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Background A delayed and recurrent complete atrioventricular block (CAVB) is a life‐threatening complication of transcatheter aortic valve replacement (TAVR). Post‐TAVR evaluation may be important in predicting delayed and recurrent CAVB requiring permanent pacemaker implantation (PPI). The impact of new‐onset right bundle‐branch block (RBBB) after TAVR on PPI remains unknown. Methods and Results In total, 407 patients with aortic stenosis who underwent TAVR were included in this analysis. Intraprocedural CAVB was defined as CAVB that occurred during TAVR. A 12‐lead ECG was evaluated at baseline, immediately after TAVR, on postoperative days 1 and 5, and according to the need to identify new‐onset bundle‐branch block (BBB) and CAVB after TAVR. Forty patients (9.8%) required PPI, 17 patients (4.2%) had persistent intraprocedural CAVB, and 23 (5.7%) had delayed or recurrent CAVB after TAVR. The rates of no new‐onset BBB, new‐onset left BBB, and new‐onset RBBB were 65.1%, 26.8%, and 4.7%, respectively. Compared with patients without new‐onset BBB and those with new‐onset left BBB, the rate of PPI was higher in patients with new‐onset RBBB (3.4% versus 5.6% versus 44.4%, P

Abstract Background This study aimed to investigate the effect of glycemic variability (GV), determined using a continuous glucose monitoring system (CGMS), on left ventricular reverse remodeling (LVRR) after ST-segment elevation myocardial infarction (STEMI). Methods A total of 201 consecutive patients with STEMI who underwent reperfusion therapy within 12 h of onset were enrolled. GV was measured using a CGMS and determined as the mean amplitude of glycemic excursion (MAGE). Left ventricular volumetric parameters were measured using cardiac magnetic resonance imaging (CMRI). LVRR was defined as an absolute decrease in the LV end-systolic volume index of > 10% from 1 week to 7 months after admission. Associations were also examined between GV and LVRR and between LVRR and the incidence of major adverse cardiovascular events (MACE; cardiovascular death, acute coronary syndrome recurrence, non-fatal stroke, and heart failure hospitalization). Results The prevalence of LVRR was 28% (n = 57). The MAGE was independent predictor of LVRR (odds ratio [OR] 0.98, p = 0.002). Twenty patients experienced MACE during the follow-up period (median, 65 months). The incidence of MACE was lower in patients with LVRR than in those without (2% vs. 13%, p = 0.016). Conclusion Low GV, determined using a CGMS, was significantly associated with LVRR, which might lead to a good prognosis. Further studies are needed to validate the importance of GV in LVRR in patients with STEMI.

Background Contradictions between management modalities of type A acute aortic dissection (TAAAD) and ST‐elevation–myocardial infarction (STEMI) may result in clinical catastrophe. Therefore, we aimed to explore which 2‐dimensional echocardiography (2DE) findings are optimal for differentiating TAAAD from STEMI. Methods and Results This study included 340 patients with STEMI and 340 patients with TAAAD who underwent 2DE in the emergency department between 2012 and 2021. The proximal ascending aorta (PAA) diameter and other echocardiographic parameters were analyzed. PAA diameters were measured at 4 levels in the parasternal view: Valsalva, the sinotubular junction (STJ), the PAA at 1 cm above the STJ, and the PAA at 2 cm above the STJ. Receiver‐operating characteristic curve analysis showed that Valsalva, STJ, PAA at 1 cm above the STJ, and PAA at 2 cm above the STJ were significant predictors of TAAAD (areas under the curve: 0.777, 0.924, 0.965, and 0.975, respectively; P

Abstract Aims Reduced skeletal muscle mass is a major component of sarcopenia, associated with impaired exercise capacity and poor prognosis in patients with heart failure (HF). Measurement of skeletal muscle mass by dual‐energy X‐ray absorptiometry may be affected by fluid retention, typically in the patients' lower extremities. The aim of the present study was to elucidate the association between upper and lower extremity skeletal muscle mass (USM and LSM) and all‐cause mortality in hospitalized patients with HF, after discharge. Methods This was a single‐centre observational cohort study of 418 patients (59% were men) admitted with a diagnosis of HF (71 ± 13 years), with a left ventricular ejection fraction of 39 ± 16%. USM and LSM were measured by dual‐energy X‐ray absorptiometry with patients in a stable state after decongestion therapy. Results The USM and LSM were 5.29 ± 1.18 and 13.78 ± 3.20 kg for men and 3.37 ± 0.68 and 9.19 ± 1.80 kg for women. A positive correlation was obtained between USM and LSM with mid‐upper arm circumference (r = 0.684, P

