Glaucoma, recognized as optic neuropathy is the second largest cause of blindness worldwide. The disease is characterized by progressive loss of retinal ganglion cells and visual field defects. The pathophysiological factors involved in the onset and progression of glaucoma are not fully understood. However, it is now well accepted that elevated intraocular pressure is not the only causative factor. The pathophysiology of glaucoma involves multiple factors that interact in a highly complex manner to favor development of glaucomatous optic neuropathy. As the knowledge of molecular mechanisms involved is expanding, more and more therapeutic targets are being recognized for the development of safe and effective pharmacotherapy of glaucoma. Although at present the intraocular pressure lowering drugs are still the first line of treatment, the prospect of introducing neuroprotective therapies that can directly protect and perhaps stimulate regeneration of dying and dead retinal ganglion cells, shows considerable promise. This review presents recent developments in the pathophysiology and pharmacotherapy of glaucoma.
Heart failure (HF) is a major burden in almost all countries. The prevalence of symptomatic HF is still high. Despite our best understanding of its pathophysiologic mechanisms and the recent advances in pharmacologic therapy, it remains a highmortality and morbidity disease. About 30-50% of patients with HF have concurrent electrical delay in the electrocardiogram (ECG), mainly in the form of LBBB.1 This kind of conduction delay commonly occurs in patients with idiopathic dilated cardiomyopathy and ischemic cardiomyopathy as well. The abnormality of left ventricle (LV) conduction will lead to a change in LV contraction pattern resulting dyssynchronized with right ventricle) contraction. Thus, a dyssynchronous LV contractile pattern usually manifested by late activation of the LV lateral wall which in turn impairs LV systolic function, reduces cardiac output, raises filling pressure and worsens mitral regurgitation2. Cardiac resynchronization therapy (CRT) improves cardiac function and exercise capacity leading to an improved survival in patients with advanced heart failure and ventricular conduction delay.3 The underlying mechanisms of these beneficial effects are not fully understood, but they appear to be related to a restored coordination of the left (LV) and right ventricular (RV) contraction and relaxation.4 These effects may directly lead to augmented contractility and reduction of LV filling pressures.5 Echocardiography has been widely used to identify patients who are candidates for CRT and to monitor the response in LV function at follow-up after device implantation. This review addresses the applications of CRT in patients with moderate– severe heart failure and the role of echocardiography in optimizing CRT including patient selection, risk and benefit of CRT and appropriate measures.