bluuebunny/crossref_metadata_2025_split huggingface dataset:
P3632Prognostic impact of aortic valve stenosis in patients with acute myocardial infarction
Authors: Mizutani H , Kurita T , Kasuya S , Mori T , Ito H , Tanimura M , Ichikawa K , Goto I , Masuda J , Sawai T , Ito M , Dohi K 
Published: October 2019

Abstract

Background
Aortic valve stenosis (AS) is associated with the presence and severity of coronary artery disease independently of clinical risk factors, which leads to increased cardiovascular mortality. However, the prevalence of AS and its prognostic value among patients with acute myocardial infarction (AMI) remain unknown.

Purpose
The purpose of this study was to investigate the prevalence and prognostic impact of AS in AMI patients.

Methods
We studied 2,803 AMI patients using data from Mie ACS registry, a prospective and multicenter registry. Patients were divided into subgroups according to the presence and severity of AS based on maximal aortic flow rate by Doppler echocardiography before hospital discharge: non-AS <2.0 m/s, 2.0 m/s≤mild AS <3.0 m/s, 3.0 m/s≤moderate AS <4.0m/s and severe AS≥4.0 m/s. The primary outcome was defined as 2-year all-cause mortality.

Results
AS was detected in 79 patients (2.8%) including 49 mild AS, 23 moderate AS and 6 severe AS. AS patients were significantly older (79.9±9.8 versus 68.3±12.6 years), and higher killip classification than non-AS patients (P<0.01, respectively). However, left ventricular ejection fraction, and prevalence of primary PCI was similar between the 2 groups. During the follow-up periods (median 725 days), 333 (11.9%) patients experienced all-cause death. AS patients demonstrated the higher all-cause mortality rate compared to that of non-AS patients during follow up (47.3% versus 11.3%, P<0.0001, chi square). Kaplan-Meier curves showed that the probability of all-cause mortality was significantly higher among AS patients than non-AS patients, and was highest among moderate and severe AS (See figure A and B). Cox regression analyses for all-cause mortality demonstrated that the severity of AS was the strongest and independent poor prognostic factor (HR 1.71, 95% CI 1.30–2.24, P<0.001, See table).
Cox hazard regression analysis Hazard ratio 95% Confidential interval P-value Severity of aortic valve stenosis 1.71 1.30–2.24 <0.001 Killip classification 1.63 1.46–1.82 <0.001 Age 1.07 1.06–1.09 <0.001 Serum creatinine level 1.05 1.03–1.08 <0.001 Max CPK level 1.00 1.00–1.01 <0.001 Left ventricular ejection fraction 0.96 0.95–0.97 <0.001 Primary percutaneous coronary intervention 0.67 0.47–0.96 0.03 CPK suggests creatinine phosphokinase.
All cause mortality

Conclusions
The presence of AS of any severity contributes to worsening of patients' prognosis following AMI independently of other known risk factors.

Acknowledgement/Funding
None
P3634Cancer patients have a higher long-term risk of death and myocardial infarction after percutaneous coronary intervention - A matched cohort analysis of 3,560 patients
Authors: Guo W , Lewis B , Johnson M , Lerman A , Herrmann J 
Published: October 2019

Abstract

Background
Cancer patients have a higher risk of thromboembolic events but it is not well known if these patients also have a higher risk of death, myocardial infarction (MI) or repeat revascularization after percutaneous coronary intervention (PCI) is unknown.

Methods
Cancer patients who underwent first-time single vessel PCI from January 1, 2003, through December 31, 2013 were identified by cross-matching of institutional cancer and PCI registries. These cancer patients were matched 4:1 to non-cancer patients, likewise undergoing first-time single vessel PCI in the time period. The combined primary endpoint was death, MI and revascularization at 5 year follow-up. Secondary endpoints were death and MI combined and the individual components of the primary endpoint. Both time dependent and non-time-dependent analyses were conducted.

