bluuebunny/crossref_metadata_2025_split huggingface dataset:
P5731Optimal blood pressure in diabetic hypertensive patients with overt proteinuria
Authors: Lee C J , Hwang J , Kang C Y , Kim H , Ha J , Chun K.-H , Oh J , Lee S.H.- , Kang S.-M , Park S , Yoo T.-H 
Published: October 2019

Abstract

Background
Evidence for the benefit of intensive blood pressure lowering in diabetic nephropathy is not clear at this time. The objective of this study was to demonstrate whether lower mean blood pressure (BP) in treated hypertensive patients with diabetic nephropathy is associated with better prognosis.

Methods
From the National Health Insurance Service (NHIS) Health Examination Database, diabetic hypertensive subjects with proteinuria between 2009 and 2010 were selected and followed-up until 2015 (N=8,663). Mean of the recorded systolic and diastolic BP during follow-up health examinations were stratified into five categories (SBP: <120, 120 to <130, 130 to <140, 140 to <150, and ≥150 mmHg; DBP: <70, 70 to <80, 80 to <90, 90 to <100, and ≥100 mmHg). All-cause death, myocardial infarction (MI), stroke, and renal outcome (progression to end stage renal disease or doubling of serum creatinine) were examined by Cox proportional hazard models with the propensity scores adjusted method.

Results
Compared to SBP of 130 to <140 mmHg, SBP of 120 to <130 mmHg was associated with lower risk of all-cause death (HR=0.78; 95% CI, 0.64–0.95), stroke (HR: 0.65; 95% CI, 0.45–0.94), and renal outcome (HR: 0.81; 95% CI, 0.68–0.97). SBP of <120 mmHg was associated with benefit for renal outcomes (HR: 0.69; 95% CI 0.55–0.88) but not with elevated risk of other outcomes. Compared to DBP of 80 to <90 mmHg, DBP of 70 to <80 mmHg were associated with lower risk of all-cause death (HR: 0.75; 95% CI, 0.64–0.88) but with higher risk of MI (HR: 1.52; 95% CI, 1.05–2.21). DBP of <70 mmHg was associated with reduced risk of all-cause death (HR: 0.79; 95% CI, 0.64–0.98).

Conclusion
In diabetic hypertensive subjects with overt proteinuria, deterioration of renal function decreased with decreasing SBP and the lowest risk of all-cause death and stroke were observed in SBP <130 mmHg. Low DBP was associated with low risk of all-cause death but there was a J curve phenomenon for MI in DBP of 70 to <80 mmHg.
P5738Multicenter analysis of left ventricular unloading on top of VA-ECMO for treatment of cardiogenic shock
Authors: Schrage B , Dabboura S , Bezerra H , Sinning J M , Thiele H , Pauschinger M , Frank D , Schulze P C , Pappalardo F , Morrow D , Li Y , Eitel I , Nordbeck P , Skurk C , Westermann D 
Published: October 2019

Abstract

Background
Veno-arterial extracorporeal membrane oxygenation therapy (VA-ECMO) is increasingly used for treatment of severe cardiogenic shock, although it causes an increase in left ventricular (LV) afterload and might therefore hamper myocardial recovery. Recently, the addition of catheter-based left ventricular assist device (cLVAD) on top of VA-ECMO has been used to unload the LV and to improve outcome measures. However, there is limited data on predictors of outcome in this high-risk population.

Aim
The aim of this study was to evaluate predictors of 30-day survival in a multicentre cohort of severe cardiogenic shock patients treated with cLVADon top of VA-ECMO.

Material and methods
We report on consecutive patients from six tertiary care centers being treated with cLVAD in addition to VA-ECMO for treatment of cardiogenic shock. The primary endpoint is 30-day all-cause mortality. To identify predictors of the primary endpoint, multivariate analysis using an “elastic net” variable selection algorithm was done after imputation of missing variables.

