atrial systole

The effect of atrial contraction on left ventricular function in six patients with varying degrees of mitral stenosis was determined by utilizing the pressure gradient technique to measure instantaneous aortic blood flow and pressure. Aortic flow was measured as ventricular rate was controlled by right ventricular pacing to create A-V (atrioventricular) dissociation at varying rates (90-150 beats/min). At each heart rate, beats with preceding P waves, effective atrial systole, were grouped according to the duration of the P-R interval. Beats without P waves served as controls. There was always a significant increase in stroke volume,

In order to evaluate the effects of atrial contraction on left ventricular function, the pressure gradient technique was used to measure instantaneous aortic blood flow and pressure in nine patients, six having complete heart block and three having normal sinus rhythm. From these data both left ventricular stroke volume and stroke work were calculated. Ventricular rate was controlled by transvenous right ventricular pacing over a range of 50-158

Background: Measurement of mitral annulus (MA) dynamics is an important component of the evaluation of left ventricular (LV) diastolic function; MA velocities are commonly measured using tissue Doppler imaging (TDI). This study aimed to examine the clinical potential of a semi-automated cardiovascular magnetic resonance (CMR) technique for quantifying global LV diastolic function, using 3D volume tracking of the MA with conventional cine-CMR images. Methods: 124 consecutive patients with normal ejection fraction underwent both clinically indicated transthoracic echocardiography (TTE) and CMR within 2 months. Interpolated 3D reconstruction of the MA over time was performed with semi-automated atrioventricular junction (AVJ) tracking in long-axis cine-CMR images, producing an MA sweep volume over the cardiac cycle. CMR-based diastolic function was evaluated, using the following parameters: peak volume sweep rates in early diastole (PSR E ) and atrial systole (PSR A ), PSR E /PSR A ratio, deceleration time of sweep

AS: atrial systole; BRISK: block regional interpolation scheme of k-space; CITP: C-terminal telopeptide of type I collagen CMR cardiovascular magnetic resonance imaging; CV: cardiovascular; CVA: cardiovascular accident; DD: diastolic dysfunction; LGE: late gadolinium enhancement; LGE CMR: late gadolinium enhancement cardiovascular magnetic resonance; E: early filling; EF: ejection fraction; HCM: hypertrophic cardiomyopathy; HF: heart failure; ICD, implantable cardioverter-defibrillator; LA: left atrium; LV: left ventricle; LVH: left ventricular hypertrophy; LVOT: left ventricular outflow tract; PC: phase contrast; PFR: peak filling rate; PICP: C-terminal propeptide of type I procollagen; RV: right ventricle; SAM: systolic anterior motion; SCD: sudden cardiac death; SERCA: sarcoplasmic reticulum Ca2+ ATPase; SICAD: small- vessel intramural coronary artery disease; VF: ventricular fibrillation; VT: ventricular tachycardia.

This study was designed to assess the independent effects of stroke volume and heart rate on the phases of systole and other selected hemodynamic parameters. By means of the pressure gradient technique instantaneous blood pressure and flow were recorded in the ascending aorta at fixed ventricular rates in five patients with complete heart block and in four patients with atrio-ventricular dissociation induced by ventricular pacing. Because of the variable contribution of atrial systole to ventricular filling, a wide range of stroke volumes were observed at each heart rate. The results indicate that the duration of ejection bears a close direct linear relationship to stroke volume while heart rate has only a weak but

Abstract-This project proposes a new approach to estimate the cardiac cycle phases in 2-D echocardiographic images as a first step in cardiac volume estimation. We focused on analyzing the atrial systole and diastole events. The proposed metohd is based on a tandem of image processing methods and artificial neural networks as a classifier to robustly extract anatomical information. The aforementioned approach is performed in two denoising scenarios. In the first scenario, the images are corrupted with Gaussian noise, and in the second one with Rayleigh noise distribution. A dataset of 20 images that include both normal and infarct cardiac pathologies were used. The results of the employed methods are qualitatively and quantitatively compared in terms of efficiency for both scenarios. This method allows improving the time efficiency. In this method, feature extraction was assessed for both the analyzed cardiac phases, and then the images belonging to our database were classified by the instrumentality of an ANN. The cardiac cycle phase estimation is performed in apical two- chamber long-axis 0◦ view (LAX0) of 2-D echocardiographic images. The experimental images were divided into two sets corresponding to two analyzed cardiac cycles (systole and diastole). The experimental echocardiographic images came from a blend of healthy and cardiac patients that suffer from myocardial infarction. Once artificial neural network is trained, the detection becomes very fast.

