ヒト心臓由来脂肪酸結合蛋白 heart-type fatty acid binding protein

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the 8th letter of the Roman alphabet (同)h

PrepTutorEJDIC

hydrogenの化学記号
鉛筆の硬度 / 《俗》heroin

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/05/18 13:27:57」(JST)

wiki en

Heart-type fatty acid binding protein (hFABP) also known as mammary-derived growth inhibitor is a protein that in humans is encoded by the FABP3 gene.^[1]^[2]

Structure

The HADHB gene is located on chromosome 1, with its specific location being 1p33-p32.^[2] The gene contains 5 exons. HADHB encodes a 51.2 kDa protein that is composed of 133 amino acids; 124 peptides have been observed through mass spectrometry data.^[3]^[4]

Function

Heart-type Fatty Acid-Binding Protein (H-FABP) is a small cytoplasmic protein (15 kDa) released from cardiac myocytes following an ischemic episode.^[5] Like the nine other distinct FABPs that have been identified, H-FABP is involved in active fatty acid metabolism where it transports fatty acids from the cell membrane to mitochondria for oxidation.^[5] See FABP3 for biochemical details.

The intracellular fatty acid-binding proteins (FABPs) belongs to a multigene family. FABPs are divided into at least three distinct types, namely the hepatic-, intestinal- and cardiac-type. They form 14-15 kDa proteins and are thought to participate in the uptake, intracellular metabolism and/or transport of long-chain fatty acids. They may also be responsible in the modulation of cell growth and proliferation. Fatty acid-binding protein 3 gene contains four exons and its function is to arrest growth of mammary epithelial cells. This gene is also a candidate tumor suppressor gene for human breast cancer.^[2]

Interactions

FABP3 is known to interact with TNNI3K in the context of interacting with cardiac troponin I.^[6] The protein also interacts with , VPS28, KIAA159,^[7]NUP62,^[8] PLK1, UBC, and Xpo1.^[2]

In HIV, a synthetic peptide corresponding to the immunosuppressive domain (amino acids 574-592) of HIV-1 gp41 downregulates the expression of fatty acid binding protein 3 (FABP3) in peptide-treated PBMCs.^[9]

Clinical significance

Diagnostic potential

H-FABP is a sensitive biomarker for myocardial infarction^[10]^[11] and can be detected in the blood within one to three hours of the pain.^[12]^{[unreliable medical source?]}

The diagnostic potential of the biomarker H-FABP for heart injury was discovered in 1988 by Professor Jan Glatz (Maastricht, Netherlands).^[13] H-FABP is 20 times more specific to cardiac muscle than myoglobin,^[13] it is found at 10-fold lower levels in skeletal muscle than heart muscle and the amounts in the kidney, liver and small intestine are even lower again.^[14]^[15]

H-FABP is recommended to be measured with troponin to identify myocardial infarction and acute coronary syndrome in patients presenting with chest pain. H-FABP measured with troponin shows increased sensitivity of 20.6% over troponin at 3-6 hours following chest pain onset.^[16] This sensitivity may be explained by the high concentration of H-FABP in myocardium compared to other tissues, the stability and solubility of H-FABP, its low molecular weight; 15kDa compared to 18, 80 and 37kDa for MYO, CK-MB and cTnT respectively,^[17]^[18]^[19] its rapid release into plasma after myocardial injury - 60 minutes after an ischemic episode,^[20] and its relative tissue specificity.^[21] Similarly this study showed that measuring H-FABP in combination with troponin increased the diagnostic accuracy and with a negative predictive value of 98% could be used to identify those not suffering from MI at the early time point of 3-6 hours post chest pain onset.^[16] The effectiveness of using the combination of H-FABP with troponin to diagnose MI within 6 hours is well reported.^[22]^[23]^[24]

