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Indwelling urethral catheters (IUCs) are used to measure urine volume, keep patients on bed rest, or keep the groin area clean in patients with acute myocardial infarction (AMI). However, the association between IUC use and in-hospital urinary-related complications is unknown.This was a single-center retrospective analysis of 303 patients admitted to our hospital in 2018-2020 who had AMI without cardiogenic shock. An IUC was inserted in the emergency room upon initiation of invasive catheter treatment and removed as soon as possible. The primary outcome was in-hospital adverse urinary event (IHAUE), which consisted of in-hospital urinary tract infection and in-hospital gross hematuria.Of 303 patients, 243 patients (80.2 %) underwent IUC insertion. A lower proportion of patients with IUCs were male (72 % vs. 85 %, p = 0.044). A higher proportion had Killip classification 2 or 3 (13 % vs. 0 %, p = 0.003) or ST-elevation myocardial infarction (65 % vs. 32 %, p 0.001). IHAUEs occurred significantly more commonly in patients with IUCs than without IUCs (11 % vs. 2 %, p = 0.023). Kaplan-Meier analysis showed that IHAUEs occurred more frequently in patients with IUCs than patients without IUCs (log-rank test p = 0.033). Furthermore, IUC use longer than the median of 2 days was associated with a higher odds ratio (OR) for IHAUE when compared with those without IUC use (OR, 3.65; 95 % confidence interval, 1.28-10.4; p = 0.015). There were no significant differences in in-hospital mortality by IUC status.IUC use is associated with a higher risk of IHAUEs in patients with uncomplicated AMI. Routine IUC use might not be recommended.

This study aimed to evaluate the early and intermediate-term outcomes of patients who underwent concomitant off-pump coronary artery bypass grafting (CABG) and transcatheter aortic valve replacement (TAVR).Between January 2014 and June 2021, 49 patients underwent concomitant off-pump CABG and TAVR via median sternotomy (TAVRCAB group) and 143 underwent concomitant on-pump CABG and surgical aortic replacement. Of the 143 patients who underwent on-pump surgery, 80 (SAVRCAB group) were eligible for comparison. The composite event included all-cause death, heart failure rehospitalisation, repeat revascularisation, brain infarction, and repeat aortic valve replacement.The Society of Thoracic Surgeons' predicted risk for mortality and age were higher in the TAVRCAB group than in the SAVRCAB group (7.1% vs 3.1% [p0.001]; 81 years vs 75 years [p0.001], respectively), while the surgical time was shorter (289 min vs 352 min; p0.001). There was no conversion to on-pump surgery in the TAVRCAB group. The postoperative maximum creatinine kinase-MB value was lower in the TAVRCAB group. There was no deep sternal wound infection or repeat revascularisation in either group. Hospital death and brain infarction developed in one patient (1.3%) each in the SAVRCAB group, but in no patients in the TAVRCAB group. The rates of freedom from the composite event were similar between the two groups during the follow-up period.Concomitant off-pump CABG and TAVR would be a less-invasive alternative procedure for treating intermediate or high surgical risk patients with aortic stenosis and coronary artery disease unsuitable for percutaneous coronary intervention.

We present the case of an 82-year-old man whose left coronary ostium became obstructed 15 months after transcatheter aortic valve replacement (TAVR) with a balloon-expandable valve. The patient underwent TAVR for symptomatic severe aortic stenosis with no complications. Fifteen months after the initial TAVR, the patient complained of chest pain while exercising, and the exercise stress myocardial perfusion scintigraphy demonstrated the development of regional myocardial ischemia in the region of the left coronary artery. Coronary angiography implied severe stenosis in the ostium of the left coronary artery. Computed tomography angiography and intravascular ultrasonography indicated a soft tissue component along with stent struts, which was considered to cause delayed coronary obstruction. Our report emphasizes the importance of having a low threshold for clinically suspecting delayed coronary obstruction in patients who have undergone TAVR, even after several years of the procedure. Learning objective Delayed coronary obstruction (DCO) should be suspected in patients presenting with new ischemic symptoms after transcatheter aortic valve replacement (TAVR). DCO may occur even in the case of TAVR with a balloon-expandable prosthetic valve, on antithrombotic regimens, and several years after the initial procedure.