Results
A total of 220 patients treated with cLVAD on top of VA-ECMO were included in the analysis. Of these, 79.1% were male with a median age of 55.5 (25thpercentile 48.0, 75thpercentile 65.6) years. In 60.5% of the patients, acute myocardial infarction was the underlying cause of cardiogenic shock and in 44.6% VA-ECMO was used for refractory cardiac arrest (eCPR). In the multivariable analysis, the following baseline parameters were significantly associated with the primary endpoint: Age (odds ratio of 1.68 per standard deviation), duration of cardiopulmonary resuscitation (OR 2.08 per SD), lactate (OR 1.04 per SD) and time from onset of shock to VA-ECMO (OR 1.30 per SD).

Conclusion and outlook
In this large-scale multicentre analysis of severe cardiogenic shock patients treated with VA-ECMO plus additional cLVAD unloading, age, duration of cardiopulmonary resuscitation, lactate and time from onset of shock to VA-ECMO were significantly associated with 30-day all-cause mortality.
To further investigate this topic, we will evaluate predictors of outcome in distinct patient populations such as acute myocardial infarction vs. acute heart failure and patients without vs. patients with prior cardiopulmonary association.
P5975Diminished LV systolic velocity on tissue Doppler imaging is linked to an amplified risk of lethal arrhythmias independently of LV ejection fraction
Authors: Barakat M F , Sunderland N , Chehab O , Kaura A , Hayat S , Amin-Youssef G , Scott P , Okonko D O 
Published: October 2019

Abstract

Background
Life threatening arrhythmias (LTA) can trigger sudden cardiac death, or provoke implantable cardioverter defibrillator (ICD) discharges that escalate morbidity and mortality. Longitudinal myofibrils predominate in the subendocardium which is uniquely sensitive to arrhythmogenic triggers.

Objectives
To test the hypothesis that mitral annular systolic velocity (S'), a tissue Doppler index of LV long-axis systolic function, might predict lethal arrhythmias irrespective of LVEF.

Methods
We analysed data from diverse ICD and cardiac resynchronization therapy defibrillator (CRT-D) patients at 2 London centres. Channelopathies were excluded. S' was averaged from medial and lateral mitral annuli velocities. Primary outcome was time to sustained ventricular tachycardia (VT) or fibrillation (VF) needing device therapy.

Results
In 302 patients (mean age 68 years, LVEF 32%, 77% male, 52% ischemic, 35% primary prevention, and 53% CRT-D), median S' was 5.1 (IQR: 4.0–6.2) cm/s and lower in CRT-D than ICD subjects. After a median follow-up of 15 months, 56 (19%) subjects had LTA and those who did had a lower S' than those who did not (4.6±1.4 cm/s vs. 5.4±1.7 cm/s, P=0.003-Fig A). Each 1cm/s lower S' correlated to a 43% increased risk of LTA (HR: 0.70, 95% CI: 0.57–0.87, P=0.001) independently of age, gender, β-blocker use, centre, ICD use and LVEF. Adding S' to the baseline model improved net reclassification (P=0.02) implying incremental utility (Fig B). An S' ≤5.6cm/s was the best cut-off, conferring a 2.4-fold higher LTA risk than an S'>5.6 cm/s (95% CI: 1.17–4.37, P=0.02–Fig C).

Conclusion
A lower S' forecasts an enhanced probability of LTA in cardiac device recipients irrespective of LVEF, and could be used to titrate medical, device and ablative therapies to mitigate future arrhythmic risk.
P5978Mechanical dispersion is a predictor of 30-day permanent pacemaker implantation after transcatheter aortic valve replacement
Authors: Manshad A S , Hemu M , Ballout F A , Zimmerman A , Hein K Z , Kavinsky C J 
Published: October 2019

Abstract

Background
Transcatheter aortic valve replacement (TAVR) related conduction disturbance resulting in permanent pacemaker (PPM) implantation is a common complication. The mechanical effects of these conduction abnormalities can be measured as regional heterogeneity of contraction by myocardial strain imaging.