Prognostic potential

In addition to its diagnostic potential, H-FABP also has prognostic value. Alongside D-dimer, NT-proBNP and peak troponin T, it was the only cardiac biomarker that proved to be a statistically significant predictor of death or MI at one year. This prognostic information was independent of troponin T, ECG and clinical examination.^[23] The risk associated with raised H-FABP is dependent upon its concentration.^[25]^[26] Patients who were TnI negative but H-FABP positive had 17% increased risk of all cause mortality within one year compared to those patients who were TnI positive but H-FABP negative.^[25] Currently these TnI positive patients are prioritised for angioplasty, and the TnI negative patients are considered to be of a lower priority, yet the addition of the H-FABP test helps identify patients who are currently slipping through the net and allows physicians to more appropriately manage this hidden high risk group. If both biomarkers were negative, there is 0% mortality at 6 months, in the authors own words this “represents a particularly worthwhile clinical outcome, especially because it was observed in patients admitted into hospital for suspected ACS.” H-FABP indicates risk across the ACS spectrum including UA, NSTEMI or STEMI where low H-FABP concentrations confer low risk whereas high H-FABP concentrations indicate patients who are at a much higher risk of future events.^[25]

H-FABP in other diseases

H-FABP has been proven to significantly predict 30 day mortality in acute pulmonary embolism.^[27] H-FABP is more effective than Troponin T in risk stratifying Chronic Heart Failure patients.^[28] H-FABP is beginning to create interest with researchers who have found emerging evidence that indicates a role in differentiating between different neurodegenerative diseases.^[29]^[30]

H-FABP Point of care testing

To obtain diagnostic and prognostic information a precise and fully quantitative measurement of H-FABP is required. Commercial tests include Cardiac Array on Evidence MultiStat (Randox Laboratories Ltd.).

