ABSTRACT
PRCIES: Empowering glaucoma patients to access their individual glaucoma related health data by using a digital health application leads to a significant improvement in quality of life and adherence. PURPOSE: Evaluate the effectiveness of improvement of glaucoma associated quality of life and adherence in patients using a digital health application. PATIENTS AND METHODS: A prospective randomized monocentric controlled study of 77 patients with primary open angle glaucoma. Patients were recruited at the University Hospital Erlangen. Patients in the intervention group tracked their intraocular pressure, symptoms and therapy using a digital application. Based on the collected data the SmartTonoTracker® gave patients simple statistics and basic recommendations for further treatment. An increasing score on the GlauQol-36 item questionnaire and the MMAS-8 score, conducted at baseline and follow-up by the intervention group, was considered successful. Statistical analysis was conducted using the unpaired t-test, paired t-test, Man-Whitney-U test, frequency analysis, frequency distribution and Pearson-correlation. RESULTS: Significant difference in the patients´ glaucoma-associated quality of life between the intervention group (rate of improvement: 7.6%, P =0.047), and the control group (rate of improvement: 0.17%, P =0.047) was shown. Also, a significant difference in adherence between the intervention group, showing a 9.8% rate of improvement ( P =0.002), and the control group, showing a 3.8% rate of improvement ( P =0.002), was shown. CONCLUSION: Enabling patients to access individual health related glaucoma data by using a digital health application and supporting them with information on their disease led to an improvement in glaucoma-associated quality of life and adherence.
ABSTRACT
Voltage dependent anion channel 2 (VDAC2) is an outer mitochondrial membrane porin known to play a significant role in apoptosis and calcium signaling. Abnormalities in calcium homeostasis often leads to electrical and contractile dysfunction and can cause dilated cardiomyopathy and heart failure. However, the specific role of VDAC2 in intracellular calcium dynamics and cardiac function is not well understood. To elucidate the role of VDAC2 in calcium homeostasis, we generated a cardiac ventricular myocyte-specific developmental deletion of Vdac2 in mice. Our results indicate that loss of VDAC2 in the myocardium causes severe impairment in excitation-contraction coupling by altering both intracellular and mitochondrial calcium signaling. We also observed adverse cardiac remodeling which progressed to severe cardiomyopathy and death. Reintroduction of VDAC2 in 6-week-old knock-out mice partially rescued the cardiomyopathy phenotype. Activation of VDAC2 by efsevin increased cardiac contractile force in a mouse model of pressure-overload induced heart failure. In conclusion, our findings demonstrate that VDAC2 plays a crucial role in cardiac function by influencing cellular calcium signaling. Through this unique role in cellular calcium dynamics and excitation-contraction coupling VDAC2 emerges as a plausible therapeutic target for heart failure.
