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Background The role of cyclic guanosine 3′,5′-monophosphate (cGMP) after acute myocardial infarction (AMI) is not well understood despite its significance as a second messenger of natriuretic peptides (NPs) in cardiovascular disease. We investigated the association between the NP-cGMP cascade and left ventricular reverse remodelling (LVRR) in anterior AMI.Methods 67 patients with their first anterior AMI (median age, 64 years; male, 76%) underwent prospective evaluation of plasma concentrations of the molecular forms of A-type and B-type natriuretic peptide (BNP) and cGMP from immediately after primary percutaneous coronary intervention (PPCI) to 10 months post-AMI. The estimated mature BNP (emBNP) concentration was calculated as the difference between total BNP and prohormone of BNP (proBNP) concentrations. Patients were divided into LVRR and non-LVRR groups on the basis of residuals between observed change in left ventricular end-systolic volume index on MR during the first 11 months after AMI and change adjusted for proBNP concentration immediately post-PPCI, which was calculated with regression. The LVRR group (n=33) had residuals below the median; the non-LVRR group (n=34) had residuals at or above the median.Results The LVRR group had higher freedom from major adverse cardiac and cerebrovascular events (MACCEs) than the non-LVRR group during a median follow-up of 9.9 years (p=0.008). The presence of LVRR (HR 0.256; 95% CI 0.081 to 0.809; p=0.028) and peak creatine phosphokinase–myocardial band level (per 100 IU/L) (HR 1.22; 95% CI 1.02 to 1.46; p=0.027) were independent predictors of MACCE after adjusting for age, male sex, infarct size and hypertension. Multivariable analyses identified logarithmic proBNP and emBNP concentrations from 12 hours to 5 days post-AMI and logarithmic cGMP concentration from immediately post-PPCI to 3 days post-AMI as independent predictors of LVRR (p

Abstract Aims The incidence and prognosis of symptomatic heart failure following acute myocardial infarction (AMI) in the primary percutaneous coronary intervention era have rarely been reported in the literature. This study aimed to (i) determine the incidence of heart failure admission among AMI survivors, (ii) compare 1 year outcomes between patients with heart failure admission and those without, and (iii) identify the independent risk factors associated with heart failure admission. Methods and results The Japan Acute Myocardial Infarction Registry is a prospective multicentre registry from which data on consecutively enrolled patients with AMI from 50 institutions between 2015 and 2017 were obtained. Among the 3411 patients enrolled, 3226 who survived until discharge were included in this study. The primary endpoint was all‐cause mortality. The secondary endpoints were major adverse cardiovascular events (defined as cardiovascular mortality, non‐fatal myocardial infarction, or non‐fatal cerebral infarction) and major bleeding events corresponding to Bleeding Academic Research Consortium Type 3 or 5. Clinical outcomes were compared between the patients who were and were not admitted for heart failure. Over a median follow‐up of 12 months, 124 patients (3.8%) were admitted due to heart failure. Independent risk factors for heart failure admission included older age, female sex, Killip class ≥2 on admission, left ventricular ejection fraction

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.

Abstract Aims The relationship between diabetic microvascular complications and the incidence of two types of heart failure—heart failure with reduced ejection fraction (HFrEF) (left ventricular ejection fraction [LVEF]

Abstract Background Although screening for coronary artery disease (CAD) using computed tomography coronary angiography in patients with stable chest pain has been reported to be beneficial, patients with chronic kidney disease (CKD) might have limited benefit due to complications of contrast agent nephropathy and decreased diagnostic accuracy as a result of coronary artery calcifications. Cardiac magnetic resonance (CMR) has emerged as a novel imaging modality for detecting coronary stenosis and high-risk coronary plaques without contrast media that is not affected by coronary artery calcification. However, the clinical use of this technology has not been robustly evaluated. Methods AQUAMARINE-CKD is an open parallel-group prospective multicenter randomized controlled trial of 524 patients with CKD at high risk for CAD estimated based on risk factor categories for a Japanese urban population (Suita score) recruited from 6 institutions. Participants will be randomized 1:1 to receive a CMR examination that includes non-contrast T1-weighted imaging and coronary magnetic angiography (CMR group) or standard examinations that include stress myocardial scintigraphy (control group). Randomization will be conducted using a web-based system. The primary outcome is a composite of cardiovascular events at 1 year after study examinations: all-cause death, death from CAD, nonfatal myocardial infarction, nonfatal ischemic stroke, and ischemia-driven unplanned coronary intervention (percutaneous coronary intervention or coronary bypass surgery). Discussion If the combination of T1-weighted imaging and coronary magnetic angiography contributes to the risk assessment of CAD in patients with CKD, this study will have major clinical implications for the management of patients with CKD at high risk for CAD. Trial registration Japan Registry of Clinical Trials (jRCT) 1,052,210,075. Registered on September 10, 2021.

