bluuebunny/crossref_metadata_2025_split huggingface dataset:
P1721 Reversible heart right failure. Pulmonary hypertension induced by Tyrosine Kinase Inhibitors
Authors: Fernandez Valledor A , Cepas Guillen P , Izquierdo M , Vidal P , Arjona R , Carbonell B , Flores Umanzor E , Lorenzatti D , Jorda P 
Published: January 2020

Abstract

BACKGROUND
Pharmacologically induced pulmonary hypertension (PH) is infrequent nowadays and it is included in the type 1 of the classification of PH.
Tyrosine kinase inhibitors (TKI) are the cornerstone of the treatment of many haemotopoietic stem cell diseases. Dasatinib is a second-generation TKI used in chronic myeloid leukemia (CML) and as an infrequent cardiovascular side-effect (&lt; 0,50%) could induce PH, usually reversible but life threatening. Only a few case series are published.
CASE DESCRIPTION: We present a 51-year-old woman who was diagnosed of a CML when she was 46. Initially, she underwent therapy with imatinib but after 5 years of treatment she developed resistance to this drug, and dasatinib was prescribed as a second line drug. After 3 months of continuous treatment, she started with dry cough and effort dyspnea. Blood analysis, EKG and Chest X-Ray were made but did not show outstanding findings. An unspecific viral infection was the final diagnosis. The patient clinical condition deteriorated with major dyspnea and edemas in the lower limbs. A TTE showed moderate tricuspid regurgitation and severe HP systolic pulmonary artery pressure (sPAP) of 80 mmHg. The pulmonary acceleration time was shortened and a mesosistolic knock was present. Systolic dysfunction of the right ventricle and pericardial effusion (image 1,2,3,4) were noted. The right atrium was not dilated. Cava vein was dilated but with inspiratory collapse &gt;50%. The left ventricular function was preserved, but first degree diastolic dysfunction was found. Other causes of PH were excluded (types 2, 3, 4). A CT pulmonary angiogram did not show segmental perfusion defects. Finally, a right heart catheterization confirmed the TTE findings: severe precapillary PH without postcapillary component. After the diagnosis was confirmed, TKI was stopped and double targeted therapy with ambrisentan + tadalafil was started. After 6 months of treatment a new TTE was made with complete reversal of the secondary changes in the myocardium induced by the PH. No tricuspid regurgitation was detected nor any indirect sign of PH was found. (image 5,6).

CONCLUSIONS
Drug-induced PH is rare nowadays and most cases were described in the seventies in the USA related with the epidemic of anorexigenic drugs. Although the pathogenesis still remains unclear, treatment includes immediately stopping the offending agent.
Echocardiography due to its accessibility, reproducibility, consistence and low cost should be the first diagnostic tool to be considered, because as it is known, in the early stages of the disease, before developing right disfunction, clinical and conventional tests are non-specific.
Abstract P1721 Figure. Echo images: previous and afte treatment
P1723 Spectacular left ventricle post infarction aneurysm
Authors: Bednarek A , Wieczorek J , Elzbieciak M , Deja M , Mizia-Stec K 
Published: January 2020

