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Aim: To assess the effect of the intravitreal dexamethasone implant (DEX) Ozurdex on the best corrected visual acuity (BCVA) and central retinal thickness (CRT) in patients with diabetic macular edema (DME)., Methods: Totally 43 eyes (24 naïve and 19 previously treated) were included in the study. Retrospective and single-center study involved patients with a clinical diagnosed of DME, who received treatment with DEX implant and had a follow-up of at least 12mo. Primary endpoints included changes in BCVA and CRT., Results: At month 12, mean improvement in BCVA from baseline was 20.4±20.8 letters and 6.8±6.9 letters in naïve and previously treated patients, respectively ( P =0.0132). The naïve patients achieved the BCVA improvement significantly faster (2.4±1.5mo) than the previously treated ones (3.5±2.4mo, P =0.0298; Mann-Whitney test). The proportion of eyes gaining ≥15 letters was 54.2% and 21.1% in the non-previously treated and previously treated groups, respectively ( P =0.0293). CRT was significantly reduced from 484.0±119.8 and 487.5±159.9 µm to 272.0±39.2 and 233.5±65.7 µm in the naïve and previously treated patients, respectively; P <0.0001 each, respectively. The presence of subretinal fluid was significantly associated with the proportion of patients achieving a BCVA improvement ≥5 letters [HR (95%CI), 1.23 (1.04 to 1.45), P =0.0145]; ≥10 letters [HR (95%CI), 1.75 (1.10 to 2.77), P =0.0182]; and ≥15 letters [HR (95% CI), 2.04 (1.03 to 4.02), P =0.0407]. Naïve patients received less DEX implants throughout the study than the previously treated ones (1.8±0.6 vs 2.3±0.6, P =0.0172, respectively). Totally 9 patients (20.9%) have developed ocular hypertension, which was successfully controlled with topical hypotensive drugs. Of the 23 phakic eyes at baseline, 5 eyes (21.7%) either had new onset lens opacity or progression of an existing opacity during the study follow-up. Four of them (2 in the naïve group and 2 in the previously treated one) required cataract surgery at months 4, 6, 6, and 6, respectively., Conclusion: The results obtained in this study may support the early use of DEX Ozurdex as first line therapy in naïve patients., (International Journal of Ophthalmology Press.)

Polypoidal choroidal vasculopathy (PCV) is a subtype of neovascular age-related macular degeneration characterised by an abnormal branching vascular network with aneurysmal polypoidal choroidal vascular lesions. PCV is more prevalent in Asian populations than in Caucasians, which may explain its underdiagnosis in Western countries. Evidence regarding the efficacy of different anti-vascular endothelial growth factor (anti-VEGF) agents on PCV is scarce, with most of these studies being conducted in Asian treatment-naïve patients. Ranibizumab was the first anti-VEGF agent to demonstrate the superiority of a combination of photodynamic therapy (PDT) and anti-VEGF over PDT or anti-VEGF monotherapy for inducing polyp regression in Asian patients with PCV. The efficacy of other anti-VEGF agents has been less studied. Resistance to ranibizumab has been described. Aflibercept offers another mechanism of targeting choroidal neovascular lesions. A 75-year-old Caucasian woman presenting to our office was diagnosed with PCV using indocyanine green angiography. Combination therapy with a loading dose of 0.5 mg intravitreal ranibizumab followed by PDT at standard fluence at month 4 and a fourth dose of ranibizumab at month 5 yielded no visual or anatomic outcomes. Treatment was switched to intravitreal aflibercept at month 6 (3 monthly loading doses of 2.0 mg) followed by half-fluence PDT (month 9). Optical coherence tomography revealed remission of the anatomic lesions. Right-eye visual acuity increased to 0.6. Aflibercept injections were administered bimonthly afterwards. Follow-up during 1 year has shown functional and anatomic stability.

Percutaneous mitral balloon valvotomy (PMV) was performed in 10 female patients with mitral stenosis; their mean age was 31 +/- 1 years. All patients underwent echophonocardiography (Echophono) before and less than 24 hours after PMV1. Cardiac catheterization and Echophono were repeated 10 and 22 months after PMV1. Eight patients with suboptimal results (defined as a post-PMV mitral valve area [MVA]/less than 1.0 cm2 and mean gradient greater than/10 mm Hg) underwent repeat PMV (PMV2) 10 months after PMV1. The Echophono data are correlated with clinical and hemodynamic changes produced by PMV1 and PMV2. MVA increased from 0.6 +/- 0.1 to 1.1 +/- 0.01 cm2 (p = 0.0009) when PMV1 was performed with a mean effective balloon dilating area (EBDA) of 5 +/- 0.19 cm2. MVA increased from 1.0 +/- 0.1 to 1.7 +/- 0.2 cm2 (p = 0.0002) when PMV2 was performed with larger EBDA (6.4 +/- 0.34 cm2). Two factors related to the learning curve account for the superior result of PMV2: (1) use of larger EBDA and (2) optimal position of the balloons parallel to the long axis of the left ventricle. PMV1 resulted in Echophono changes consistent with decreased severity of mitral stenosis: shortening of Q-S1 from 93 +/- 4 to 82 +/- 4 msec (p less than 0.05) and (Q-S1)-(S2-OS) from 1.8 +/- 0.8 to -0.9 +/- 0.6 (p less than 0.01); prolongation of S2-OS from 75 +/- 5 to 91 +/- 5 msec (p less than 0.05) and increase of EF slope from 7 +/- 1 to 17 +/- 4 mm/sec (p less than 0.05). Compared with PMV1, post PMV2 Echophono showed a further decrease in the severity of mitral stenosis: Q-S1 decreased to 78 +/- 3 msec and (Q-S1)-(S2-OS) decreased to -0.5 +/- 0.3 msec. S2-OS increased to 86 +/- 5 msec and EF slope increased to 22 +/- 4 mm/sec. The hemodynamic and Echophono changes produced by PMV1 and PMV2 persisted at the corresponding follow-up studies. There was no evidence of restenosis. Thus Echophono is a simple, low cost method helpful in the evaluation and follow-up of patients undergoing PMV.