Abstract Background Cachexia, characterized by loss of muscle with or without loss of fat mass, is a poor prognostic factor in patients with heart failure (HF). However, there is limited investigation on the prognostic impact of muscle and fat mass separately in HF. We hypothesized that muscle and fat mass have different effects on the prognosis of HF. Methods This was an observational cohort study of 418 patients (59% were men) admitted with a diagnosis of HF (71 ± 13 years [mean ± standard deviation]), with left ventricular ejection fraction (LVEF) of 39 ± 16%, including 31.3%, 14.8%, and 53.8% of patients with preserved LVEF (LVEF ≥ 50%), mid‐range LVEF (40–50%), and reduced (

Background: The role of left ventricular (LV) mechanical dispersion estimated after an ST elevation acute myocardial infarction (STEMI) remains unclear. Methods: The study participants were 208 consecutive patients (152 men, age = 72 years) presenting with STEMI for the first time who underwent primary percutaneous coronary intervention (PCI) within 12 h of STEMI onset. Within 48 h of PCI (mean = 24 h), 2D and 3D speckle-tracking echocardiography were performed. The global longitudinal strain (GLS) was calculated using 3D (3D-GLS) and 2D (2D-GLS) speckle tracking. Mechanical dispersion was defined using the standard deviation (SD) of the time to regional peak longitudinal strain (LS) for all 16 segments for both 2D-STE and 3D-STE (2D-LS-SD, 3D-LS-SD). Infarct size was estimated by Tc99m-sestamibi as the total area of 56.7 ms was a significant predictor of MACEs (hazard ratio = 1.991, 95% confidence interval 1.033–3.613, p = 0.03), but 2D-LS-SD > 58.1 ms was not an independent predictor of MACEs (hazard ratio = 1.577, 95% confidence interval 0.815–3.042, p = 0.1). Furthermore, the combination of 3D-GLS and 3D-LS-SD had accurate predictability for MACE, as shown by the Kaplan-Meier curves (log rank, χ2 = 94.1, p

Background Myocardial bridge (MB), common anatomic variant, is generally considered benign, while previous studies have shown associations between MB and various cardiovascular pathologies. This study aimed to investigate for the first time possible impact of MB on long‐term outcomes in patients with implantable cardioverter defibrillator, focusing on life‐threatening ventricular arrhythmia (LTVA). Methods and Results This retrospective analysis included 140 patients with implantable cardioverter defibrillator implantation for primary (n=23) or secondary (n=117) prevention of sudden cardiac death. Angiographically apparent MB was identified on coronary angiography as systolic milking appearance with significant arterial compression. The primary end point was the first episode(s) of LTVA defined as appropriate implantable cardioverter defibrillator treatments (antitachyarrhythmia pacing and/or shock) or sudden cardiac death, assessed for a median of 4.5 (2.2–7.1) years. During the follow‐up period, LTVA occurred in 37.9% of patients. Angiographically apparent MB was present in 22.1% of patients; this group showed younger age, lower rates of coronary risk factors and ischemic cardiomyopathy, higher prevalence of vasospastic angina and greater left ventricular ejection fraction compared with those without. Despite its lower risk profiles above, Kaplan–Meier analysis revealed significantly lower event‐free rates in patients with versus without angiographically apparent MB. In multivariate analysis, presence of angiographically apparent MB was independently associated with LTVA (hazard ratio, 4.24; 95% CI, 2.39–7.55; P

Abstract Background Impaired glucose metabolism is an established risk factor for coronary artery disease. Previous studies revealed that glycemic variability (GV) is also important for glucose metabolism in patients with acute coronary syndrome (ACS). We explored the association between GV and prognosis in patients with ACS. Methods A total of 417 patients with ACS who received reperfusion wore a continuous glucose monitoring system (CGMS) in a stable phase after admission and were monitored for at least 24 consecutive h. The mean amplitude of glycemic excursion (MAGE) was calculated as a marker of GV. We divided into two groups based on the highest tertile levels of MAGE (MAGE = 52 mg/dl). The groups were followed up for a median of 39 months [IQR 24–50 months]. The primary endpoint was the incidence of major adverse cardiovascular and cerebrovascular events (MACCE). Result During follow-up, 66 patients experienced MACCE (5 patients had cardiovascular death, 14 had recurrence of ACS, 27 had angina requiring revascularization, 8 had acute decompensated heart failure, and 16 had a stroke). MACCE was more frequently observed in the high MAGE group (23.5% vs. 11.6%, p = 0.002). In multivariate analysis, high MAGE was an independent predictive factor of poor prognosis for MACCE (odds ratio, 1.84; 95% confidence interval, 1.01–3.36; p = 0.045). Conclusion Glycemic variability determined with a CGMS is a predictor of prognosis in patients with ACS without severe DM. Trial registration UMIN 000010620. Registered April 1st 2012