left atrium posterior to the interatrial groove. The point of attachment of the tumour to the atrium was determined by inspection and exploration of the tumour with the index finger. An oblique right atriotomy was made and the interior of the right atrium examined in case a second tumour is present. The IAS was then opened with a knife near the center of the fossa ovalis, and with the finger in the left atrium as a guide to the attachment of the tumour, a sufficient amount of atrial septum is excised to include the tumour attachment and if possible uninvolved tissue 5 mm beyond it. The defect in the IAS was closed by direct technique or with a pericardial or PTFE patch.

(FGF-21) is discovered as a new type of cyto- kine in fibroblast growth factor (FGF) family that regulates glucose and lipid metabolism in the recent [9, 10]. It showed that FGF-21 can im- prove the endothelial function in early stage of atherosclerosis, and prevent the development of coronary heart disease [11]. Clinical studies showed that FGF-21 increased in plasma of patients with coronary heart disease and was related to lipid metabolism and glucose metab- olism [12]. Recently, Han et al. demonstrated that serum FGF-21 levels was elevated in AF patients and associated with left atrial diame- ter, which indicated that FGF-21 may be an independent risk factor for AF [13]. However, whether the levels of plasma and cardiac FGF- 21 could reflect the degree of myocardial fibro- sis respectively, whether associated with atrial fibrosis as a biological indicator in patients with atrial fibrillation and rheumatic heart disease is still unclear. Therefore, this study aimed to investigate the relationship of FGF-21 and atrial fibrosis in patients with atrial fibrillation and rheumatic heart disease.

Electrical phenomena and its surrogate, the propagation of myocardial contraction, are three-dimensional events with variable sites of origin and distribution patterns. Next generation maps must be able to map the full thickness of the atrial and ventricular wall. One major challenge in clinical electrophysiology is to precisely visualize target cardiac structures and simultaneously depict electrical events. Using intracardiac ultrasound with high TDI frame rates, TDI is suitable for displaying more rapid changes in tissue motion related to the onset and propagation of electrical excitation in the myocardium at a very early stage with high temporal resolution. This ultrasound imaging technique should have an important impact on the diagnosis and management of cardiac arrhythmias. Such technology will foster simultaneous single modality visualization of anatomy, function and electrical events for the purpose of refining the proper intervention.

Myocyte contraction during systole leads to the ob- served circumferential and longitudinal shortening of the ventricle and concomitant radial thickening, along with the twisting of the apex relative to the base that comprises a torsional component of the ventricular con- traction. Interestingly, myocytes isovolumically shorten by ~15% during systole, which only accords with an ~8% increase in myocyte radius (Figure 1B). This is insuffi- cient to account for the observed radial wall thickening, which is upwards of 25%. Hence, to generate >8% wall thickening another mechanism is needed. The work of Spotnitz et al. [4] was the first to highlight the fact that the countable number of myocytes across the ventricular wall increases from end diastole to end systole, at a given level! For this to be possible, the myocardium must undergo a large shear deformation that rearranges the relative position of the myocytes and accounts for the large amounts of wall thickening (Figure 1B). This

(no syncope, no dizziness, no hemodynamic compromise) the occurrence of “atrial commotio cordis ” is underreported. Moreover, it is plausible that “ lone AF ” reported in otherwise healthy athletes could be triggered by a previous blunt chest trauma; therefore, a careful history should be taken when evaluating young athletes with a history of palpitation or evidence of AF.