Background Acute myocardial infarction (AMI) infrequently occurs after acute stroke. The Heart‐brain team approach has a potential to appropriately manage this poststroke cardiovascular complication. However, clinical outcomes of AMI complicating acute stroke (AMI‐CAS) with the heart‐brain team approach have not been characterized. The current study investigated cardiovascular outcomes in patients with AMI‐CAS managed by a heart‐brain team. Methods and Results We retrospectively analyzed 2390 patients with AMI at our institute (January 1, 2007–September 30, 2020). AMI‐CAS was defined as the occurrence of AMI within 14 days after acute stroke. Major adverse cerebral/cardiovascular events (cardiac‐cause death, nonfatal myocardial infarction, and nonfatal stroke) and major bleeding events were compared in subjects with AMI‐CAS and those without acute stroke. AMI‐CAS was identified in 1.6% of the subjects. Most AMI‐CASs (37/39=94.9%) presented ischemic stroke. Median duration of AMI from the onset of acute stroke was 2 days. Patients with AMI‐CAS less frequently received primary percutaneous coronary intervention (43.6% versus 84.7%; P

Abstract Aims Percutaneous veno‐arterial extracorporeal membrane oxygenation (VA‐ECMO) is utilized for patients with cardiogenic shock or cardiac arrest. However, the procedure protocol for weaning from VA‐ECMO has not been well established. The present study aimed to determine the usefulness of echocardiographic and pulmonary artery catheter parameters for predicting successful weaning from VA‐ECMO in patients with refractory cardiogenic shock. Methods and results We retrospectively studied 50 patients who were hospitalized and supported by VA‐ECMO for >48 h between January 2013 and March 2017. Patients successfully weaned from VA‐ECMO without reintroduction of VA‐ECMO or left ventricular assist device implantation were defined as 30 day survivors. Echocardiographic and pulmonary artery catheter parameters were evaluated when ECMO flow was limited to a maximum of 1.5–2.0 L/min. Twenty‐four patients were successfully weaned from VA‐ECMO, whereas 26 were not. Fractional shortening, corrected left ventricular ejection time (LVETc, defined as LVET divided by the square root of heart rate), left ventricular outflow tract velocity time integral, and LVETc divided by pulmonary artery wedge pressure (PAWP) were significantly larger in the 30 day survivor groups. Multivariable analysis revealed LVETc∕PAWP as a significant independent predictor of successful weaning (LVETc∕PAWP, odds ratio 0.82, 95% confidence interval 0.71–0.94, P = 0.005). Receiver operating characteristic curve analysis revealed 15.9 as the optimal LVETc∕PAWP for predicting successful weaning (area under the curve 0.82). Conclusions The present findings indicate that LVETc∕PAWP is a potential predictor of successful weaning from VA‐ECMO.

A 75-year-old female patient on hemodialysis presented with non–ST-segment elevation myocardial infarction. After successful primary percutaneous coronary intervention, in-stent restenosis (ISR) occurred 3 consecutive times. Intravascular imaging assessment during the repeated percutaneous coronary intervention indicated that the ISR was not associated with neointimal hyperplasia but was mainly attributed to a calcified nodule, which protruded into the lumen. We applied excimer laser catheter ablation to avoid another ISR. (Level of Difficulty: Intermediate.)