References

^ Phelan CM, Larsson C, Baird S, Futreal PA, Ruttledge MH, Morgan K et al. (May 1996). "The human mammary-derived growth inhibitor (MDGI) gene: genomic structure and mutation analysis in human breast tumors". Genomics 34 (1): 63–8. doi:10.1006/geno.1996.0241. PMID 8661024.
^ ^a ^b ^c ^d "Entrez Gene: FABP3 fatty acid binding protein 3, muscle and heart (mammary-derived growth inhibitor)".
^ ]Zong NC, Li H, Li H, Lam MP, Jimenez RC, Kim CS et al. (Oct 2013). "Integration of cardiac proteome biology and medicine by a specialized knowledgebase". Circulation Research 113 (9): 1043–53. doi:10.1161/CIRCRESAHA.113.301151. PMC 4076475. PMID 23965338.
^ "Fatty acid-binding protein, heart". Cardiac Organellar Protein Atlas Knowledgebase (COPaKB).
^ ^a ^b Kleine AH, Glatz JF, Van Nieuwenhoven FA, Van der Vusse GJ (Oct 1992). "Release of heart fatty acid-binding protein into plasma after acute myocardial infarction in man". Molecular and Cellular Biochemistry 116 (1-2): 155–62. doi:10.1007/BF01270583. PMID 1480144.
^ Zhao Y, Meng XM, Wei YJ, Zhao XW, Liu DQ, Cao HQ et al. (May 2003). "Cloning and characterization of a novel cardiac-specific kinase that interacts specifically with cardiac troponin I". Journal of Molecular Medicine 81 (5): 297–304. doi:10.1007/s00109-003-0427-x. PMID 12721663.
^ Stelzl U, Worm U, Lalowski M, Haenig C, Brembeck FH, Goehler H et al. (Sep 2005). "A human protein-protein interaction network: a resource for annotating the proteome". Cell 122 (6): 957–68. doi:10.1016/j.cell.2005.08.029. PMID 16169070.
^ Svendsen JM, Smogorzewska A, Sowa ME, O'Connell BC, Gygi SP, Elledge SJ et al. (Jul 2009). "Mammalian BTBD12/SLX4 assembles a Holliday junction resolvase and is required for DNA repair". Cell 138 (1): 63–77. doi:10.1016/j.cell.2009.06.030. PMID 19596235.
^ Denner J, Eschricht M, Lauck M, Semaan M, Schlaermann P, Ryu H et al. (2013). "Modulation of cytokine release and gene expression by the immunosuppressive domain of gp41 of HIV-1". PloS One 8 (1): e55199. doi:10.1371/journal.pone.0055199. PMID 23383108.
^ Tanaka T, Hirota Y, Sohmiya K, Nishimura S, Kawamura K (Apr 1991). "Serum and urinary human heart fatty acid-binding protein in acute myocardial infarction". Clinical Biochemistry 24 (2): 195–201. doi:10.1016/0009-9120(91)90571-U. PMID 2040092.
^ Watanabe K, Wakabayashi H, Veerkamp JH, Ono T, Suzuki T (May 1993). "Immunohistochemical distribution of heart-type fatty acid-binding protein immunoreactivity in normal human tissues and in acute myocardial infarct". The Journal of Pathology 170 (1): 59–65. doi:10.1002/path.1711700110. PMID 8326460.
^ Dobson R (2010-04-06). "At last, the pacemaker that lets you have a lifesaving body scan". Health. Daily Mail.
^ ^a ^b Glatz JF, van Bilsen M, Paulussen RJ, Veerkamp JH, van der Vusse GJ, Reneman RS (Jul 1988). "Release of fatty acid-binding protein from isolated rat heart subjected to ischemia and reperfusion or to the calcium paradox". Biochimica Et Biophysica Acta 961 (1): 148–52. doi:10.1016/0005-2760(88)90141-5. PMID 3260112.
^ Ghani F, Wu AH, Graff L, Petry C, Armstrong G, Prigent F et al. (May 2000). "Role of heart-type fatty acid-binding protein in early detection of acute myocardial infarction". Clinical Chemistry 46 (5): 718–9. PMID 10794758.
^ Pelsers MM, Hermens WT, Glatz JF (Feb 2005). "Fatty acid-binding proteins as plasma markers of tissue injury". Clinica Chimica Acta; International Journal of Clinical Chemistry 352 (1-2): 15–35. doi:10.1016/j.cccn.2004.09.001. PMID 15653098.
^ ^a ^b McMahon G, Lamont J, Curtin E, McConnell RI, Crockard M, Kurth MJ et al. (2011). "Diagnostic accuracy of H-FABP for the early diagnosis of acute myocardial infarction". American Journal of Emergency Medicine: in press.
^ Glatz JF, Kleine AH, van Nieuwenhoven FA, Hermens WT, van Dieijen-Visser MP, van der Vusse GJ (Feb 1994). "Fatty-acid-binding protein as a plasma marker for the estimation of myocardial infarct size in humans". British Heart Journal 71 (2): 135–40. doi:10.1136/hrt.71.2.135. PMC 483632. PMID 8130020.
^ Wodzig KW, Kragten JA, Hermens WT, Glatz JF, van Dieijen-Visser MP (Mar 1997). "Estimation of myocardial infarct size from plasma myoglobin or fatty acid-binding protein. Influence of renal function". European Journal of Clinical Chemistry and Clinical Biochemistry 35 (3): 191–8. doi:10.1515/cclm.1997.35.3.191. PMID 9127740.
^ Michielsen EC, Diris JH, Kleijnen VW, Wodzig WK, Van Dieijen-Visser MP (2006). "Interpretation of cardiac troponin T behaviour in size-exclusion chromatography". Clinical Chemistry and Laboratory Medicine 44 (12): 1422–7. doi:10.1515/CCLM.2006.265. PMID 17163817.
^ Van Nieuwenhoven FA, Kleine AH, Wodzig WH, Hermens WT, Kragten HA, Maessen JG et al. (Nov 1995). "Discrimination between myocardial and skeletal muscle injury by assessment of the plasma ratio of myoglobin over fatty acid-binding protein". Circulation 92 (10): 2848–54. doi:10.1161/01.cir.92.10.2848. PMID 7586251.
^ Alhadi HA, Fox KA (Apr 2004). "Do we need additional markers of myocyte necrosis: the potential value of heart fatty-acid-binding protein". Qjm 97 (4): 187–98. doi:10.1093/qjmed/hch037. PMID 15028848.
^ Azzazy HM, Pelsers MM, Christenson RH (Jan 2006). "Unbound free fatty acids and heart-type fatty acid-binding protein: diagnostic assays and clinical applications". Clinical Chemistry 52 (1): 19–29. doi:10.1373/clinchem.2005.056143. PMID 16269514.
^ ^a ^b McCann CJ, Glover BM, Menown IB, Moore MJ, McEneny J, Owens CG et al. (Dec 2008). "Novel biomarkers in early diagnosis of acute myocardial infarction compared with cardiac troponin T". European Heart Journal 29 (23): 2843–50. doi:10.1093/eurheartj/ehn363. PMID 18682444.
^ Li CJ, Li JQ, Liang XF, Li XX, Cui JG, Yang ZJ et al. (Mar 2010). "Point-of-care test of heart-type fatty acid-binding protein for the diagnosis of early acute myocardial infarction". Acta Pharmacologica Sinica 31 (3): 307–12. doi:10.1038/aps.2010.2. PMID 20140003.
^ ^a ^b ^c Kilcullen N, Viswanathan K, Das R, Morrell C, Farrin A, Barth JH et al. (Nov 2007). "Heart-type fatty acid-binding protein predicts long-term mortality after acute coronary syndrome and identifies high-risk patients across the range of troponin values". Journal of the American College of Cardiology 50 (21): 2061–7. doi:10.1016/j.jacc.2007.08.021. PMID 18021874.
^ Viswanathan K, Kilcullen N, Morrell C, Thistlethwaite SJ, Sivananthan MU, Hassan TB et al. (Jun 2010). "Heart-type fatty acid-binding protein predicts long-term mortality and re-infarction in consecutive patients with suspected acute coronary syndrome who are troponin-negative". Journal of the American College of Cardiology 55 (23): 2590–8. doi:10.1016/j.jacc.2009.12.062. PMID 20513600.
^ Kaczyñska A, Pelsers MM, Bochowicz A, Kostrubiec M, Glatz JF, Pruszczyk P (Sep 2006). "Plasma heart-type fatty acid binding protein is superior to troponin and myoglobin for rapid risk stratification in acute pulmonary embolism". Clinica Chimica Acta; International Journal of Clinical Chemistry 371 (1-2): 117–23. doi:10.1016/j.cca.2006.02.032. PMID 16698008.
^ Niizeki T, Takeishi Y, Arimoto T, Takabatake N, Nozaki N, Hirono O et al. (Mar 2007). "Heart-type fatty acid-binding protein is more sensitive than troponin T to detect the ongoing myocardial damage in chronic heart failure patients". Journal of Cardiac Failure 13 (2): 120–7. doi:10.1016/j.cardfail.2006.10.014. PMID 17395052.
^ Mollenhauer B, Steinacker P, Bahn E, Bibl M, Brechlin P, Schlossmacher MG et al. (2007). "Serum heart-type fatty acid-binding protein and cerebrospinal fluid tau: marker candidates for dementia with Lewy bodies". Neuro-Degenerative Diseases 4 (5): 366–75. doi:10.1159/000105157. PMID 17622779.
^ Lescuyer P, Allard L, Zimmermann-Ivol CG, Burgess JA, Hughes-Frutiger S, Burkhard PR et al. (Aug 2004). "Identification of post-mortem cerebrospinal fluid proteins as potential biomarkers of ischemia and neurodegeneration". Proteomics 4 (8): 2234–41. doi:10.1002/pmic.200300822. PMID 15274117.