Abstract
Sixty six-y.o. woman 2 months after anterior wall ST-segment elevation myocardial infraction and PCI LAD + 3DES (TIMI 1) was re-admitted to the clinic because of progressive severe heart failure (NYHA III/IV). In admission NT-proBNP level was 14 000 pg/ml, INR 1,7, bilirubin 4,5mg/dl. The electrocardiogram showed persistent ST elevation on anterior leads. Transthoracic echocardiography (TTE) revealed spectacular finding: aneurysm of left ventricle (LV) involving ½ distal part of interventricular septum, apex, inferior, anterior and lateral wall with LVEF 24%, LVEDV 272ml. Thickness of intraventricular septum (IVS) on aneurysm level was only 2,5-3,5mm. In the middle part of IVS a minimal ventricular septal defect (VSD) was showed. Cardiac magnetic resonance examination confirmed TTE findings. The course of the disease was dynamic. The diameter of VSD was increased during consecutive days of hospitalization with maximum width 6,5mm. The patient was hemodynamical unstable, she needed pressure amines, diuretics and intra-aortic balloon pumping. The patient underwent several Heart Team consultations. She was disqualified from percutaneous VSD closing because of thickness of IVS and spiral shape of VSD. Due to potentially too small LV volume after LV plastic surgery the patient was also disqualified from that procedure. We reported the patient to heart transplantation (HTX). There was no transplant donor. In next days we observed progressive signs of a cardiogenic shock with right ventricle decompensation secondary to widening of VSD. Because of unstable stage and growing decompensation, no possibility of HTX patient had life—saving cardiac surgery of LV with mitral valve and tricuspid valve anuloplasthies. The patient survived operation.
Abstract P1723 Figure.
P1724 Bidimensional echocardiographical radial strain abnormalities mandate differential diagnosis between athlete heart syndrome and incipient genetic cardiomyopathy
Authors: Cojocaru C , Pupaza A , Radu D A , Onciul S , Vatasescu R G 
Published: January 2020

Abstract
Background
Left ventricular dilation and mild systolic dysfunction at rest in young endurance athletes may mandate differential diagnosis between adaptive physiology and various forms of incipient non-ischemic dilated cardiomyopathies, especially if family history is positive. Multimodal imaging (i.e. bidimensional echocardiography (TTE), speckle tracking echography (STE) and cardiac magnetic resonance (CMR)) can accurately diagnose "true" underlying heart disease.
Purpose
We sought to outline the efficacy of multimodality imaging in dilated left ventricular phenotypes with mild systolic dysfunction of athletes.
Methods
We present the case of a 45 year old Caucasian male, rock climbing athlete (14 hours of training per week), with no prior personal medical history, who was admitted for fast palpitations leading to syncope immediately after a training session. Family history revealed maternal non-ischemic cardiomyopathy with complete atrioventricular (AV block requiring permanent pacing at a similar age. Stable, clinically asymptomatic, nodal complete AV block ∼ 40 bpm was diagnosed by ECG. TTE revealed a dilated LV (61 mm left ventricular end-diastolic diameter (LVIDd)) with no hypertrophy, with decreased diffuse contractility (LVEF ∼ 43%). Exercise echocardiography showed no improvement in LVEF, despite transition from complete AV block to first AV grade block. Moreover, moderate mitral regurgitation by posterior mitral leaflet (PML) prolapse was discovered. STE demonstrated normal global longitudinal strain (GLS), but decreased interventricular septum (IVS) radial strain (RS) (figure A). Late gadolinium enhancement was evident along the interventricular septum and the right ventricular insertion points in CMR (figure B), with no edema.
Results
The association of LV dilation (with multiple apparent causes – endurance training, genetic substrate, PML prolapse) with mild systolic dysfunction that persisted during echocardiographic exercise testing and a reduced IVS RS (with physiological GLS) was observed. Subsequently, mid-myocardial septal scarring in CMR was consistent with a diagnosis of "true" dilated cardiomyopathy. A cardiac resynchronization defibrillator device was implanted and genetic testing is in progress (lamin disease suspicion).
Conclusions
Athlete’s heart syndrome phenotypes may overlap with forms of genetic dilated cardiomyopathy.
1. The diagnostic suspicion of structural heart disease derived from echocardiography (radial strain & exercise echocardiography abnormalities), with subsequent confirmation by late gadolinium enhancement myocardial fibrosis.
2. The prospective sudden cardiac death risk requires careful assessment. The presence of clinical arrhythmic syncope, septal CMR fibrosis and specific genetic mutation lead to the decision of ICD (internal cardioverter defibrillator) implantation.
Abstract P1724 Figure. A - 2D Radial strain B - LGE CMR
P1734 Surprising image in the aortic root, is it zebra ?
Authors: Alak C , Cirgamis D , Badak O , Ozpelit E 
Published: January 2020

