Type 2 diabetes mellitus (T2DM) is a major risk factor of coronary artery diseases (CAD). Clinical outcomes in CAD with T2DM are poor despite improvement in medications and intervention devices. Coronary artery bypass grafting (CABG) is superior to percutaneous coronary intervention (PCI) in treating diabetic patients with multivessel coronary artery diseases (MVD). However, selecting a revascularization strategy should depend not only on the lesion complexity but also on the patient’s background and comorbidities. In addition, comprehensive risk management with medical and non-pharmacological therapies is important, as is confirmation of whether risk managements are appropriately achieved. Recently, novel anti-diabetic drugs have been demonstrated to have effectiveness in reducing cardiovascular events, which was independent of their glucose-lowering effect. Furthermore, non-pharmacological interventions using exercise and diet during the earlier stages of abnormal glucose metabolism might be beneficial in preventing the development or progression of T2DM and reducing the incidence of cardiovascular events.
The aim of this study was to investigate the antiplatelet effects of eicosapentaenoic acid (EPA) at a sufficient dose following coronary stent implantation. Thirty-one patients on dual antiplatelet therapy with aspirin and clopidogrel were treated with highly purified EPA-E (Epadel®) for 12 weeks. Based on our previous study, patients with a high baseline EPA/arachidonic acid (AA) ratio (≥ 0.37; n = 11) were given a standard dose (1800 mg daily) of EPA-E, whereas those with a low EPA/AA ratio (< 0.37; n = 20) were given a high dose (2700 mg daily) to reach the target value of > 0.92. Platelet function was then evaluated with agonist-induced aggregation using light transmittance aggregometry and VerifyNow®. After EPA-E treatment, the EPA/AA ratio significantly increased from 0.28 to 1.31 (P < 0.001). Collagen (1, 2, and 4 μg/mL)-induced maximal platelet aggregation (MPA) was significantly suppressed after EPA-E administration (from 28.0 to 24.0, P = 0.033; from 44.0 to 40.0, P = 0.016; from 60.0 to 56.0, P = 0.010; respectively). However, there were no changes in MPA induced by adenosine diphosphate and AA and in P2Y12 reaction units (PRU) and aspirin reaction units. After EPA-E treatment, PRU was significantly suppressed in 8 patients showing high on-treatment platelet reactivity (HTPR) (baseline 305; 266–321 versus on-treatment 256; 233–261, P = 0.012), but not in those without HTPR (201; 156–220 versus 183; 159–233, P = 0.212). In conclusion, EPA treatment at a sufficient dose suppressed platelet aggregation and showed possible add-on effects in patients with clopidogrel hyporesponsiveness.
The prognostic significance of atrial fibrillation (AF) on mortality in ST-segment elevation myocardial infarction (STEMI) patients is not clearly understood. To elucidate the clinical significance of AF on mortality for 1 year in STEMI patients, we retrospectively analyzed the Korea Acute Myocardial Infarction Registry (KAMIR) database, which spans January 2008 to September 2010 and includes 14,329 patients with acute myocardial infarction. We selected 5,556 patients with marked ECG rhythm (NSR, normal sinus rhythm or AF) on emergency room arrival, < 12 hours of symptom onset, and who underwent primary percutaneous coronary intervention (PCI) within 90 minutes of arriving at the hospital. Patients who had been followed-up for at least for 1 year were analyzed (2,636 of NSR, 119 of AF). At enrollment, AF patients were older (70.7 versus 65.5 years, P < 0.001) and had lower systolic blood pressure (120.6 versus 125.9 mmHg, P = 0.050), a higher heart rate (80.4 versus 75.6/minute, P = 0.009), and a higher rate of Killip III, IV (25.0 versus 14.2%, P = 0.002). Patients with AF showed clearly higher all-cause mortality (22.7 versus 9.5%, HR 2.51, 95%CI 1.68~3.76, P < 0.001) and cardiac death rate (17.7 versus 7.5%, HR 2.49, 95%CI 1.59~3.90, P < 0.001) at 1 year after admission compared patients with NSR. AF induced significantly higher all-cause mortality and cardiac mortality rate in STEMI patients who were appropriately revascularized with primary PCI compared to NSR at 1 year.
Treatment of ventricular arrhythmias (VAs) commonly involves ablating sites showing electrograms with the earliest activity relative to the VA, but there is no threshold value for prematurity guaranteeing success. Ablation of sites with great prematurity can still result in failure.
