Heart and Vessels最新文献

The role of preoperative hyperamylasemia in the perioperative enzyme levels in patients undergoing cardiac surgery is unclear. The primary outcome of this observational clinical study was to determine whether patients with preoperative hyperamylasemia undergoing on-pump cardiac surgery document an increase in serum amylase levels perioperatively compared with patients with normal serum amylase levels preoperatively. This prospective study evaluated serum total, pancreatic, and salivary amylase levels, estimated glomerular filtration rate (eGFR), and serum creatinine before the operation at postoperative days (POD) 1, 2, 3, and 7. We also followed up on any perioperative symptoms, including abdominal pain and lower ear or jaw swelling. We preoperatively had 157 patients with normal amylase levels (Normal group) and 45 with hyperamylasemia (Hyperamylasemia group). The Hyperamylasemia group demonstrated continuously lower eGFR and higher creatinine values at the preoperative time, postoperative days 1, 2, 3, and 7, compared with the Normal group. The Hyperamylasemia group showed higher serum total, pancreatic, and salivary amylase levels at preoperative (total 70 [55-90] [Normal] vs. 142 [107 to 162] [Hyperamylasemia] IU/L, median [25-75th percentile], P < 0.001) and postoperative periods compared with the Normal group. The relationship between renal dysfunction and serum amylase levels in all patients was significant in the preoperative, but not postoperative, periods. We noted no patients demonstrating clinical symptoms. Preoperative hyperamylasemia in patients undergoing on-pump cardiac surgery was associated with renal dysfunction without needing hemodialysis. However, whether the relation affects postoperative serum amylase levels is inconclusive.

Since many people die of either cancers or cardiovascular diseases worldwide, it is important to find the clinical pitfall that provokes cardiovascular diseases and cancer overall. Since metabolic syndrome (MetS) is largely linked to cardiovascular diseases, we have come to consider that MetS, even in its early state, may prime the occurrence of cancers overall. Indeed, the importance of MetS in causing pancreatic cancer has been proved using our large medical database. We analyzed Japanese healthcare and clinical data in 2005, who were followed up until 2020 and we examined the incidence of major cancers. At the enrollment, we examined the presence or absence of MetS judged by either Japanese criteria or NCEP/ATPIII. Of 2.7 million subjects without missing data, 102,930; 200,231; 237,420; 63,435; 76,172; and 2,422 subjects suffered lung, stomach, colon, liver and prostate cancer, respectively, and myelogenous leukemia during follow-up. MetS, defined by Japanese criteria, increased (p < 0.005 each) the incidence of cancer with a hazard ratio (HR) of 1.03-1.47 for lung, stomach, colon, liver, prostate cancers, and myelogenous leukemia. According to Japanese criteria, cancer incidence in the pre-stage MetS group was comparable to the MetS group. The results were almost identical when we defined MetS using NCEP ATP III. Taken together, we conclude that MetS is linked to majority of cancers.

Preoperative left ventricular (LV) ejection fraction (LVEF) and LV end-systolic dimension (LVESD) are established predictors of LV dysfunction (LVD) after mitral valve repair (MVr) for mitral regurgitation (MR). Although elevated estimated right ventricular systolic pressure (eRVSP) indicating pulmonary hypertension is the best proposed additional predictor, we hypothesized that transthoracic echocardiography (TTE) parameters more directly reflecting left atrial pressure (LAP) would more accurately predict LVD than eRVSP. Furthermore, predictors of a significant decline in LVEF remain unknown. We retrospectively studied 622 patients, aged 20-87 years, who underwent MVr for severe chronic primary MR. As previously reported predictors of postoperative LVD, we collected seven preoperative TTE parameters, including LVESD, LVEF, eRVSP, LV end-diastolic dimension, left atrial volume index (LAVI), early transmitral annular (e') velocity, and atrial fibrillation. Furthermore, as LAP-related TTE parameters, we collected left atrial dimension, E-wave velocity, and E/e' ratio, in addition to eRVSP and LAVI. Using multivariate logistic regression and receiver operating characteristic curve analyses, we explored predictors of early postoperative LVD, defined as LVEF < 50% measured on postoperative day 7. We further explored predictors of a significant decline in LVEF, defined as an absolute decline in LVEF of > 12 percentage points, the third quintile of the data. Incidences of postoperative LVD and a significant LVEF decline were 12.9% and 23.2%, respectively. In addition to LVESD and LVEF, E-wave velocity, but not eRVSP, remained a significant predictor of postoperative LVD. E-wave velocity, LVESD, and LVEF had additive effects in risk prediction. Furthermore, E-wave velocity was the strongest predictor of a significant LVEF decline. E-wave velocities > 121.5 cm/s and > 101.5 cm/s were associated with increased risks of postoperative LVD (odds ratio [OR], 2.896; 95% confidence interval [95%CI], 1.792-4.681; p < 0.001) and a significant LVEF decline (OR, 6.345; 95%CI, 3.707-10.86; p < 0.001), respectively. After adjustment for multiple TTE parameters, E-wave velocity, but not eRVSP, remained significant predictors of postoperative LVD and a significant LVEF decline after MVr. These results were reproducible in 461 patients who underwent follow-up TTE at 1 year, suggesting an important role of E-wave velocity in risk prediction.

