関連する実験動画
アセトアミノフェンは,冠動脈疾患の患者に血圧を上昇させます
Isabella Sudano1, Andreas J Flammer, Daniel Périat
1Cardiovascular Center Cardiology University Hospital Zurich, Rämistrasse 100, CH-8091 Zurich, Switzerland.
Circulation
|October 20, 2010
まとめ
アセトアミノフェンは,痛みを和らげるために推奨され,冠動脈疾患の患者の血圧を大幅に上昇させる. この発見は,アセトアミノフェンは,特に高リスクの個人に,NSAIDと同様に,厳格な心血管安全性評価を必要とすることを示唆しています.
科学分野:
- 心臓病学 心臓病学
- 薬理学 薬理学とは
- クリニック・トライアル 臨床試験
背景:
- アセトアミノフェンは,NSAIDよりも心血管の安全性が想定されているため,第一線鎮痛剤として推奨されます.
- アセトアミノフェンの心血管安全性に関する予測データは限られており,特に高リスク集団では限られている.
- 冠動脈疾患 (CAD) の患者は,鎮痛剤の安全性を評価するための重要なグループです.
研究 の 目的:
- 既存の冠動脈疾患を有する患者のアセトアミノフェンの心血管安全性を評価する.
- この患者コホートにおけるアセトアミノフェンが重要な心血管のパラメータに影響を与えるかどうかを判断する.
主な方法:
- ランダム化,ダブルブラインド,プラセボ対照,クロスオーバー研究.
- CADの33人の患者は,標準治療に加えて2週間アセトアミノフェン (1g TID) またはプラセボを投与されました.
- 評価されたパラメータには,歩行式血圧,心拍数,内皮機能,血小板機能が含まれていました.
主要な成果:
- アセトアミノフェンは,プラセボと比較して,シストリックおよびダイアストリックの平均歩行血圧を有意に増加させた.
- 心拍数,内皮機能,血小板機能の有意な変化は観察されなかった.
- また,レニン=アニオテンシン系,炎症,酸化ストレスに関する特定のマーカーも評価した.
結論:
- アセトアミノフェンは,冠動脈疾患の患者において,循環器の血圧を著しく上昇させます.
- アセトアミノフェンの心血管安全性については,NSAIDやCOX-2阻害剤と同様の厳格な評価が必要である.
- 心血管疾患のリスクが高い患者にアセトアミノフェンを処方する際には注意が必要です.
関連する概念動画
Antihypertensive Drugs: Angiotensin II Receptor Blockers
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Drug toxicity: Drug–Drug Interaction
Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...
Coronary Artery Disease IV: Preventive Measures
Effective preventive measures for coronary artery disease (CAD) focus on controlling modifiable risk factors, including cholesterol abnormalities and lifestyle changes.Cholesterol ManagementFirst, the Mediterranean diet and the American Heart Association advocate for maintaining low-density lipoprotein (LDL) cholesterol levels below 100 mg/dL, with a more stringent recommendation of below 70 mg/dL for individuals at high risk. LDL cholesterol, often termed "bad cholesterol," can lead to the...
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers
Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...