Hypertrophic cardiomyopathy (HCM) is a heterogeneous genetic disorder most often caused by sarcomeric mutations resulting in left ventricular hypertrophy, fibrosis, hypercontractility, and reduced compliance. It is the most common inherited monogenic cardiac condition, affecting 0.2% of the population. Whereas currently available therapies for HCM have been effective in reducing morbidity, there remain important unmet needs in the treatment of both the obstructive and non‐obstructive phenotypes. Novel pharmacotherapies directly target the molecular underpinnings of HCM, while innovative procedural techniques may soon offer minimally‐invasive alternatives to current septal reduction therapy. With the advent of embryonic gene editing, there now exists the potential to correct underlying genetic mutations that may result in disease. This article details the recent developments in the treatment of HCM including pharmacotherapy, septal reduction procedures, mitral valve manipulation, and gene‐based therapies.

The pathogenesis of Alzheimer's disease is characterized by aggregation of the amyloid-β protein (Aβ) into neurotoxic plaques. Recent in vivo studies have suggested the non-proteolytic clearance of Aβ via receptor-mediated transport across the blood-brain barrier (BBB). The aim of this study was to investigate the role of p-glycoprotein (Pgp) and the low-density lipoprotein receptor-related protein (LRP) in Aβ efflux across the BBB. We developed an in vitro BBB-like model using Madin Darby Canine Kidney (MDCK) cells seeded on filters separating apical (blood) and basolateral (brain) compartments. MDCK cells were stably transfected with Pgp or mLRP4, an LRP mini-receptor. When compared to empty vector-transfected cells, MDCK-Pgp cells did not transcytose radiolabeled Aβ in the basolateral-to-apical direction. MDCK-mLRP4 cells were found to endocytose and degrade, but not to trasncytose intact radiolabeled Aβ. These results implicate LRP as a mediator of Aβ degradation, but indicate that overexpression of LRP or Pgp alone is insufficient for nonproteolytic transcytosis of intact Aβ.

A 60 year-old man with a history of prostate cancer who underwent radical prostatectomy is currently being treated with androgen-deprivation therapy and is on a clinical trial with bevacizumab (Avastin, an antiangiogenic and anti-vascular endothelia growth factor [VEGF] chemotherapy) for an elevated prostate-specific antigen. At clinic visits after starting bevacizumab, he was noted to have new hypertension, with blood pressure as high as 178/98 mm Hg. After his second cycle of bevacizumab, he had sudden onset of palpitations, with workup revealing atrial fibrillation. He spontaneously cardioverted back to sinus rhythm but was referred to our institution's cardiology clinic for oncology patients (Cardio-Oncology Clinic) for management of hypertension and atrial fibrillation in the setting of bevacizumab therapy.Angiogenesis, the formation of new blood vessels from preexisting ones, is required for the growth and metastases of solid tumors.