We hypothesized that isochronal map area (ISCA), derived from isochrones indicating electrogram prematurity, could help identify ablation targets in VA patients, as well as predict outcome. Specifically, we hypothesized that smaller ICSA for a given prematurity value would indicate a shallower arrhythmogenic focus leading to a higher likelihood of successful ablation.
We studied ICSA in 29 patients (12 males, 57 [17-65] years old) undergoing VA ablation. The VAs originated from the right and left ventricles in 11 and 18 patients, respectively. The earliest activation site of the VAs, ECG morphology of sinus beats and premature ventricular complexes (PVCs), and ISCA of activation preceding PVCs were evaluated.
RF ablation at the site showing earliest prematurity resulted in VA elimination in 21 patients (success group). The 5-ms ISCA was smaller in the success group than in the failure group (0.2 [0.1-0.6] versus 1.0 [0.8-1.5] cm2, respectively; P < 0.01). No significant difference was noted in prematurity itself (36 [30-45] versus 30 [29-33] ms, respectively; P = 0.07). The cut-off value of the 5 ms ISCA for successful RF ablation was 0.7 cm2 with 87.5% sensitivity and 85.6% specificity.
Isochrones of activity preceding PVCs appear to contain information beyond prematurity values and may help dictate suitable areas for successful ablation of VAs.
Radiofrequency catheter ablation (RFCA) in the treatment of AF is currently based on pulmonary vein isolation (PVI). Some studies have investigated the efficacy of empiric SVC isolation (SVCI) in addition to conventional PVI in order to improve success rates and reduce recurrence rates. However, the results of the studies have given conflicting data.
We performed a meta-analysis to evaluate the efficacy and safety of the empiric SVCI compared with conventional SVCI for paroxysmal atrial fibrillation (PAF) ablation.
We searched MEDLINE, EMBASE, the Web of Science, and the Cochrane Database from the period January 1986 to August 2016 and identified qualified studies. The primary clinical outcome was the recurrence rate of atrial tachyarrhythmias, and the secondary clinical outcomes were procedure time, fluoroscopy time, and complications.
We identified 3 randomized controlled trials (RCTs) and one nonrandomized, observational study (nROS) involving 245 patients with empiric SVCI and 269 patients with conventional SVCI. The empiric SVCI group had a lower recurrence rate of atrial tachyarrhythmia after a single procedure compared with the conventional SVCI group (16.7% versus 29.4%, OR: 0.48, 95%CI: 0.31 to 0.74, P = 0.0009). There was no significant difference in fluoroscopic time (P = 0.22), procedure time (P = 0.32), or clinical complications (P = 0.33) between the two groups.
Empiric SVCI is more effective than conventional SVCI in terms of the long-term outcomes of PAF patients after a single PVI procedure, with the same fluoroscopic time, procedure time, and clinical complications.
The effects of smoking on the prognosis of non-valvular atrial fibrillation (NVAF) patients are unclear.
The Shinken Database 2004-11 (n = 17,517) includes all new patients visiting the Cardiovascular Institute between June 2004 and March 2012. Among these cases, 2,102 NVAF patients were identified. The effects of smoking on ischemic stroke (IS), intracranial hemorrhage (ICH), and coronary artery events including percutaneous coronary intervention (PCI) and acute coronary syndrome (ACS) were analyzed. Smokers were younger and had lower risk profiles compared with non-smokers. A similar tendency was observed between current and former smokers. In contrast, patients with high tobacco consumption were older and had higher risk profiles, including uncontrolled hypertension, compared with those with low tobacco consumption. In 8,159 patient-years, IS, ICH, PCI, and ACS occurred at rates of 7.7, 2.7, 12.4, and 3.0 per 1000 patient-years. In multivariate Cox regression analysis, smoking was not significantly associated with any adverse event. However, different effects of smoking were observed when stratified by age. In patients ≥ 65 years old, current smokers were independently associated with PCI. Moreover, current smokers and smokers with a total tobacco amount ≥ 800 were marginally and independently associated with IS. In patients < 65 years, current smokers were independently associated with ICH.
Age appears to be one of the contributors to differentiation of the effects of smoking on cardiovascular events in our NVAF patients. In elderly patients who still smoke, smoking was associated with the promotion of atherosclerosis or thromboembolism, whereas in young patients it was associated with bleeding.
Fungal endocarditis (FE) is a rare and fatal disease. The contemporary in-hospital and long-term surgical outcomes of FE have not been adequately evaluated. This study describes our experience with the surgical management of FE.