Abstract Pulmonary tumor thrombotic microangiopathy (PTTM) is a rapidly progressive subtype of pulmonary hypertension (PH) associated with impaired right ventricular adaptation and very poor prognosis in cancer, and its rapid progression makes antemortem diagnosis and treatment extremely difficult. We describe the case of a 35‐year‐old woman who developed severe PH with subsequent circulatory collapse. The patient was clinically diagnosed with PTTM induced by lung adenocarcinoma harboring the c‐ros oncogene 1 (ROS1) rearrangement within 1–2 weeks, while hemodynamics were stabilized by rescue venoarterial extracorporeal membrane oxygenation support. Crizotinib, an oral tyrosine kinase inhibitor targeting anaplastic lymphoma kinase, MET, and ROS1 kinase domains dramatically resolved PH, resulting in more than 3 years of survival. Targeted gene‐tailored therapy with mechanical support can improve survival in PTTM.

OBJECTIVES:. To determine the characteristics of thyroid storm patients with acute decompensated heart failure who should be candidates for temporary percutaneous mechanical circulatory support in addition to beta-blocker treatment to prevent cardiogenic shock. DESIGN:. A single-center, retrospective review of treatment details and data collected from electronic medical records. SETTING:. Thyrotoxicosis complicated with acute decompensated heart failure. PATIENTS:. Eight consecutive patients who were admitted to our hospital for acute decompensated heart failure with thyroid storm between December 2011 and August 2020 were retrospectively reviewed. Of the eight patients, four were treated with percutaneous mechanical circulatory support. INTERVENTIONS:. None. MEASUREMENTS AND MAIN RESULTS:. Compared with thyroid storm patients who did not require percutaneous mechanical circulatory support, those who did had a significantly higher initial plasma brain natriuretic peptide level (1,231 [911–3,387] vs 447 pg/mL [243–653 pg/mL], respectively; p = 0.015), as well as a significantly larger left ventricular end-diastolic diameter (56 [54–63] vs 48 mm [38–48 mm], respectively; p = 0.029) and end-systolic diameter (50 [49–58] vs 28 mm [28–30 mm], respectively; p = 0.029) on echocardiogram. In terms of thyroid storm severity, the Burch-Wartofsky score was higher in patients with percutaneous mechanical circulatory support than in those without, although the difference was not significant. All patients survived this index admission. CONCLUSIONS:. In thyroid storm patients, the presence of a high brain natriuretic peptide level, “left ventricular dilatation,” or both may necessitate hemodynamic assessment to determine the indication of percutaneous mechanical circulatory support before beta-blocker administration.

In the original publication of this article [1] the wording of ‘3Di-PMR’ was different between the text and figures.

Abstract Background Periprocedural myocardial injury (pMI) is a common complication of elective percutaneous coronary intervention (PCI) that reduces some of the beneficial effects of coronary revascularization and impacts the risk of cardiovascular events. We developed a 3-dimensional volumetric cardiovascular magnetic resonance (CMR) method to evaluate coronary high intensity plaques and investigated their association with pMI after elective PCI. Methods Between October 2012 and October 2016, 141 patients with stable coronary artery disease underwent T1-weighted CMR imaging before PCI. A conventional 2-dimensional CMR plaque-to-myocardial signal intensity ratio (2D-PMR) and the newly developed 3-dimensional integral of PMR (3Di-PMR) were measured. 3Di-PMR was determined as the sum of PMRs above a threshold of > 1.0 for voxels in a target plaque. pMI was defined as high-sensitivity cardiac troponin T > 0.07 ng/mL. Results pMI following PCI was observed in 46 patients (33%). 3Di-PMR was significantly higher in patients with pMI than those without pMI. The optimal 3Di-PMR cutoff value for predicting pMI was 51 PMR*mm3 and the area under the receiver operating characteristic curve (0.753) was significantly greater than that for 2D-PMR (0.683, P = 0.015). 3Di-PMR was positively correlated with lipid volume (r = 0.449, P

Background Statin‐mediated efficacy of lowering low‐density lipoprotein (LDL) cholesterol varies in each individual, and its diminished response is associated with worse outcomes. However, there is no established approach to predict hyporesponse to statins. PCSK9 (proprotein convertase subxilisin/kexin type 9) is a serine‐protease associated with LDL metabolism, which circulates as mature and furin‐cleaved PCSK9. Since mature PCSK9 more potently degrades the LDL receptor, its evaluation may enable the identification of statin hyporesponders. Methods and Results We analyzed 101 statin‐naive patients with coronary artery disease who commenced a statin. PCSK9 subtypes at baseline and 1 month after statin use were measured by ELISA. Hyporesponse to statins was defined as a percent reduction in LDL cholesterol 228 ng/mL is associated with hyporesponse to statins. This finding suggests that mature PCSK9 might be a potential determinant of hyporesponse to statins.

