補完系は,心不全性疾患における補完系である
M Yasuda1, K Takeuchi, M Hiruma
1First Department of Internal Medicine, Osaka City University Medical School, Japan.
Circulation
|January 1, 1990
まとめ
コンプリメントシステムの活性化は,急性心筋梗塞 (AMI) で発生し,心臓損傷に関連しています. 軽度のアクティベーションは不安定なアンギナでは見られますが,心臓機能障害のない安定したアンギナでは見られません.
科学分野:
- 心血管医学 心血管医学
- 免疫学 免疫学とは
- バイオケミストリー バイオケミストリー
背景:
- 急性心筋梗塞 (AMI) の後の組織損傷のメカニズムは不明である.
- 実験的なモデルは,AMIに関連するマイクロ血管およびマクロ血管損傷における補完系関与を示唆しています.
- 胸痛における補完体活性化の役割はよく定義されていません.
研究 の 目的:
- 心筋炎症の媒介者としてのコンプレメントシステムの役割を調査する.
- AMI,不安定性アンギナ,安定性アンギナ,および健康なボランティアの患者におけるコンプリメント活性化製品の定量化.
- コンプリメント活性化と心筋損傷の関連性を評価する.
主な方法:
- プラズマサンプルにおけるコンプレメント活性化製品 (C3d,C4d,Bb,SC5b-9) の定量化.
- 研究対象は,AMI患者31人,アンスタブルなアンギナ患者17人,安定したアンギナ患者19人,正常なボランティア20人でした.
- SC5b-9レベルとピーククレアチン・フォスフォキナーゼ,エジェクション分数,心不全状態の間の相関を分析した.
主要な成果:
- プラズマC3d濃度は,AMIおよび不安定性胸痛患者で上昇した (p<0.01).
- C4d,Bb,SC5b-9の血濃度は,AMI患者においてのみ増加した (p<0.01).
- 血SC5b-9濃度は,クレアチン・フォスフォキナーゼ (r=0.71) と逆のエジェクション分数 (r=-0.71) と相関しており,心不全のAMI患者では高かった.
結論:
- 補完系活性化はAMI後に明らかであり,心筋損傷と関連しています.
- 軽度の補完系活性化は,心機能障害のない不安定な胸痛で起こります.
- コンプリメントシステムは,安定した胸痛では活性化されません.
関連する概念動画
Ischemic Heart Disease: Overview
Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...
Complement System
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
Myocarditis I: Introduction
Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
Acute Coronary Syndrome IV: Interprofessional Care
IntroductionThe management of Acute Coronary Syndrome (ACS) aims to minimize myocardial damage, preserve myocardial function, and prevent complications.Initial ManagementInpatient management involves continuous cardiac monitoring, preferably in an ICU, focusing on blood pressure, serum sodium, potassium, and creatinine levels, and urine output. Ongoing pharmacologic management is crucial for stabilizing the patient.Supplemental Oxygen: Administer supplemental oxygen if oxygen saturation is...
Ischemic Stroke ll: Pathophysiology
An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...