UpToDate Contents

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1. トロポニンおよびクレアチンキナーゼ以外の心筋障害を示唆するバイオマーカー biomarkers suggesting cardiac injury other than troponins and creatine kinase
2. 非ST上昇型心筋梗塞後の有害転帰の危険因子 risk factors for adverse outcomes after non st elevation acute coronary syndromes
3. 心筋障害のバイオマーカーとしてのトロポニンおよびクレアチンキナーゼ troponins and creatine kinase as biomarkers of cardiac injury

English Journal

Species-specific expression of various proteins in meat tissue: Proteomic analysis of raw and cooked meat and meat products made from beef, pork and selected poultry species.

Montowska M, Pospiech E.SourceInstitute of Meat Technology, Poznań University of Life Sciences, Wojska Polskiego 31, 60-624 Poznań, Poland. Electronic address: magdalena.montowska@gmail.com.
Food chemistry.Food Chem.2013 Feb 15;136(3-4):1461-9. doi: 10.1016/j.foodchem.2012.09.072. Epub 2012 Oct 2.
The aim was to search for proteins differentiating the six species (cattle, pig, chicken, turkey, duck and goose) and relatively stable during the meat aging and only slightly degraded in ready-made products. The two-dimensional electrophoresis was used for analysis of the protein profiles from raw
PMID 23194549

Clinical and analytical evaluation of an immunoturbidimetric heart-type fatty acid-binding protein assay.

