The Cardiovascular effects of chocolate.

The antioxidants as polyphenols, especially flavanols present in cocoa, exert a favorable effect on endothelium vasodilation, modulate inflammatory markers, and decrease platelet aggregation, lipid oxidation and insulin resistance. Recent nutritional intervention trials and molecular studies demonstrate that consumption of cocoa, particularly rich in flavanols, is beneficial to promote cardiovascular health. This review describes the cardiovascular effects of chocolate.

Current State of Platelet-rich Plasma in the Treatment of Rheumatic Disease: A Retrospective Review of the Literature.

INTRODUCTION: Rheumatic diseases are a spectrum of autoimmune or inflammatory diseases that cause damage to the musculoskeletal system as well as vital organs, such as the heart, lungs, kidneys, and central nervous system. METHODS: The study of rheumatic disease has made great progress in the understanding and management of these conditions in the last few decades using disease-modifying antirheumatic drugs and synthesized biological immunomodulating therapies. However, one potential treatment that has not been well investigated in rheumatic disease is platelet-rich plasma (PRP). PRP is proposed to facilitate the healing of injured tendons and ligaments through a variety of mechanisms, including mitogenesis, angiogenesis and macrophage activation via cytokine release, although its exact mechanism is unclear. RESULT: There has been a great deal of work in determining the exact preparation method and composition of PRP for regenerative purposes in orthopedic surgery, sports medicine, dentistry, cardiac surgery, pediatric surgery, gynecology, urology, plastic surgery, ophthalmology, and dermatology. Despite this, there is a paucity of research on the impact of PRP on rheumatic disease. CONCLUSION: This study aims to summarize and evaluate the current research concerning the use of PRP in rheumatic disease.

The Role of False Tendons in Left Ventricular Remodeling and Secondary Mitral Regurgitation After Acute Myocardial Infarction.

BACKGROUND: Left ventricular false tendons (LVFT) are common structures visualized on transthoracic echocardiography (TTE). The present study tested the hypothesis that LVFT, via a possible 'constraint' mechanism, attenuate left ventricular (LV) remodeling and secondary mitral regurgitation after acute myocardial infarction. METHODS: Seventy-one patients admitted to the Coronary Care Unit following an ST-elevation (n = 63) or non-ST-elevation (n = 8) myocardial infarction were analyzed; 29 (41%) had LVFT, and 42 (59%) did not (no-LVFT). All had a TTE and at least 1 follow-up study after revascularization. The χ² analysis, Student's t-test, and Mann Whitney U test were used for the statistical analyses. RESULTS: The mean age (64 vs. 66 years), left ventricular ejection fraction (LVEF) (41% vs. 39%), left ventricular end-diastolic diameter (LVEDd) index (23 mm/m² for both), and prevalence of ≥ moderate secondary/functional mitral regurgitation (MR) (17% vs. 14%) were similar between the LVFT and no-LVFT groups. At 1-year follow-up, there was no significant difference in chamber remodeling amongst the LVFT versus no-LVFT group when assessed by: 1) ≥ 10% decrease in the relative LVEF (24% vs. 26%; p = 0.83); 2) ≥ 10% increase in the LVEDd index (41% vs. 38%, p = 0.98); and, 3) ≥ 10% increase in the LV mass index (48% vs. 41%, p = 0.68). There was no difference in the prevalence of ≥ moderate secondary/functional MR (17% vs. 12%, p = 0.77). Outcomes remained similar when stratifying by LVFT morphology or ischemic territory. CONCLUSIONS: In patients with mild to moderate LV dysfunction and normal chamber size, LVFT do not affect the development of LV remodeling or secondary/functional MR post-myocardial infarction.