Introduction: Differentiation of tachycardia-induced cardiomyopathy (TIC) from dilated cardiomyopathy (DCM) in patients admitted for heart failure (HF) with left ventricular dysfunction and supraventricular tachyarrhythmia (SVT) remains challenging. The role of tissue tracking (TT) in this setting remains unknown.

Methods: Forty-three consecutive patients admitted for HF due to SVT with left ventricular ejection fraction (LVEF) < 50% undergoing CMR were retrospectively included. Those eventually evolving to LVEF > 50% at follow-up were classified as TIC and those maintaining a LVEF < 50% were classified as DCM. Clinical, echocardiography, and CMR findings, including TT, were analyzed to predict LVEF recovery.

Results: Twenty-five (58%) patients were classified as TIC. Late gadolinium enhancement (LGE) was more frequent in DCM group (61% vs 16%, p = 0.004). Left ventricle (LV) peak systolic radial velocity and peak diastolic radial strain rate were lower in DCM group (7.24 ± 4.44 mm/s vs 10.8 ± 4.5 mm/s; p = 0.015 and -0.12 ± 0.33 1/s vs -0.48 ± 0.51 1/s; p = 0.016, respectively). Right ventricle (RV) peak circumferential displacement was lower in patients with TIC (0.2 ± 1.3 vs 1.3 ± 0.9°; p = 0.009). In the multivariate analysis, diabetes (p = 0.046), presence of LGE (p = 0.028), LV peak systolic radial velocity < 7.5 mm/s (p = 0.034), and RV peak circumferential displacement > 0.5° (p = 0.028) were independent predictors of lack of LVEF recovery.

Conclusion: In the setting of acute HF with LV dysfunction related to SVT, diabetes, LGE, LV peak systolic velocity, and RV peak circumferential displacement are independent predictors of lack of LVEF recovery and, therefore, represent clinically useful parameters to differentiate TIC from DCM.

NEXT [NOBORI biolimus-eluting stent (BES) versus XIENCE/PROMUS everolimus-eluting stent (EES) trial] was a multicenter, randomized, prospective trial that included 3235 patients with 8-12 months of follow-up imaging at 18 centers. IB-IVUS images were analyzed at an interval of 0.5 mm using a motorized pull-back system in each plaque that required stent implantation. We analyzed seven cross-sections at the site of minimal lumen area and ten cross-sections in proximal and distal peripheral sites prior to the procedure, after stent implantation and after 8 months. We averaged the relative blue volume, relative green volume, relative yellow volume, and relative red volume across seven cross-sections using the manufacturer's default setting. Fifty-four lesions in 50 patients were analyzed. There were 28 lesions in 25 patients in the EES group and 26 lesions in 25 patients in the BES group. The patient characteristics did not differ significantly between the two groups except high-density lipoprotein cholesterol. There were no significant differences before and after stent implantation after 8 months in relative red volume, relative yellow volume, relative green volume or relative blue volume. Although the present study was likely underpowered for statistical analyses and larger populations are needed to confirm the conclusions, the vascular response regarding tissue characterization was similar between EES and BES, even though the thickness and releasing materials differed between the stents.