Results
A total of 712 cancer patients were identified and matched to 2,848 non-cancer patients (one third women in either group). Bare-metal stents were used in one third of patients in both groups. The combined primary study endpoint was significantly more frequently encountered in the cancer than in the non-cancer group in both time-dependent (Figure 1) and non-time dependent analyses (5-year event rate 48.6% vs. 31.2%, p<0.001). This was driven by a higher 5-year event rate of death (39.0% vs. 20.1%) and MI (14.8% vs 4.86%) in the cancer group. The 5-year rate of revascularization did not differ significantly between the two groups (10.5% vs 10.3%).
Figure 1. MI + revascularization-survival

Conclusion
Cancer patients have a two times higher rate of death and a three times higher rate of MI over the first 5 years after PCI. Future studies will need to define the etiology and factors accounting for this higher event rate in cancer patients, especially of these patients are predisposed to stent thrombosis and need longer term dual antiplatelet therapy.
P3637Relationship between serial measurements of NT-proBNP and cardiovascular events in patients with acute coronary syndrome
Authors: Jang J Y , Ahn J H , Bae J S , Kang M G , Kim K , Park H W , Koh J S , Park Y , Hwang S J , Kwak C H , Hwang J Y , Jeong Y H 
Published: October 2019

Abstract

Background
Increased level of natriuretic peptides has been known as an important predictors of adverse cardiovascular (CV) outcomes in patients with acute coronary syndrome (ACS). We sought to evaluate clinical implication of N-terminal pro-brain natriuretic peptide (NT-proBNP) measured at initial and follow-up periods.

Methods
Serial NT-proBNP levels (on-admission and one-month post-PCI) were measured in ACS patients undergoing PCI (n=2,290). High NT-proBNP levels were determined according to the predefined age-specific criteria. Patients were stratified into 4 groups according to NT-proBNP levels (on-admission & one-month): (1) normal-normal group (n=1234, 53.9%); (2) high–normal group (n=257, 11.2%); (3) normal-high group (n=376, 16.4%); and (4) high-high group (n=423, 18.5%). Clinical events were defined as all-cause death and MACE (a composite of CV death, non-fatal MI, and ischemic stroke).

Results
With a median follow-up of 35.9 (IQR: 16.8, 54.5) months, all-cause death and MACE were occurred in 4.1% and 7.2%, respectively. NT-proBNP on-admission vs. at one-month did not differ significantly (median 391.6 [IQR: 143.9, 1402.3] vs. median 619.1 [IQR 240.1, 1616.1]; p=0.622), but the prevalence of high NT-proBNP was increased over time (25.3% to 34.9%; p<0.001). The rates of all-cause death and MACE significantly increased only in the high-high group compared with other groups (log-rank test, all p values <0.001, Figure). After adjustment, the high-high group remained significantly risky in terms with the occurrence of all-cause death (HR, 2.99; 95% CI, 1.65 to 5.41; p<0.001) and MACE (HR, 1.96; 95% CI, 1.28 to 3.01; p=0.002).
Figure 1

Conclusion
Serial measurements of NT-proBNP at on-admission and follow-up can help to stratify the risks of all-cause death and adverse CV events following PCI in ACS patients. About two-fifths of patients having high NT-proBNP level during hospitalization can be classified into the low-risk group for all-cause death and adverse CV events.

Acknowledgement/Funding
None
P3648Plasma glutamate are increased in non-smoker patients with vasospastic angina pectoris and associated with plasma cystine and antioxidant capacity
Authors: Fujibayashi K , Oda M , Wakasa M , Takano S , Kuzume Y , Saeki Y , Sawaguchi J , Fujita W , Saito R , Kawai Y , Kajinami K 
Published: October 2019

