This bachelor assignment will be executed commis- sioned by Demcon. The goal of the assignment is to improve one of the evaluated points of the by Demcon developed Proof of Principle (POP) of a Total Epicardial Delivery Device. This improvement will be tested with a new POP which is also realized during the assignment. The TEDD is a device which will be used for pacemaker lead placement on the left ventricle (LV) with a minimal invasive surgery. Minimal invasive surgery means that there will be no open chest, but small incisions in which a camera and instrument are inserted to perform the surgery. After the leads have been placed on the LV they will be connected to the pacemaker. Demcon is coop- erating closely with the Universitair Medisch Centrum Groningen (UMCG) and with the surgeons that work there for insights from the field. Those doctors will be using the TEDD in the future so it is of great importance that they are able to use it very well in order to treat the patient as good as possible. The patient does also have an important role in the development of this product. The entire product is developed in order to reduce the recovery period afterwards. The purpose of the device is to make it possible for the patient to receive a pacemak- er with a minimal invasive surgery instead of an open chest surgery. It is unacceptable if the success rate of the operation will be reduced or the change of implications will increase with the TEDD. What is more, the TEDD has to make it easier for the doctor to place the lead, and also to place the lead on the desired location. There- fore the change of a successful lead placement should increase. Demcon is developing the TEDD from a POP to a certified medical product. At the moment they are at the phase were they delivered a POP. However, there are some components that need improvement in order to reach maximum functionality. The functionality and usability have to be improved to assure that doctors can use it safely and easily.
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Current method that using the Doppler technique did provide the imaging blood flow with presenting of Continuous Wave, PW, and Color Wave. Since left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the heart wall which main pumping chamber (left ventricle), left ventricular hypertrophy can develop in response to some factors such as high blood pressure or a heart condition that causes the left ventricle to work harder. As the workload increases, the muscle tissue in the chamber wall thickens, and sometimes the size of the chamber itself also increases. This situation will produce an abnormal blood flow, with using PW, it can be measured by increment and decrement of blood velocity value, the change in direction flow and presence of turbulence flow. Thus, the goal of this work is to assess the parameter of early diastole, E wave (Ew), end diastole, A wave (Aw), Deceleration time (Dct). E/A ratio, E/e' (medial), E/e' (lateral) for the blood flow vector at left ventricle with the assist of the Pulsed Wave (PW).
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Both E/e' ratio (as an expression of LV filling pres- sures) and GLS (as a marker of LV subendocardial func- tion) can be easily measured in most patients with AS and have the potential of becoming useful tools for risk assessment in clinical practice. However, their incremen- tal prognostic value over well-known haemodynamic pa- rameters of AS severity was not clearly demonstrated. After accounting for the severity of AS, neither indexed LV mass nor any TDI derived parameter of LV function provided additional predictive information in asymptom- atic patients . On the other hand, low values of GLS were independently associated to increased all-cause mortality when adjusting for several established risk fac- tors (including symptoms, LVEF and haemodynamic se- verity) [66,68].
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In necroscopic studies, cardiac fat is often seen in the RV, with a frequency of up to 85% . Adipose tissue in the left heart chamber, except at the ventricular apex, in healthy individuals has been rarely reported. The necro- scopic finding of adipose tissue in the LV in 95% of the cases in the present study reinforces the growing evi- dence that emerged in the last decade from imaging tests, the presence of fat cells in the heart of healthy people, as well as in people with cardiovascular and non-cardiovascular diseases .
thalassemia there is a larger left ventricular end-systolic diameter, end-diastolic and end-systolic volume, left ven- tricular mass index, and mitral early/late diastolic flow vel- ocity ratio (p < 0.05). Strain and strain rate imaging study of the basal lateral wall of the left ventricle was higher in pa- tients than in controls. They concluded that LV volume and mass index parameters might be more sensitive than the other conventional and strain/strain rate imaging parame- ters during childhood. However, the adulthood strain and strain rate imaging values may be lower than those of the controls [20, 21]. Parsaee and colleagues have shown than STI is helpful for detecting early stages of left ventricular dysfunction in thalasemic patients . In their study, they noticed that there was a significant reduction in GLS (− 20.9% ± 1.9 vs. -22.2 ± 1.03) and also basal segments longitu- dinal strain compared to normal subjects group (− 17.4% ± 2.7 vs. -19.6% ± 1.2). They noticed that circumferential strain is not associated with left ventricular dysfunction. However, Ari et al. have noticed that an abnormal strain value, espe- cially circumferential, may be detected as the first finding of abnormal iron load and related to T2* values .