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

Abstract Background Despite the success of HMG-CoA reductase inhibitor (statin) therapy in reducing atherosclerotic cardiovascular events, a residual risk for cardiovascular events in patients with coronary artery disease (CAD) remains. Long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFAs), especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are promising anti-atherosclerosis agents that might reduce the residual CAD risk. Non-contrast T1-weighted imaging (T1WI) with cardiac magnetic resonance (CMR) less invasively identifies high-risk coronary plaques as high-intensity signals. These high-intensity plaques (HIPs) are quantitatively assessed using the plaque-to-myocardium signal intensity ratio (PMR). Our goal is to assess the effect of EPA/DHA on coronary HIPs detected with T1WI in patients with CAD on statin treatment. Methods/design This prospective, controlled, randomized, open-label study examines the effect of 12 months of EPA/DHA therapy and statin treatment on PMR of HIPs detected with CMR and computed tomography angiography (CTA) in patients with CAD. The primary endpoint is the change in PMR after EPA/DHA treatment. Secondary endpoints include changes in Hounsfield units, plaque volume, vessel area, and plaque area measured using CTA. Subjects are randomly assigned to either of three groups: the 2 g/day EPA/DHA group, the 4 g/day EPA/DHA group, or the no-treatment group. Discussion This trial will help assess whether EPA/DHA has an anti-atherosclerotic effect using PMR of HIPs detected by CMR. The trial outcomes will provide novel insights into the effect of EPA/DHA on high-risk coronary plaques and may provide new strategies for lowering the residual risk in patients with CAD on statin therapy. Trial registration The University Hospital Medical Information Network (UMIN) Clinical Trials Registry, ID: UMIN000015316 . Registered on 2 October 2014.

A 76-year-old man who had been diagnosed with long-QT syndrome type 2 had frequent syncopal attacks. The electrocardiogram was monitored, and frequent torsades de pointes (TdP) was detected despite administration of conventional medications: oral propranolol, verapamil, intravenous magnesium sulfate, verapamil, and lidocaine. In contrast, 2 μg/kg/min landiolol could completely suppress TdP. Subsequently, an implantable cardioverter defibrillator was placed, and he was diagnosed with silent myocardial ischemia using myocardial perfusion scintigraphy and coronary angiography. This is the first case report wherein landiolol effectively suppressed TdP due to long-QT syndrome with silent myocardial ischemia.

Abstract Follistatin‐like 1 (Fstl1) is a secreted protein that is acutely induced in heart following myocardial infarction (MI). In this study, we investigated cell type‐specific regulation of Fstl1 and its function in a murine model of MI. Fstl1 was robustly expressed in fibroblasts and myofibroblasts in the infarcted area compared to cardiac myocytes. The conditional ablation of Fstl1 in S100a4‐expressing fibroblast lineage cells (Fstl1‐cfKO mice) led to a reduction in injury‐induced Fstl1 expression and increased mortality due to cardiac rupture during the acute phase. Cardiac rupture was associated with a diminished number of myofibroblasts and decreased expression of extracellular matrix proteins. The infarcts of Fstl1‐cfKO mice displayed weaker birefringence, indicative of thin and loosely packed collagen. Mechanistically, the migratory and proliferative capabilities of cardiac fibroblasts were attenuated by endogenous Fstl1 ablation. The activation of cardiac fibroblasts by Fstl1 was mediated by ERK1/2 but not Smad2/3 signaling. This study reveals that Fstl1 is essential for the acute repair of the infarcted myocardium and that stimulation of early fibroblast activation is a novel function of Fstl1.