Eight FE patients who underwent surgery in our center from January 2004 to November 2016 were included in this study. Seven had fungal prosthetic valve endocarditis (PVE) and one fungal native valve endocarditis (NVE). The Bentall operation, Cabrol operation, and mitral valve replacement were performed in 4, 3, and 1 patient, respectively. The overall in-hospital mortality rate was 25% (2/8). The follow-up was completed in all surviving patients and the mean follow-up time was 55.5 ± 63.3 (range, 1-154) months. Two late deaths occurred at 2 months and 4 months after discharge. The other patients recovered well during the follow-up.
FE is a devastating disease and surgical treatment has acceptable in-hospital and long-term mortality rates.
Dilated cardiomyopathy (DCM), the most common form of primary myocardial disease, is a leading cause of congestive heart failure and the most common indication for heart transplantation. Recently, NKX2-5 mutations have been involved in the pathogenesis of familial DCM. However, the prevalence and spectrum of NKX2-5 mutations associated with sporadic DCM remain to be evaluated. In this study, the coding regions and flanking introns of the NKX2-5 gene, which encodes a cardiac transcription factor pivotal for cardiac development and structural remodeling, were sequenced in 210 unrelated patients with sporadic adult-onset DCM. A total of 300 unrelated healthy individuals used as controls were also genotyped for NKX2-5. The functional effect of the mutant NKX2-5 was investigated using a dual-luciferase reporter assay system. As a result, two novel heterozygous NKX2-5 mutations, p.R139W and p.E167X, were identified in 2 unrelated patients with sporadic adult-onset DCM, with a mutational prevalence of approximately 0.95%. The mutations were absent in 600 referential chromosomes and the altered amino acids were completely conserved evolutionarily across species. Functional assays revealed that the NKX2-5 mutants were associated with significantly reduced transcriptional activity. Furthermore, the mutations abrogated the synergistic activation between NKX2-5 and GATA4 as well as TBX20, two other cardiac key transcription factors that have been causally linked to adult-onset DCM. This study is the first to associate NKX2-5 loss-of-function mutations with enhanced susceptibility to sporadic DCM, which provides novel insight into the molecular etiology underpinning DCM, and suggests the potential implications for the genetic counseling and personalized treatment of the DCM patients.
QRS duration has been associated with the response to cardiac resynchronization therapy (CRT). However, the methods for defining QRS duration to predict the outcome of CRT have discrepancies in previous reports. The aim of this study was to determine an optimal measurement of QRS duration to predict the response to CRT.
Sixty-one patients who received CRT were analyzed. All patients had class III-IV heart failure, left ventricular ejection fraction not more than 35%, and complete left bundle branch block. The shortest, longest, and average QRS durations from the 12 leads of each electrocardiogram (ECG) were measured. The responses to CRT were determined using the changes in echocardiography after 6 months. Thirty-five (57.4%) patients were responders and 26 (42.6%) patients were non-responders. The pre-procedure shortest, average, and longest QRS durations and the QRS shortening (ΔQRS) of the shortest QRS duration were significantly associated with the response to CRT in a univariate logistic regression analysis (P = 0.002, P = 0.03, P = 0.04 and P = 0.04, respectively). Based on the measurement of the area under curve of the receiver operating characteristic curve, only the pre-procedure shortest QRS duration and the ΔQRS of the shortest QRS duration showed significant discrimination for the response to CRT (P = 0.002 and P = 0.038, respectively). Multivariable logistic regression showed the pre-procedure shortest QRS duration is an independent predictor for the response to CRT.
The shortest QRS duration from the 12 leads of the electrocardiogram might be an optimal measurement to predict the response to CRT.
Adaptive servo-ventilation (ASV) is a recently-developed non-invasive therapy that improves the clinical course of heart failure (HF) patients. However, the precise hemodynamic response and predictors of ASV therapy remain uncertain. Overall, 69 patients with New York Heart Association HF class II-IV underwent 10-minute ASV testing along with hemodynamic studies. Among them, 21 (30%) achieved an acute response, which was defined as an increase in the cardiac index (CI) during ASV. ΔLeft ventricular end-diastolic pressure (LVEDP) did not correlate with ΔCI, whereas Δtransmural LVEDP, which was calculated by subtracting right ventricular end-diastolic pressure (RVEDP) from LVEDP, and ΔCI were positively correlated, similar to the ascending limb of Frank-Starling’s law (P = 0.009, r = 0.311). Among baseline data, higher RVEDP and higher LVEDP were significant predictors of an acute response by logistic regression analyses (P < 0.05 for both). RVEDP had a significantly higher area under the curve than LVEDP in the receiver operating characteristic analyses (0.846 versus 0.673, P = 0.028). Higher baseline RVEDP was significantly associated with a greater decrease in RVEDP during ASV (P < 0.001, r = -0.604). In conclusion, in HF patients with elevated RVEDP, ASV increased cardiac output through a decrease in RVEDP and an increase in transmural LVEDP, according to the ascending limb of Frank-Starling’s law.