Calcified nodule (CN) is an eruptive calcified mass causing acute coronary syndrome (ACS). Since coronary calcification is associated with an elevated cardiac event's risk, ACS attributable to CN may exhibit worse clinical outcome following percutaneous coronary intervention (PCI).We retrospectively analyzed 657 ACS patients receiving PCI with newer-generation drug-eluting stent (DES) implantation under intravascular ultrasound (IVUS) guidance. CN was defined as (1) protruding calcification with its irregular surface and (2) the presence of calcification at adjacent proximal and distal segments. The primary endpoint was a composite of major adverse cardiac event [MACE = cardiac death + ACS recurrence + target lesion revascularization (TLR)].CN was identified in 5.3% (=35/657) of the study subjects. CN patients were more likely to have coronary risk factors including hypertension (p = 0.005), chronic kidney disease (p 0.001), maintenance hemodialysis (p 0.001) and a history of PCI (p 0.001). During the observational period (median = 1304 days), CN was associated with an increased risk of MACE (HR = 7.68, 95%CI = 4.61-12.80, p 0.001), ACS recurrence (HR = 12.32, 95%CI = 6.05-25.11, p 0.001) and TLR (HR = 10.48, 95%CI = 5.80-18.94, p 0.001). These cardiac risks related to CN were consistently observed by Cox proportional hazards model (MACE: p 0.001, ACS recurrence: p 0.001, TLR: p 0.001) and a propensity score-matched cohort analysis (MACE: p = 0.002, ACS recurrence: p = 0.01, TLR: p = 0.005). Of note, over 80% of TLR at the CN lesion was driven by its re-appearance within the implanted DES.ACS patients attributable to CN have an increased risk of ACS recurrence and TLR, mainly driven by the continuous growth and protrusion of the calcified mass.

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.), Graphical abstract

A 75-year-old man had recurrent in-stent restenosis (ISR) attributable to calcified nodule. Near-infrared spectroscopy (NIRS) showed a gradual decrease in yellow signals during the process of repeated percutaneous coronary intervention for recurrent ISR that eventually halted. The case indicates that NIRS signals may represent lesion instability even in calcified nodule, and may be potentially predictive of recurrent ISR.

Abnormal liver function test results are often observed in acute decompensated heart failure (ADHF). However, the prognostic value of bilirubin fractionation has not been elucidated. The prognostic value of direct bilirubin (DB), in comparison with total bilirubin (TB), was examined in 556 consecutive patients with ADHF. Patients with elevated DB showed mostly similar patient characteristics including signs of elevated right-sided pressure (frequent hepatomegaly, jugular venous distention, dilated inferior vena cava, and elevated gamma-glutamyltransferase) and decreased cardiac output (cold extremities, decreased pulse pressure, and lower blood pressure) and other parameters of heart failure (HF) severity (increased plasma renin activity, decreased sodium, total cholesterol, and ejection fraction) to elevated TB; however, only patients with elevated DB showed a significant difference in the frequency of HF history and alkaline phosphatase value. Kaplan-Meier analysis showed that patients with elevated DB had a significantly higher rate of the composite end point of all-cause mortality or HF readmission (p = 0.021) compared with those with normal DB, whereas patients with elevated TB did not show a statistically significant difference compared with those with normal TB (NS). A multivariate Cox hazards model showed that DB was an independent predictor of adverse events (adjusted hazard ratio 1.052, 95% confidence interval 1.001 to 1.099, p = 0.034), whereas TB was not (adjusted hazard ratio 1.017, 95% confidence interval 0.985 to 1.046, p = 0.27). Adding DB to existing prognostic variables resulted in higher C-statistics than adding TB (C-statistics: 0.670 to 0.675, 0.670 to 0.674, respectively). In conclusion, elevated DB in ADHF was an independent prognostic predictor that was superior to TB. DB may be useful for further risk stratification in ADHF.

The prognostic value of nutritional status is poorly understood and evidence-based nutritional assessment indices are required in acute heart failure (AHF). We investigated the prognostic value of malnutrition assessed by the Controlling Nutritional Status (CONUT) score (range 0-12, higher=worse, consisting of serum albumin, cholesterol and lymphocytes) in AHF patients.The CONUT score was measured on admission in 635 consecutive AHF patients. The primary outcome was all-cause death.Median CONUT score was 3 (interquartile range 2 to 5). During the median follow-up of 324days, CONUT score was independently associated with death (HR 1.26, 95% CI 1.11-1.42, P0.001) after adjustment for confounders in a multivariate Cox model. The CONUT score demonstrated the best C-statistic for predicting death (0.71) among other common nutritional markers in HF. Furthermore, addition of the CONUT score to an established risk prediction model from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure study significantly increased the C-statistic from 0.75 to 0.77 (P=0.02). The net reclassification improvement afforded by CONUT score was 21% for all-cause death, 27% for survival and 49% overall (P0.001).Malnutrition assessed by the CONUT score on admission was an independent determinant of long-term death in AHF, and its prognostic value outweighed that of other nutritional indices. Moreover, addition of the score to the existing risk prediction model significantly increased the predictive ability for death, indicating beneficial clinical application of the CONUT score in AHF patients.