Abstract
CASE
80 year old-man patient was admitted our emergency department with dyspnea and chest pain. Transthoracic echocardiography (TTE) was performed.Ejection fraction was %60.Severe tricuspid regurtation was observed and pulmonary artery pressure was 55 mmHg.TTE showed mobile, hyperdense, flap-like appearance (Figure 1-A) Thorax computerized tomography (CT) angiography scan was performed with the suspicion of aortic dissection.CT angiography showed that there is no aortic dissection.(Figure 1-B) Transesophageal echocardiography (TEE) was planned. TEE showed an appearance consistent with the prosthetic material extending from the ascending aorta to the left main coronary artery.(Figure 1-C,D) When the patient"s history was investigated in detail, it was learned that the patient underwent coronary angiography six months ago.The patient was recommended bypass surgery, but he refused bypass surgery. Due to his rejection of bypass surgery, percutaneous intervention was attempted to the left anterior descending artery. Percutaneous coronary intervention was unsuccessful due to the severely calcified lesions. After learning this information, it was decided to perform imaging with fluoroscopy and chest CT without contrast.Because the image mimicking aortic dissection was thought to be the material related to previous unsuccesfull percutaneous coronary intervention. CT showed linear, hyperdense metallic densities that mimicked aortic dissection,extending form the left main coronary artery orifice to the ascending aorta. (Figure 1-E) The patient underwent imaging under fluoroscopy. In the imaging of the patient under fluoroscopy, it was observed that the image was consistent with the stent extending from the aorta to the left main coronary. (Figure 1-F) The mystery was solved and it was understood that during the unsuccessfull percutaneous coronary intervention the stent was removed from the balloon in the ascending aorta.
CONCLUSİON
In patients presenting with shortness of breath and chest pain, differantial diagnoses should always be life-threatening conditions such as aortic dissection, myocardial infarction and pulmonary embolism. When you hear hoofbeats, think of horses not zebras as taught in the early years of medical schools. Everything is never as it seems.Sometimes the sound of hoofbeats may also belong to the zebras.It is very important to evaluate the patient and medical history together with different perspectives.
Abstract P1734 Figure.
P1739 Diameter of the pulmonary artery in relation to the ascending aorta: a promising parameter for the diagnosis of pulmonary hypertension
Authors: Schneider M , Ran H , Pistritto A M , Gerges C , Heidari H , Hengstenberg C , Bergler-Klein J , Lang I , Binder T , Goliasch G 
Published: January 2020

Abstract

Background
Pulmonary hypertension (PH) is a disease with significant morbidity and mortality. The first imaging modality in the diagnostic algorithm is transthoracic echocardiography (TTE). Despite significant technological advances in recent years, there are still patients with PH who are missed by TTE. The pulmonary artery to ascending aorta ratio (PA/Ao-R) has been evaluated in cardiac magnetic resonance (CMR) and computed tomography (CT) studies. The ratio was able to detect patients with PH, it correlated with hemodynamics, and it was predictive for mortality. We sought to evaluate the diagnostic accuracy of PA/Ao-R measured by TTE in the detection of PH.

Methods
We evaluated consecutive patients who received quasi-simultaneous transthoracic echocardiography and right heart catheterization (RHC) for evaluation of pulmonary hypertension between July 2015 and July 2016.

Results
A total of 84 patients fulfilled the inclusion criteria, 47 were female, mean age was 65 years. Median PA/Ao-R was 0.8 (Q1;Q3 0.69;0.94). Seventy patients had PH (median mean pulmonary artery pressure (mPAP) was 35.5 mmHg, Q1;Q3 27;47). The area under the curve for the diagnosis of PH via PA/Ao-R was 0.853. A cut-off of 1 was chosen for further analysis. Sensitivity for the diagnosis of PH was 100%, specificity was 23%. PA/Ao-R correlated with mPAP (r = 0.65, p &lt; 0.001), and pulmonary vascular resistance (r = 0.68, p &lt; 0.001). In the subgroup of patients with PH, those patients with a PA/Ao-R of ≥1 had significantly (p &lt; 0.001) higher pulmonary pressures than those below, with a mean mPAP of 53 mmHg as compared to 38.5 mmHg.