The clinical impact of left ventricular (LV) segmental wall motion abnormalities (SWMA) in patients with idiopathic dilated cardiomyopathy (IDCM) has not been well elucidated.
Among 100 consecutive IDCM patients with follow-up visits, we enrolled 85 after excluding those with left bundle branch block and/or ventricular pacemaker implantation. LV wall motion was assessed using left ventriculography scored for 7 segments according to the American Heart Association classification as follows: 0, normokinesis; 1, hypokinesis; 2, akinesis; and 3, dyskinesis. SWMA were defined as a score dispersion of more than 1 degree among the segments.
SWMA was exhibited by 26 patients. Kaplan-Meier curves demonstrated that the patients with SWMA (SWMA+) had a significantly higher cardiac event-free rate than the patients without SWMA (P < 0.001). Cox proportional hazards analysis showed that SWMA+ was an independent predictor of cardiac events (P = 0.03; hazard ratio = 3.38; 95% confidence interval [CI], 1.11–10.8). Furthermore, multiple regression analysis showed that SWMA+ was an independent predictor of decreased LV end-systolic dimension index after optimal pharmacotherapy (β = -0.24; 95%CI, -9.12 to -0.73; P = 0.02).
SWMA is common in patients with IDCM and is independently associated with a poor prognosis and less morphometric and functional improvement of LV in response to pharmacotherapy.
Autonomic imbalance in hypertension induces excessive blood pressure (BP) elevation during exercise, thereby increasing left ventricular mass (LVM). Although muscle weakness enhances autonomic imbalance by stimulating muscle sympathetic activity during exercise, it is unclear whether muscle weakness is associated with an increase of LVM in patients with hypertension. This study aimed to investigate the relationships between muscle weakness, BP elevation during exercise, and LVM in these patients. Eighty-six hypertensive patients aged 69 ± 8 years with controlled resting BP (ie, < 140/90 mmHg) were recruited. Plasma brain natriuretic peptide (BNP), left ventricular mass index (LVMI), and knee extension muscle strength were measured. Changes in plasma noradrenaline (NORA) and brachial-ankle pulse wave velocity (ba-PWV) were assessed before and after an ergometer exercise test performed at moderate intensity (ΔNORA and ΔPWV, respectively). A difference between baseline and peak systolic BP during the exercise test was defined as BP elevation during exercise (ΔSBP). Relationships between muscle strength, ΔNORA, ΔPWV, ΔSBP, BNP, and LVMI were analyzed, and significant factors increasing LVM were identified using univariate and multivariate regression analyses. Muscle strength was negatively correlated with ΔNORA (r = -0.202, P = 0.048), ΔPWV (r = -0.328, P = 0.002), ΔSBP (r = -0.230, P = 0.033), BNP (r = -0.265, P = 0.014), and LVMI (r = -0.233, P = 0.031). LVMI was positively correlated with ΔPWV (r = 0.246, P = 0.023) and ΔSBP (r = 0.307, P = 0.004). Muscle strength was a significant independent factor associated with LVMI (β = -0.331, P = 0.010). Our findings suggest that muscle weakness is associated with an increase of LVM through excessive BP elevation during exercise in patients with hypertension.
Adverse cardiovascular events after lung transplantation (LT) increase the mortality in patients with pulmonary arterial hypertension (PAH). Long-term intravenous prostacyclin is the usual treatment in severe patients with PAH, but it may increase the risk of hemorrhage due to its antiplatelet aggregation effect or thrombocytopenia. We investigated the impact of length of intravenous prostacyclin therapy on acute adverse cardiovascular events including hemorrhagic complication after LT. We retrospectively compared the incidence of adverse events (death, intrathoracic hematoma and bleeding, cardiac congestion or shock, cerebral infarction and pulmonary embolism) within 30 days after LT between no/short-term (median 0.6 years, n = 13) and long-term (median 3.7 years, n = 15) intravenous prostacyclin groups. There were no differences in the dose of intravenous prostacyclin and pulmonary artery pressure between the two groups. Among 22 adverse events (0.8 ± 1.1 events/patient), 4 events occurred in the no/short-term intravenous prostacyclin group and 18 occurred in the long-term intravenous prostacyclin group. The event rate per patient in the long-term intravenous prostacyclin group (1.2 ± 1.3 events/patient) was significantly higher than that in the no/short-term intravenous prostacyclin group (0.3 ± 0.5 events/patient) (P < 0.05). Intrathoracic hematoma and bleeding was the most frequent adverse event (9 events, 41%). Preoperative long-term intravenous prostacyclin therapy increases acute adverse cardiovascular events after LT in patients with PAH.