Carless DR, Wnęk M, Knox C, Harrison KR, Calder N, Hall AS, Barth JH.SourceBlood Sciences.
Scandinavian journal of clinical and laboratory investigation.Scand J Clin Lab Invest.2013 Feb;73(1):48-53. doi: 10.3109/00365513.2012.734396. Epub 2012 Nov 1.
Abstract Background. Heart-type fatty acid-binding protein (H-FABP) is a low molecular weight protein involved in the intracellular uptake and buffering of long chain fatty acids in the myocardium. It is an early marker for ACS. We have evaluated the Randox Laboratories immunoturbidimetric assay o
PMID 23113681

Japanese Journal

Heart Type Fatty Acid Binding Protein Is More Sensitive Than Troponin I and Creatine Kinase Myocardial Band at Early Stage in Determining Myocardial Injury Caused by Percutaneous Coronary Intervention

Ozdemir Levent,Elonu Orhan Hakan,Gocmen Ayse Yesim
International Heart Journal 52(3), 143-145, 2011
… Heart type fatty acid binding protein (H-FABP) is a relatively novel marker for the diagnosis of myocardial injury. … The purpose of the present study was to compare H-FABP with Troponin I (cTnI) and creatine kinase myocardial band (CK-MB) in determining myocardial injury in patients with early stage of percutaneous coronary intervention (PCI). …
NAID 130000770911

Soluble Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 as an Early Biomarker for ST Elevation Myocardial Infarction : – Time-Dependent Comparison With Other Biomarkers –

Kobayashi Nobuaki,Hata Noritake,Kume Noriaki,Seino Yoshihiko,Inami Toru,Yokoyama Shinya,Shinada Takuro,Tomita Kazunori,Kaneshige Toshihiko,Mizuno Kyoichi
Circulation Journal 75(6), 1433-1439, 2011
… Background: The diagnostic sensitivity of myocardial necrosis markers, such as creatine kinase-MB (CK-MB), cardiac troponins, myoglobin and heart-type fatty acid-binding protein (H-FABP) for the earliest stage of ST-elevation myocardial infarction (STEMI), remains insufficient. … Time-dependent changes in sLOX-1, H-FABP, myoglobin, troponin T and CK-MB were analyzed in 27 STEMI patients. …
NAID 130000743552

Related Pictures

FABP | What is H-FABP? – Heart-Type FABP nieuwe myocard infarct sneltest H Protein (H-FABP) Kit – Hotgen Biotech Assay procedure for MARKIT-M H-FABP 心脑血管疾病快速诊断系列 FABP | Clinical Value of H-FABP 酸结合蛋白（H-FABP）的临床意义

★リンクテーブル★

リンク元	「急性心筋梗塞」「ヒト心臓由来脂肪酸結合蛋白」「脂肪酸結合蛋白質」
関連記事	「FAB」「FA」「H」「FABP」

「急性心筋梗塞」

Fatty acid binding protein 3, muscle and heart (mammary-derived growth inhibitor)
	; PDB rendering based on 1g5w.
Available structures
PDB	Ortholog search: PDBe, RCSB
List of PDB id codes
	1G5W, 1HMR, 1HMS, 1HMT, 2HMB, 3RSW, 3WBG
Identifiers
Symbols	FABP3 ; FABP11; H-FABP; M-FABP; MDGI; O-FABP
External IDs	OMIM: 134651 MGI: 95476 HomoloGene: 68379 IUPHAR: 2533 ChEMBL: 3344 GeneCards: FABP3 Gene
Gene ontology
Molecular function	• long-chain fatty acid transporter activity; • protein binding; • cytoskeletal protein binding; • long-chain fatty acid binding; • icosatetraenoic acid binding; • oleic acid binding;
Cellular component	• extracellular space; • cytosol; • sarcoplasm; • extracellular vesicular exosome;
Biological process	• fatty acid metabolic process; • negative regulation of cell proliferation; • response to insulin; • response to drug; • cholesterol homeostasis; • long-chain fatty acid import; • regulation of fatty acid oxidation; • phospholipid homeostasis; • response to fatty acid; • positive regulation of phospholipid biosynthetic process;
	Sources: Amigo / QuickGO
RNA expression pattern
	More reference expression data
Orthologs
	This box: view; talk; edit;

　　[★]