Conclusion
PA/Ao-R correlates with mPAP. A ratio of ≥1 should prompt suspicion for the presence of PH. PA/Ao-R should be reported in every patient who is evaluated for PH.
P1742 Occurrence of right ventricle dysfunction in patients with Brugada syndrome: a follow-up study by echocardiography and electrophysiological examination
Authors: Mizumoto A , Amano M , Kamakura T , Hashimoto S , Oonishi E , Tanaka N , Izumi C 
Published: January 2020

Abstract
Background
Brugada syndrome (BrS) has been characterized by no apparent structural abnormalities in both ventricles, but, recently, the presence of subtle right ventricular (RV) structural abnormalities in patients with BrS has been reported.
Purpose
The aim of this study was to evaluate the occurrence of RV dysfunction in patients with BrS and their characteristics.
Methods
We enrolled 49 consecutive patients (54 ± 11 years old) diagnosed with Brs and underwent echocardiography from 2017 to 2018. The echocardiographic parameters and electrophysiological examinations were evaluated including RV size and function such as RV outflow and inflow tract diameter, TAPSE, S’, and FAC. Abnormality threshold for parameters of RV dysfunction is defined as followed: a TAPSE of &lt;17 mm, an S’ of &lt;9.5 cm, and an FAC of &lt;35%.
Results
Among 49 patients, one patient showed a TAPSE of &lt;17 mm, 5 patients an S’ of &lt;9.5 cm, and 10 patients an FAC of &lt;35%. Evaluating characteristics of Brs patients with RV dysfunction, all patients were divided into 2 groups by the value of RV FAC; 39 patients showing FAC &gt;35% (group A), 10 patients FAC ≤35% (group B). The comparison of each parameter between 2 groups is shown in Table. TAPSE and S’ in group B were lower than in group A. RV inflow tract diameter in group B was larger than in group A, although there was no differences in RV out tract diameter. There were no significant differences in left ventricular parameters, and grade of tricuspid regurgitation. QRS duration prolonged and the rate of ICD implantation was higher in group B than in group A. Moreover, all patients in group B showed RV wall motion abnormalities and the distribution was as followed: diffuse (n = 2), RV mid (n = 2), RV apex (n = 6).
Conclusions
BrS patients frequently showed RV dysfunction during follow-up, and it may be related to the prolongation of QRS duration. We should pay much attention to the occurrence of RV dysfunction in follow-up echocardiography.
Group A (FAC &gt;35%) N = 39 Group B (FAC ≤35%) N = 10 p-value TAPSE, mm 22.9 ± 2.1 20.4 ± 2.6 0.009 S", cm/s 12.8 ± 2.0 11.1 ± 1.4 0.010 RV outflow tract, mm 29.7 ± 4.4 31.2 ± 5.0 0.49 RV mid inflow tract, mm 30.4 ± 2.9 33.8 ± 3.7 0.008 RV basal inflow tract, mm 38.5 ± 3.2 43.7 ± 4.0 0.001 QRS duration, ms 112.9 ± 12.9 136.3 ± 28.4 0.006 Late potential positive, n (%) 25 (64) 8 (80) 0.34 ICD implantation, n (%) 19 (68) 9 (90) 0.019
P1744 Motion and velocity of the different parts of the AV plane. Relation to site and wall length
Authors: Stoylen A , Molmen H E , Dalen H E 
Published: January 2020

Abstract

Background
Displacement (MAPSE) and peak systolic velocity (S") of the various parts of the mitral annulus differ. Also, both indices are higher in the right ventricular free wall. We aimed to investigate the relations between wall motion, wall lengths and sites in the left ventricle, as well as comparing to the right ventricle to assess the influence on systolic deformation of the AV-plane.

