Low-coherence optical diffraction tomography using a ferroelectric liquid crystal spatial light modulator.

Optical diffraction tomography (ODT) is a three-dimensional (3D) label-free imaging technique. The 3D refractive index distribution of a sample can be reconstructed from multiple two-dimensional optical field images via ODT. Herein, we introduce a temporally low-coherence ODT technique using a ferroelectric liquid crystal spatial light modulator (FLC SLM). The fast binary-phase modulation provided by the FLC SLM ensures the high spatiotemporal resolution. To reduce coherent noise, a superluminescent light-emitting diode is used as an economic low-coherence light source. We demonstrate the performance of the proposed system using various samples, including colloidal microspheres and live epithelial cells.

Generalized quantification of three-dimensional resolution in optical diffraction tomography using the projection of maximal spatial bandwidths.

Optical diffraction tomography (ODT) is a three-dimensional (3D) quantitative phase imaging technique, which enables the reconstruction of the 3D refractive index (RI) distribution of a transparent sample. Due to its fast, non-invasive, and quantitative imaging capability, ODT has emerged as a powerful tool for various applications. However, the spatial resolution of ODT has only been quantified along the lateral and axial directions for limited conditions; it has not been investigated for arbitrary-oblique directions. In this paper, we systematically quantify the 3D spatial resolution of ODT by exploiting the spatial bandwidth of the reconstructed scattering potential. The 3D spatial resolution is calculated for various types of systems, including the illumination-scanning, sample-rotation, and hybrid scanning-rotation methods. In particular, using the calculated 3D spatial resolution, we provide the spatial resolution as well as the arbitrary sliced angle. Furthermore, to validate the present method, the point spread function of an ODT system is experimentally obtained using the deconvolution of a 3D RI distribution of a microsphere and is compared with the calculated resolution.

Left ventricular diastolic dyssynchrony in patients with treatment-naive hypertension and the effects of antihypertensive therapy.

AIMS: The presence of left ventricular diastolic dyssynchrony is well known to be a frequent and important manifestation in heart failure. We investigated diastolic dyssynchrony in patients with treatment-naive hypertension, compared with normal controls; the determinants of the presence of diastolic dyssynchrony by performing comprehensive studies including laboratory, arterial stiffness, central blood pressure (BP), ambulatory BP monitoring (ABPM), and transthoracic echocardiography (TTE) evaluations; the effects of 6-month antihypertensive therapy on diastolic dyssynchrony; and the predictors associated with the change of diastolic dyssynchrony after medical therapy. METHODS: A total of 325 treatment-naive hypertensive patients and 172 normal controls were prospectively enrolled. Hypertensive patients were followed up at 6 months after medical therapy, and were assessed by serial TTE (at baseline and 6-month follow-up visit) and clinical evaluations. The time-to-peak myocardial early diastolic velocity (Te) of the 12 left ventricular segments was measured with reference to the QRS complex. The standard deviation (SD) of Te of all 12 left ventricular segments (Te-SD12) and the maximal difference in Te between any two of the 12 left ventricular segments (Te-Max) were calculated. A Te-SD12 at least 34 or Te-Max at least 113 ms was regarded as indicating the presence of diastolic dyssynchrony. RESULTS: Diastolic dyssynchrony was more prevalent in treatment-naive hypertensive patients, compared with normal controls (15.4 versus 7.0%, P = 0.007). Male sex [odds ratio (OR), 9.36 (1.93-45.41)], magnesium [OR per 1 SD, 2.54 (1.32-4.90)], night-time heart rate [HR; OR per 1 SD, 2.44 (1.18-5.05)], and mitral E/A [OR per 1 SD, 0.13 (0.04-0.45)] were independent determinants for the diastolic dyssynchrony in hypertensive patients. A 6-month follow-up, echocardiography was performed in 74 of 275 patients without diastolic dyssynchrony (group 1) and 26 of 50 patients with diastolic dyssynchrony (group 2). Diastolic dyssynchrony (Te-SD12, Δ = -8.3 ms; Te-Max, Δ = -27.6 ms; prevalence, Δ = -42.3%; all P < 0.05) improved in group 2, whereas it did not in group 1. Baseline daytime HR (P = 0.008) and magnesium levels (P = 0.029) and changes of the midwall fractional shortening (P = 0.026), mitral E/A (P = 0.003), mean annulus Ea (P = 0.003), mean annulus Ea/Aa (P = 0.020), and mitral peak E (P = 0.042) were independent predictors for changes of Te-SD12. CONCLUSION: Diastolic dyssynchrony is not rare in treatment-naive hypertensive patients. Male sex, magnesium levels, night-time HR, and mitral E/A are independent determinants for the impaired diastolic dyssynchrony. Antihypertensive therapy reduces both the severity and prevalence of diastolic dyssynchrony in patients with impaired diastolic dyssynchrony. Daytime HR, magnesium levels, and indications of systolic or diastolic dysfunction are independent predictors for improvements in diastolic dyssynchrony. Thus, magnesium levels, HR, and diastolic dysfunction seem to have important implications for diastolic dyssynchrony in hypertensive patients, whereas left ventricular hypertrophy, office BPs, arterial stiffness, central BPs, and ABPM parameters do not.

The effect of cilostazol on stent thrombosis after drug-eluting stent implantation.

BACKGROUND AND OBJECTIVES: Placement of drug-eluting stents (DES) can be complicated by stent thrombosis; prophylactic antiplatelet therapy has been used to prevent such events. We evaluated the efficacy of cilostazol with regard to stent thrombosis as adjunctive antiplatelet therapy. SUBJECTS AND METHODS: A total of 1,315 patients (846 males, 469 females) were prospectively enrolled and analyzed for the frequency of stent thrombosis. Patients with known risk factors for stent thrombosis, except diabetes and acute coronary syndrome, were excluded from the study. All patients maintained antiplatelet therapy for at least six months. To evaluate the effects of cilostazol as another option for antiplatelet therapy, triple antiplatelet therapy (aspirin+clopidogrel+cilostazol, n=502) was compared to dual antiplatelet therapy (aspirin+clopidogrel, n=813). Six months after stent placement, all patients received only two antiplatelet drugs: treatment either with cilostazol+aspirin (cilostazol group) or clopidogrel+aspirin (clopidogrel group). There were 1,033 patients (396 in cilostazol group and 637 in clopidogrel group) that maintained antiplatelet therapy for at least 12 months and were included in this study. Stent thrombosis was defined and classified according to the definition reported by the Academic Research Consortium (ARC). RESULTS: defined and classified according to the definition reported by the Academic Research Consortium (ARC). RESULTS: During follow-up (561.7+/-251.4 days), 15 patients (1.14%) developed stent thrombosis between day 1 to day 657. Stent thrombosis occurred in seven patients (1.39%) on triple antiplatelet therapy and four patients (0.49%) on dual antiplatelet therapy (p=NS) within the first six months after stenting. Six months and later, after stent implantation, one patient (0.25%) developed stent thrombosis in the cilostazol group, and three (0.47%) in the clopidogrel group (p=NS). CONCLUSION: During the first six months after DES triple antiplatelet therapy may be more effective than dual antiplatelet therapy for the prevention of stent thrombosis. However, after the first six months, dual antiplatelet treatment, with aspirin and cilostazol, may have a better cost benefit ratio for the prevention of stent thrombosis.