The mechanism mediating the development of ventricular arrhythmia (VA) after acute myocardial infarction (AMI) is still un- certain. Thrombin receptor (TR) activation has been proven to be arrhythmogenic in many other situations, and we hypothesize that it may participate in the genesis of post-AMI VA. Using a left coronary artery ligation rat model of AMI, we found that a local injection of hirudin into the left ventricle (LV) significantly reduced the ratio of VA durations to infarction sizing, whereas injection of thrombin receptor–activating peptide (TRAP) increased the ratios of VA duration to infarction sizing. The effects of TR activa- tion on whole-cell currents were investigated in isolated myocytes. TRAP increased a glibenclamide-sensitive outward current. Pretreatment of rats with glibenclamide (4 mg/kg intraperitoneally) eliminated the effects of a local injection of TRAP on the ra- tios of VA durations to infarction sizing. TR mRNA and protein expression in the ischemic left ventricle had reached its peak by 20 min postligation in the rat AMI model (P < 0.05). TR-immunoreactive myocytes were observed in infarcted LV but were seldom seen in the right ventricle or in the normal heart. By 60 min, TR transcript levels had returned to control levels. We conclude that increased TR activation and expression in the infarcted LV after AMI may contribute to VA through a mechanism involving gliben- clamide-sensitive potassium channels.
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Objective: Bicuspid Aortic Valve (BAV) is normally asymptomatic for a long time in both the general population and regularly-trained athletes. The study aimed to evaluate the role of physical stress echocardiography in early identifica- tion of any possible dissimilarities in the Left Ventricle (LV) performance and the valve functioning of asymptomatic BAV athletes as compared to the Tricuspid Aortic Valve (TAV) athletes. Design: Data were collected for BAV and TAV athletes from echocardographic examinations to evaluate any possible differences between them. Setting: Sport Medi- cine Center - University of Florence-Italy. Participants: 66 male BAV athletes and 45 TAV athletes Assessment of risk factors: decrease in LV performance and aortic valve dysfunction during stress test. Main outcome measures: Measure of the standard echocardiographic parameters. Comparison of LV Ejection Fraction (EF) and Aortic Peak Flow Veloc- ity (APFV) data in the two groups at rest and after stress. Results: At rest, values were normal in both groups, although LV systolic diameters tended to be higher in BAV. After physical effort, APFV and EF showed a significant increase in both groups, and for the former the values were at the upper limits in BAV (2.55 m/s BAV 2.12 m/s TAV ). Conclusions:
One month later on follow-up, the patient reported a marked improvement of his exercise capacity (NYHA II). Electrode values remained stable. An unscheduled echo- cardiogramm (Philips iE33) revealed a marked reduction of left ventricular dimensions with an improved mono- plane ejection fraction (51%). However, through the mitral valve leaflets a thick electrode proceeded into the apex of the left ventricle. An additional transesophageal echocar- diographic examination demonstrated the coronary sinus (CS) electrode in place (Figure 3a) but a malposition of the RV electrode passing the patent foramen ovale (PFO) via an Eustachian valve into the left ventricle (3 b-d).
Echocardiograms were performed 6 ± 3 days before and 10 ± 4 days following PTE. A Vivid cardiovascular ultra- sound system (GE VingMed, Horton, Norway) was used for all cases. Studies included measurements of the left atrial volume (LAVI), mitral E/A ratio, and mitral annular E/E’ ratio. Measurements of the left ventricle were also ac- quired, including cardiac index (CI) and end-systolic and end-diastolic diameters. All echocardiographic techniques followed the recommendations of the American Society of Echocardiography . Maximum left atrial volume was measured at end-systole and then indexed using body sur- face area, a technique that has demonstrated the strongest correlation to cardiovascular risk stratification .
