[Coronary artery aneurysms].
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Coronary Aneurysm↗
Biomedical subjects
Marie Stugaard
Publications and source records attributed to Marie Stugaard.
Failure to prevent progressive dilation of ascending aorta by aortic valve replacement in patients with bicuspid aortic valve: comparison with tricuspid aortic valve.
BACKGROUND: Patients with bicuspid aortic valve (BAV) have been frequently complicated with ascending aortic dilation possibly because of hemodynamic burdens by aortic stenosis (AS) or regurgitation (AR) or congenital fragility of the aortic wall. METHODS AND RESULTS: To clarify if the aortic dilation could be prevented by aortic valve replacement (AVR) in BAV patients, we studied 13 BAV (8 AR dominant, 5 AS dominant) and 14 tricuspid aortic valve (TAV) patients (7 AR, 7 AS) by echocardiography before and after AVR (9.7+/-4.8 years). We also studied 18 BAV (11 AR, 7 AS) without AVR. Diameters of the sinuses of Valsalva, sinotubular junction and the proximal aorta were measured. The annual dilation rate was calculated by dividing changes of diameters during the follow-up period by the body surface area and the observation interval. We found that aortic dilation in BAV patients tended to be faster than that in TAV patients, although a significant difference was found only at the proximal aorta (0.18+/-0.08 versus -0.08+/-0.08 mm/(m2/year), P=0.03). BAV patients with and without AVR showed similar progressive dilation. AR dominant group showed tendency of more progressive dilation than AS dominant group in BAV, although it did not reach statistical significance. TAV patients did not show further aortic dilation after AVR. CONCLUSIONS: AVR could not prevent progressive aortic dilation in BAV. Since the aorta did not dilate in TAV, progressive aortic dilation in BAV seems mainly due to the fragility of the aortic wall rather than hemodynamic factors.
Adult↗
Quantitative assessment of short axis wall motion using myocardial strain rate imaging.
Although left ventricular wall motion has been usually assessed with four-point scale (1 = normal; 2 = hypokinesis; 3 = akinesis; 4 = dyskinesis) based on the visual assessment, this method is only qualitative and subjective. Recently, a new echocardiographic system that enables calculation of myocardial strain rate based on tissue Doppler information has been developed. We investigated whether myocardial strain rate could quantify regional myocardial contraction in 17 patients with and without wall motion abnormalities including 6 patients undergoing dobutamine stress echocardiography. Left ventricular short-axis wall motion was assessed with standard two-dimensional echocardiography at basal, mid-ventricular, and apical levels. The same levels were imaged with tissue Doppler method to determine regional myocardial strain rate. Sixty-four segments were judged normokinesis, 53 segments hypokinesis, and 18 segments akinesis at rest; 16 segments were judged normokinesis and 6 segments hypokinesis at stress. No segments characterized dyskinesis. Strain rates of normokinetic, hypokinetic, and akinetic wall segments at rest were significantly different each other (-2.0 +/- 0.6 for normokinesis,-0.6 +/- 0.5 for hypokinesis,P < 0.0001 vs. normokinesis, and-0.008 +/- 0.3 for akinesis, P < 0.0001 vs. normokinesis and hypokinesis). Further, strain rates well reflected the change in wall motion induced by dobutamine challenge: strain rates in the 15 segments revealing augmented wall motion changed from -2.0 +/- 0.7 to -4.7 +/- 1.7 (1/sec) (P < 0.0001) and those in the 7 segments revealing deteriorated or unchanged wall motion changed from -2.1 +/- 1.0 to -1.7 +/- 0.8 (1/sec) (P < 0.05). In conclusion, strain rate agreed well with assessed wall motion. Strain rate imaging may be a new powerful tool to quantify regional wall contraction.
Adult↗
Mechanisms of diastolic intraventricular regional pressure differences and flow in the inflow and outflow tracts.