Mean serum uric acid (SUA) levels are higher in men than women. In addition, recent studies have suggested that the SUA threshold at which the cardiovascular risk might increase may vary between women and men. In the current retrospective study, by analyzing the data from 219 female and 519 male patients who were free from uric acid-lowering medication, we investigated whether SUA is associated with left ventricular mass index (LVMI), left ventricular ejection fraction (LVEF), and plasma levels of B-type natriuretic peptide (BNP) independent of confounding factors, such as serum calcium, inorganic phosphate, and fibroblast growth factor 23 (FGF23), in a gender-specific manner.
In multivariate stepwise linear regression analysis in which age, blood pressure, eGFR, corrected calcium, inorganic phosphate, and FGF23 were entered as potential covariates, SUA was selected as a factor significantly associated with LVEF, LVMI, and plasma levels of BNP in both genders. On the other hand, however, after adding diuretic use as a potential covariate, the association between SUA and LVEF lost statistical significance in both genders, and that between SUA and BNP lost significance among female patients. These findings suggest that diuretic use is a non-negligible confounder in understanding the observed association between SUA and cardiac dysfunction and heart failure.
In summary, SUA is associated with left ventricular hypertrophy independent of confounding factors including FGF23 and diuretic use in female and male patients. Whether lowering SUA can influence the progression of cardiac remodeling awaits further investigation.
The efficacy and safety of direct oral anticoagulants (DOAC) with antiplatelet therapy compared to warfarin are unclear. The subjects were 280 patients who received antiplatelet therapy with oral anticoagulation (OAC) for the treatment of or protection from thromboembolism between January 2012 and September 2015. Among the 280 subjects, 79 (28.2%) received dual therapy (OAC plus aspirin or P2Y12 inhibitor) with DOAC, 75 (26.8%) dual therapy with warfarin, 46 (16.4%) triple therapy (OAC plus aspirin and P2Y12 inhibitor) with DOAC, and 80 (28.6%) triple therapy with warfarin.
Compared to triple therapy with warfarin, triple therapy with DOAC had slightly lower bleeding (3.5 versus 12.0/100 persons-years, HR: 0.24, 95%CI: 0.03 to 1.96, P = 0.183), and similar benefit outcomes (cardiac death, acute myocardial infarction or stroke) and thromboembolism (7.0 versus 10.5, HR: 0.53, 95%CI: 0.10 to 2.75, P = 0.453; 7.0 versus 7.5, HR: 0.96, 95%CI: 0.18 to 5.22, P = 0.964, respectively). Compared to dual therapy with warfarin, dual therapy with DOAC had slightly lower bleeding (3.0 versus 8.4, HR: 0.38, 95%CI: 0.07 to 2.18, P = 0.279), and similar benefit outcomes and thromboembolism (4.6 versus 4.2, HR: 1.66, 95%CI: 0.30 to 9.25, P = 0.565; 4.6 versus 1.4, HR: 3.11, 95%CI: 0.23 to 42.84, P = 0.397, respectively). Bleeding mainly occurred after 3 months (16/17, 94.1%).
Triple therapy and dual therapy with DOAC were not inferior to triple therapy and dual therapy with warfarin in terms of major bleeding, benefit outcomes, and thromboembolism. Bleeding mainly occurred in the late phase.
Resveratrol has been reported to have potent anti-atherosclerotic effects in animal studies. However, there are few interventional studies in human patients with atherosclerogenic diseases. The cardio-ankle vascular index (CAVI) reflects arterial stiffness and is a clinical surrogate marker of atherosclerosis. The aim of the present study was to investigate the effect of resveratrol on arterial stiffness assessed by CAVI in patients with type 2 diabetes mellitus (T2DM).
In this double-blind, randomized, placebo-controlled study, 50 patients with T2DM received supplement of a 100mg resveratrol tablet (total resveratrol: oligo-stilbene 27.97 mg/100 mg/day) or placebo daily for 12 weeks. CAVI was assessed at baseline and the end of study. Body weight (BW), blood pressure (BP), glucose and lipid metabolic parameters, and diacron-reactive oxygen metabolites (d-ROMs; an oxidative stress marker) were also measured.