protect against ischemia and reperfusion injury [23]. It is believed that amputation of both atrial appendages in the original Cox-maze procedure is a major cause of postoperative ANP decrease [17]. Therefore, according to Yoshihara et al. preservation of RAA in the modified maze procedure effectively protects against postoperative decrease of ANP and it has beneficial impact on the postoperative course [21]. Hypothetically, an elevated ANP level after HIFU ablation may have a beneficial ef- fect on postoperative course, but this question requires further investigations. In our study we amputated RAA in 100% and LAA in 21.4% of cases, therefore the in- creased ANP levels on POD 1 must be associated with other factors than preservation of atrial auricles. Since increased ANP levels from POD 7 to 3 months in follow-up were also observed in the control group with SR, we suspect that immediate postoperative ANP in- crease is rather a reaction to surgical trauma, periopera- tive higher volume load and atrial stretch. Other studies revealed also similar increase of ANP levels observed on POD 1 and 2 after CABG [24]. Surprisingly, cardiopul- monary bypass and its duration did not influence plasma ANP levels significantly [25]. Among patients with AF, we observed a significant increase in postoperative ANP levels only in the ablation group, but not in the control group without ablation. We might hypothesize that higher ANP concentrations could also be derived from necrotizing wall injury due to ablation. Nevertheless, among the individuals who did not undergo HIFU abla- tion, we observed that patients in the SR control group had a much greater increase in ANP levels on POD 1 than patients in the AF control group without ablation, (83% vs 24% increase from baseline level). This might suggest an impaired capability of the atria to release ANP, when they are fibrillating. Systemic ANP level depends not only on atrial stretching secondary to hemodynamic changes, but also on structural state and remodeling of atria. Previous study suggested that plasma ANP levels in patients with AF reflected degen- erative changes and inversely correlated with the level of LA fibrosis [15]. Probably because the degenerative changes are most expressed in LsPe AF, only in these pa- tients preoperative plasma ANP levels were independent predictors of cardiac rhythm after ablation in the present study. While patients with Pa and Pe AF with intermit- tent burden of atrial wall-stretch are heterogeneous as for factors stimulating ANP release. It might explain, why in our population we found the lowest basal plasma ANP levels in the SR control group, increased in pa- tients with paroxysmal and persistent and highest in pa- tients with longstanding persistent AF. This data partially confirmed the findings by Cao, which showed elevated plasma ANP levels in paroxysmal and persistent AF compared to SR group [5].

LV systolic dysfunction is commonly differentiated from LV diastolic dysfunction by the presence of a reduced LVEF [17, 18]. This differentiation is potentially erroneous as abnormalities of contractile function and diastolic dys- function have been shown to coexist, and diastolic dys- function often has its genesis in systole [19]. The idea of isolated diastolic function can, therefore, be questioned and it can be suggested that heart failure should be viewed as an individual disease where systolic and diastolic dys- function are the extremes on a spectrum of different phe- notypes of the same disease [19, 20]. In this study, systolic and diastolic function are shown to go hand-in-hand, i.e. a patient with poor systolic function is also shown to have poor diastolic function. This relationship is clearly depicted when using total average diastolic LD as a marker of diastolic dysfunction (Fig. 4), indicating that LD is a potentially valid substitute for present velocity-based determinations of diastolic dysfunction.

The Pitx2 gene encodes a homeobox transcription factor that is required for mammalian development. Disruption of PITX2 expression in humans causes congenital heart diseases and is associated with atrial fibrillation; however, the cellular and molecular processes dictated by Pitx2 during cardiac ontogeny remain unclear. To characterize the role of Pitx2 during murine heart development we sequenced over 75,000 single cardiac cell transcriptomes between two key developmental timepoints in control and Pitx2 null embryos. We found that cardiac cell composition was dramatically altered in mutants at both E10.5 and E13.5. Interestingly, the differentiation dynamics of both anterior and posterior second heart field-derived progenitor cells were disrupted in Pitx2 mutants. We also uncovered evidence for defects in left-right asymmetry within atrial cardiomyocyte populations. Furthermore, we were able to detail defects in cardiac outflow tract and valve development associated with Pitx2. Our findings offer insight into Pitx2 function and provide a compilation of gene expression signatures for further detailing the complexities of heart development that will serve as the foundation for future studies of cardiac morphogenesis, congenital heart disease and arrhythmogenesis.