英: acute myocardial infarction, AMI
関: 心筋梗塞

症状

胸痛：デルマトームC7-T1への放散痛(PHD.179)。デルマトームT1-T4への放散痛(IMD.418)→胸骨裏側、左上肢の尺側側、頚部、下顎部

痛みは虚血により生じた代謝産物(アデノシン、乳酸)が局所の神経終末を刺激することで生じる

PDH.179

心筋梗塞の症候

特徴的な疼痛	持続性で、ひどい痛み、典型的には胸骨下痛
交感神経による作用	発汗
交感神経による作用	皮膚が湿って冷たく感じられる
副交感神経による作用	悪心・嘔吐
副交感神経による作用	倦怠感
炎症反応	中程度の発熱
心臓の所見	IV音ギャロップ(うっ血性心不全があればIII音も)
その他	運動異常を伴う膨隆(前壁梗塞なら)
	心膜摩擦音(心膜炎があれば)
	収縮期雑音(僧帽弁閉鎖不全症や心室中隔欠損があれば)
	肺のラ音(うっ血性心不全があれば)
	頚動脈の拡大(右室梗塞)

身体所見(ST-segment elecation MI HIM.1533)

不安、不穏、ベットの上で場所を変えたり身体を曲げたりして痛みを和らげようとしている。
蒼白
四肢の冷感
30分以上持続する後胸骨痛 + 発汗　→　ST上昇心筋梗塞を示唆
多くの患者は最初の1時間は脈拍、血圧、正常
前壁梗塞の患者の1/4は交感神経が興奮　→　頻脈、高血圧

about one-fourth of patients with anterior infarction have manifestations of sympathetic nervous system hyperactivity (tachycardia and/or hypertension)

下壁梗塞の1/2は副交感神経興奮　→　徐脈±低血圧

up to one-half with inferior infarction show evidence of parasympathetic hyperactivity (bradycardia and/or hypotension)

検査

血液生化学検査: マーカー

	上昇	正常化
ミオグロビン	1-2時間	2-3日
H-FABP	1-2時間	24時間
WBC	2-3時間	7日
CK-MB	3-4時間	3-7日
トロポニンT	3-4時間	14-21日
心筋ミオシン軽鎖I	4-6時間	7-14日
AST	6-12時間	3-7日
LDH1,2	12-24時間	8-14日
CRP	1-3日	21日

時系列

→→→→→→→→→→→→→→→→→→
myo	W	TnT	myo	AST	LDH	CRP
H		CK
2-3時間　～～～～～～半日～　1日

心電図

PECG.168

(超急性期：発症直後～数時間)T波先鋭化、非特異的ST上昇
(急性期　：数時間～12時間)特異的ST上昇(上に凸)、R波減高、異常Q波出現
(亜急性期：24時間～1週間)ST上昇は減高、T波が陰転化(冠性T波:左右対称な陰性T波)。しばしばQT延長を伴う。
全層虚血でのST上昇は対側誘導でST低下が見られる。
異常Q波　+　ST上昇　が数週間持続　→　高度の壁運動の異常　→　心室瘤の形成を示唆

診断

心筋梗塞を疑ったら診察は、病歴、心電図変化、心筋マーカーの上昇で行う。心エコーで心筋壁の障害が認められ、CAGで冠動脈の閉塞または狭窄所見が見られたら確実(YN.C81)

治療

初期治療

PHD.187 ガイドライン1

アスピリン：治療開始から退院後も継続的に服用。
未分画ヘパリン：冠動脈の開存性を保つ。
βブロッカー：酸素需要減少。拡張期の延長による障害心筋への灌流を改善。静脈投与→経口投与。

禁忌：喘息、低血圧、著しい徐脈。

硝酸薬：前負荷・後負荷軽減による心筋酸素需要量低減、冠攣縮の解除・予防、側副路の血流増加。

使用不可：収縮期血圧＜90mmHg or 通常血圧より30mmHg以上血圧低下、高度徐脈(＜50bpm)、頻脈(＞100bpm)、下壁梗塞・右室梗塞合併疑い例

禁忌：勃起不全治療薬服用後24時間以内。

未分画ヘパリン：PCIが施行される場合にはヘパリンをactivated clotting timeが250を越えるように使用。tPAを使用した血栓溶解を行った後にはヘパリン48時間投与し、APTTを50-70秒に保つ。
鎮痛薬：塩酸モルヒネ：硝酸薬使用後も疼痛が持続する場合。

再灌流療法

適応：発症後12時間以内 (救急医療パーフェクトマニュアル p.43)