Objectives
The aim of this study was to investigate whether post-TAVR left ventricular mechanical dispersion (MD) can predict PPM implantation.

Methods
We retrospective analyzed 137 patients (48% men, 80±9 years) who underwent TAVR at our institution after excluding patients with pre-existing PPM. 2D speckle-tracking echocardiography was used to assess MD (SD of time from Q/R on the ECG to peak strain in 16 LV segments) immediately after TAVR (median, 1 day). Images were analyzed offline using a vendor-independent software (TomTec).

Results
At 30-days post-TAVR, 14 (10.2%) patients underwent PPM implantation. Patients requiring PPM had more pronounced MD (p=0.012), pre-existing RBBB (p=0.017), pre-existing LAHB (p<0.001), and peri-procedural AVB (p=0.005). Multivariate Cox regression analysis of important clinical covariates (model 1 = age, sex, RBBB, LAHB, AVB) showed significant predictive value for PPM implantation (chi-square 41.8, p<0.001). Addition of MD to the model resulted in a significant chi-square increase (from 41.8 to 47.3, p=0.01).

Conclusion
Left ventricular MD, measured immediately after TAVR, was associated with 30-day PPM and provided incremental predictive value to important clinical variables.
P5980Etiology of perioperative myocardial injuries after non-cardiac surgery and associated outcomes
Authors: Puelacher C , Gualandro D M , Lurati Buse G , Marbot S , Gueckel J , Hidvegi R , Wildi K , Espinola J , Kindler C , Lampart A , Bolliger D , Osswald S , Mueller C 
Published: October 2019

Abstract

Background
Perioperative myocardial injuries (PMI) are a common complication following non-cardiac surgery associated with significantly increased postoperative mortality. Due to its mostly asymptomatic presentation it is currently often missed in clinical routine. With the advent of routine screening PMI will be an increasingly recognised. Therefore, a more detailed understanding of the different etiologies causing PMI is needed to guide management.

Methods
We included consecutive high-risk patients (defined as known cardiovascular disease or aged ≥65 years) undergoing major non-cardiac surgery at two hospitals into this prospective multicenter observational study. All patients received a systematic screening using cardiac troponin (cTn) in clinical routine for detection of PMI, defined as an absolute cTn-rise from baseline values within 3 days of surgery. Patients were contacted to assess occurrence of major adverse events (MACE) including all-cause death at 30-days. First, we identified preoperative existing comorbidities as well as perioperative factors associated with PMI by multivariable regression analysis. Second, PMI were centrally adjudicated to identify predefined subtypes (“type I myocardial infarction (T1MI)”, “acute heart failure” (AHF), “tachyarrhythmia”, “extra-cardiac” triggers, “unknown”) by two independent reviewers using all clinical information available, and subtypes tested for association with 30-day (MACE).

Results
From 2014 to 2016 we enrolled 4250 patients undergoing 5375 surgeries. PMI occurred after 785 (14,5%) surgeries. Occurrence of PMI was more frequent with older age and cardiovascular comorbidities, especially insulin-dependent diabetes mellitus and chronic kidney disease. Perioperatively multiple known type II triggers (hypotension, bleeding, hypoxemia, tachycardia, length of surgery) were associated with PMI. Only 5,0% of PMI were adjudicated as “T1MI”, 4,3% as “AHF”, 4,3% as “tachyarrhythmia”, 12,0% “extra-cardiac” and the majority of 74,4% as “unknown”. The subtypes were associated increased MACE-rates (24% for T1MI, 40% for “AHF”, 22% for “tachyarrhythmia”, 24% for “extra-cardiac”, 7,1% for “unknown”) compared to non-PMI patients (1,8%, p<0,001 see Figure).
MACE within 30 days following surgery

Conclusion
PMI occurs more likely in patients with preoperative existing comorbidities, PMI are associated with type II triggers in the intra- as well as postoperative period. We identified subtypes allowing a risk-stratification to identify high-risk types and guide clinical management.