Background: Both native T1 time and extracellular volume (ECV) fraction have been shown to be important measures for the detection of myocardial fibrosis. However, ECV determination requires the administration of an intravenous contrast agent, whereas native T1 mapping can be performed without a contrast agent. Methods: Here, we conducted a meta-analysis of myocardial native T1 data obtained for non-ischemic cardiomyopathy (NIC) patients and controls. A literature review included studies that applied T1 mapping using modified Look–Locker inversion recovery to measure myocardial fibrosis, and the results were validated by comparing datasets for dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM) patients and healthy controls (HCs). Results: We identified 16 eligible studies. Pooled mean differences (MDs) and 95% confidence intervals (CIs) were estimated as follows. Native T1 at 1.5-T, DCM vs. HC: MD = 45.26 (95% CI: 30.92–59.59); HCM vs. HC: MD = 47.09 (95% CI: 32.42–61.76). Native T1 at 3.0-T, DCM vs. HC: MD = 82.52 (95% CI: 47.60–117.44); HCM vs. HC: MD = 115.87 (95% CI: 50.71–181.04). ECV at 1.5-T, DCM vs. HC: MD = 4.26 (95% CI: 3.06–5.46); HCM vs. HC: MD = 1.49 (95% CI: −1.45–4.43). ECV at 3.0-T, DCM vs. HC: MD = 8.40 (95% CI: 2.94–13.86); HCM vs. HC: MD = 8.02 (95% CI: 5.45–1–0.59). Conclusion: In conclusion, native T1 values were significantly different between NIC patients and controls. Native T1 mapping may be a useful noninvasive method to detect diffuse myocardial fibrosis in NIC patients. Keywords: Native T1 mapping, Extracellular volume fraction, Dilated cardiomyopathy, Hypertrophic cardiomyopathy, Systematic review, Meta-analysis

BackgroundThe biphasic inflammation after ST‐segment elevation myocardial infarction (STEMI) plays an important role in myocardial healing and progression of systemic atherosclerosis. The purpose of this study is to investigate the impact of fever during the first and second phases of post‐STEMI inflammation on long‐term cardiac outcomes. Methods and ResultsA total of 550 patients with STEMI were enrolled in this study. Axillary body temperature (BT) was measured and maximum BTs were determined for the first (within 3 days: max‐BT1–3d) and second (from 4 to 10 days after admission: max‐BT4–10d) phases, respectively. Patients were followed for cardiac events (cardiovascular death, acute coronary syndrome, and rehospitalization for heart failure) for a median 5.3 years. During the follow‐up period, 80 patients experienced cardiac events. A high max‐BT4–10d was strongly associated with long‐term cardiac events (hazard ratio, 95% CI) for a 1°C increase in the max‐BT4–10d: 2.834 (2.017–3.828), P

Background: Blood glucose variability is receiving considerable attention as a new risk factor for coronary artery disease. This study aimed to investigate the association between blood glucose variability and coronary plaque tissue characteristics. Methods: In 57 patients with acute coronary syndrome, integrated backscatter intravascular ultrasound (IB-IVUS) and gray-scale IVUS were performed before balloon dilatation or stent implantation in the culprit vessels. Standard IVUS indices were evaluated for volume index (volume/length), and plaque components were measured by IB-IVUS for percent tissue volume. In addition to conventional glucose indicators, blood glucose variability in a stable state was determined by calculating the mean amplitude of glycemic excursions (MAGE) using a continuous glucose monitoring system. Results: Higher MAGE values were significantly correlated with larger percent plaque volumes (r = 0.32, p = 0.015), and increased lipid (r = 0.44, p = 0.0006) and decreased fibrous (r = -0.45, p = 0.0005) plaque components. In contrast, HbA1c or fasting plasma glucose values were not significantly correlated with plaque volumes and percent plaque components. Homeostasis model assessment of insulin resistance values were positively correlated with vessel (r = 0.35, p = 0.007) and plaque (r = 0.27, p = 0.046) volumes, but not with percent plaque components. In multiple regression analysis, higher MAGE values were independently associated with increased lipid (β = 0.80, p = 0.0035) and decreased fibrous (β = -0.79, p = 0.0034) contents in coronary plaques. Conclusions: Among all glucose indicators studied, only higher blood glucose variability was an independent determinant of increased lipid and decreased fibrous contents with larger plaque burden, suggesting blood glucose variability as one of the important factors related to coronary plaque vulnerability. [ABSTRACT FROM AUTHOR]