The strain analysis was done on an offline basis (Fig. 1). Generally, we traced a region of interest by point-and- click approach on the endocardium at end-diastole in RV from the RV-focused view. A second larger region of interest was further produced and manually fine-tuned near the epicardium. The region of interest was carefully adjusted using visual assessment to assure that every segment was tracked perfectly. The right ventricle was partitioned into 6 standard segments at 3 levels (i.e., the basal, middle, and apical levels), correspondingly gener- ating 6 time-strain curves (Fig. 1). RV free wall longitu- dinal peak systolic strain (RV LPSS) was evaluated in the basal, midventricular, and apical segments of the RV free Table 3 Changes of recommended measures of left ventricle in 48 studied participants over the time
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Methods: Seven slaughterhouse pig hearts were installed in the MRI-compatible isolated beating pig heart platform. First, Langendorff perfusion mode was established; then, the system switched to working mode, in which blood was actively pumped by the left ventricle. A pacemaker ensured a stable HR during 3-T MRI scanning. All hearts were submitted to human physiological conditions of cardiac output and stayed vital for several hours. Aortic flow was measured from which stroke volume, cardiac output, and regurgitation fraction were calculated. Results: 4D flow MRI acquisitions were successfully conducted in all hearts. Stroke volume was 31 ± 6 mL (mean ± standard deviation), cardiac output 3.3 ± 0.9 L/min, and regurgitation fraction 16% ± 9%. With 4D flow, intracardiac and coronary flow patterns could be visualised in all hearts. In addition, we could study valve function and regurgitation in two hearts after TAVR.
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CMR: cardiovascular magnetic resonance; CRT: Cardiac resynchronization therapy; HF: heart failure; LV: left ventricle; LBBB: left bundle branch block; NYHA: New York Heart Association; ICM: ischemic cardiomyopathy; SSFP: steady state free precession; TE: echo time; TR: repetition time; FOV: field of view; LGE: late gadolinium enhancement; CSPAMM: complementary spatial modu- lation of magnetization; IL-AS: inferolateral to antero- septal; AL-IS: anterolateral to inferoseptal; A-I: anterior to inferior; IVCD: interventricular conduction delay; T12SD: Standard deviation of time to peak systole cir- cumferential strain in the 12 segments of basal and mid ventricular slices; %S: percent shortening.
Under aseptic conditions, the right femoral artery was cannulated with an introducer sheath (7.5 Fr, Arrow International Inc., Reading, PA, USA) by the Seldinger method, and the aortic blood pressure was re- corded continuously with a micromanometer-tipped catheter (5 Fr., Millar Instruments, Inc., Houston, TX, USA) introduced into the femoral artery. After the right cervical dissection, the right carotid artery was cannulated with an introducer sheath (7.5 Fr) by the Seldinger method, and the left ventricle (LV) pressure was recorded continuously with a micromanometer- tipped catheter (5 Fr., Millar Instruments, Inc., Houston, TX, USA) introduced into the right carotid artery. Two introducer sheaths were placed in the right
Conclusions: Patients with aortic stenosis most often develop symmetric hypertrophy; however, a small subset has asymmetric septal hypertrophy leading to left ventricular outflow tract obstruction. In cases of severe aortic stenosis, however, evidence of left ventricular outflow tract obstruction via both symptoms and echocardiographic findings may be minimized due to extremely high afterload on the left ventricle. Diagnosing a left ventricular outflow tract obstruction as the cause of hemodynamic instability during transcatheter aortic valve replacement, in the absence of abnormal findings on echocardiogram preoperatively, requires a high index of clinical suspicion. The
A 16-month old Caucasian girl (weight 12 kg, height 95 cm, body surface area (BSA) – 0.56 m 2 ) with a diag- nosis of right atrial aneurysm (RAA) was transferred to our clinic. She was diagnosed with RAA at the age of two months. At that time, a computed tomography scan showed a 3.9x3.4x3.4 cm cavity directly connected to the right atrium (RA) (Fig. 1). Parents declined surgical treatment. At the time of hospitalisation she presented with “ progressive ” heart failure, dyspnoea and pallor. Ar- terial blood saturation was 98 % on room air. Initial ECG showed ectopic atrial tachycardia, which later be- came atrial fibrillation. Pulse rate was 110 – 160 beats per minute, arterial blood pressure was 96/68 mmHg. The lower margin of the liver was palpable at 4.5 cm below the right costal arch. Pre-operative chest X-ray showed severe cardiomegaly (Fig. 2a). Transthoracic echocardiography (TTE) revealed a large dilated RAA (7.3x5.3 cm) that was compressing both ventricles and interfering with left ventricular filling and ejection frac- tion (left ventricle (LV) ejection fraction (EF) was 30 %). The next day her condition started to worsen. She re- fused to eat. Her haemodynamics became unstable,
