Low Quantitative Blush Evaluator score predicts larger infarct size and reduced left ventricular systolic function in patients with STEMI regardless of diabetes status.

Type 2 diabetes mellitus (T2DM) and diminished myocardial perfusion increase the risk of heart failure (HF) and/or all-cause mortality during 6-year follow up following primary percutaneous coronary intervention (pPCI) for ST elevation myocardial infarction (STEMI). The aim of the present study was to evaluate the impact of myocardial perfusion on infarct size and left ventricular ejection fraction (LVEF) in patients with T2DM and STEMI treated with pPCI. This is an ancillary analysis of an observational cohort study of T2DM patients with STEMI. We enrolled 406 patients with STEMI, including 104 with T2DM. Myocardial perfusion was assessed with the Quantitative Myocardial Blush Evaluator (QUBE) and infarct size with the creatine kinase myocardial band (CK-MB) maximal activity and troponin area under the curve. LVEF was measured with biplane echocardiography using Simpson's method at admission and hospital discharge. Analysis of covariance was used for modeling the association between myocardial perfusion, infarct size and left ventricular systolic function. Patients with T2DM and diminished perfusion (QUBE below median) had the highest CK-MB maximal activity (252.7 ± 307.2 IU/L, P < 0.01) along with the lowest LVEF (40.6 ± 10.0, P < 0.001). Older age (p = 0.001), QuBE below median (p = 0.026), and maximal CK-MB activity (p < 0.001) were independent predictors of LVEF. Diminished myocardial perfusion assessed by QuBE predicts significantly larger enzymatic infarct size and lower LVEF among patients with STEMI treated with pPCI, regardless of diabetes status.

Preservative-free triamcinolone acetonide injectable suspension versus "traditional" triamcinolone preparations: impact of aggregate size on retinal biocompatibility.

PURPOSE: To evaluate the biocompatibility of the three currently most commonly used triamcinolone acetonide (TA) preparations on retinal cells. METHODS: Preservative containing KL (Kenalog-40; Bristol-Myers Squibb, Princeton, NJ), compounded preservative-free triamcinolone acetonide (PFTA; compounded from Volon A; Dermapharm, Vienna, Austria), and preservative-free triamcinolone acetonide injectable suspension (TRIESENCE; Alcon, Inc, Fort Worth, TX) (0.01-1 mg/mL) were either added directly on top or separated by a Boyden chamber filter or by a layer of vitreous to confluent cell cultures of retinal pigment epithelial cells (ARPE19) or retinal ganglion cells (RGC5). The distribution pattern of the TA crystals was assessed microscopically. Cell viability was assessed using MTT-ELISA and Live/Dead-Assay. RESULTS: Sedimentation of triamcinolone acetonide injectable suspension, KL, or PFTA caused a pronounced decrease in cell viability. Cytotoxicity was most pronounced when triamcinolone acetonide injectable suspension and PFTA were used. Without direct sedimentation of TA crystals on top of the cells, none of the three formulations were cytotoxic. Triamcinolone acetonide injectable suspension showed the largest and most dense TA crystal aggregates on top of the cells. CONCLUSION: Retinal cytotoxicity of TA seems only to occur when there is intimate contact of TA crystals with the cellular membrane. Cytotoxicity depends on the number and size of TA crystal aggregates-with larger conglomerates being more harmful. Of the TA formulations tested, triamcinolone acetonide injectable suspension had the strongest tendency to form large TA crystal conglomerates and to gravitate downward.

Effect of Diabetes Mellitus and Left Ventricular Perfusion on Frequency of Development of Heart Failure and/or All-cause Mortality Late After Acute Myocardial Infarction.

Type 2 diabetes mellitus (DM) has a detrimental impact on cardiovascular outcomes, with implications for prognosis following ST elevation myocardial infarction (STEMI).The aim was to evaluate the impact of DM and myocardial perfusion on the long-term risk of heart failure (HF) and/or all-cause mortality following primary percutaneous coronary intervention (pPCI) for STEMI. A total of 406 STEMI patients (104 with DM) treated with pPCI were enrolled in this observational study. Myocardial perfusion was reassessed with the Quantitative Myocardial Blush Evaluator. Follow-up data on HF (ICD10 [International Statistical Classification of Diseases] codes I50.0 - I50.9) and all-cause mortality were obtained from the National Health Fund. During a 6-year follow-up, 36 (35%) patients with DM died compared with 45 (15%) patients without DM (p <0.001). Also, 24 (23%) patients with DM developed HF compared with 51 (17%) patients without DM (p = 0.20). Patients with DM and HF had the highest mortality rate (75%), and those with DM and a QuBE score below the median value (9.0 arb. units) had significantly higher risk of HF (hazard ratio [HR] =1.96, 95% CI 1.18 to 3.27, p = 0.0099) and the composite of HF and/or all-cause mortality (HR = 1.89, 95% CI 1.33 to 2.69, p = 0.0004). In conclusion DM (type 2) and diminished myocardial perfusion increase the risk of HF and/or all-cause mortality during a 6-year follow-up after pPCI for STEMI.