BACKGROUND:High-sensitive cardiac troponin T (hsTnT) is a sensitive biomarker of myocardial damage and predictor of acute decompensated heart failure (ADHF). However, there is little information on changes over time in hsTnT level during ADHF management. The aim of this prospective study was to evaluate changes in hsTnT levels between admission and at discharge in patients with ADHF, and identify factors that determine such levels and their prognostic significance. METHODS AND RESULTS:We evaluated 404 ADHF patients with abnormal hsTnT levels (≥0.0135 ng/ml) on admission. The median (interquartile ranges) hsTnT levels on admission, at discharge, and percent changes in hsTnT levels were 0.038 (0.026 to 0.065), 0.032 (0.021 to 0.049) ng/ml, and -12.0 (-39.8 to 7.4) % respectively. The numbers of patients with falling (hsTnT decrease > -15%), stable (hsTnT change between -15 and +15%) and rising (hsTnT increase > +15%) hsTnT level at discharge were 190, 146, and 68, respectively. The percent change in B-type natriuretic peptide (BNP) levels was greater in the falling group, compared to the stable (p

BackgroundThe histological diagnosis of cardiac sarcoidosis (CS) is based on the presence of myocardial granulomas; however, the sensitivity of endomyocardial biopsy is relatively low. We investigated whether immunocompetent cells including dendritic cells (DC) and macrophages in nongranuloma sections of endomyocardial biopsy samples could be histopathological surrogates for CS diagnosis. Methods and ResultsThe numbers of DC and macrophages were investigated in 95 consecutive CS patients and 50 patients with nonischemic cardiomyopathy as controls. All patients underwent endomyocardial biopsy, and immunohistochemical staining was performed on all samples. We examined these immunocompetent cells in nongranuloma sections in CS patients diagnosed by the presence of myocardial granulomas (n=26) and in CS patients without myocardial granulomas diagnosed by the Japanese Ministry of Health Welfare 2007 criteria (n=65) or the Heart Rhythm Society 2014 criteria (n=26). In CS patients with and without myocardial granulomas, CD209+ DC and CD68+ macrophages were more frequently observed (P

Circulating polyunsaturated fatty acid (PUFA) levels are associated with clinical outcomes in cardiovascular diseases including coronary artery disease and chronic heart failure (HF). However, their clinical implications in acute decompensated HF (ADHF) remain unclear. The aim of this study was to investigate the clinical roles of circulating PUFAs in patients with ADHF.Circulating levels of PUFAs, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), arachidonic acid (AA) and dihomo-gamma linoleic acid (DGLA), were measured on admission in 685 consecutive ADHF patients. Adverse events were defined as all-cause death and worsening HF.During a median follow-up period of 560 days, 262 (38.2%) patients had adverse events. Although patients with adverse events had lower n-6 PUFA (AA + DGLA) level than those without, n-3 PUFA (EPA + DHA) level was comparable between the groups. Kaplan-Meier analyses showed that lower n-6 PUFA level on admission was significantly associated with the composite of all-cause death and worsening HF, all-cause death, cardiovascular death and worsening HF (p < 0.001, p = 0.005, p = 0.021, p = 0.019, respectively). In a multivariate Cox model, lower n-6 PUFA level was independently associated with increased risk of adverse events (HR 0.996, 95% CI: 0.993-0.999, p = 0.027).Lower n-6 but not n-3 PUFA level on admission was significantly related to worse clinical outcomes in ADHF patients. Measurement of circulating n-6 PUFA levels on admission might provide information for identifying high risk ADHF patients.