Acute kidney injury (AKI) often occurs in patients with acute myocardial infarction (AMI), and is associated with adverse outcomes. However, it remains unclear how timing of AKI affects it. This study assessed impact of timing of AKI on prognosis after AMI.This study consisted of 760 patients with AMI who were admitted within 48h after symptom onset. AKI was diagnosed as increase in creatinine ≥0.3mg/dl or ≥50% within any 48h after admission. Patients were classified into 3 groups according to the occurrence and timing of AKI: no-AKI, early-AKI (within 48h after admission) and late-AKI (48h). Early-AKI was classified into transient early-AKI, defined as creatinine returning to the level below the criteria of AKI, and persistent early-AKI.Early-AKI occurred in 64 patients (9%) and late-AKI in 32 patients (4%). Patients with early-AKI had significantly higher mortality (35%) than those with late-AKI (7%, p0.001) and no-AKI (3%, p0.001). Multivariate analysis showed early-AKI was an independent predictor of in-hospital mortality (OR: 3.38, 95% CI: 1.30-8.76, p=0.013), but late-AKI was not. Among patients with early-AKI, mortality was significantly higher even if AKI was transient (23%, p0.001). Patients with persistent early-AKI had the highest mortality (66%, p0.001).Early-AKI was associated with worse outcome. Even if renal function once returned to baseline level, patients with early-AKI tended to be at high risk of mortality.

Background Delirium is a serious syndrome in critically ill patients. However, the prognostic impact of delirium and its determinants in acute heart failure (AHF) patients have not been fully elucidated. Methods We examined 611 AHF patients who were admitted to our institution. Delirium was diagnosed based on the Intensive Care Delirium Screening Checklist (ICDSC). Results Delirium developed in 139 patients (23%) during hospitalization. Patients with delirium had higher incidence of non-cardiovascular death (p=0.046) and worsening heart failure (p Conclusion In patients with AHF, the development of delirium was associated with poor clinical outcomes, suggesting the importance of early screening and careful monitoring of delirium in such patients.

Background Coronary high-intensity plaques detected by noncontrast T1-weighted imaging may represent plaque instability. High-intensity plaques can be quantitatively assessed by a plaque-to-myocardium signal-intensity ratio (PMR). Objectives This pilot, hypothesis-generating study sought to investigate whether intensive statin therapy would lower PMR. Methods Prospective serial noncontrast T1-weighted magnetic resonance imaging and computed tomography angiography were performed in 48 patients with coronary artery disease at baseline and after 12 months of intensive pitavastatin treatment with a target low-density lipoprotein cholesterol level Results In the statin group, 12 months of statin therapy significantly improved low-density lipoprotein cholesterol levels (125 to 70 mg/dl; p Conclusions Statin treatment significantly reduced the PMR of high-intensity plaques. Noncontrast T1-weighted magnetic resonance imaging could become a useful technique for repeated quantitative assessment of plaque composition. (Attempts at Plaque Vulnerability Quantification with Magnetic Resonance Imaging Using Noncontrast T1-weighted Technique [AQUAMARINE]; UMIN000003567 )

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, p0.001) and in-hospital mortality (9.8% vs 1.6%, p0.001). 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% confidence interval 1.05 to 1.27, p0.001), 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, p0.001) 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.

An 85-year-old man with chronic kidney disease (estimated glomerular filtration rate 28.9 ml/min/1.73 m2) underwent percutaneous coronary intervention with optical coherence tomographic (OCT) guidance (ILUMIEN OPTIS, Abbott Laboratories, Abbott Park, Illinois) using low–molecular-weight dextran

Although percutaneous coronary intervention (PCI) routinely achieves good angiographic success, 5% to 30% of patients experience periprocedural myocardial injury (pMI), which is associated with long-term adverse outcomes and immediate adverse events [(1)][1]. Because coronary high-intensity

FSTL1 is an extracellular glycoprotein whose functional significance in physiological and pathological processes is incompletely understood. Recently, we have shown that FSTL1 acts as a muscle-derived secreted factor that is up-regulated by Akt activation and ischemic stress and that FSTL1 exerts favorable actions on the heart and vasculature. Here, we sought to identify the receptor that mediates the cellular actions of FSTL1. We identified DIP2A as a novel FSTL1-binding partner from the membrane fraction of endothelial cells. Co-immunoprecipitation assays revealed a direct physical interaction between FSTL1 and DIP2A. DIP2A was present on the cell surface of endothelial cells, and knockdown of DIP2A by small interfering RNA reduced the binding of FSTL1 to cells. In cultured endothelial cells, knockdown of DIP2A by small interfering RNA diminished FSTL1-stimulated survival, migration, and differentiation into network structures and inhibited FSTL1-induced Akt phosphorylation. In cultured cardiac myocytes, ablation of DIP2A reduced the protective actions of FSTL1 on hypoxia/reoxygenation-induced apoptosis and suppressed FSTL1-induced Akt phosphorylation. These data indicate that DIP2A functions as a novel receptor that mediates the cardiovascular protective effects of FSTL1.