Abstract

Background
Endothelial dysfunction of the coronary arteries caused by oxidative stress plays an important role in the pathogenesis of vasospastic angina pectoris (VSAP). Glutamate, a non-essential amino acid, exerts endothelial dysfunction by oxidative stress production through N-methyl-D-aspartate receptor activation. Besides oxidative stress, decrease of antioxidant may be responsible for endothelial dysfunction. Glutathione (GSH), an important antioxidant, is synthesized from imported cystine through the cystine/glutamate antiporter system (XC-) in association with the export of glutamate. Glutamate also competitively inhibits cystine import into the endothelial cells through the XC-leading to GSH depletion. Thus the extracellular glutamate and cystine are crucial for the intracellular redox status. However, it remains unclear whether glutamate and/or cystine are implicated in the pathogenesis of VSAP. As smoking induces powerful oxidant stresses in the whole body, we investigated plasma glutamate, cystine, oxidative stress markers and antioxidant capacity in non-smoker patients with VSAP.

Methods and results
Sixty-two consecutive non-smoker patients suspected having VSAP were performed coronary angiograms (CAG). Forty-nine patients who did not show any significant coronary stenosis (<50%) were performed the intracoronary acetylcholine provocation test. Patients were categorized into the VSAP-positive group (n=27) and the VSAP-negative group (n=22) on the basis of test results. Blood samples were collected from the femoral sheath before the CAG. Plasma glutamate, cystine, nitrotyrosine (NT), reactive oxygen metabolites (d-ROMs) and biological antioxidant potential (BAP) were measured. The levels of plasma glutamate and cystine in the VSAP-positive group were significantly higher than those in the VSAP-negative group (59.8±25.7 vs 43.5±18.7 nmol/L, p=0.0054, and 35.3±14.2 nmol/L vs 25.2±9.1 nmol/L, p=0.0018, respectively). The levels of plasma glutamate showed significant and positive association with the levels of plasma cystine (r=0.40, p=0.005). There were no significant differences in the levels of NT and d-ROMs as oxidative stress markers, and BAP as an antioxidant capacity between the two groups, respectively. However, the levels of plasma glutamate showed significant and negative association with BAP values (r=−0.3, p=0.038).

Conclusions
Plasma levels of glutamate were increased in non-smoker patients with VSAP and positively associated with plasma cystine levels and negatively associated with antioxidant capacity, suggesting that plasma glutamate modulate plasma cystine levels and antioxidant capacity through the XC- inhibition, and could be a novel risk factor of VSAP.
P3655Right ventricular volume off-loading following atrial septal defect closure or pulmonary valve replacement: impact on tricuspid regurgitation and mid-term remodeling
Authors: Martin Garcia A C , Dimopoulos K , Boutsikou M , Kempny A , Alonso-Gonzalez R , Swan L , Uebing A , Babu-Narayan S V , Martin-Garcia A , Sanchez-Fernandez P L , Castro Garay J C , Li W , Shore D F , Gatzoulis M A 
Published: October 2019

Abstract

Introduction
Cardiac surgery or catheter intervention is nowadays commonly performed to abolish volume loading of the right ventricle (RV) in adults with congenital heart disease (ACHD).

Purpose
Little is known, however, of their impact on the preexisting tricuspid regurgitation (TR) following such procedures (atrial septal defect [ASD] closure and pulmonary valve replacement [PVR]), which was the aim of our study.

Methods
Demographics, clinical and echocardiographic characteristics were analyzed from 162 consecutive patients undergoing such interventions between July 2005 and December 2014, who had at least mild preoperative TR.