Quantitative myocardial blush score (QuBE) allows the prediction of heart failure development in long-term follow-up in patients with ST-segment elevation myocardial infarction: Proof of concept study.

BACKGROUND: Acute myocardial infarction (AMI) might lead to left ventricular remodeling. Adequate myocardial perfusion is critical to prevent this adverse remodeling. Quantitative myocardial blush evaluator (QuBE) software, available on-line, is a simple analysis tool which enables the precise quan-tification of myocardial perfusion in the infarct area immediately after interventional treatment. The aim of this study was to assess whether the results of QuBE analysis might predict the development of heart failure (HF) in AMI patients in 3 year-long follow-up. METHODS: Ninety five patients with first AMI, single vessel coronary artery disease, Killip class I at presentation were enrolled in the study. Angiograms were reanalyzed using the on-line QuBE software. Data on heart failure development (ICD 10 codes I50) provided by the National Health Fund were considered as primary outcome. RESULTS: QuBE values ranged from 0.0 to 25.3 arbitrary units, mean value was 9.9 ± 5.2 arbitrary units. QuBE correlated positively with myocardial blush grade (MBG; Spearman R = 0.342 at p < 0.05). Multivariate Cox proportional hazard modeling, adjusted for initial Thrombolysis in Myocardial In-farction (TIMI flow, and TIMI thrombus grade indicated QuBE score (1 unit increase - HR 0.919, 95% CI 0.846-0.999, p = 0.049) and left ventricular ejection fraction at discharge (1% increase - HR 0.936, 95% CI 0.902-0.971, p = 0.000) as independent predictors of HF development. CONCLUSIONS: The QuBE assessment of myocardial perfusion allows the prediction of HF development in the post-infarction period in this highly selective group of patients.

Cost assessment of treatment of acute myocardial infarction and angiographically visible coronary thrombus.

AIM: Study was aimed to assess the real-world costs of manual thrombectomy (MT) in selected ST-segment elevation myocardial infarction patients with intracoronary thrombus (IT). METHODS: Study group (IT+) comprised 51 patients with MT applied and control group (IT-) comprised 56 patients without IT who underwent angioplasty alone. Costs comprised hospital care and cost of disposable materials used during primary angioplasty. RESULTS: Complex management of patients with IT is more expensive, though allows to achieve clinical outcomes comparable to low-risk ST-segment elevation myocardial infarction patients without IT. CONCLUSION: A complex pharmaco-interventional strategy, with glycoprotein IIB/IIIA inhibitor and MT, though more expensive, may prove cost-effective.

Cyclosporine a protects RGC-5 cells from excitotoxic cell death.

PURPOSE: Cyclosporine A (CSA) is a widely used immunosuppressive drug. Furthermore, CSA showed neuroprotective properties in several neurological disorders. However, nearly no data exist regarding CSA and its possible neuroprotective effect on retinal ganglion cells (RGCs). METHODS: RGC-5 cells were stressed with 10 mM glutamate for 24 hours with or without adding varying concentrations of CSA (1, 3, 6, or 9 µg/mL) to the medium. Cell viability and cell density were analyzed by MTS assay and crystal violet staining, respectively. Induction of apoptosis was determined through caspase 3/7 activity and Annexin V+/PI- flow cytometry. RESULTS: The incubation of RGC-5 cells with 10 mM glutamate for 24 hours induced a 3.1-fold and a 3.4-fold decrease in overall cell viability and cell density, respectively, compared with controls. The supplementation of 9 µg/mL CSA to 10 mM glutamate led to a 2.7-fold increase in overall cell viability (P<0.0005) and a 2.5-fold increase in cell density (P<0.0005) compared with RGC-5 cells treated only with 10 mM glutamate. Furthermore, the addition of 9 µg/mL CSA to 10 mM glutamate significantly reduced caspase 3/7 activity by 1.3-fold (P<0.0005) and the amount of Annexin V+/PI- cells by 2.8-fold compared with RGC-5 cells incubated with 10 mM glutamate alone. The neuroprotective effect of CSA dose-dependently decreased with lower concentrations. CONCLUSIONS: CSA can effectively protect RGC-5 cells against glutamate-induced excitotoxicity. Therefore, CSA should be tested in further experiments to evaluate its potential as a neuroprotective substance against RGC disorders.