Acknowledgement/Funding
Swiss National Science Foundation, Swiss Heart Foundation, Cardiovascular Research Foundation Basel, Roche
P5981Impact of radiotherapy on myocardial function and paravalvular leaks after transcatheter aortic valve implantation (TAVI)
Authors: Cicenia M , Marchetta S , Dulgheru R , Ilardi F , Bouziane M , Cimino S , Mancone M , Fedele F , Lancellotti P 
Published: October 2019

Abstract

Introduction
Thanks to the anticancer therapies, the life expectancy of the oncologic patients has noticeably increased, but several cardiac diseases can be observed in these patients as the result of the cardiotoxic effects.

Purpose
To investigate the impact of radiotherapy on the clinical and echocardiographic outcomes, in patients with severe aortic stenosis (AS) and preserved left ventricle ejection fraction (LVEF) treated with transcatheter aortic valve implantation (TAVI).

Methods
We recruited patients with severe AS and left ventricular ejection fraction (LVEF) ≥50‰ treated with TAVI and who received prior radiotheraphy. Patients with LVEF <50‰, treated with valve in valve, with inadequate acoustic windows or the absence of echocardiographic images pre-TAVI and after 3–6 months were excluded. Demographic, clinical and echocardiographic data were recorded.

Results
102 patients were included in the present analysis. They were divided in two groups: 19 (18‰) with an oncologic history treated with previous left thoracic/mediastinal radiotherapy and 83 (82‰) patients without an oncologic history. The two groups were homogeneous in terms of demographic and clinical data, brain natriuretic peptide (BNP), echocardiographic data pre-TAVI. They only differed for a greater prevalence of mitral stenosis and calcifications in the oncologic patients versus the non-oncologics (respectively 36‰ vs. 12‰ p=0,016; 73‰ vs. 29‰ p=0,001). No differences in terms of in-hospital clinical outcomes were observed. The echocardiographic evaluation in both groups showed a significant decrease of the peak velocities and of the transprosthetic gradients. There was a higher incidence of at least moderate degree paraprosthetic leaks in the oncologic group vs. the non-oncologic one: 6 (31‰ total leaks, 37‰ leaks >2+) vs. 7 (8‰ total leaks, 12‰ leaks >2+); p=0.029. After 3–6 months, there was not a statistically significant improvement of ejection fraction (EF) in neither of the two groups but there was a statistically significant improvement of transmural, subepicardial and subendocardial longitudinal strain values in the non-oncologic group compared to pre-TAVI values, respectively −19±4 vs. −17±4 (p<0.001); −17±3 vs. −15±3 (p<0.001); −22±4 vs. −19.8±4 (p<0.001). Any statistically significant improvement was detected in the group with history of anticancer treatments between the longitudinal strain values post and pre-TAVI (−18±3‰ vs. −16±3‰; −14±3‰ vs. −20±5‰; −20 ±± 5‰ vs. −19±4‰).

Conclusions
Patients affected by severe AS treated with TAVI and who received received prior radiotheraphy, showed the absence of statistically significant improvement of multilayer strain values, at 3–6 months after TAVI. Oncologic patients also had a higher incidence of haemodynamically relevant paravalvular leaks after the intervention, compared to the non-oncologic patients.
P5992Why aortic valve disease may persist after surgery? A joint basic science - Clinical effort
Authors: Petersen J , Kloth B , Grammatika-Pavlidou N , Eschenhagen T , Reichenspurner H , Nikolaev V O , Christ T , Molina C E , Girdauskas E 
Published: October 2019

Abstract

Background
Diseases of the aortic valve are a common reason for heart surgery. Aortic stenosis (AS) is associated with pressure and aortic regurgitation (AR) with a volume overload of the left ventricle (LV). Over time both pathologies lead to systolic and diastolic heart failure, while progressive downregulation of β-adrenoceptors occurs. While LV re-remodeling occurs in the majority of patients after aortic valve surgery, LV dysfunction persists in one fourth of such patients and leads to a terminal heart failure. We aimed to investigate whether differential remodeling in the protein kinase A (PKA) dependent inotropic response in myocytes and myocardial tissue obtained from patients undergoing aortic valve surgery is associated with the LV re-remodeling after surgery.