This study examined the anti-inflammatory and endothelial function-enhancing effects of proprotein convertase subtilisin/kexin 9 (PCSK9) inhibitor therapy in the early phase after acute myocardial infarction (AMI) by assessing changes in tumor necrosis factor-α (TNF-α) levels and the L-arginine/asymmetric-dimethylarginine (ADMA) ratio. This retrospective, single-center cohort study included patients who underwent successful timely primary percutaneous coronary intervention (PCI) for first-onset AMI between September 2017 and March 2018. The PCSK9 inhibitor group comprised patients who received 75 mg alirocumab up to 7 days after AMI, while the standard therapy group comprised patients who did not. We evaluated the change in TNF-α levels and the L-arginine/ADMA ratio at the time of hospital admission and prior to discharge. PCSK9 inhibitor therapy in the early phase after AMI suppressed TNF-α levels (standard therapy group, 1.64 ± 2.14 pg/mL vs. PCSK9 inhibitor group, 0.26 ± 0.33 pg/mL; p = 0.033) and increased the L-arginine/ADMA ratio (standard therapy group, - 13.0 ± 39.7 vs. PCSK9 inhibitor group, 23.2 ± 39.7; p = 0.042). Upon multiple regression analysis adjusted for sex, age, and peak creatine kinase levels, PCSK9 inhibitor therapy was associated with TNF-α suppression (p = 0.025; β = - 0.235, 95% confidence interval [CI], - 0.436 to - 0.033). The L-arginine/ADMA ratio was also analyzed using multiple regression, adjusted for sex, age, peak creatine kinase levels, and smoking, showing a significant improvement in the ratio (p = 0.018; β = 41.913, 95% CI, 10.337-73.491). Moreover, a weak negative correlation was suggested between the change in TNF-α levels and the change in L-arginine/ADMA ratio (r = - 0.393, p = 0.058). PCSK9 inhibitor therapy in the early phase after AMI suppresses TNF-α levels and improves the L-arginine/ADMA ratio, potentially indicating anti-inflammatory and endothelial function-enhancing effects.

Endothelial dysfunction may trigger coronary spastic angina (CSA). However, the risk factors for CSA in young patients remain unclear. This study aimed to investigate the age-dependent role of serum uric acid levels in patients with CSA. We enrolled 423 patients who underwent an ergonovine tolerance test during coronary angiography for the CSA evaluation. We categorized the patients as (1) young (age ≤ 65 years) CSA-positive (n = 33), (2) young CSA-negative (n = 138), (3) elderly (age > 66 years) CSA-positive (n = 42), and (4) elderly CSA-negative (n = 210) groups. In the young groups, the smoker proportion (57.6 vs. 38.4%, p = 0.04) and serum uric acid levels (6.3 ± 1.4 vs. 5.4 ± 1.5 mg/dl, p = 0.006) were significantly higher in the CSA-positive compared with the CSA-negative group. Conversely, in the elderly group, the male proportion (66.6 vs. 47.1%, p = 0.02) and alcohol consumption level (40.5 vs. 21.0%, p = 0.01) were significantly higher in the CSA-positive compared with the CSA-negative group. The multivariate analysis in young groups revealed the independent association between the serum uric acid level (p = 0.02) and the presence of CSA. Our results indicate that elevated serum uric acid levels may affect CSA development in young patients.

Background: The global use of angiotensin receptor neprilysin inhibitor (ARNI) in clinical practice, especially in patients with heart failure and below-normal ejection fraction (HFbnEF), has not been thoroughly evaluated. We aimed to investigate the characteristics, outcomes, and adverse events in patients treated with ARNI for HF with reduced (HFrEF), below-normal (HFbnEF), and supranormal left ventricular EF (HFsnEF).

Methods: This observational study analyzed data from the electronic healthcare records (EHR) of patients with HF treated with ARNI between 2015 and 2022 in North and South America, Europe, the Middle East, Africa, and Asia-Pacific. Based on the left ventricular EF, patients were categorized as HFrEF (< 40%), HFbnEF (40-60%), and HFsnEF (> 60%). Mortality and the incidence of adverse events were investigated.

