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Sökning: WFRF:(Shahgaldi K)

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  • Gudmundsson, P, et al. (författare)
  • Parametric quantification of myocardial ischaemia using real-time perfusion adenosine stress echocardiography images, with SPECT as reference method.
  • 2010
  • Ingår i: Clinical Physiology and Functional Imaging. - 1475-0961. ; 30:1, s. 30-42
  • Tidskriftsartikel (refereegranskat)abstract
    • Summary Background: Real-time perfusion (RTP) adenosine stress echocardiography (ASE) can be used to visually evaluate myocardial ischaemia. The RTP power modulation technique, provides images for off-line parametric perfusion quantification using Qontrast((R)) software. From replenishment curves, this generates parametric images of peak signal intensity (A), myocardial blood flow velocity (beta) and myocardial blood flow (Axbeta) at rest and stress. This may be a tool for objective myocardial ischaemia evaluation. We assessed myocardial ischaemia by RTP-ASE Qontrast((R))-generated images, using 99mTc-tetrofosmin single-photon emission computed tomography (SPECT) as reference. Methods: Sixty-seven patients admitted to SPECT underwent RTP-ASE (SONOS 5500) during Sonovue((R)) infusion, before and throughout adenosine stress, also used for SPECT. Quantitative off-line analyses of myocardial perfusion by RTP-ASE Qontrast((R))-generated A, beta and Axbeta images, at different time points during rest and stress, were blindly compared to SPECT. Results: We analysed 201 coronary territories [corresponding to the left anterior descendent (LAD), left circumflex (LCx) and right coronary (RCA) arteries] from 67 patients. SPECT showed ischaemia in 18 patients. Receiver operator characteristics and kappa values showed that A, beta and Axbeta image interpretation significantly identified ischaemia in all territories (area under the curve 0.66-0.80, P = 0.001-0.05). Combined A, beta and Axbeta image interpretation gave the best results and the closest agreement was seen in the LAD territory: 89% accuracy; kappa 0.63; P<0.001. Conclusion: Myocardial isachemia can be evaluated in the LAD territory using RTP-ASE Qontrast((R))-generated images, especially by combined A, beta and Axbeta image interpretation. However, the technique needs improvements regarding the LCx and RCA territories.
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  • Naar, J., et al. (författare)
  • Heart rate and dyssynchrony in patients with cardiac resynchronization therapy : a pilot study
  • 2017
  • Ingår i: Scandinavian Cardiovascular Journal. - : Taylor and Francis Ltd. - 1401-7431 .- 1651-2006. ; 51:3, s. 143-152
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: The objective of this pilot study was to describe the impact of paced heart rate on left ventricular (LV) mechanical dyssynchrony in synchronous compared to dyssynchronous pacing modes in patients with heart failure. Methods: Echocardiography was performed in 14 cardiac resynchronization therapy (CRT) patients at paced heart rates of 70 and 90 bpm in synchronous- (CRT), and dyssynchronous (atrial pacing + wide QRS activation) pacing modes. LV dyssynchrony was quantified using the 12-segment standard deviation model (Ts-SD) derived from Tissue Doppler Imaging. In addition, cardiac cycle intervals were assessed using cardiac state diagrams and stroke volume (SV) and filling pressure were estimated. Results: Ts-SD decreased significantly with CRT at 90 bpm (25 ± 12 ms) compared to 70 bpm (35 ± 15 ms, p =.01), but remained unchanged with atrial pacing at different paced heart rates (p =.96). The paced heart rate dependent reduction in Ts-SD was consistent when Ts-SD was indexed to average Ts and systolic time interval. Cardiac state diagram derived analysis of cardiac cycle intervals demonstrated a significant reduction of the pre-ejection interval and an increase in diastole with CRT compared to atrial pacing. SV was maintained at the higher paced heart rate with CRT pacing but decreased with atrial pacing. Discussion: Due to the small sample size in this pilot study general and firm conclusions are difficult to render. However, the data suggest that pacing at higher heart rates acutely reduces remaining LV dyssynchrony during CRT, but not during atrial pacing with dyssynchronous ventricular activation. These results need confirmation in a larger patient cohort.
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  • Venkateshvaran, Ashwin, et al. (författare)
  • The impact of arterial load on left ventricular performance : An invasive haemodynamic study in severe mitral stenosis
  • 2015
  • Ingår i: Journal of Physiology. - : Wiley. - 0022-3751 .- 1469-7793. ; 593:8, s. 1901-1912
  • Tidskriftsartikel (refereegranskat)abstract
    • Key points: A hallmark of mitral stenosis (MS) is the markedly altered left ventricular (LV) loading. As most of the methods used to determine LV performance in MS patients are influenced by loading conditions, previous studies have shown conflicting results. The present study calculated LV elastance, which is a robust method to quantify LV function. We demonstrate that LV loading in MS patients is elevated but normalizes after valve repair and might be a result of reflex pathways. Additionally, we show that the LV in MS is less compliant than normal due to a combination of right ventricular loading and the valvular disease itself. Immediately after valve dilatation the increase in blood inflow into the LV results in even greater LV stiffness. Our findings enrich our understanding of heart function in MS patients and provide a simple reproducible way of assessing LV performance in MS. Left ventricular (LV) function in rheumatic mitral stenosis (MS) remains an issue of controversy, due to load dependency of previously employed assessment methods. We investigated LV performance in MS employing relatively load-independent indices robust to the altered loading state. We studied 106 subjects (32 ± 8 years, 72% female) with severe MS (0.8 ± 0.2 cm2) and 40 age-matched controls. MS subjects underwent simultaneous bi-ventricular catheterization and transthoracic echocardiography (TTE) before and immediately after percutaneous transvenous mitral commisurotomy (PTMC). Sphygmomanometric brachial artery pressures and TTE recordings were simultaneously acquired in controls. Single-beat LV elastance (Ees) was employed for LV contractility measurements. Effective arterial elastance (Ea) and LV diastolic stiffness were measured. MS patients demonstrated significantly elevated afterload (Ea: 3.0 ± 1.3 vs. 1.5 ± 0.3 mmHg ml-1; P < 0.001) and LV contractility (Ees: 4.1 ± 1.6 vs. 2.4 ± 0.5 mmHg ml-1; P < 0.001) as compared to controls, with higher Ea in subjects with smaller mitral valve area (≤ 0.8 cm2) and pronounced subvalvular fusion. Stroke volume (49 ± 16 to 57 ± 17 ml; P < 0.001) and indexed LV end-diastolic volume (LVEDVindex: 57 ± 16 to 64 ± 16 ml m-2; P < 0.001) increased following PTMC while Ees and Ea returned to more normal levels. Elevated LV stiffness was demonstrated at baseline and increased further following PTMC. Our findings provide evidence of elevated LV contractility, increased arterial load and increased diastolic stiffness in severe MS. Following PTMC, both LV contractility and afterload tend to normalize.
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