PCI
血栓溶解薬
CABG

二次予防

一般療法

患者教育
禁煙指導
食事療法：血圧管理、脂質管理、体重管理、糖尿病管理
運動療法

薬物療法

抗血小板薬
脂質異常症治療薬
RAA系阻害薬
βブロッカー
カルシウム拮抗薬：血圧管理や狭心症が他の薬剤でコントロールできない場合に限る(心筋梗塞発症早期での短時間作用型カルシウム拮抗薬投与による総死亡低下に対する有効性が確認されなかったため)。，STEMI患者への短時間作用型ジヒドロピリジン系カルシウム拮抗薬投与は通常禁忌。(ガイドライン1)
ニコランジル
ワルファリン

合併症

心室細動：発症一時間以内に起こりやすい。

機械的合併症

NSU.424 SSUR.397

心筋梗塞の破裂は全心筋梗塞例の2-4%でみられ、3/4の例で左室自由壁破裂、1/4の例で心室中隔穿孔、僧帽弁乳頭筋断裂はごく稀(SSUR.397)。

2週間以内に生じうる

1. 心室中隔穿孔

心室中隔を栄養する血流の途絶により中隔の壊死を来たす。左右シャントを生じ、原疾患である心筋梗塞による心不全を増悪させ、前方不全、すなわち低心拍出量症候群をきたす。増悪すれば、心原性ショックに陥る。右室は容量負荷をうけ右心不全をきたすことがある。症状は苦悶、血液低下、尿量減少を来たし、半数例においては心原性ショックが見られる。治療は循環が悪化している場合にはドパミン、ドブタミン、ニトログリセリンが用いられるが一時的であり、大動脈内バルーンパンピングによって循環動態を安定させる。その後、速やかに手術を施行する。循環動態が安定している例では2－3週間後に手術を行う(NSU.424)。手術は心停止下に左室梗塞部を切開して中隔穿孔部をダクロンパッチで閉鎖する。

2. 虚血性僧帽弁不全症(急性：乳頭筋断裂、慢性：乳頭筋機能不全)

乳頭筋断裂の75%は下壁梗塞に合併して後乳頭筋に発生し、残りは前乳頭筋に生ずる。僧帽弁尖の逸脱が起こり急性僧帽弁閉鎖不全症の病態を呈する。原疾患の心筋梗塞による心不全に加え、急性僧帽弁閉鎖不全症により心原性ショックに陥る。治療はIABPを挿入して循環動態を安定化後、僧帽弁置換術を行う。

3. 心室自由壁破裂

自由壁破裂は左室に多く、健常部と梗塞部位の境界に多い。病型は急激に大出血するblow-out型とじわじわ出血するoozing型がある。いずれの場合でも出血による心タンポナーデを来たし、低心拍出量の低下、さらに心原性ショックに陥る。症状は血圧低下、意識消失、呼吸停止、徐脈、心停止に至る。治療は直ちにPCPSにより循環の維持を図り(oozing型の場合は心嚢穿刺によるタンポナーデの解除を行う)、開胸手術により出血部のフェルトを用いた縫合閉鎖を行う。

2週間以降に生じうる

4. 左心室瘤

ガイドライン

1. 急性心筋梗塞（ST上昇型）の診療に関するガイドライン

http://www.j-circ.or.jp/guideline/pdf/JCS2008_takano_h.pdf

国試

103A035

「ヒト心臓由来脂肪酸結合蛋白」

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英: heart type fatty acid-binding protein H-FABP
同: 心臓型脂肪酸結合蛋白、心臓由来脂肪酸結合蛋白
関: 脂肪酸結合蛋白

[show details]

心臓型脂肪酸結合蛋白 : 約 3,270 件
心臓由来脂肪酸結合蛋白 : 約 22,000 件
ヒト心臓型脂肪酸結合蛋白 : 28 件
ヒト心臓由来脂肪酸結合蛋白 : 約 11,900 件

「脂肪酸結合蛋白質」

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英: fatty acid-binding protein, FABP
関: ヒト心臓由来脂肪酸結合蛋白

心臓型(H-FABP)

「FAB」

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「FA」

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「H」

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「FABP」

　　[★] 脂肪酸結合蛋白質 fatty acid-binding protein

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匿名

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案内

H-FABP