Exercise training outcomes in patients with chronic heart failure with reduced ejection fraction depend on patient background.

Background: The aim of this study was to identify significant factors affecting the effectiveness of exercise training using information of the HF-ACTION (Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training) study. Methods: Background factors influencing the effect of exercise training were comprehensively surveyed for 2,130 patients by multivariable Cox regression analysis with the stepwise variable selection, and only significant factors were selected that were statistically distinguished from dummy noise factors using the Boruta method. Results: The analysis suggested that the use of beta-blockers, pulse pressure, hemoglobin level, electrocardiography findings, body mass index, and history of stroke at baseline potentially influenced the exercise effect on all-cause death (AD). Therefore, a hypothetical score to estimate the effect of exercise training was constructed based on the analysis. The analysis suggested that the score is useful in identifying patients for whom exercise training may be significantly effective in reducing all-caused death and hospitalization (ADH) as well as AD. Such a subpopulation accounted for approximately 40% of the overall study population. On the other hand, in approximately 45% of patients, the effect of exercise was unclear on either AD or ADH. In the remaining 15% of patients, it was estimated that the effect of exercise might be unclear for ADH and potentially rather increase AD. Conclusions: This study is the first analysis to comprehensively evaluate the effects of various factors on the outcome of exercise training in chronic heart failure, underscoring the need to carefully consider the patient's background before recommending exercise training. However, it should be noted that exercise training can improve many outcomes in a wide variety of diseases. Therefore, given the limitations involved in post-hoc analyses of a single clinical trial, the characteristics of patients to whom the results of this analysis can be applied need attention, and also further research is necessary on the relationship between the degree of exercise and the outcomes. A new clinical trial would be needed to confirm the factors detected and the appropriateness of the score.

Influence of myocardial bridge on atherosclerotic plaque distribution and characteristics evaluated by near-infrared spectroscopy intravascular ultrasound.

BACKGROUND: This study aims to clarify whether myocardial bridge (MB) could influence atherosclerotic plaque characteristics assessed using near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) imaging. METHODS: One hundred and sixteen patients who underwent percutaneous coronary intervention (PCI) using NIRS-IVUS imaging were included. MB was defined as an echo-lucent band surrounding left anterior descending artery (LAD). In MB patients, LAD was divided into three segments: proximal, MB, and distal segments. In non-MB patients, corresponding three segments were defined based on the average length of the above segments. Segmental maximum plaque burden and lipid content derived from NIRS-IVUS imaging in the section of maximum plaque burden were evaluated in each segment. Lipid content of atherosclerotic plaque was evaluated as lipid core burden index (LCBI) and maxLCBI4mm. LCBI is the fraction of pixels indicating lipid within a region multiplied by 1000, and the maximum LCBI in any 4-mm region was defined as maxLCBI4mm. RESULTS: MB was identified in 42 patients. MB was not associated with maximum plaque burden in proximal segment. LCBI and maxLCBI4mm were significantly lower in patients with MB than those without in proximal segment. Multivariable analysis demonstrated both MB and maximum plaque burden in proximal segment to be independent predictors of LCBI in proximal segment. CONCLUSIONS: Lipid content of atherosclerotic plaque assessed by NIRS-IVUS imaging was significantly smaller in patients with MB than those without. MB could be considered as a predictor of lipid content of atherosclerotic plaque when assessed by NIRS-IVUS imaging.

Impact of perioperative antithrombotic strategies on clinical events in non-cardiac surgery.