To examine the involvement of diacylglycerol kinase (DGK) and phosphatidic acid phosphatase (PAP) in pressure overloaded cardiac hypertrophy, rats were subjected to either ascending aortic banding for 3, 7, and 28 days or sham operation. In comparison with sham-operated rats, the left ventricular (LV) weight of the aortic-banded rats increased progressively. At 28 days after surgery, the expression of DGKepsilon mRNA but not DGKzeta or PAP2b mRNA in the LV myocardium significantly decreased in the aortic-banded rats compared with the sham-operated rats. DGKzeta protein in the LV myocardium translocated from the particulate to the cytosolic compartment in the aortic-banded rats. Furthermore, the myocardial content of 1,2-diacylglycerol and PKCdelta protein expression in the particulate fraction of the LV myocardium significantly increased in aortic-banded rats compared with sham-operated rats. These results suggest that DGKepsilon and DGKzeta play distinct roles in the development of pressure overloaded cardiac hypertrophy and that the two isozymes are differentially regulated.

Proprotein convertase subtilisin/kexin type 9 (PCSK9), an important contributor to low-density lipoprotein metabolism in heterozygous familial hypercholesterolemia (HeFH), exhibits direct proatherogenic effects. PCSK9 circulates as mature and furin-cleaved forms, which differ in its biological activity. However, it remains to be elucidated whether each PCSK9 subtype has different atherogenic properties.To investigate the association of each PCSK9 subtype with coronary atherosclerosis in HeFH.About 204 nonculprit segments in 138 HeFH subjects with coronary artery disease were evaluated by using intravascular ultrasound. Mature, furin-cleaved PCSK9 and total concentration of PCSK9 subtypes were measured by using enzyme-linked immunosorbent assay (BML Inc., Tokyo, Japan). The relationship of these PCSK9 values with intravascular ultrasound measures was investigated.Mature PCSK9 level was positively associated with percent atheroma volume (PAV: r = 0.78, P = .003). Despite extensive atheroma under a higher mature PCSK9 level, vessel volume did not change across any mature PCSK9 levels (r = 0.05, P = .78). These responses resulted in smaller lumen volume, which was negatively correlated to mature PCSK9 level (r = 0.65, P = .009). By contrast, there were no significant relationships of PAV with furin-cleaved (r = 0.12, P = .45) and total PCSK9 (r = 0.37, P = .25) levels. On multivariate analysis, mature PCSK9 level independently contributed to PAV (odds ratio: 1.45, 95% confidence interval: 1.11-1.67, P = .01). Even in subjects with low-density lipoprotein cholesterol level2.6 mmol/L, greater PAV was still observed in association with an elevated mature PCSK9 level (P = .003).Mature PCSK9 associated with atheroma volume and impaired vessel remodeling in HeFH patients with coronary artery disease. These findings suggest the potential role of mature PCSK9 in propagation of coronary atherosclerosis in HeFH.

Background Dendritic cells ( DC ) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted heart and its immunoprotective roles in the post‐infarction healing process after experimental myocardial infarction ( MI ). However, its clinical significance has not been determined. Methods and Results The degree of DC infiltration and its correlation with the post‐infarction healing process in the human infarcted heart were investigated in 24 autopsy subjects after ST ‐elevation MI . Patients were divided into two groups according to the presence (n=13) or absence (n=11) of cardiac rupture. The numbers of infiltrated DC and macrophages and the extent of fibrosis in the infarcted area were examined. In the rupture group, CD 68 + macrophage infiltration was increased and CD 209 + DC , and CD 11c + DC infiltration and the extent of reparative fibrosis were decreased compared with the non‐rupture group, under matched baseline characteristics including the time from onset to death and use of revascularization. Furthermore, there was a significant positive correlation between the number of infiltrating CD 209 + DC , and CD 11c + DC and the extent of reparative fibrosis. Conclusions Decreased number of DC in human‐infarcted myocardial tissue was associated with increased macrophage infiltration, impaired reparative fibrosis, and the development of cardiac rupture after MI . These findings suggest a protective role of DC in post‐ MI inflammation and the subsequent healing process.

Acute kidney injury (AKI) often occurs during early after acute myocardial infarction (AMI) and is associated with unfavorable outcomes. Acute hyperglycemia deteriorates myocardial damage. However, impact of acute hyperglycemia on the development of AKI after AMI remains unclear. This study