reasonable for aneurysms greater than 5 mm but less than 10 mm . Surgical interventions, such as aneurysm ligation with distal bypass grafting, isolate CABG, aneurysm plication and saphenous vein patch re- pair of the aneurysm, are generally accepted as the pre- ferred treatment for giant CAA with any symptoms. A specific surgical approach must be selected in accord- ance with the size and anatomy of the aneurysm to per- form safe and effective corrections, and the closure of the fistula is also mandatory if giant CAAs are combined with a fistula . In this patient, the left giant CAA contributed to the restricted cardiac dysfunction and the left-to-right shunting of the RCA-to-PA fistula aggra- vated the pulmonary congestion. Owing to the left giant CAA originates from a branch of LAD and no signs of myocardial ischemia can be detected according to coronary angiography, we completely debrided thrombi in the left CAA sac and subsequently closed the prox- imal orifice, in order to relieve its oppression to left ventricle. As for the diffuse and extensive right CAA, surgical resection combined with CABG could be an effective and reasonable strategy. However, the poor pre- operative condition of this patient prevented us from performing these time-consuming procedures. Moreover, the main trunk of the RCA was angiographically normal, and therefore we decided to merely ligate the RCA-PA fistula and leave the right CAA untreated. In order to prevent further thrombosis in delated coronary arteries, lifelong antiplatelet therapy is mandatory. The follow-up coronary CTA and TTE demonstrated no abnormalities.
Using the electronical database of the echocardiography laboratory of the department of cardiac, thoracic and vascular sciences of the University of Padua, 94 patients with severe FMR and complete transthoracic echocardi- ography performed between November 2010 and March 2018, have been retrospectively selected. Inclusion cri- teria were: age > 18 years; severe FMR according to current guidelines ; availability of good quality 3D data sets of both the left ventricle (LV) and the MV. We excluded patients with organic MR, mitral stenosis, aor- tic stenosis, more than moderate aortic regurgitation, or those with valve prostheses. Each patient was assigned to the IMR or nIMR subgroup according to his/her clin- ical history and the documentation of presence/absence
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Fractional-SFD is defined as SFD divided by the end- diastolic SF dimension. The unusually high end-systolic pressure in the lumen of the RV in patients with PH affects the cross-sectional shape of the cavity. Whereas it normally tends to be crescent shaped in cross section, it adopts a more circular cross section when contracting against pressure that approaches or exceeds that of the left ventricle (Figure 1). This alteration of geometry mainly affects transverse rather than longitudinal dimen- sions, and therefore contributes more to reduction of fractional-SFD rather than fractional-TAAD. In addition to any impairment of RV myocardial contractility, this "transverse" dilation may contribute to the large differ- ence between PH patients and controls.
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The most recent trial addressing this issue was the ECHO – CRT trial 11 . This was a randomized multicenter trial involving Patients in NYHA Class III or IV heart failure with LVEF <= 35%, diastolic LV dimension greater than 5.5cm, QRS duration < 130 milliseconds and dyssynchrony assessed by tissue Doppler and speckle tracking. All eligible patients underwent biventricular ICD with randomization to CRT on versus CRT off. The study was terminated prematurely. The CRT group had higher death which was statistically significant.
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a useful marker of LV diastolic function and a robust index of clinical outcome risk including atrial fibrillation, stroke, and heart failure [1-3,5,14-16]. One likely mech- anism is LA remodeling in response to increased LV fill- ing pressure . Therefore a cross-sectional evaluation of LA size is viewed as a marker of LV filling pressure over time. Most published epidemiologic and clinical studies rely on maximal LA volume at LV end systole (LAV max ) [13,14,17-19]. But a recent clinical study ex-