Planimetry of Mitral Valve Stenosis by Magnetic Resonance Imaging

Djavidani, Behrus; Debl, Kurt; Lenhart, Markus; Seitz, Johannes; Paetzel, Christian; Schmid, Franz X.; Nitz, Wolfgang R.; Feuerbach, Stefan; Riegger, Günter A.J.; Luchner, Andreas

doi:10.1016/j.jacc.2005.03.036

Cited by 70 publications

(38 citation statements)

References 14 publications

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“…[23][24][25][26][27][28][29][30][31] In patients with mitral stenosis, inflow velocities as assessed by Doppler echocardiography and CMR phasecontrast imaging correlate well (Table 3). 23,[32][33][34][35][36][37] If not stated in the publication, statistics were calculated from the data provided in the manuscript. If this was not performed or data were not provided, a designation of "not available" (...) was given.…”

Section: Peak Antegrade Velocity and Pressure Gradientmentioning

confidence: 99%

“…These comparisons are most appropriate when measurements based on similar concepts are compared (Tables 2 and 3). [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37] For evaluation of mitral stenosis, 2 methods are commonly used to determine valve area: planimetry and pressure halftime. 39 A trend can be identified for CMR to overestimate the If not stated in the publication, statistics were calculated from the data provided in the manuscript.…”

Section: Valve Areamentioning

confidence: 99%

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Cardiovascular Magnetic Resonance Imaging for Valvular Heart Disease

2009

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Section: Peak Antegrade Velocity and Pressure Gradientmentioning

confidence: 99%

Section: Valve Areamentioning

confidence: 99%

Cardiovascular Magnetic Resonance Imaging for Valvular Heart Disease

2009

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“…In patients with AS, valve area was assessed by direct planimetry as described previously. [13][14][15][16][17] All imaging studies were analysed separately by two observers (KD and BD). Only studies in which both readers agreed on the presence of hyperenhancement were analysed quantitatively for volumes and distribution of hyperenhancement by a single reader (KD).…”

Section: Mri Protocolmentioning

confidence: 99%

Delayed hyperenhancement in magnetic resonance imaging of left ventricular hypertrophy caused by aortic stenosis and hypertrophic cardiomyopathy: visualisation of focal fibrosis

Debl

Djavidani²,

Büchner³

et al. 2006

Heart

105

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Objective: To compare the extent and distribution of focal fibrosis by gadolinium contrast-enhanced magnetic resonance imaging (MRI; delayed hyperenhancement) in severe left ventricular (LV) hypertrophy in patients with pressure overload caused by aortic stenosis (AS) and with genetically determined hypertrophic cardiomyopathy (HCM). Methods: 44 patients with symptomatic valvular AS (n = 22) and HCM (n = 22) were studied. Cine images were acquired with fast imaging with steady-state precession (trueFISP) on a 1.5 T scanner (Sonata, Siemens Medical Solutions). Gadolinium contrast-enhanced MRI was performed with a segmented inversion-recovery sequence. The location, extent and enhancement pattern of hyperenhanced myocardium was analysed in a 12-segment model. Results: Mean LV mass was 238.6 (SD 75.3) g in AS and 205.4 (SD 80.5) g in HCM (p = 0.17). Hyperenhancement was observed in 27% of patients with AS and in 73% of patients with HCM (p , 0.01). In AS, hyperenhancement was observed in 60% of patients with a maximum diastolic wall thickness > 18 mm, whereas no patient with a maximum diastolic wall thickness , 18 mm had hyperenhancement (p , 0.05). Patients with hyperenhancement had more severe AS than patients without hyperenhancement (aortic valve area 0.80 (0.09) cm 2 v 0.99 (0.3) cm 2 , p , 0.05; maximum gradient 98 (22) mm Hg v 74 (24) mm Hg, p , 0.05). In HCM, hyperenhancement was predominant in the anteroseptal regions and patients with hyperenhancement had higher end diastolic (125.4 (36.9) ml v 98.8 (16.9) ml, p , 0.05) and end systolic volumes (38.9 (18.2) ml v 25.2 (1.7) ml, p , 0.05). The volume of hyperenhancement (percentage of total LV myocardium), where present, was lower in AS than in HCM (4.3 (1.9)% v 8.6 (7.4)%, p, 0.05). Hyperenhancement was observed in 4.5 (3.1) and 4.6 (2.7) segments in AS and HCM, respectively (p = 0.93), and the enhancement pattern was mostly patchy with multiple foci. Conclusions: Focal scarring can be observed in severe LV hypertrophy caused by AS and HCM, and correlates with the severity of LV remodelling. However, focal scarring is significantly less prevalent in adaptive LV hypertrophy caused by AS than in genetically determined HCM. R emodelling in left ventricular (LV) hypertrophy is accompanied by several structural changes. Interstitial and replacement fibrosis are among the morphological alterations that have been observed in LV hypertrophy caused by pressure overload and in genetically determined hypertrophic cardiomyopathy (HCM).

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“…CMR can be used to perform planimetry of the mitral orifice and pressure half-time assessment, although it tends to overestimate MVA when compared with TTE and cardiac catheterisation [53]. The reproducibility of CMR planimetry is acceptable [53], although use of CMR is hampered by the common association of MS with atrial fibrillation and with signal void caused by calcification.…”

Section: Mitral Stenosismentioning

confidence: 99%

“…The reproducibility of CMR planimetry is acceptable [53], although use of CMR is hampered by the common association of MS with atrial fibrillation and with signal void caused by calcification. CT reliably detects MV calcification [54], and may have accuracy similar to that of echocardiography in assessing severity, although the case series analysed to date are small [55].…”

Section: Mitral Stenosismentioning

confidence: 99%