Resveratrol supplementation decreased systolic BP (-5.5 ± 13.0 mmHg), d-ROMs (-25.6 ± 41.8 U.CARR), and CAVI (-0.4 ± 0.7) significantly (P < 0.05) and decreased BW (-0.8 ± 2.1 kg, P = 0.083) and body mass index (-0.5 ± 0.8 kg/m2, P = 0.092) slightly compared to baseline, while there were no significant changes in the placebo group. Decreases in CAVI and d-ROMs were significantly greater in the resveratrol group than in the placebo group. Multivariate logistic regression analysis identified resveratrol supplementation as an independent predictor for a CAVI decrease of more than 0.5.
In conclusion, 12-week resveratrol supplementation may improve arterial stiffness and reduce oxidative stress in patients with T2DM. Resveratrol may be beneficial in preventing the development of atherosclerosis induced by diabetes. However, a large-scale cohort study is required to validate the present findings.
Balloon pulmonary angioplasty (BPA) has been an attractive strategy for chronic thromboembolic pulmonary hypertension (CTEPH), even though it occasionally causes lung injury. However, predictive factors of lung injury after BPA have not been established. Pulmonary artery (PA) dilatation is often observed in patients with pulmonary hypertension. We investigated the association between PA diameter and complications after BPA.
The subjects were 19 CTEPH patients who underwent BPA. Patients were divided into two groups: patients with lung injury including asymptomatic lung infiltration on computed tomography (CT) images or mild hemoptysis (group L, n = 9) and no complications (group N, n = 10). PA diameter was measured on CT and corrected by the body surface area (PA diameter index).
There were no significant differences in hemodynamic indices or the number of treated vessels between the two groups. Right, left, and main PA diameter indices were higher in group L than in group N. Among the clinical variables, the right, left, and main PA diameter indices were significant predictors for lung injury caused by BPA (right PA: OR 1.819, 95%CI 1.056-3.135, P < 0.05; left PA: OR 1.857, 95%CI 1.091-3.159, P < 0.05; main PA: OR 1.399, 95%CI 1.001-1.956, P < 0.05).
The PA diameter index can be used to effectively predict the risk of lung injury after BPA.
The integral changes of coagulation and fibrinolysis, and their relationships with inflammation in patients with Takayasu arteritis (TA) remain undetermined. The purpose of this study was to analyze the changes of coagulation and fibrinolysis process in patients with TA by thrombelastography (TEG).
A total of 127 patients with TA and 55 healthy controls were enrolled. Patients with TA were grouped according to disease activity. The routine hematological parameters, traditional coagulation assays, and TEG parameters were summarized retrospectively.
A shorter K time, larger alpha angle, and higher levels of MA, MA(A), G, and TPI were found in patients with TA, especially in those at the active stage. The R time, EPL, LY30, and CL30 were similar between patients with TA and healthy controls, as well as TA patients with different disease activity. Spearman’s correlation showed that ESR was correlated with PLT (r = 0.206, P = 0.020), K (r = -0.353, P < 0.001), alpha angle (r = 0.328, P < 0.001), MA (r = 0.474, P < 0.001), MA (A) (r = 0.623, P < 0.001), G (r = 0.475, P < 0.001), and TPI (r = 0.458, P < 0.001).
In conclusion, inflammation was associated with platelet coagulation function rather than enzymatic coagulation function in patients with TA. Physicians should focus on antiplatelet treatment for improving the prognosis of patients with TA.
Tolvaptan, a vasopressin type 2 receptor antagonist, does not affect kidney circulation or cause worsening of renal function (WRF) in patients with acute decompensated heart failure (ADHF). Bioelectrical impedance analysis (BIA) can be used to evaluate intravascular volume by calculating the ratio of extracellular water (ECW) to intracellular water (ICW). There have been no reports examining the mechanisms of tolvaptan-induced diuresis using BIA. We investigated whether tolvaptan decreases excess volume while maintaining intravascular volume in ADHF patients.
Study patients included 29 ADHF patients (age 48-95, men 69%) diagnosed between April 2013 and May 2016 and who underwent BIA before and after treatment. Fifteen patients were treated with tolvaptan in addition to conventional diuresis therapy (tolvaptan group), and 14 patients were treated with conventional diuresis therapy only (control group). In the control group, the numerical value of serum creatinine (Cre) significantly increased from 0.89 ± 0.22 mg/ dL to 1.07 ± 0.29 mg/dL (P = 0.004), and the ECW/ICW significantly decreased from 0.696 ± 0.036 to 0.673 ± 0.032 (P = 0.004). These values were not significantly different from those obtained for the tolvaptan group. Furthermore, regression analysis showed a negative correlation between ΔCre and ΔECW/ICW, which are the differences between values before and after treatment (ΔCre = -0.002-5.668 × ΔECW/ICW, r2 = 0.306, P = 0.002).