Methods
The HUNT study examined 1266 subjects without evidence of heart disease from a mixed urban/rural population of North Trøndelag county, S", linear diastolic left ventricular annulus to apex distance (WL) and MAPSE was measured in the septal, anterior, lateral and inferior points of the mitral annulus. Intra individual variance and relative variance (variance / mean) of S" and MAPSE was calculated and compared to the same variance of the values normalised for wall length (S"/WL and MAPSE/WL).

Results
Wall lengths, velocities and MAPSE are shown in figure 1. Wall lengths were associated with both MAPSE and S". Both wall lengths and motion were greatest in the free walls of the LV, but smallest in the septal parts of the AVplane. Variances are shown in table 1. Even if intra-individual variances are larger for S" than MAPSE, relative variance for both decreased by 80 - 90% when normalised for wall length.

Conclusion
There is an intra-individual variability of MAPSE and S" of the LV, corresponding to WL, when the values normalised for WL most of the variability disappears. Intra individual variability of strain and strain rate per wall is less than MAPSE and S" as shown earlier. As the apex is located centrally, walls corresponding to the free walls are longer than those closest to the septum, thus motion and wall length are both greatest corresponding to the LV free walls.
Motion of the right ventricular free wall was higher than the LV free wall; TAPSE 2.8 cm, and S" 12.6 cm/s as shown previously. The relation of TAPSE and S" of the right ventricle to wall length will be different, as the afterload in the RV is far less. But as both lateral parts of the AV plane move more than the centre, givinga systolic bending of the AV-planealso as the central part of the AV-plane is centrally anchored to the large arteries as shown in fig. 1.
Table 1 WL (cm) MAPSE (cm) MAPSE / WL (% points) S" (cm/s) S" / WL (/s) Mean of 4 walls 9.5 1.6 0.16 8.4 0.87 Variance 0.04 0.04 0.0004 1.2 0.01 Relative variance (%) 2.8 2.7 0.25 12.1 1.4 Wall lengths (WL), displacement(MAPSE), Systolic velocity (S") and mAPSE and S" normalised for WL. Means and intra individual variances.
Abstract P1744 Figure. Fig. 1
P1745 Changes in diastolic function in patients with heart failure with reduced ejection fraction treated with sacubitril/valsartan
Authors: Mas Llado C , Ramis Barcelo M F , Pericas Ramis P , Valadron Sucasas C I , Noris Mora M , Forteza Alberti J F , Pasamar L , Morcuende A , Rodriguez Fernandez A , Gonzalez Codino R , Peral Disdier V 
Published: January 2020

Abstract

Introduction
Sacubitril/valsartan (S/V) has shown to improve mortality and reduce hospitalizations for heart failure in patients with reduced ejection fraction (HFrEF). It has been analysed its improvement in ejection fraction and left ventricle volumes. Very few studies have analysed its effect on diastolic dysfunction. The aim of this study is to determine if the treatment with S/V in patients with HFrEF produces changes in diastolic function.
Methods
We performed a prospective observational study in ambulatory patients with HFrEF and sinus rhythm that, according to the ESC guidelines, had indication to initiate S/V. An echocardiographic examination was done previous to start with S/V and 6 month after having been treated with it.
Results
A total of 67 patients were included in the study (Figure 1). After six months of starting with S/V, there was a statistically significant improvement in diastolic parameters (results are illustrated in table 1): it was observed better values of E/A, E/e’, left atrial maximal volume and deceleration time, leading to a reduction in filling pressures and diastolic dysfunction. Furthermore, we analysed recent parameters that have been postulated as new predictors of diastolic dysfunction, such as left atrial minimal volume (LAVmin), left atrial ejection fraction (LAEF) and left atrial strain (LAStr). There was a statistically significant reduction in LAVmin and values of LAStr after treatment with S/V, but no significant differences were observed in LAEF (table 1).