In apical four-chamber view, the pulsed Doppler sample volume was placed at the level of the LV lateral mitral annulus, and subsequently at the septal mitral annulus and right ventricular tricuspid annulus. The sampling window was positioned as parallel as possible with the myocardial segment of interest to obtain the optimal angle of imaging. Atrial electromechanical coupling was defined as the time interval from the onset of P wave on the surface electrocardiogram to the beginning of the late diastolic wave (Am wave), i.e. PA interval and was measured from the lateral mitral annulus (PA lateral), septal mitral annulus (PA septum), and right ventricular tricuspid annulus (PA tricuspid) [9]. All PA intervals were averaged over three consecutive beats. The dif- ference between the lateral and tricuspid PA intervals was defined as interatrial electromechanical delay, and the difference between the septal and tricuspid PA

Quantitative analysis with MPR yielded high diagnostic accuracies in both systole and diastole (AUC: 0.92 and 0.94 respectively). The optimal MPR cut-off values for detecting significant CAD (1.75 for systole and 2.02 for diastole) were within the range of 1.50–2.06 reported in previous 2D-perfusion CMR studies [9,13,20,21,27]. Re- cently, in 2D-perfusion CMR, Huber et al (n = 31) showed that the use of stress MBF alone had a similar diagnostic accuracy as MPR (AUC 0.92 vs. 0.84 respectively; p < 0.18) [11]. Our study has shown a similar finding in 3D- perfusion CMR and the implication is that a rest perfusion sequence could potentially be omitted in quantitative studies, thus reducing both scanning and post-processing times without a loss in diagnostic yield (Figure 3).

For all subjects analyzed, 4D flow data was successfully registered to short-axis cine images for through-plane velocity mapping. Figure 2 shows examples of through- plane velocity and KE mapping at peak systole in a representative control subject and in a representative subject with an anterior AMI. Compared to the control subject, the anterior AMI subject has lower through- plane velocities in all LV regions. In both subjects, the KE map is dominated by regions near the left ventricular outflow tract. Figure 3 shows average through-plane flow-time curves in each region for anterior AMI pa- tients and controls. Figure 4 shows representative visual- izations of flow compartment analysis in a control (a, b) and AMI subject (d, e). The AMI subject had a lower fraction of pathlines in the direct flow compartment and a higher fraction of pathlines in the residual volume compartment. Subpanels c) and f) show group-average pie charts of the distribution of flow among compart- ments. Among all subjects, the median number of path- lines passing through the ventricular wall (and therefore discarded) was 24%. Table 3 shows the average 12 LV flow parameters in controls and anterior AMI patients, along with P-values for the comparison. Compared to controls, anterior AMI subjects had significantly lower through-plane flow in the mid-ventricle at peak systole and in the apex at peak systole and diastole. There were no significant differences in KEi EDV measures between

At the end of the systole propagates not a sine wave, but a group of waves. In dispersive system, such as the blood, the wave phase velocity varies with frequency. Higher-frequency waves travel faster than the lower-fre- quency ones. Speed differences causes dispersion of the group wave packets: different particles in the substance in individual wavelets travel at different speeds and directions, that is dissipates blood cell aggregates, the me- chanical energy of the viscous flow. Group wave at the frequency dispersion forms the structural rearrangement of the aggregates of the red, white blood cells, platelets, but on the vessel wall reflection it causes the wall dam- age: at the “stagnation” point on the outer curvature of the aortic isthmus, denudating the wall (Figure 6(d)).

time; PEP/ET: Pre-ejection period/Ejection time; IVSD: Interventricular septal dimension in diastole; LVPWD: Left ventricular posterior wall dimension in diastole; IVSS: Interventricular septal dimension in systole; LVPWS: Left ventricular posterior wall dimension in systole; LVEDD: Left ventricular end-diastolic dimension; LVESD: Left ventricular end-systolic dimension; EF: Ejection fraction; SF: Shortening fraction; AO: Aorta diameter;LA: Left atrium diameter; AO/LA: Aorta/Left atrium diameter; ICT: Isovolumic contraction time; IRT: Isovolumic relaxation time; AT: Acceleration time; DS: Deceleration slope; DT: Deceleration time; Peak E: Peak E velocity; Peak A: Peak A velocity; E/A: E/A velocity ratio.

Of 6 cases which showed a normal PR inter al prior to the attack, only 3 showed a prolongation during the acute episode. Those which shoved a pro- longed PR interval prior to the pericar[r]