Antithrombotic therapy including antiplatelet agents and anticoagulants are prescribed for secondary prevention in patients with established cardiovascular disease. Although antithrombotic therapy is often interrupted before non-cardiac surgery with or without perioperative bridging anticoagulation, the impact on thrombotic and bleeding events remains uncertain. A total of 360 patients chronically treated with antithrombotic therapy for secondary prevention underwent elective non-cardiac surgery under general anesthesia, with the complete interruption of antithrombotic agents. The study endpoints included all-cause death, thrombotic events, and major bleeding complications after surgical procedures. Of 360 patients, 190 (52.8%) and 200 (55.6%) received antiplatelet and anticoagulation perioperatively. Atrial fibrillation (32.8%) and coronary artery disease (22.5%) were the major indications for antithrombotic regimens. Antithrombotic therapy was interrupted from 5 [2, 7] days before the surgery to 4 [2, 7] days postoperatively. Perioperative bridging therapy with unfractionated heparin was employed in 113 (31.4%) patients. During the hospitalization, one (0.3%) patient died due to non-cardiovascular causes. Thrombotic events and major bleeding occurred in two (0.6%) and eight (2.2%) patients. Bridging therapy with heparin was significantly associated with an increased risk of bleeding events (5.3% vs. 0.8%, p = 0.02). Pre-operative bridging therapy with heparin and operative duration were significantly associated with bleeding complications. In the present study, complete interruption of antithrombotic therapy resulted in a few thrombotic events in patients undergoing elective non-cardiac surgery. Bridging therapy with heparin and longer operative duration were significantly associated with post-operative bleeding complications.

Extent of lipid core plaque in patients with Achilles tendon xanthoma undergoing percutaneous coronary intervention for coronary artery disease.

BACKGROUND: It has been reported that Achilles tendon xanthoma (ATX), being one of the important diagnostic criteria for familial hypercholesterolemia, is independently associated with the severity of coronary artery disease (CAD). The aim of this study was to investigate plaque vulnerability in CAD patients with ATX. METHODS: Patients with CAD who underwent percutaneous coronary intervention (PCI) with near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) guidance were enrolled. Soft X-ray radiography of the Achilles tendon was performed, and a maximum thickness of 9 mm or more was regarded as ATX. Using NIRS-IVUS, the degree of lipid core plaque (LCP) was evaluated by calculating the maximum value of lipid core burden index (LCBI) for any of the 4-mm segments (maxLCBI4mm) in the target lesion and non-target vessel. RESULTS: In a total of 156 patients, 14 patients (9.0%) had ATX. MaxLCBI4mm in the ATX group was significantly greater in the target lesion (p<0.001) and in the non-target vessel (p=0.032) compared to the non-ATX group. When patients were divided into tertiles according to Achilles tendon thickness, maxLCBI4mm was progressively increased in favor of thickness, although there was only a tendency in the target lesion (p=0.062), and no statistical significance in the non-target vessel (p=0.189). Multiple linear regression analysis determined ATX as an independent predictor for maxLCBI4mm in the target lesion and non-target vessel. CONCLUSIONS: ATX was associated with the degree of LCP in CAD patients requiring PCI. High-risk patients with lipid-rich vulnerable plaque can possibly be detected by evaluating Achilles tendon thickness.

Successful Leadless Pacemaker Implantation in an Elderly Patient With Dextrocardia and Situs Inversus.

Leadless pacemaker is indicated in patients with symptomatic bradycardia as an alternative therapy when transvenous pacemaker implantation is considered difficult or at high risk. The experience of implanting leadless pacemaker in patients with dextrocardia and situs inversus is limited. A 94-year-old male was transferred to our hospital due to advanced atrio-ventricular block with episode of syncope. Chest radiograph and computed tomography revealed dextrocardia with situs inversus. Emergency cardiac catheterization was performed and a temporary pacemaker was inserted, but the patient removed it due to delirium. So, a leadless pacemaker was implanted to him. Shorter time of bed-rest after the implantation and shorter hospital stay would be beneficial of implanting a leadless pacemaker. Precise anatomical evaluation would be important to perform implantation efficiently and safely.

Utility of near-infrared spectroscopy to detect the extent of lipid core plaque leading to periprocedural myocardial infarction.