Results
Mean age at intervention was 42±16 years (38.3% male); 101 patients underwent ASD closure, whereas 61 patients PVR. Only 11.1% receiving concomitant tricuspid valve surgery (repair). There was significant overall improvement in severity of TR, from 38 (23.5%) patients having moderate or severe TR preoperatively to only 11 (6.8%) and 20 (12.3%) at 6 and 12 months of follow-up, respectively (p<0.05) (Figure 1) (Table 1). Improvement in TR was observed in patients who did not have concomitant TV repair, from 15.3% to 6.9% and 11,8%, 6 and 12 months, respectively (p<0.05).
Echocardiographic data Echo 1 (baseline) Echo 2 (6 months) Echo 3 (12 months) p-value† ‡Echo 1 ‡Echo 2 ‡Echo 3 TR grade (none = 1, mild = 2, moderate = 3, severe = 4) 2.3±0.6 1.6±0.6 1.7±0.8 <0.0001 A B B End-diastolic tricuspid annulus diameter (cm) 4.3±0.6 3.6±0.6 3.5±0.5 <0.0001 A B B Systolic tenting area (cm2) 0.7±0.5 0.5±0.2 0.5±0.3 <0.0001 A B B Coaptation distance (cm) 0.6±0.2 0.4±0.2 0.4±0.2 <0.0001 A B B End-diastolic area (cm2) 30.3±7.5 21.7±6.0 20.6±6.0 <0.0001 A B C Fractional area change (%) 39.4±8.4 39.0±8.0 39.9±8.1 0.58 A A A RV mid diameter (cm) 4.2±0.7 3.3±0.7 3.2±0.6 <0.0001 A B B RVOT end-diastolic proximal diameter (cm) 4.4±0.6 3.8±0.6 3.6±0.5 <0.0001 A B C TAPSE (cm) 2.1±0.6 1.4±0.5 1.4±0.4 <0.0001 A B B Lateral TDi S (cm/s) 12.4±3.3 8.8±3.0 9.2±3.0 <0.0001 A B B Systolic pulmonary artery pressure (mmHg) 42.4±13.4 34.8±10.1 35.1±11.6 <0.0001 A B B LVEF (normal = 1, mild LV dysfunction = 2, moderate = 3, severe = 4) 1.0±0.2 1.0±0.2 1.0±0.2 0.80 A A A RA area (cm2) 26.1±9.6 19.5±6.6 19.2±6.7 <0.0001 A B B *One-way ANOVA comparison. ‡Tukey pairwise comparison between Echos 1, 2 and 3: means that do not share a letter are significantly different (i.e. p<0.05).
Figure 1

Conclusions
ASD closure or PVR are commonly associated with significant reduction of preoperative functional tricuspid regurgitation event amongst patients who did not undergo concomitant tricuspid valve surgery.
P3660Investigating the role of neutrophils and NETs in staphylococcus aureus endocarditis
Authors: Meyers S , Liesenborghs L , Lox M , De Meyer S F , Vanassche T , Verhamme P , Martinod K 
Published: October 2019

Abstract

Background/Introduction
Infective endocarditis (IE) remains one of the deadliest cardiac diseases. Despite optimal antibiotic and surgical treatment, still one in three patients do not survive Staphylococcus aureus (S. aureus) IE. In order to cause this disease, bacteria need to first overcome shear stress and adhere to cardiac valves. Secondly, they need be able to progress into a complex lesion. Previously, we have shown that S. aureus adheres to cardiac valves via platelets and von Willebrand factor. However, the process of progression from initial bacterial adhesion to a complex vegetation, particularly how bacteria bypass the immune system and thrive in the host environment, remains unclear.

Purpose
We aimed to determine the role of neutrophils and neutrophil extracellular traps (NETs) in IE progression using a novel mouse model.

Methods
We intravenously injected mice with S. aureus and locally stimulated the endothelium with histamine, resulting in IE lesions that originate on inflamed heart valves. After three days we determined the development of IE on the aortic valves with Gram staining and echocardiography. We investigated the presence of NETs in 14 mice by immunostaining for citrullinated histone H3 (H3Cit), extracellular DNA, and myeloperoxidase. Of these 14 mice, 9 developed endocarditis. In a separate set of experiments, we investigated the role of neutrophils in IE development by injecting a neutrophil-depleting or control antibody 24h before surgery.