Our findings suggest that WRF is caused by a reduction in intravascular volume and that tolvaptan treatment can decrease the excess volume while maintaining intravascular volume.
The aim of the present study was to evaluate the effects of hypertonic saline solution (C-HSS) with high dose furosemide on hospitalization time, readmission, and mortality in patients with New York Heart Association (NYHA) class III heart failure.
Decompensated heart failure patients (NYHA III) with chronic ischemic or nonischemic cardiomyopathy and ejection fraction < 40% were divided into 2 groups in an open-label random manner: the first group received a 1-hour intravenous infusion of furosemide (100 mg) plus compound C-HSS (100 mL) twice daily and underwent serious water restriction (500 mL/day); the second group received furosemide intravenous bolus (100 mg) twice a day and water restriction (500 mL/day), without C-HSS. Both groups had normal sodium (120 mmol sodium) intake. After discharge, the two groups continued to receive 120 mmol Na/day and 500-1000 mL water/day.
The first group (132 C-HSS patients) had an increase in urination, a reduction in hospitalization time (4 ± 2 versus 7 ± 2 days, P < 0.01), and a reduction in hospitalization costs (2210 RMB versus 3506 RMB, P < 0.01) compared with the second group (132 without C-HSS patients). During the follow-up period (36 ± 12 months), the first group had a significantly higher average readmission time (31.84 ± 7.58 months versus 15.60 ± 6.25 months, P < 0.01) and lower mortality rate (16.5% versus 31.9%, P < 0.01).
The results suggest that periodical C-HSS administration, combined with serious water restriction and a normal sodium diet, significantly reduces the hospitalization time, readmission rate, and mortality in patients with NYHA class III HF.
The aim of the present study was to investigate the effects of glucose fluctuation on neointimal proliferation after stent implantation by optical coherence tomography (OCT) in a diabetic/hypercholesterolemic (DM/HC) swine model.
A total of 24 everolimus-eluting stents (EES) were implanted in the right coronary artery (RCA) of the animals using a 20% overstretch ratio. The 24 swines were divided into a DM-high glucose fluctuation (HGF) group (n = 8), DMlow glucose fluctuation (LGF) group (n = 8), and a control group (n = 8). Percent diameter stenosis (%DS), late loss (LL), percent area stenosis (%AS), and neointimal thickness (NIT) were analyzed. The differences in neointimal characteristics and circulating oxidative stress and inflammation biomarkers were assessed and measured.
At 28 days, the highest values of %DS, LL, %AS, and NIT were achieved in the HGF group followed by the LGF group (P < 0.05) and the control group (P < 0.05). The highest frequency of the heterogeneous pattern was in the HGF group followed by the LGF group (P < 0.05) and the control group (P < 0.05). This was also the case for the oxidative stress and inflammation biomarkers.
DM might have a deleterious impact on neointimal proliferation after EES implantation in this DM/HC swine model. The extent of glucose fluctuation may be related to the degree of neointimal proliferation and this needs to be further confirmed by long-term follow-up and histology.
Left ventricular (LV) remodeling after myocardial infarction (MI) causes heart failure. Although medical therapies including angiotensin converting enzyme inhibitors show inhibitory effects on post-infarct LV remodeling, the prognosis of patients with post-infarct heart failure is still poor. Accumulating evidence suggests that an inflammatory response is implicated in the process of post-infarct LV remodeling. Therefore, we hypothesized that anti-inflammatory therapy by nanoparticle-mediated monocyte/macrophage-targeting delivery of pitavastatin may protect the heart from post-infarct LV remodeling.
Male C57BL/6 mice were subjected to permanent coronary ligation and pitavastatin-incorporating nanoparticles (Pitavastatin-NPs) were intravenously injected for 3 to 5 consecutive days. Pitavastatin-NPs were delivered to CD11b+ monocytes/macrophages, but not to cardiomyocytes. Treatment with Pitavastatin-NPs after establishment of MI attenuated post-infarct LV remodeling accompanied by a reduction of monocytes/macrophages in the heart, whereas pitavastatin solution treatment did not. Pitavastatin-NPs inhibited mobilization of monocytes from the spleen after MI. In mice after splenectomy, Pitavastatin-NPs still decreased the number of monocytes/macrophages in the infarcted heart and inhibited post-infarct LV remodeling.