BACKGROUND: Cardiovascular events still occur at intermediate stenosis with fractional flow reserve (FFR) ≥0.81, underscoring the additional measure to evaluate this residual risk. A reduction in distal coronary artery pressure/aortic pressure (Pd/ Pa) from baseline to hyperemia (ie, change in Pd/Pa) reflects lipidic burden within vessel walls. We hypothesized that this physiological measure might stratify the risk of future cardiac events at deferrable lesions. METHODS: Lesion- (899 intermediate lesions) and patient-based (899 deferred patients) analyses in those with FFR ≥0.81 were conducted to investigate the association between change in Pd/Pa and target lesion failure (TLF) and major adverse cardiac events at 7 years, respectively. RESULTS: The occurrence of TLF and major adverse cardiac events was 6.7% and 13.4%, respectively. The incidence of target lesion--related nonfatal myocardial infarction was 0.6%. Lesions with TLF had a greater change in Pd/Pa (0.11±0.03 versus 0.09±0.04; P=0.002), larger diameter stenosis (51.0±9.2% versus 46.4±12.4%; P=0.048), and smaller FFR (0.84 [0.82--0.87] versus 0.86 [0.83--0.90]; P=0.02). Change in Pd/Pa (per 0.01 increase) predicted TLF (odds ratio, 1.16 [95% CI, 1.05--1.28]; P=0.002) and major adverse cardiac event (odds ratio, 1.08 [95% CI, 1.01--1.16]; P=0.03). Lesions with change in Pd/Pa ≥0.10 had 2.94- and 1.85-fold greater likelihood of TLF (95% CI, 1.30--6.69; P=0.01) and major adverse cardiac event (95% CI, 1.08--3.17; P=0.03), respectively. Lesions with FFR ≤0.85 had a substantially higher likelihood of TLF when there is a change in Pd/Pa ≥0.10 (12.4% versus 2.9%; hazard ratio, 3.60 [95% CI, 1.01--12.80]; P=0.04). However, change in Pd/Pa did not affect TLF risk in lesions with FFR ≥0.86 (3.8% versus 3.7%; hazard ratio, 0.56 [95% CI, 0.06--5.62]; P=0.62). CONCLUSIONS: Despite deferrable FFR values, lesions and patients with a change in Pd/Pa ≥0.10 had higher cardiovascular risk. Change in Pd/Pa might help stratify lesion- and patient-level risks of future cardiac events in those with FFR ≥0.81. GRAPHIC ABSTRACT: A graphic abstract is available for this article. [ABSTRACT FROM AUTHOR]

Aims: The prognostic impact of chronic total coronary occlusion (CTO) on implantable cardioverter-defibrillator (ICD) recipients remains unclear.Methods and Results: Eighty-four consecutive patients with ischaemic heart disease who received ICD therapy for primary or secondary prevention were analysed. We investigated all-cause mortality and major adverse cardiac events (MACEs) including cardiac death, appropriate device therapy, hospitalization for heart failure, and ventricular assist device implantation. Of the study patients (mean age 70 ± 8 years; 86% men), 34 (40%) had CTO. There were no significant differences in age, left ventricular ejection fraction (LVEF), New York Heart Association functional class III or IV status, and proportion who underwent secondary prevention between patients with CTO (CTO group) and without CTO (non-CTO group). During a median follow-up of 3.8 years (interquartile range 2.7-5.4 years), the CTO group tended to have a higher MACE rate (log-rank P = 0.054) than the non-CTO group. Within the CTO group, there was no difference in the MACE rate between patients with and without viable myocardium. In patients with ICD for secondary prevention (n = 47), 16 patients (34%) with CTO had a higher MACE rate than patients without CTO (log-rank P < 0.01). Cox proportional hazards regression analysis showed that the presence of CTO, but not LVEF, was associated with a higher MACE rate. Multivariate analysis showed that the presence of CTO was a predictor of MACE (P < 0.05).Conclusion: In patients with ischaemic heart disease receiving ICD implantation, the presence of CTO has an adverse impact on long-term prognosis, especially as secondary prevention. [ABSTRACT FROM AUTHOR]

