itself in CAD.

Long-term Survival Benefit of Statin in Patients with Coronary Chronic Total Occlusion without Revascularization.

BACKGROUND: Limited data are available on the efficacy of statin therapy in stable ischemic heart disease with chronic total occlusion (CTO) without revascularization. We investigated whether statin therapy could be beneficial in stable patients with CTO without revascularization. METHODS: From March 2003 to February 2012, 2,024 patients with at least one CTO were enrolled in a retrospective, single-center registry; 664 of these patients were managed conservatively without an initial revascularization strategy. Among them, we excluded CTO cases involving acute coronary syndrome, in-hospital death or incomplete data and classified 551 patients into statin (n = 369) and non-statin (n = 182) groups according to use of statin at discharge. Propensity score matching analysis was also performed in 148 pairs. The primary outcome was cardiac death. RESULTS: The median overall follow-up duration was 45.7 months (interquartile range: 19.9-70.5 months). Cardiac death occurred in 22 patients (6.0%) in the statin group vs. 24 patients (13.2%) in the non-statin group (P < 0.001). In propensity score matching analysis, statin therapy was associated with a low risk of cardiac death (adjusted hazard ratio [HR], 0.39; 95% confidence interval [CI], 0.18-0.85; P = 0.022) and major adverse cardiac events (adjusted HR, 0.66; 95% CI, 0.43-0.98; P = 0.043). On multivariate analysis, independent predictors for cardiac death were age > 70 years, renal insufficiency, prior myocardial infarction, left ventricular ejection fraction < 40%, proximal-to-mid CTO location, and no use of statin in CTO patients. CONCLUSION: Statin therapy at discharge may be associated with a reduction in long-term cardiac mortality in stable CTO patients without revascularization.

Patent foramen ovale, paradoxical embolism and fatal coronary obstruction.

A 75-year-old woman was admitted to the emergency room with chest pain and vomiting. An electrocardiogram and laboratory results were suggestive for myocardial infarction of the posterior cardiac wall. Echocardiography was indicative of aortic dissection, and a CT scan of the thoracic arteries showed a massive pulmonary thromboembolism and thrombotic occlusion of the right coronary artery (RCA). The woman died shortly after admission. Autopsy confirmed the presence of thromboemboli in the right pulmonary artery and its lobar branches. Also, the anterior aortic sinus was filled with a 9 cm long thromboembolus that extended into the RCA, making it dilated and completely occluded. Another 3.5 cm long thromboembolus extended from the beginning of the left subclavian artery. A patent foramen ovale (PFO) was present. On the posterior wall of the left ventricle, there was an area suggestive of myocardial infarction, and histopathological examination confirmed that it was 24-48 hours old. The coronary circulation was "co-dominant". The sources of thrombotic masses were the deep veins of the lower limbs. The cause of death was myocardial infarction, caused by RCA occlusion with thromboembolus originating from the deep veins of the left lower leg after paradoxical embolism via PFO. This case illustrates that although deep venous thrombosis, pulmonary thromboembolism, and PFO are not rare findings at autopsy, their combination could be a relatively rare cause of fatal coronary artery occlusion after paradoxical embolism.

Plaque morphology predictors of side branch occlusion after provisional stenting in coronary bifurcation lesion: Results of optical coherence tomography bifurcation study (ORBID).

OBJECTIVES: The aim of this study was to identify the predictors of side branch (SB) ostial stenosis developed after provisional stenting of the main vessel (MV) using optical coherence tomography (OCT). BACKGROUND: Provisional stenting remains the main approach to treatment of bifurcation lesions; however, it may result in the narrowing of SB ostium. There is little information about underlying plaque morphology of the MV lesion and its potential impact on the SB after provisional stenting. METHODS: Patients with stable coronary disease with angiographic MV lesion not involving SB were included in a prospective single center study. The primary outcome was significant SB ostium stenosis (SBOS), defined as residual stenosis of >50% after MV stenting. RESULTS: Thirty bifurcation lesions in 30 patients were analyzed in the study. Poststenting significant SBOS was observed in 30% of patients. The MV lesions with SBOS > 50% were characterized by a higher prevalence of lipid rich plaques (100 vs. 64%, p = 0.040) and spotty calcifications (60 vs. 0%, p = 0.005). Maximal lipid arcs were greater (257° vs. 132°, p = 0.001) and lipid volume index was higher (1380 vs. 574, p = 0.012) in the SBOS >50% group. Multivariate logistic regression analysis identified maximal lipid arc (odds ratio (OR): 1.014, p = 0.038) and the presence of lipid plaque contralateral to SB ostium (OR: 8.14, p = 0.046) before stenting as independent predictors of significant SBOS after PCI. CONCLUSIONS: High lipid content of the MV lesion and a contralateral location of lipid in the bifurcation area may contribute to SBOS after provisional stenting. © 2016 Wiley Periodicals, Inc.

Enhancement patterns detected by multidetector computed tomography are associated with microvascular obstruction and left ventricular remodelling in patients with acute myocardial infarction.

AIMS: This study evaluated the clinical value of myocardial contrast-delayed enhancement (DE) with multidetector computed tomography (MDCT) for detecting microvascular obstruction (MVO) and left ventricular (LV) remodelling revealed by DE magnetic resonance imaging after acute myocardial infarction (AMI). METHODS AND RESULTS: In 92 patients with first AMI, MDCT without iodine reinjection was performed immediately following successful percutaneous coronary intervention (PCI). Delayed-enhancement magnetic resonance imaging performed in the acute and chronic phases was used to detect MVO and LV remodelling (any increase in LV end-systolic volume at 6 months after infarction compared with baseline). Patients were divided into two groups according to the presence (n = 33) or absence (n = 59) of heterogeneous enhancement (HE). Heterogeneous enhancement was defined as concomitant presence of hyper- and hypoenhancement within the infarcted myocardium on MDCT. Microvascular obstruction and LV remodelling were detected in 49 (53%) and 29 (32%) patients, respectively. In a multivariable analysis, HE and a relative CT density >2.20 were significant independent predictors for MVO [odds ratio (OR) 13.5; 95% confidence interval (CI), 2.15-84.9; P = 0.005 and OR 12.0; 95% CI, 2.94-49.2; P < 0.001, respectively). The presence of HE and relative CT density >2.20 showed a high positive predictive value of 93%, and the absence of these two findings yielded a high negative predictive value of 90% for the predictive value of MVO. Heterogeneous enhancement was significantly associated with LV remodelling (OR 6.75; 95% CI, 1.56-29.29; P = 0.011). CONCLUSION: Heterogeneous enhancement detected by MDCT immediately after primary PCI may provide promising information for predicting MVO and LV remodelling in patients with AMI.