ABSTRACT
Hyperlipidemia is a common metabolic disorder and one of risk factors for cardiovascular disease. Clinical studies have shown that hyperlipidemia increases the risk of non-ischemic heart failure, while decreasing serum lipids can reverse heart dysfunction. Apart from indirectly affecting the function of the heart by promoting the development of atherosclerosis, hyperlipidemia also affects the systolic function and cardiac electrophysiological response of the heart directly, which may be related to gradual accumulation of cardiac lipids and consequent systemic oxidative stress, proinflammatory state and mitochondrial dysfunction. However, the mechanism underlying direct effects of hyperlipidemia on the heart are not fully understood. In this review, we provide an updated summary of recent experimental and clinical studies that focus on elucidating the mechanisms of the action of hyperlipidemia on cardiac function, the relationship between heart failure and serum lipids, and protective effects of lipid-lowering drugs on the heart. The exciting progress in this field supports the prospect of guiding early protection of the heart to benefit the patients with chronic hyperlipidemia and familial hyperlipidemia.
Subject(s)
Hyperlipidemias/complications , Hyperlipidemias/drug therapy , Myocardium/pathology , Heart Failure/etiology , Heart Failure/metabolism , Heart Failure/pathology , Humans , Hyperlipidemias/metabolism , Hypolipidemic Agents/therapeutic use , Myocardium/metabolism , Oxidative Stress/physiologyABSTRACT
Restenosis is a pathologic re-narrowing of a coronary artery lesion after mechanical injury. Its pathophysiological mechanisms have not been fully elucidated at present, but are thought to include inflammation, vascular smooth muscle cell (VSMC) proliferation, and matrix remodeling, beginning with insufficient endothelium healing. Restenosis presents with angina symptoms or acute coronary syndromes and lead to a revascularization, either with coronary artery bypass or repeat percutaneous coronary intervention. Some studies have reported that hypoadiponectinemia has been an independent risk factor for the onset of acute coronary syndromes and restenosis. Accumulating evidence shows that low concentrations of adiponectin may be involved in impairing endothelium functions, inflammation, and VSMC proliferation that lead to restenosis. Preclinical studies have proven that adiponectin promotes endothelium healing, effectively inhibits inflammation, and maintains contractile phenotypes of VSMCs, indicating that it may be developed as a new therapeutic target for the treatment of restenosis.
Subject(s)
Adiponectin/metabolism , Cardiovascular Agents/metabolism , Coronary Restenosis/metabolism , Drug Delivery Systems/trends , Adiponectin/agonists , Adiponectin/deficiency , Animals , Cardiovascular Agents/administration & dosage , Cell Proliferation/drug effects , Cell Proliferation/physiology , Coronary Restenosis/drug therapy , Humans , Metabolism, Inborn Errors/drug therapy , Metabolism, Inborn Errors/metabolism , Muscle, Smooth, Vascular/drug effects , Muscle, Smooth, Vascular/metabolism , Treatment OutcomeABSTRACT
BACKGROUND: Atrial myxoma accounts for approximately 50% of all cardiac tumors. The majority of myxomas are located in the left atrium and present variable clinical manifestation. CASE PRESENTATION: A young man was transferred to our hospital with sudden onset of resting pain, pallor and numb in right leg. An atrial mobile mass was detected by transthoracic echocardiography. Anticoagulant and antithrombotic therapy were administered, a timely surgery was performed and the mass was confirmed as a myxoma. The patient did not discharge any discomfort post-operation. CONCLUSION: For patients with atrial myxoma, early diagnosis is essential, anticoagulant or antithrombotic therapy and surgery have a great importance to prevent further embolism.