Results
Echocardiography revealed real IE lesions attached on inflamed aortic valves. Mice with endocarditis had significantly (P=0.005) more detectable H3Cit (9/9) than those without (1/5). More specifically, four mice had H3Cit+ neutrophils within thrombi, indicating early NETosis. Seven mice had an extracellular H3Cit staining pattern within the thrombus. These extracellular H3Cit-positive regions were associated with DNA and myeloperoxidase, indicating the presence of a network of NETs. When we depleted neutrophils, mice developed significantly more endocarditis (7/16 vs. 1/15, P=0.03).

Conclusion
Endocarditis lesions contained NETs or neutrophils undergoing NETosis, and neutrophil depletion led to increased IE incidence. Further investigating these two players in IE could potentially provide new strategies to combat this deadly disease.

Acknowledgement/Funding
FWO SB
P3661Two-fold increase in incidence of infective endocarditis in the period 1997–2016: a Danish nationwide study
Authors: Dalsgaard Jensen A , Ostergaard L , Eske Bruun N , Voldstedlund M , Torp-Pedersen C , Gislason G , Koeber L , Loldrup Fosboel E 
Published: October 2019

Abstract

Background
Infective Endocarditis (IE) is a disease with high mortality. Previous studies have shown considerable differences and contradicting trends in overall incidence and mortality why data from an unselected nationwide cohort is needed.

Purpose
We investigated temporal trends in the incidence rate and in-hospital mortality of IE in Denmark in the period of 1997–2016.

Methods
We included cases of first-time IE (1997–2016) using Danish nationwide registries. Crude incidence rates were given for each calendar year. Further, incidence rates were reported for subgroups of age and sex. For the analysis of patient characteristics and in-hospital mortality, the study cohort was grouped into four 5-year intervals (1997–2001, 2002–2006, 2007–2011, 2012–2016). Multivariable adjusted Cox proportional hazard model was used to compare in-hospital mortality between groups.

Results
A total of 8,147 patients with IE were identified in the period of 1997–2016. The median age and proportion of males increased from 64.3 years (P25-P75: 48–75.5) and 59.1% to 71.8 years (P25-P75: 62.1–79.9) and 67.1% in 1997–2001 and 2012–2016, respectively. The overall incidence rate (Figure 1) increased from 4.68/100.000-person-years (PY) (CI95: 4.17–5.26) to 8.23/100.000 PY (CI95: 7.53–8.99) in 1997 and 2016, respectively. Male incidence increased from 5.35/100.000 PY (CI95: 4.59–6.23) to 11.03/100.000 PY (CI95: 9.9–12.29) and female incidence increased from 4.03/100.000 PY (CI95: 3.38–4.8) to 5.44/100.000 PY (CI95: 4.67–6.35) in 1997 and 2016 respectively. Incidence rates increased more than seven-fold for the oldest age group (≥80 years) from 1997 to 2016 (6.95/100.000 PY [CI95: 5.32–9.08] to 51.19/100.000 PY [CI95: 43.41–60.38], respectively). In-hospital mortality was significantly lower for patients with IE in the period of 2011–2016 compared with 1997–2001 HR: 0.8 (CI95: 0.69–0.92).
Figure 1

Conclusion
Infective endocarditis incidences are increasing mostly among men and elderly patients. In order to prevent this disease as best as possible, we need more knowledge on causes for this increasing incidence.
P3667Diagnostic value of cardiac CT scan in patients with suspected infective endocarditis
Authors: Simoni A S S , Di Biceglie M D B , Alessandrini M A , Resseguier N R , Casalta A C C , Pradier J P , Casalta J P C , Gouriet F G , Riberi A R , Raoult D R , Drancourt M D , Collart F C , Jacquier A J , Habib G H 
Published: October 2019

Abstract

Background
Infective endocarditis (IE) is a severe disease requiring early diagnosis and treatment. Although echocardiography (ECHO) is the key diagnostic method, CT-scan (CT) has recently been added as a new ESC diagnostic criterion. However, published data are scarce and included few patients

Purpose
To assess the additional value of CT over ECHO for the diagnosis of IE

Methods
Between 2014 and 2017, 246 pts with suspected IE underwent both ECHO and CT. Using the expert consensus of the Endocarditis Team after a 3-month follow-up as gold standard, 222 IE were confirmed (112 native [NVE] and 110 prosthetic [PVE]) and 24 were rejected.
The primary end-point was the comparison between ECHO and cardiac CT (CCT) findings.
The secondary end-point was the change in diagnostic criteria sensitivity and specificity associated with the addition of CT results.