OBJECTIVES: We sought to investigate the mechanisms of left ventricular (LV) intracavitary early diastolic flow during changes in contractility and loading. BACKGROUND: There is limited understanding of how intracavitary flow velocities relate to intraventricular driving pressures. METHODS: In 12 anesthetized dogs, we measured pressures in the left atrium (LA), LV at the mitral tip, apex, and subaortic region; intraventricular velocities by color M-mode Doppler echocardiography (CMD); and volume by sonomicrometry. We also investigated responses to isoprenaline, ischemic failure, and volume loading. RESULTS: During rapid, early filling, the mitral to apical pressure gradient (LVP(mitral-apex)) correlated with the peak mitral to apical velocity (r = 0.92). The LVP(mitral-apex) increased from 1.4 +/- 0.6 (SD) to 3.2 +/- 1.8 mm Hg during isoprenaline (p < 0.05) and decreased to 0.6 +/- 0.5 during ischemic failure (p < 0.01). The pressure gradient correlated positively with the time constant of isovolumic relaxation (tau) (r = 0.82) and negatively with LV end-systolic volume (ESV) (r = -0.77). Volume loading increased LA pressure, tau, and ESV, but caused no significant change in LVP(mitral-apex). At baseline and during isoprenaline, tau was shorter (p < 0.05) at the apex than at the base. When the mitral to apical gradient approached zero, filling velocities were directed toward the LV outflow tract, and a pressure gradient was established between the apex and subaortic region. CONCLUSIONS: Changes in LVP(mitral-apex) induced by inotropic stimuli, loading, and ischemia appeared to reflect dependency of the pressure gradient on the rate of relaxation, ESV, and LA pressure. Regional differences in the rate of relaxation may also contribute to intraventricular pressure gradients. These findings have implications for how to interpret intraventricular filling in a clinical context.
Animals↗
Postsystolic shortening in ischemic myocardium: active contraction or passive recoil?
BACKGROUND: Postsystolic shortening in ischemic myocardium has been proposed as a marker of tissue viability. Our objectives were to determine if postsystolic shortening represents active fiber shortening or passive recoil and if postsystolic shortening may be quantified by strain Doppler echocardiography (SDE). METHODS AND RESULTS: In 15 anesthetized dogs, we measured left ventricular (LV) pressure, myocardial long-axis strains by SDE, and segment lengths by sonomicrometry before and during LAD stenosis and occlusion. Active contraction was defined as elevated LVP and stress during postsystolic shortening when compared with the fully relaxed ventricle at similar segment lengths. LAD stenosis decreased systolic shortening from 10.4+/-1.2% to 5.9+/-0.9% (P<0.05), whereas postsystolic shortening increased from 1.1+/-0.3% to 4.2+/-0.7% (P<0.05). In hypokinetic and akinetic segments, LV pressure-segment length and LV stress-segment length loop analysis indicated that postsystolic shortening was active. LAD occlusion resulted in dyskinesis, and postsystolic shortening increased additionally to 8.2+/-1.0% (P<0.05). After 3 to 5 minutes with LAD occlusion, the dyskinetic segment generated no active stress, and the postsystolic shortening was attributable to passive recoil. Elevation of afterload caused hypokinetic segments to become dyskinetic, and postsystolic shortening remained partly active. Postsystolic shortening by SDE correlated well with sonomicrometry (r=0.83, P<0.01). CONCLUSIONS: Postsystolic shortening is a relatively nonspecific feature of ischemic myocardium and may occur in dyskinetic segments by an entirely passive mechanism. However, in segments with systolic hypokinesis or akinesis, postsystolic shortening is a marker of actively contracting myocardium. SDE was able to quantify postsystolic shortening and might represent a clinical method for identifying actively contracting and hence viable myocardium.
Animals↗
Distinction between well-differentiated liposarcoma and intramuscular lipoma by power Doppler ultrasonography.
BACKGROUND: This study evaluates the feasibility of ultrasonography in the distinction between well-differentiated liposarcoma (WDLS) and intramuscular lipoma (IL). MATERIALS AND METHODS: Three WDLSs and 9 ILs were included. Gray scale images were assessed for echogenicity, textural pattern and margins. Power Doppler ultrasonography was used to assess the number of detectable flow velocity signals in a 3 x 3 cm area. Furthermore, the ratio of the area occupied by colour flow signals relative to the selected area was determined. RESULTS: Gray scale images showed no differences between WDLSs and ILs. However, power Doppler showed more than 2 flow velocity signals in all WDLSs, whereas only 11% of the ILs had 2 signals. In all WDLSs, colour flow signals occupied more than 30% of the selected area. In contrast, ILs were characterized by a low color-dot ratio. Histologically, increased vascularity was found close to malignant cell invasions. CONCLUSION: Power Doppler ultrasonography is feasible to evaluate increased vascularity and thus differentiate WDLSs from ILs.
Aged↗