Understanding the mechanisms that underlie age-related macular degeneration (AMD) has led to the identification of key molecules. Hypoxia-inducible transcription factors (HIFs) have been associated with choroidal neovascularization and the progression of AMD into the neovascular clinical phenotype (nAMD). HIFs regulate the expression of multiple growth factors and cytokines involved in angiogenesis and inflammation, hallmarks of nAMD. This knowledge has propelled the development of a new group of therapeutic strategies focused on gene therapy. The present review provides an update on current gene therapies in ocular angiogenesis, particularly nAMD, from both basic and clinical perspectives.

A patient in their 70s with a history of paroxysmal atrial fibrillation and a structurally normal heart was prescribed flecainide, 100 mg twice a day, for rhythm control. The patient presented to the emergency department with complaints of dizziness. Their blood pressure was 60/44 mm Hg, heart rate was 166 beats/min, and oxygen saturation was 100% on ambient air. Serum sodium level was 138 mEq/L; serum potassium level, 4.4 mEq/L; and serum creatinine level, 0.86 mg/dL. The electrocardiogram (ECG) at presentation (Figure 1) showed a regular monomorphic wide complex tachycardia (WCT) at a rate of 160 beats/min.Question: What is the diagnosis?

Premature ventricular complexes (PVCs) are a common finding in general population and can be even considered physiologic in most cases. Nevertheless, very frequent isolated PVCs may lead to the development of a usually reversible left ventricular dysfunction or be a manifestation of an underlying cardiac condition that could be associated with more severe ventricular arrhythmias, heart failure or cardiac death. Three causative mechanisms of the PVCs have been proposed: abnormal automaticity, triggered activity and reentry supposing different diagnostic and therapeutic implications. Although many patients with PVCs remain completely asymptomatic, others may suffer from a wide range of symptoms like palpitations, fatigue, dyspnoea or dizziness of a variable degree. Proper characterisation of the PVCs, their burden and features, as well as the identification of their sites of origin and mechanisms should be pursued to establish the convenience of a conservative or therapeutic approach. Specific treatment with medical therapy or catheter ablation must be contemplated in symptomatic patients or in those who develop related systolic dysfunction or other kind of complications.

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