Background--The efficacy and prognosis of percutaneous coronary intervention (PCI) as secondary revascularization in patients with previous coronary artery bypass graft surgery remain uncertain. Methods and Results--We retrospectively evaluated 434 consecutive patients with previous coronary artery bypass graft surgery hospitalized for PCI between 2004 and 2011 (men 84%, age 71 (interquartile range, 66-76) years) and calculated the coronary artery bypass graft Synergy Between Percutaneous Coronary Intervention With Taxus score (CSS) before (baseline CSS) and after PCI (post-PCI CSS). Patients were divided into 2 groups based on median post-PCI CSS: low-score (≤23; n=217) and high-score groups (>23; n=217). Major adverse cardiovascular events (MACE) were defined as the composite of cardiovascular death, myocardial infarction, and unplanned repeat revascularization for myocardial ischemia. The median baseline and post-PCI CSS were 30 (interquartile range, 21-40) and 23 (interquartile range, 14.5-33.5), respectively. During a median follow-up of 69 months, the prevalence of MACE and cardiac death differed significantly between the 2 post-PCI CSS groups (MACE: low, 13.8%; high, 28.6%; P<0.001; cardiac death: low, 6.2%; high, 16.7%; P=0.002). In multivariable analysis, the high post-PCI CSS divided by the median was associated with substantially greater cumulative MACE (hazard ratio, 2.09; 95% confidence interval, 1.31-3.34; P=0.002) and cardiac death (hazard ratio, 2.02; 95% confidence interval, 1.03-3.98; P=0.042) compared with the low post-PCI CSS. Net reclassification improvement analysis revealed that post-PCI CSS resulted in significantly improved prediction of MACE and cardiac death compared with baseline CSS. Conclusions--In this external validation study, the CSS was a potential prognostic factor after subsequent PCI, even for previous coronary artery bypass graft surgery patients. [ABSTRACT FROM AUTHOR]

Aims: Although previous reports suggest that an elevated endogenous erythropoietin (EPO) level is associated with worse clinical outcomes in chronic heart failure (HF) patients, the prognostic implication of EPO in patients with acute decompensated HF (ADHF) and underlying mechanisms of the high EPO level in severe HF patients who have a poor prognosis remain unclear. Methods and results: We examined 539 consecutive ADHF patients with EPO measurement on admission from our registry. During a median follow-up period of 329 days, a higher EPO level on admission was independently associated with worse clinical outcomes [hazard ratio (HR) 1.25, 95% confidence interval (CI) 1.06-1.48, P = 0.008], and haemoglobin level was the strongest determinant of EPO level (P < 0.001), whereas estimated glomerular filtration rate (eGFR) was not significant in multivariate regression analysis. In the anaemic subgroup of 318 patients, a higher EPO level than expected on the basis of their haemoglobin level was related to increased adverse events (HR 1.63, 95% CI 1.05-2.49, P = 0.028). Moreover, estimated plasma volume excess rate was positively associated with EPO level (P = 0.003), and anaemic patients with a higher than expected EPO level tended to have a higher estimated plasma volume excess rate and plasma lactate level, and lower systemic oxygen saturation level with the preservation of the reticulocyte production index than those with a lower than expected EPO level. Conclusion: A high EPO level predicts long-term worse clinical outcomes in ADHF patients, independent of anaemia and impaired renal function. Anaemia and hypoxia due to severe congestion may synergistically contribute to a high EPO level in high-risk HF patients. [ABSTRACT FROM AUTHOR]

This study was undertaken to assess the impact of acute hyperglycemia (acute-HG) and chronic hyperglycemia (chronic-HG) on short-term outcomes in patients with acute myocardial infarction (AMI). This study consisted of 696 patients with AMI. Acute-HG was defined as admission plasma glucose ≥200 mg/dl and chronic-HG as hemoglobin A1c ≥6.5%. Acute-HG was associated with higher peak serum creatine kinase (4,094 ± 4,594 vs 2,526 ± 2,227 IU/L, p <0.001) and in-hospital mortality (9.8% vs 1.6%, p <0.001). On the contrary, there was no significant difference in peak creatine kinase (2,803 ± 2,661 vs 2,940 ± 3,181 IU/L, p = 0.59) and mortality (3.3 vs 3.7%, p = 0.79) between patients with chronic-HG and those without. Multivariate analysis showed that admission plasma glucose was an independent predictor of in-hospital mortality (odds ratio 1.15, 95% con-fidence interval 1.05 to 1.27, p <0.001), but hemoglobin A1c was not. When only patients with acute-HG were analyzed, chronic-HG was associated with a significantly smaller infarct size (3,221 ± 3,001 vs 5,904 ± 6,473 IU/L, p <0.001) and lower in-hospital mortality (5.5 vs 18.9%, p = 0.01). In conclusion, these results suggested that acute-HG, but not chronic-HG, was associated with adverse short-term outcomes after AMI. Paradoxically, in patients with acute-HG, chronic-HG might abate the adverse effects of acute-HG. [ABSTRACT FROM AUTHOR]