Aims We sought to compare the morphological features of non-culprit plaques with >50% diameter stenosis in patients with acute coronary syndromes (ACS) with those of culprit plaques in patients with ACS and stable angina pectoris (SAP) using optical coherence tomography (OCT) and integrated backscatter intravascular ultrasound (IB-IVUS). Methods and results A total of 150 culprit and non-culprit coronary plaques (non-culprit vessels) in 150 patients with coronary artery disease were interrogated by OCT before percutaneous coronary intervention (PCI). Patients were categorized as follows: 73 culprit plaques in patients with ACS (ACS-C), 32 non-culprit plaques in patients with ACS (ACS-NC), and 45 culprit plaques in patients with SAP. The fibrous cap thickness was thinner in the ACS-C and ACS-NC groups than in the SAP group and was thinnest in the ACS-C group (ACS-C vs. ACS-NC vs. SAP, 60 vs. 82 vs. 114 µm, P < 0.001). IB-IVUS sub-analysis of 95 patients demonstrated that% lipid volume was greater and % fibrous volume was lower in the ACS-NC group than those in the SAP group (ACS-C vs. ACS-NC vs. SAP, 56.3 ± 11.0 vs. 59.9 ± 11.2 vs. 50.1 ± 13.9%, P < 0.05 and 39.5 ± 9.0 vs. 35.0 ± 9.0 vs. 43.9 ± 11.3%, P < 0.01, respectively). Conclusion Plaques of non-culprit vessels in patients with ACS had a thinner fibrous cap and a higher percentage of lipid content than culprit plaques in patients with SAP. However, the fibrous cap thickness was thinner in the culprit lesions in patients with ACS than in the non-culprit lesions in patients with ACS, while plaque compositions were not significantly different between the groups. [ABSTRACT FROM AUTHOR]

Pacemaker. QT interval (QTI) may change when cardiac junction is improved by optimizing the AV delay. QTI is used as the sensor for rate responsive pacemakers. Evoked (e)QTI is measured as the time duration from the ventricular pace-pulse to the T sense point, which is the steepest point of the intracardiac T wave. The relationship between AV delay and eQTI and cardiac function was studied in 13 patients (74.2 ± 9.3 [SD] years old) with an implanted QT-driven DDDR pacemaker. A special pacemaker software module was downloaded into the pacemaker memory for eQTI data logging. AV delay was set at 100, 120, 150, 180, 210, and 240 ms. Cardiac output (CO) was measured by' continuous Doppler echocardiography eQTI was 343.3 ± 22.5, and 343.4 ± 23.2 ms (P < 0.01. repeated ANOVA) and CO was 4.2 ± 0.8, 4.6 ± 0.8, and 4.2 ± 0.8 L/min (P < 0.0001, repeated ANOVA) when AV delay was set at the AV delay shortened by one step (AV[-]) and prolonged by one step (AV[+]) from the AV delay at which QT interval was maximum (AV[max]) in seven patients, in whom the peak AV delay at which the eQTI was maximal could be identified. eQTI decreased from 345.1 ± 20.9 to 339.4 ± 21.1 ms (P < 0.0001) and CO decreased from 4.4 ± 1.4 to 4.1 ± 1.3 L/min (P <0.005) when AV delay was prolonged from AV(max) to AV(+) in all patients. eQTI decreased from 345.1 ± 22.5 to 343.3 ± 22.4 ms (P < 0.0005) and CO decreased from 4.6 ± 0.8 to 4.2 ± 0.8 L/min (P < 0.05) when AV delay was shortened from AV(max) to AV(-) in seven patients. Thus, CO was maximal when AV delay was set at the AV delay at which eQTI was maximal. In conclusion, the optimal AV delay can be predicted from the eQTI sensed by an implanted pacemaker. and automatic setting of the optimal A V delay can be achieved by the QT sensor of an implanted pacemaker. [ABSTRACT FROM AUTHOR]