Methods
Preoperatively, pro BNP levels were measured and left ventricular strain analysis via echocardiography was performed. Interventricular septal biopsy was obtained intraoperatively in 10 patients who underwent aortic valve surgery. In-vitro contractility was analyzed in myocardial tissue paced with 4 Hz at 37 °C. Freshly isolated cells were transduced with an adenovirus expressing a cytosolic Förster resonance energy transfer (FRET) based cAMP biosensor (Epac1-camps). After 48 hours of culture, Föster-resonance energy transfer (FRET) was used for the first time to measure cAMP in 60 isolated human ventricular myocytes. Isoprenaline (10 nM – 10 μM) was used for β-adrenoceptor activation and forskolin (10 μmol) to activate adenylyl cyclase directly.

Results
We found a significantly downregulated β-adrenergic sensitivity in cardiomyocytes of patients with aortic valve disease, although contractile response to forskolin was maintained. Furthermore, we found a clear association between reduced sensitivity to isoprenaline (i.e., high EC50 values) and low maximum effect size to isoprenaline in myocardial tissue of patients with aortic valve disease, pointing out relevant β-adrenoceptor dysfunction. There were no significant differences in basal myocardial force between tissue samples of patients with AR and AS.

Conclusion
Collectively, our data show a profound remodelling in the cAMP/PKA pathway in patients with aortic valve disease. These disturbances may have an impact on the postoperative ventricular function and possibly on the long-term LV re-remodelling after aortic valve surgery.
P6001Inflammation, coronary microvascular function and diastolic function - Is there a link?
Authors: Suhrs H E , Schroder J , Bove K B , Mygind N D , Frestad D , Michelsen M M , Lange T , Gustafsson I , Kastrup J , Prescott E 
Published: October 2019

Abstract

Background
It has been proposed that multiple comorbidities including diabetes, hypertension and dyslipidemia contribute to a pro-inflammatory state that induces oxidative stress in the microvascular endothelium, leading to coronary microvascular dysfunction (CMD) and cardiac diastolic dysfunction.

Purpose
We tested the hypothesis that subclinical inflammation is an underlying cause of both CMD and diastolic dysfunction and that the effect of inflammation on diastolic function is partly mediated by CMD.

Methods
In a cross-sectional study design, we included women with angina but no flow limiting coronary artery stenosis (180 with diabetes, 156 without diabetes) and 95 asymptomatic controls. Blood samples were analysed for 91 mainly inflammatory cardiovascular biomarkers. Coronary microvascular function was assessed as coronary flow velocity reserve (CFVR) by transthoracic Doppler echocardiography. Correlation of each biomarker with CFVR and E/e' as a marker of diastolic function, was examined by age adjusted linear regression and mediation analysis was conducted to assess if any effect of inflammation on E/e' was mediated by impaired CFVR.

Results
CFVR was lowest in patients with diabetes and highest in controls and, conversely, E/e' was highest in patients with diabetes (both test for trend p<0.001). Of the 91 biomarkers, 29 had a significant negative correlation with CFVR, 26 had a significant positive correlation with E/e' and 14 were associated with both CFVR and E/e'. CFVR and E/e' were correlated in a subgroup of patients with more pronounced CMD and higher E/e' (p=0.012) but not in the total population (p=0.818). A mediation analysis did not indicate that any effect of inflammation on E/e' was mediated by impaired CFVR.
Population charachteristics compared across groups with trend test (unadjusted linear regression) Diabetes (n=180) No diabetes (n=156) Control (n=95) p for trend Age, mean (min, max) 64 (36,80) 62 (32,80) 61 (32,81)* 0.003 BMI, mean (min, max) 30.7 (15.2, 45.5) 26.1 (18.6,40.0)* 24.7 (18.6,38.4)* <0.001 Hypertension, n (%) 133 (75%) 85 (55%)* 15 (18%)* <0.001 CFVR, median (IQR) 2.22 (1.90, 2.56) 2.35 (1.96, 2.74) 2.63 (2.22, 3.08)* <0.001 E/e' ratio, median (IQR) 9.79 (8.14, 12.21) 8.07 (6.85, 9.95)* 7.86 (6.89, 9.58)* <0.001 *p<0.005 compared with the diabetes group. BMI: body mass index; CFVR: coronary flow velocity reserve.
Generic directed acyclic graph