OBJECTIVES: The aim of this study was to investigate whether lipid core plaque (LCP) in the entire stented segment detected by near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) could predict procedural myocardial infarction (PMI) in patients undergoing percutaneous coronary artery intervention (PCI). BACKGROUND: NIRS-IVUS can identify LCP, described as high lipid core burden index (LCBI). Previously, the highest LCBI contained only in the 4-mm segment (maxLCBI4mm ) was reported to predict PMI. METHODS: Patients who underwent NIRS-IVUS examination during PCI for coronary artery disease at Chiba University Hospital were included. The extent of LCP in the stented segment derived from NIRS-IVUS analysis was presented as LCBI, maxLCBI4mm , and LCP area index (LAI), reflecting the total amount of LCP in the entire stented segment calculated as LCBI×lesion length. PMI was defined as an elevation of creatine kinase MB > 3 times upper reference level (URL), and periprocedural myocardial injury (PMInj) was defined as an elevation of troponin I>5 times URL within 12 to 24 h after PCI. RESULTS: Out of 141 enrolled patients, PMI occurred in 20 (14.2%) and PMInj occurred in 62 (44.0%) patients. Receiver-operating characteristic curve analysis revealed LAI was the strongest predictor for both PMI and PMInj (area under curve 0.771, p < 0.001, and 0.717, p < 0.001, respectively). Multiple logistic regression analysis determined high LAI value as the independent predictor of both PMI and PMInj. CONCLUSIONS: Greater extent of LCP in the entire stented segment detected by NIRS-IVUS was significantly associated with PMI as well as PMInj in patients undergoing PCI.

Factors that predict ventricular arrhythmias in the late phase after acute myocardial infarction.

AIMS: Little is known regarding factors that predict the occurrence of lethal ventricular arrhythmias (VAs) occurring after acute myocardial infarction (AMI). This observational cohort study aimed to identify factors that predicted lethal VAs during the late phase after AMI in patients with reduced left ventricular ejection fraction (LVEF). METHODS AND RESULTS: Data were collected from our AMI database regarding consecutive patients with an LVEF of ≤40% after AMI (January 2012 to July 2018). The 'late phase' was defined as ≥7 days after AMI onset, and the primary endpoint was defined as lethal VAs in the late phase. The study included 136 patients (82% men; mean age: 66 ± 13 years). The average LVEF at admission was 32.7 ± 8.2%. During a mean follow-up period of 20.7 months, 14 patients (10%) experienced lethal VAs, including ventricular fibrillation (n = 8) and sustained ventricular tachycardia (n = 10). Univariate analyses revealed that lethal VAs were predicted by age and LVEF at admission. Receiver operating characteristic curve analysis indicated that the optimal cut-off value was 23% for using the LVEF at admission to predict the primary endpoint (area under the curve: 0.77, P < 0.0001). Multivariable analysis also demonstrated that LVEF at admission was an independent predictor of the primary endpoint (risk ratio = 7.12, P = 0.001). CONCLUSIONS: Lethal VAs in the late phase are common in patients with AMI, and reduced LVEF and cardiac function at admission play a significant role in the risk stratification for future lethal VAs in this population.

Greater coronary lipid core plaque assessed by near-infrared spectroscopy intravascular ultrasound in patients with elevated xanthine oxidoreductase: a mechanistic insight.

Elevated serum uric acid level was reportedly associated with greater coronary lipid plaque. Xanthine oxidoreductase (XOR) is a rate-limiting enzyme in purine metabolism and believed to play an important role in coronary atherosclerosis. However, the relation of XOR to coronary lipid plaque and its mechanism are unclear. Patients with stable coronary artery disease undergoing elective percutaneous coronary intervention under near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) guidance were prospectively enrolled. They were divided into three groups according to serum XOR activities: low, normal, and high. Coronary lipid core plaques in non-target vessels were evaluated by NIRS-IVUS with lipid core burden index (LCBI) and a maximum LCBI in 4 mm (maxLCBI4mm). Systemic endothelial function and inflammation were assessed with reactive hyperemia index (RHI) and high-sensitivity C-reactive protein, neutrophil-to-lymphocyte ratio, and platelet-to-lymphocyte ratio. Of 68 patients, 26, 31, and 11 were classified as low, normal, and high XOR activity groups. LCBI (474.4 ± 171.6 vs. 347.4 ± 181.6 vs. 294.0 ± 155.9, p = 0.04) and maxLCBI4mm (102.1 ± 56.5 vs. 65.6 ± 48.5 vs. 55.6 ± 37.8, p = 0.04) were significantly higher in high XOR group than in normal and low XOR groups. Although RHI was significantly correlated with body mass index, diabetes, current smoking, and high-density lipoprotein cholesterol, no relation was found between XOR activity and RHI. There were also no relations between XOR activity and C-reactive protein, neutrophil-to-lymphocyte ratio, or platelet-to-lymphocyte ratio. In conclusion, elevated XOR activity was associated with greater coronary lipid core plaque in patients with stable coronary artery disease, without significant relations to systemic endothelial function and inflammation.

