Cardio-oncology: cardiovascular complications of cancer therapy.

This paper focuses on three classes of commonly used anticancer drugs, which can cause cardiotoxicity: anthracyclines, monoclonal antibodies exemplified by trastuzumab and tyrosine kinase inhibitors. Anthracyclines can induce cardiomyocyte necrosis and fibrosis. Trastuzumab can cause cardiac stunning.

Therapeutic angiogenesis: angiogenic growth factors for ischemic heart disease.

Stem cells encode vascular endothelial growth factors (VEGFs), fibroblastic growth factors (FGFs), stem cell factor, stromal cell-derived factor, platelet growth factor and angiopoietin that can contribute to myocardial vascularization. VEGFs and FGFs are the most investigated growth factors. VEGFs regulate angiogenesis and vasculogenesis.

Cocaine produces cardiac hypertrophy by protein kinase C dependent mechanisms.

Background: Chronic cocaine users can have as much as a 69% increase in left ventricular muscle mass without associated increases in arterial blood pressure, heart rate, renin, aldosterone, or cortisol. We determined whether cocaine directly increases cardiomyocyte protein content and whether protein kinase C is important in this process.

Methods And Results: Adult rat cardiomyocytes were isolated and grown in cultures.

Vasoactive intestinal peptide: cardiovascular effects.

Vasoactive intestinal peptide (VIP) is present in the peripheral and the central nervous systems where it functions as a nonadrenergic, noncholinergic neurotransmitter or neuromodulator. Significant concentrations of VIP are present in the gastrointestinal tract, heart, lungs, thyroid, kidney, urinary bladder, genital organs and the brain. On a molar basis, VIP is 50-100 times more potent than acetylcholine as a vasodilator.