Results: Of the 11,141 patients analyzed, HFrEF, HFbnEF and HFsnEF accounted for 74%, 22%, and 4%, respectively. Patients with a higher EF were more likely to be older, female, and obese. Hypertension and atrial fibrillation were the most common in HFsnEF. Systolic blood pressure was lower and natriuretic peptide levels were higher in the lower EF groups. Mortality was lowest in HFbnEF (7.7 per 100 patient-years follow-up in HFrEF, 5.8 in HFmrEF, and 6.0 in HFsnEF). Similarly, hypotension and acute kidney injury were the least frequent in HFbnEF. Incidence of elevated serum potassium levels was similar between the groups.

Conclusions: In this analysis of large-scale EHR, ARNI was mainly used in HFrEF and HFbnEF, consistent with previous randomized trials and pooled analyses. Adverse events were less common in HFbnEF.

Background: We investigated whether drug-coated balloon (DCB) treatment is effective for all de novo cases of coronary artery disease (CAD) in patients with diabetes mellitus. Furthermore, we also investigated the relationship between the degree of diabetes mellitus and clinical outcomes after DCB treatment.

Methods: In this study, we included 516 consecutive patients with de novo CAD who were treated with DCB. The patients were divided into the diabetic and non-diabetic groups. Patients with diabetes mellitus were further classified into non-insulin-treated diabetes mellitus (NITDM) and insulin-treated diabetes mellitus (ITDM). The primary endpoints were major adverse cardiovascular ischemic events (MACE) and clinically driven target lesion revascularization (CD-TLR).

Results: Within a mean clinical follow-up period of 2.5 years, the incidence of MACE among patients with diabetes mellitus (22.1%) was almost twice that of non-diabetic patients (11.9%) with a relative risk of 1.86 (95% CI 1.24-2.79, p = 0.002). The 3-year CD-TLR occurred in 28 patients with diabetes mellitus (10.6%) and 13 non-diabetic patients (5.1%, p = 0.02). ITDM patients had a significantly higher rate of MACE compared with non-diabetic patients with a relative risk of 2.86 (95% CI 1.76-4.63, p = 0.0002). ITDM remained an independent predictor of 3-year MACE with an odd ratio of 1.96 (95% CI 1.00-3.83, p = 0.05).

Conclusion: In patients undergoing DCB, the presence of DM was associated with a higher risk of MACE and CD-TLR. Particularly in DCB, treatment was still inadequately effective for ITDM patients.

It remains to be elucidated whether Ca²⁺ antagonists induce pharmacological preconditioning to protect the heart against ischemia/reperfusion injury. The aim of this study was to determine whether and how pretreatment with a Ca²⁺ antagonist, azelnidipine, could protect cardiomyocytes against hypoxia/reoxygenation (H/R) injury in vitro. Using HL-1 cardiomyocytes, we studied effects of azelnidipine on NO synthase (NOS) expression, NO production, cell death and apoptosis during H/R. Action potential durations (APDs) were determined by the whole-cell patch-clamp technique. Azelnidipine enhanced endothelial NOS phosphorylation and NO production in HL-1 cells under normoxia, which was abolished by a heat shock protein 90 inhibitor, geldanamycin, and an antioxidant, N-acetylcysteine. Pretreatment with azelnidipine reduced cell death and shortened APDs during H/R. These effects of azelnidipine were diminished by a NOS inhibitor, L-NAME, but were influenced by neither a T-type Ca²⁺ channel inhibitor, NiCl₂, nor a N-type Ca²⁺ channel inhibitor, ω-conotoxin. The azelnidipine-induced reduction in cell death was not significantly enhanced by either additional azelnidipine treatment during H/R or increasing extracellular Ca²⁺ concentrations. RNA sequence (RNA-seq) data indicated that azelnidipine-induced attenuation of cell death, which depended on enhanced NO production, did not involve any significant modifications of gene expression responsible for the NO/cGMP/PKG pathway. We conclude that pretreatment with azelnidipine protects HL-1 cardiomyocytes against H/R injury via NO-dependent APD shortening and L-type Ca²⁺ channel blockade independently of effects on gene expression.