Impact of clinical presentations on lipid core plaque assessed by near-infrared spectroscopy intravascular ultrasound.

Near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) studies have demonstrated that lipid core plaque (LCP) is frequently observed in the culprit segment of myocardial infarction (MI). However, little is known about the impact of clinical presentations such as chronic coronary syndrome (CCS) and acute coronary syndrome (ACS) including unstable angina (UA), non ST-segment elevation MI (NSTEMI), and ST-segment elevation MI (STEMI) on LCP. The present prospective single-center registry included a total of 178 patients who underwent percutaneous coronary intervention under NIRS-IVUS guidance. Patients were divided into CCS and ACS groups, and ACS patients were further sub-divided into the 3 groups according to the clinical presentation. The primary endpoint was coronary LCP in the target lesion assessed by NIRS-IVUS with maximal lipid core burden index over any 4 mm segment (maxLCBI4mm). The study population included 124 and 54 patients with CCS and ACS. MaxLCBI4mm in the target lesion was significantly higher in the ACS group than in the CCS group (503 [284-672] vs. 406 [250-557], p = 0.046). Among ACS patients, MaxLCBI4mm in the target lesion was also significantly different in those with UA (n = 18), NSTEMI (n = 21), and STEMI (n = 15) (288 [162-524] vs. 518 [358-745] vs. 646 [394-848], p = 0.021). In conclusion, LCP assessed by NIRS-IVUS, a surrogate of coronary plaque vulnerability, was significantly different according to the clinical presentations such as CCS, UA, NSTEMI, and STEMI.

Vasospastic angina and overlapping cardiac disorders in patients resuscitated from cardiac arrest.

BACKGROUND: Vasospastic angina (VSA) reportedly accounts for one form of sudden cardiac arrest (SCA). Intracoronary acetylcholine (ACh) testing is useful for diagnosing VSA although invasive provocation testing after SCA is a clinical challenge. In addition, even if the ACh test is positive, any causal relationship between VSA and SCA is often unclear because patients with VSA may have other underlying cardiac disorders. METHODS: A total of 20 patients without overt structural heart disease who had been fully resuscitated from SCA were included. All patients underwent the ACh provocation test and scrutiny such as cardiac computed tomography or magnetic resonance imaging. Patients were followed up for all-cause death or recurrent SCA including appropriate implantable cardioverter defibrillator therapy. RESULTS: An ACh provocation test was performed 20 ± 17 days after cardiac arrest. Fifteen out of 20 (75.0%) patients had a positive ACh test and 2 (10.0%) had adverse events such as ventricular tachycardia and transient cardiogenic shock during the test. In patients with a positive ACh test, 6 of 15 (40.0%) patients had other overlapping cardiac disorders such as long QT syndrome, Brugada syndrome, cardiac sarcoidosis, myocarditis, or cardiomyopathy. Long-term prognosis was not different regardless of a positive ACh test or the presence of other cardiac disorders overlapping with VSA. CONCLUSIONS: Three-quarters of the patients who had been resuscitated from SCA had a positive ACh test. Further examinations revealed other overlapping cardiac disorders in addition to VSA in 40% of patients with a positive ACh test.

Coronary Flow Reserve and Glycemic Variability in Patients with Coronary Artery Disease.