Thirty-five patients with severe mitral stenosis underwent percutaneous mitral valvotomy (PMV). There were 29 female and six male patients (mean age 49 +/- 3 years, range 13 to 87). After transseptal left heart catheterization, PMV was performed with either a single- (20 patients) or double- (14 patients) balloon dilating catheter. Hemodynamic and left ventriculographic findings were evaluated before and after PMV. There was one death. Mitral regurgitation developed or increased in severity in 15 patients (43%). One patient developed complete heart block requiring a permanent pacemaker. PMV resulted in a significant decrease in mitral gradient from 18 +/- 1 to 7 +/- 1 mm Hg (p less than .0001) and a significant increase in both cardiac output from 3.9 +/- 0.2 to 4.6 +/- 0.2 liters/min (p less than .001) and in mitral valve area from 0.8 +/- 0.1 to 1.7 +/- 0.2 cm2 (p less than .0001) Effective balloon dilating diameter per square meter of body surface area correlated significantly with the decrease in mitral gradient but did not correlate with the degree of mitral regurgitation. There was no correlation of age, prior mitral commissurotomy or mitral calcification with hemodynamic results. PMV is an effective nonsurgical procedure for patients with mitral stenosis, including those with pliable valves, those with previous commissurotomy, and even those with mitral calcification.

Sixty-two patients hospitalized because of prolonged chest pain and initial electrocardiographic (ECG) changes of ST depression and T-wave inversion suggestive of acute subendocardial myocardial infarction were evaluated to determine the ability of Tc-99m-stannous pyrophosphate mycardial scintigraphy to detect the presence or absence of acute subendocardial myocardial necrosis. Three groups of patients were designated. Group A consisted of eight patients (13%) who developed reduction of R-waves of more than 25% or new Q-waves broader than 0.03 seconds; of these patients with acute transmural myocardial infarction, all had well-localized, abnormal scintigrams. Group B consisted of 30 patients with ECG changes and subsequent enzymatic documentation, including elevated serum creatine kinase-B levels as determined by radioimmunoassay, of the presence of acute subendocardial myocardial infarction. Of these, 27 had abnormal scintigrams, including 18 with well-localized patterns and nine with "poorly localized" patterns. Group C consisted of 24 patients (39%) with chest pain, but without enzymatic documentation of the presence of acute myocardial infarction (acute coronary insufficiency). Eight of these had abnormal scintigrams, including one with a well-localized pattern and seven with "poorly localized" patterns. In four of the latter, the scintigrams were "persistently positive" several weeks to months after a previous myocardial infarct. Serial myocardial imaging will be necessary to identify such patients.

The relation between global and regional left ventricular function and electrocardiographic signs of ischemia at rest and during submaximal supine exercise was studied in 27 patients 2 to 3 weeks after acute myocardial infarction. Dynamic myocardial scintigraphy was performed at rest and during submaximal exercise utilizing an in vivo method of labeling red blood cells with technetium-99m pertechnetate. Gated radionuclide blood pool scintigrams were obtained in a modified left anterior oblique, and in some patients also in the right anterior oblique projection, to measure left ventricular ejection fraction and segmental wall motion. Electrocardiographic monitoring of heart rate and rhythm was provided during the exercise. The submaximal exercise test was terminated when the patient's heart rate reached 125 beats/min or if angina, malignant ventricular ectopy or electrocardiographic evidence of myocardial ischemia developed before this rate was reached. The data demonstrate that patients with a recent anterior myocardial infarct, in contrast to patients with a recent inferior or nontransmural infarct, manifest a significant reduction in left ventricular ejection fraction with submaximal exercise. Of the eight patients with an anterior infarct, seven had segmental wall motion abnormalities at rest. Four of these eight manifested more severe abnormalities with submaximal exercise; three had abnormalities at rest that did not change with exercise. Four of the eight had a positive electrocardiographic response during exercise (two were taking digoxin). Of these four, only two had more marked wall motion abnormalities with effort. Of the 13 patients with an inferior infarct, 11 had apparently normal wall motion in the modified left anterior oblique projection at rest, including 2 who manifested segmental wall motion abnormalities with submaximal exercise; the 2 remaining patients had wall motion abnormalities at rest that, on exercise, became more marked in one and were unchanged in one. Four of the 13 had a positive electrocardiographic response with exercise (one was taking digoxin); only one of these had a detectably more severe wall motion abnormality with exercise. Of the six patients with a nontransmural infarct, four had no identifiable wall motion abnormalities at rest; in one of these, an abnormality developed with exercise. The remaining two patients had wall motion abnormalities at rest; in one, a positive electrocardiographic ischemic response developed with exercise. Patients with an anterior infarct appear to have a different functional ventricular response to submaximal exercise at the time of hospital discharge than patients with an inferior or nontransmural infarct. To identify ischemic responses with submaximal exercise in these patients one should ideally use both electrocardiographic monitoring and dynamic myocardial scintigraphy.