Conclusion
Treatment with S/V in patients with HFrEF leads to an improvement in diastolic function. More studies need to be done to analyse if S/V could have the same effect in patients with heart failure and preserved ejection fraction.
Figure 1: Population characteristics Gender (male, %) 74.6 High blood pressure (%) 53.7 Age (mean) 59.7 Diabetes mellitus (%) 40.3 Cardiomyopathy (%) Dyslipidaemia (%) 56.7 Ischemic 61.2 Smokers (%) 17.9 Non Ischemic 38.8 Treatment (%) Functional class (%) Beta-blockers 98.5 I 3 Aldosterone antagonists 91 II 71.6 Ivabradine 23.9 III 23.9 Diuretics 71.6
Abstract P1745 Table 1
P1748 Left atrial diastolic and systolic functions modulate the response to the standardised Valsalva maneuver in normal subjects
Authors: Musci R , Teodone G , Pollice P , Guaricci A I , Barbier P 
Published: January 2020

Abstract

Background
Although the Valsalva maneuver (VM) is being advocated by current guidelines to identify with echocardiography patients with increased left ventricular (LV) filling pressures using a decrease in mitral E/A velocity &gt; 0.5 as cutoff, there are limited published data for both patients and the normal response to the maneuver in healthy subjects.

Purpose
To assess LV and left atrial (LA) physiology during a standardized VM (VMs) in normal subjects.

Methods
The VMs was performed in 50 healthy subjects (M:F 38:12; age 40 ± 12 y.; HR 70 ± 11 bpm; BSA 1.81 ± 11 m2), instructed to forcefully exhale for 20 seconds without an initial deep breath into a tube connected to a sphygmomanometer, maintaining a 25-35 mmHg pressure. The VM was repeated 2 times at 5 minute intervals to record sequentially in the apical 4-chamber view: 1. LV and LA volumes; 2. Transmitral flow velocities. LA diastolic reservoir function (LAres) was calculated as: (maximum – minimum volume) / minimum volume x 100. Results. During the VMs, in all subjects LV indexed end-diastolic (-14 ± 7 ml/m2, -31 ± 15 %) and end-systolic (-6 ± 4 ml/m2, -31 ± 18 %) volumes, and stroke volume index (-9 ± 5 ml/m2, -30 ± 15 %) decreased similarly with unchanged LV ejection fraction %, and LA maximum and minimum volume indices both decreased (respectively -8 ± 6 ml/m2, -3 ± 3 ml/m2;-32 ± 25 %) with high variability. Mitral peak E velocity also decreased (-22 ± 13 cm/s, -27 ± 14 %) in all subjects, whereas peak A velocity change varied, such that a "pseudo-abnormal" decrease of E/A &gt; 0.5 was seen in 18 subjects (37 %). At baseline, this subgroup had lower heart rate (66 ± 11 vs 73 ± 10 bpm, p= .026), higher LAres (193 ± 67 vs 145 ± 47 %, p= .006), lower peak A velocity (50 ± 12 vs 58 ± 12 cm/s, p= .04) and higher E/A (1.8±.6 vs 1.4±.3, p= .004). During VMs, LV and LA volumes decreased similarly in all subjects, but increase in heart rate was higher (12 ± 8 vs 6 ± 5 bpm, p= .023), and peak A wave increased instead of decreasing (20 ± 20 % vs -8 ± 18 %, p&lt; .001) in the subjects with "pseudo-abnormal" decrease of E/A. During VMs, decrease in E/A was mainly determined (regression analysis, r: .76, p= .029) by baseline LAres (B= -.71) and change in LAres during VMs (B= -.47), whereas an increase in peak A velocity (r: .46, p= .031) was mainly determined by degree of HR increase (B= .41) and baseline LV EF (B= .3).

Conclusions
During VMs, a "pseudo-abnormal" decrease of the E/A velocity ratio is present in almost 40 % of normal subjects, and is determined by the interplay of the baseline diastolic compliance and the increase in systolic function of the LA during VM. These results may influence the accuracy of the VMs in the detection of increased LV filling pressures in patients.