Objective Glycemic variability is being increasingly recognized as an early indicator of glucose metabolic disorder and may contribute to the development of diabetic vascular complications, such as coronary microvascular dysfunction. The present study sought to investigate the relationship between coronary microvascular function assessed by intracoronary thermodilution method and glycemic variability on a continuous glucose monitoring system (CGMS). Methods We prospectively enrolled 40 patients with or without known diabetes mellitus who had epicardial coronary artery disease referred for coronary angiography and were not treated with diabetic medications. Of these, two had a significant stenosis in the left main coronary artery and were therefore excluded from the analyses. In the end, 38 patients were equipped with a CGMS and underwent intracoronary physiological assessments in the unobstructed left anterior descending artery. The mean amplitude of glycemic excursion (MAGE) and standard deviation were calculated from the obtained CGMS data as indicators of glucose variability. Results Coronary flow reserve (CFR) was negatively correlated with MAGE (r=-0.328, p=0.044) and standard deviation (r=-0.339, p=0.037) on CGMS, while the index of microcirculatory resistance showed no such correlation. Multivariable linear regression analyses showed that MAGE on CGMS was significantly associated with CFR after adjusting for age, sex, fractional flow reserve and hemoglobin A1c. Conclusion Higher MAGE on CGMS was associated with reduced CFR in stable patients with coronary artery disease, suggesting a potential effect of glycemic variability on coronary microvascular flow regulation. A further study with a larger sample size needs to be conducted to confirm our findings.

In-Hospital Blood Pressure Variability: A Novel Prognostic Marker of Renal Function Decline and Cardiovascular Events in Patients with Coronary Artery Disease.

INTRODUCTION: Several measures of blood pressure (BP) variability have been associated with kidney disease and cardiovascular events. Although BP is routinely measured during hospitalization in daily practice, the prognostic impact of in-hospital BP and its variability are uncertain. METHODS: A total of 226 participants who underwent elective percutaneous coronary intervention (PCI) for stable coronary artery disease (CAD) were included. BP was measured by trained nurses during the 4-day hospitalization for PCI. BP variability was assessed by standard deviation (SD) and coefficient variation of systolic BP. Estimated glomerular filtration rate (eGFR) was calculated at baseline and follow-up (≥6 months). The cardiovascular end point was defined as a composite of cardiovascular death, acute coronary syndrome, stroke, heart failure hospitalization, and any coronary revascularization. RESULTS: In-hospital BP was measured 9.5 ± 0.8 times. During a median follow-up period of 1.7 years, mean eGFR change was -1.7 mL/min/1.73 m2 per year, and 35 (15.5%) participants met the cardiovascular end point. Mean systolic BP and SD were negatively correlated with eGFR change. In the receiver operating characteristic curve analysis, SD of systolic BP predicted the cardiovascular end point (AUC 0.63, best cutoff value 14.2 mm Hg, p = 0.003). Kaplan-Meier analysis demonstrated a significantly higher incidence of the cardiovascular end point in patients with SD of systolic BP ≥14.2 mm Hg compared to their counterpart (p = 0.003). A multivariable analysis showed SD of systolic BP as an independent predictor for the cardiovascular end point. When assessed with coefficient variation, BP variability was similarly related to eGFR change and clinical outcomes. CONCLUSION: Greater in-hospital BP variability was associated with renal function decline and cardiovascular events in patients with stable CAD.

Mental Health Status in Patients Undergoing Intracoronary Acetylcholine Provocation Test.

BACKGROUND: Previous studies showed the relation of mental distress such as anxiety and depression to coronary vasoconstriction and myocardial ischemia. However, the mental health status of patients suspected to have vasospastic angina is unclear. METHODS: A total of 99 patients underwent intracoronary acetylcholine (ACh) provocation tests for the diagnosis of vasospastic angina and mental health assessment using the 12-item General Health Questionnaire (GHQ-12) and State-Trait Anxiety Inventory Form Y (STAI Y-2). Patients with binary GHQ-12 ≥ 4 were defined as having poor mental health. RESULTS: Median GHQ-12 and STAI Y-2 were 3 [1, 6] and 44 [36, 50]. Forty-one (41%) patients had binary GHQ-12 ≥ 4, and 48 (48%) had positive ACh provocation tests. The number of provoked vasospasms and rate of electrocardiographic change and chest pain during ACh tests were not significantly different between patients with and without GHQ-12 ≥ 4. The incidence of positive ACh provocation test was similar between the two groups (49% vs. 48%, p = 1.00). The multivariable analysis indicated that younger age, no history of percutaneous coronary intervention and no diabetes mellitus were factors associated with higher GHQ-12 and/or STAI Y-2 scores. CONCLUSIONS: More than 40% of patients who underwent ACh provocation tests had poor mental condition. No impact of mental distress on positive ACh tests was found in this study.