Results
1. Among the 110 cases of definite PVE,
– Vegetations were found in 49 (44%) pts by ECHO and 45 (40%) by CCT (agreement in 71 [64%] pts).
– Periannular lesions were found in 33 (30%) pts by ECHO and 46 (41%) by CCT (agreement in 86 [77%] pts).
– CCT found a new cardiac lesion missed by ECHO in 10 (9%) pts.
2. Among the 112 cases of definite NVE,
– Vegetations were found in 84 (76%) pts by ECHO and 90 (81%) by CCT (agreement in 84 [76%] pts).
– Periannular lesions were found in 34 (30%) pts by ECHO and 29 (26%) by CCT (agreement in 58 [52%] pts).
– CCT found a new cardiac lesion missed by ECHO in 3 (3%) pts.
3. Including CT findings as major and minor criteria increased the sensitivity of Duke criteria from 60 to 70% in 124 suspected PVE, and from 73 to 80% in 122 suspected NVE, without significant decrease in specificity.

Conclusions
1. This study is the largest prospective study assessing the value of CT in the diagnosis of IE.
2. Adding CT findings significantly increases the sensitivity of Duke criteria, both in NVE and PVE.
3. Our results support the use of ESC criteria including CT rather than Duke criteria.
P3672Effects of inhaled nitrite in addition to sildenafil in thalassemia patients with pulmonary hypertension
Authors: Sasiprapha T , Pussadhamma B , Sibmooh N , Chuncharunee S , Sritara P , Yingchoncharoen T 
Published: October 2019

Abstract

Background
Pulmonary hypertension is the major morbidity and mortality in patients with thalassemia. Recent studies have found that inhaled nebulized nitrite can significantly decrease pulmonary pressure in immediate response, but data are needed to determine its clinical benefits.

Methods
We conducted a multicenter, randomized, double-blind, placebo-controlled trial including thalassemia patients with symptomatic pulmonary hypertension, diagnosed by right heart catheterization and were currently treated with sildenafil. Patients continued the optimum dose of sildenafil and were randomly assigned into 2 groups; the treatment group and the control group. The treatment group was given 30 mg of inhaled nebulized nitrite twice a day for 3 months while the control group was given inhaled normal saline. The outcomes were the improvement of clinical and echocardiographic parameters at 1 and 3 months.

Results
A total of 12 patients were recruited, 5 were assigned to the treatment group and 7 to the control group. The median of sildenafil in both group were 60 mg/day. Treatment with the inhaled nebulized nitrite in addition to sildenafil significantly reduced the mean pulmonary artery pressure at 3 months when compared to placebo (median −7.30 mmHg in treatment group vs +2.30 mmHg in control group, P=0.016). In the treatment group, the median 6-minute walk distance was significantly increased from 380 m to 427 m. at 1 month (P=0.043) but there was no significant difference in the median change of 6-minute walk distance when compared to control group at 3 months (+48 m. in treatment group vs +17.5 m. in control group, P=0.286). No significant difference in NT-proBNP change between the two groups was detected. There were no hypotension or other major adverse effects in the treatment group.
Clinical and Echoparemeters Outcome

Conclusions
The addition of inhaled nebulized nitrite to sildenafil can decrease mean pulmonary pressure and has a tendency to improve six minutes walk distance in thalassemia patients with pulmonary hypertension.

Acknowledgement/Funding
Cooley's anemia foundation, Mahidol university research funding