Conclusion
This is the first study to link a large number of mainly inflammatory biomarkers to CMD and diastolic dysfunction in patients suspected of microvascular angina. Direct association between CMD and diastolic function was only seen in those with impaired CFVR and poorest diastolic function.

Acknowledgement/Funding
The Danish Council for Independent Research and the Danish Heart Foundation
P6002Impaired peripheral endothelial function is associated with microvascular injury assessed by cardiac magnetic resonance imaging and decreased coronary flow in patients with STEMI
Authors: Van Der Hoeven N W , Janssens G N , Nap A , Everaars H , Van De Ven P M , Van Rossum A C , Escaned J , Van Leeuwen M A H , Van Royen N 
Published: October 2019

Abstract

Background
Microvascular injury (MVI) occurs in about 50% of successfully revascularized ST-elevation myocardial infarction (STEMI) patients and is associated with a decreased clinical outcome. MVI results from myocardial reperfusion injury, subsequent inflammation and coronary endothelial dysfunction. A correlation between peripheral and coronary endothelial function has been suggested and peripheral endothelial dysfunction is associated with the occurrence of cardiovascular events. Therefore we hypothesize a relation between peripheral and coronary endothelial function.

Purpose
The primary aim of our study was to assess the relationship between peripheral endothelial function and microvascular injury in successfully resvascularized STEMI patients.

Methods
Peripheral endothelial function and laboratory values were measured in the acute and stable setting (at 1 year follow-up). Reactive hyperemia-pulse amplitude tomography on the index finger was used to assess peripheral endothelial function by means of the reactive hyperemia index (LnRHI). After revascularization of the culprit vessel, we measured intracoronary coronary flow reserve (CFR). Cardiac magnetic resonance imaging (CMR) at day 5 evaluated the occurrence of MVI defined as microvascular obstruction (MVO) or intramyocardial hemorrhage. Myocardial salvage index (MSI) was calculated as (area at risk − final infarct size) / area at risk.

Results
We included 110 STEMI patients with the age of 60.1±9.5 years. Acute LnRHI was 0.56±0.33 and stable LnRHI was 0.64±0.27 (p=0.070). In the acute setting, LnRHI was impaired in patients with MVI compared to patients without MVI (0.44±0.37 vs. 0.61±0.34, p=0.045). The quantity of MVO (in grams) correlated with acute LnRHI (rho=-0.24, p=0.028). Acute LnRHI correlated to CFR in the revascularized culprit vessel (rho=0.25, p=0.015). In patients with decreased coronary blood flow after successful revascularization (TIMI-flow≤2), stable LnRHI was decreased (0.51±0.36 vs. 0.67±0.24, p=0.019). Stable LnRHI correlated to MSI (rho=0.28, p=0.020). Acute LnRHI correlated to leukocyte count (rho=-0.21, p=0.028) and LDH (rho=-0.25, p=0.018). LnRHI was impaired in patients who were hospitalized during 1 year follow-up (0.45±0.35 vs. 0.66±0.25, p=0.024).

Conclusion(s)
In patients with successfully revascularized STEMI, impaired peripheral endothelial function is associated with microvascular injury, decreased coronary flow and an increased inflammatory status. Furthermore, impaired peripheral endothelial function was associated with the occurrence of clinical events.