Decreased Double Product at Rest in Patients With Severe Vasospasm.

BACKGROUND: Autonomic nerve system and endothelial function play important roles in vasospastic angina. Elevated heart rate (HR), blood pressure (BP), and double product (DP) can increase endothelial-dependent coronary artery dilation and blood flow. However, the impact of HR, BP, and DP on occurrence and severity of VSA in the clinical setting is unclear. METHOD: A total of 170 patients undergoing intracoronary acetylcholine (ACh) provocation test during hospitalisation was included. Resting HR, BP, and DP were measured at least four times, and their variabilities were evaluated by standard deviations (SD) and coefficient of variations (CVs). Angiographic coronary artery vasospasm was defined as total or subtotal occlusion induced by ACh provocation. RESULTS: Mean±SD HR (65.7±9.1 vs 69.6±7.9 beats per minute; p=0.003), systolic BP (122.3±13.4 vs 127.7±14.6 mmHg; p=0.01), and DP (8,001±1,229 vs 8,903±1,495; p<0.001) were significantly lower in patients with a positive ACh test than the counterpart, whereas SD and CV of both HR and systolic BP were not significantly different between the two groups. Mean HR, BP, and DP progressively decreased with increase in the number of vessels with angiographic vasospasm. Multivariate analysis showed current smoking and lower DP as independent predictors of the greater number of vessels with provoked angiographic vasospasm. CONCLUSIONS: Resting HR, BP, and DP were lower in patients with vasospastic angina, especially in those with severe vasospasm.

Relation of Plasma Xanthine Oxidoreductase Activity to Coronary Lipid Core Plaques Assessed by Near-Infrared Spectroscopy Intravascular Ultrasound in Patients With Stable Coronary Artery Disease.

Previous studies reported that elevated serum uric acid level was associated with greater coronary lipid plaque. Xanthine oxidoreductase (XOR) is a rate-limiting enzyme in purine metabolism and is believed to play important roles in coronary atherosclerosis. However, the relation between XOR and coronary lipid plaque is unclear. Patients with stable coronary artery disease who underwent elective percutaneous coronary intervention under near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) guidance were prospectively included. They were divided into 3 groups according to plasma XOR activities based on a previous report: low, normal, and high. Quantitative coronary angiography and gray-scale IVUS were analyzed. The primary end point was coronary lipid plaques in a nontarget vessel assessed by NIRS-IVUS with lipid core burden index (LCBI) and maximum LCBI in 4 mm (maxLCBI4mm). Out of 68 patients, 26, 31, and 11 patients were classified as low, normal, and high XOR activity groups. Quantitative coronary angiography demonstrated that the high XOR activity group had longer lesion length, smaller minimum lumen diameter, and higher percentage of diameter stenosis in a nontarget vessel among the 3 groups. Gray-scale IVUS analysis also showed smaller lumen area in the high XOR activity group than the others. LCBI (102.1 ± 56.5 vs 65.6 ± 48.5 vs 55.6 ± 37.8, p = 0.04) and maxLCBI4mm (474.4 ± 171.6 vs 347.4 ± 181.6, 294.0 ± 155.9, p = 0.04) in a nontarget vessel were significantly higher in the high XOR group than in the normal and low groups. In conclusion, elevated XOR activity was associated with coronary lipid-rich plaque in a nontarget vessel in patients with stable coronary artery disease.

Association between Achilles tendon xanthoma and severity of coronary artery disease in patients undergoing percutaneous coronary intervention.