Nanoparticle-mediated delivery of pitavastatin to monocytes/macrophages may be a novel therapeutic strategy to protect the heart from post-infarct LV remodeling. Inhibition of monocyte mobilization from the bone marrow is one of the major mechanisms by which Pitavastatin-NPs attenuated post-infarct LV remodeling.
The most important factor for preventing contrast-induced nephropathy (CIN) during percutaneous coronary intervention (PCI) in patients with severe renal dysfunction is to minimize the contrast volume. Herein, we report a successful case of complete revascularization after 3 separate PCI procedures using a super-low volume of contrast medium in a patient with 3-vessel disease, including two chronic total occlusions (CTOs). A 70-year-old man having exertional angina despite maximal medical therapy was referred to our hospital. He had severe renal dysfunction (estimated glomerular filtration rate 19 mL/minute/1.73 m2). Coronary angiography, in which a total volume of 15 mL (over 3 injections) of contrast medium was used after hydration with normal saline, demonstrated 2 CTOs in the proximal left circumflex artery (LCX) and the proximal right coronary artery (RCA) as well as focal stenosis in the mid left descending artery (LAD). Because the patient refused coronary artery bypass grafting, we opted for revascularization with PCI, divided into 3 procedures. We made full use of microcatheter tip injection and evaluation with intravascular ultrasound and achieved complete revascularization with a total of 31 mL of contrast medium: 9 mL for RCA, 6 mL for LAD, and 16 mL for LCX, without the occurrence of CIN. Additionally, we present tips for performing PCI using super-low contrast medium.
Congenital abnormalities of the aortic arch include interrupted aortic arch (IAA), coarctation of the aorta (CoA), and double aortic arch (DAA). Aortic arch repair is difficult and postoperative complications are common. However, postoperative tracheobronchial stenosis with respiratory insufficiency is an uncommon complication and is usually caused by increased aortic anastomotic tension. We report here a case of tracheal compression by a mediastinal hematoma following IAA surgery. The patient underwent a repeat operation to remove the hematoma and was successfully weaned off the ventilator.
In cases of tracheobronchial stenosis after aortic arch surgery, airway compression by increased aortic anastomotic tension is usually the first diagnosis considered by clinicians. Other causes, such as mediastinal hematomas, are often ignored. However, the severity of symptoms with mediastinal hematomas makes this an important entity.
Primary coronary sinus tumors are extremely rare. Herein, we present a case of a pregnant woman with a primary myxoma in the coronary sinus (CS), which was diagnosed by echocardiography and computed tomography. We reviewed the literature and found two other primary CS tumors. We summarized the gender, ages, symptoms, diagnostic methods, associated anomalies, treatments, histologic findings, and outcomes of the 3 cases. Dyspnea was a common symptom of all 3 patients. Diagnostic methods included echocardiography, computed tomography, magnetic resonance imaging, and coronary angiography. Associated anomalies included coronary artery fistulas, coronary sinus orifice atresia with persistent left superior vena cava, intra-cardiac invasion, and pericardial effusion. The 3 histologic types of primary CS tumor were haemangioma, lymphoma, and myxoma. The 3 patients received proper treatment and had good therapeutic outcomes.
Paget-Schroetter syndrome (PSS) is thrombosis of the deep veins draining the upper extremity due to anatomic abnormalities of the thoracic outlet that cause subclavian compression and subsequent thrombosis, leading to thrombus formation in the subclavian vein. Vigorous arm activity in sports is a known risk factor. Here, we report a case of Paget-Schroetter syndrome in a 31-year-old male non-professional baseball pitcher.
A 60-year-old man, who had claudication in his right limb due to total occlusion of the right superficial femoral artery, received bare metal stents. Although the bare metal stents in the superficial femoral artery did not show restenosis 5 years after stent implantation, angiography revealed significant in-stent restenosis when he developed right critical limb ischemia at 8 years post implantation. Ballooning for in-stent lesions did not result in full expansion. His right limb was amputated above the knee due to progressive limb ischemia. In the pathological findings in the superficial femoral artery, marked calcification was observed in the entire circumference of the luminal surface of the neointima. However, lipid core formation was not identified in the neointima. Although several cracks following balloon angioplasty were observed at the superficial calcified layers, injury to neointimal tissue such as compression was not observed. The neointima exhibited heavy calcification in the very late phase of in-stent restenosis after bare metal stent implantation in superficial femoral artery. Therefore, balloon angioplasty in the very late phase of in-stent restenosis potentially results in underexpansion.
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