BACKGROUND: Tendon xanthoma, represented as Achilles tendon xanthoma (ATX), is one of the important diagnostic criteria for familial hypercholesterolemia (FH). However, there are some cases with ATX who do not meet these criteria. This study aimed to investigate the severity of coronary artery disease (CAD) in patients with ATX. METHODS: A total of 394 patients with CAD undergoing percutaneous coronary intervention (PCI) at Chiba University Hospital between June 2016 and February 2018 were enrolled. Soft X-ray radiography of Achilles tendon was performed, and a maximum thickness of 9 mm or more was regarded as ATX. Heterozygous FH was diagnosed according to the diagnostic criteria proposed by the Japan Atherosclerosis Society in 2017. CAD severity was assessed by SYNTAX score before the first PCI during the study period. RESULTS: There were 43 (10.9%) patients with ATX, and 16 (4.1%) were diagnosed as FH (15 with ATX and 1 without ATX). The ATX group showed greater body mass index, lower high-density lipoprotein cholesterol level, and the higher prevalence of FH, diabetes, prior myocardial infarction, acute coronary syndrome, multivessel disease, hemodialysis, and prior statin administration. SYNTAX score and the rate of SYNTAX score ≥23 were significantly higher in the ATX group compared with the non-ATX group (p < 0.001 for each). When patients were divided into quartiles according to Achilles tendon thickness, SYNTAX score and the prevalence of SYNTAX score ≥23 were progressively increased in favor of greater Achilles tendon thickness (p < 0.001 for each). Multivariate analysis determined male, diabetes, and ATX as independent predictors for higher SYNTAX score. CONCLUSIONS: In CAD patients undergoing PCI, ATX was independently associated with severity of CAD. Detecting ATX may be useful not only for diagnosing FH, but also for identifying patients with advanced CAD.

Percutaneous Transluminal Septal Myocardial Ablation for Hypertrophic Obstructive Cardiomyopathy Under Extracorporeal Membrane Oxygenation Support.

We report the case of a 70-year-old woman with hypertrophic obstructive cardiomyopathy, who was admitted because of severe heart failure and cardiogenic shock and mechanical support requiring extracorporeal membrane oxygenation. She recovered well by percutaneous transluminal septal myocardial ablation under the extracorporeal membrane oxygenation support and was discharged without complications. (Level of Difficulty: Advanced.).

Increased platelet inhibition after switching from prasugrel to low-dose ticagrelor in Japanese patients with prior myocardial infarction.

BACKGROUND: Ticagrelor and prasugrel are novel and potent P2Y12 inhibitors. Ticagrelor 90mg or 60mg twice daily is known to reduce ischemic events but be associated with an increased risk of bleeding in patients with prior myocardial infarction in Western countries. Although ticagrelor 90mg twice daily was tested in a randomized clinical trial in East Asia, the clinical significance of ticagrelor 60mg twice daily is unclear. This study aimed to evaluate platelet inhibition of low-dose ticagrelor compared to prasugrel in Japanese patients. METHODS: A total of 33 patients with prior myocardial infarction (>3 months) who received aspirin and prasugrel 3.75mg once daily were enrolled. Prasugrel was switched to ticagrelor 60mg twice daily. Platelet inhibition was assessed by VerifyNow assay (Accumetrics, San Diego, CA, USA) at baseline and 14 days after switching to ticagrelor. P2Y12 reaction unit (PRU) ≤95 was defined as low on-treatment platelet reactivity (LPR) and PRU≥262 as high on-treatment platelet reactivity. RESULTS: Ticagrelor treatment resulted in significantly lower PRU [10 (7-39) vs. 143 (102-201), p<0.001] and a higher rate of LPR (94% vs. 24%, p<0.001), compared to prasugrel treatment. Neither patients treated with ticagrelor nor prasugrel had high on-treatment platelet reactivity. During 2-week follow-up on ticagrelor therapy, no major bleeding occurred in both groups, while four minor bleeding events were observed. CONCLUSION: In Japanese patients with prior myocardial infarction, significantly lower PRU and a higher rate of LPR were observed on ticagrelor 60mg twice daily compared to prasugrel 3.75mg once daily.