Haemostasis in acute myocardial infarction

Acute myocardial infarction (AMI) is caused by a localized arterial thrombosis, which resulted with myocardial ischemia and necrosis. This event causes the reaction of heart muscle (akinesis and dyskinesis of the ischemic parts of myocardial wall, arrhythmias, and haemodinamic disturbances) and severe systemic reaction (activation of neuroendocrine axis and inflammatory response). Haemostatis disturbances, which can be detected during the AMI and partly caused by the local coronary thrombosis, and partly by the mentioned heart and systemic reaction. A number of therapeutic procedures like venepuncture and almost all drugs commonly used, also influence the measurement of haemostatic parameters. Premorbid state, like smoking diabetes, hyperchlosterolemia, hypertension and obesity and also strong modulators of haemostatis disturbances in AMI and to light on the main factors which modulate that complicated process.

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Plaque Erosion Is a Major Substrate for Coronary Thrombosis in Acute Myocardial Infarction

Journal of the American College of Cardiology ◽

10.1016/s0735-1097(97)85356-9 ◽

1998 ◽

Vol 31 (2) ◽

pp. 379A ◽

Cited By ~ 1

Author(s):

E Arbustini

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Coronary Thrombosis ◽

Plaque Erosion

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TCTAP C-023 Contrast CT Was Useful in the Diagnosis of Acute Myocardial Infarction ue to Coronary Thrombosis

Journal of the American College of Cardiology ◽

10.1016/j.jacc.2017.03.244 ◽

2017 ◽

Vol 69 (16) ◽

pp. S112-S113

Author(s):

Gen Matsuura

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Coronary Thrombosis ◽

Contrast Ct

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Conservative Management of Subacute Contained Left Ventricular Rupture after Acute Myocardial Infarction

Indian Journal of Cardiovascular Disease in Women WINCARS ◽

10.1055/s-0038-1669784 ◽

2018 ◽

Vol 03 (01) ◽

pp. 034-038

Author(s):

Bharat Goud C ◽

Johann Christopher

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Color Doppler ◽

Regional Wall Motion ◽

Left Ventricular ◽

Mechanical Complication ◽

Inferior Wall ◽

Early Reperfusion ◽

St Segment Elevation ◽

Myocardial Wall

AbstractLeft ventricular free wall rupture (LVFWR) is a near-fatal mechanical complication of acute myocardial infarction in which an early diagnosis and emergency surgery should be of utmost priority for successful treatment. LVFWR is generally perceived to be universally fatal. Majority of LVFWR patients developing cardiac tamponade die rapidly, while in minority of cases the development of tamponade may be sufficiently slow to allow for diagnosis and successful intervention. In this article, the authors report a case of a 63-year-old male patient diagnosed with an inferoposterior wall myocardial infarction treated with early reperfusion thrombolytic therapy presenting 3 days later with diagnosis of subacute LVFWR. Patient had a history of relapse of chest pain which was severe and prolonged with 2 to 3 mm saddle-shaped ST-segment elevation in lateral leads, detected on a routine electrocardiogram, which led to an urgent bedside transthoracic echocardiogram (TTE). TTE showed regional wall motion abnormality in form of akinetic basal inferior-wall, a small echodense pericardial effusion, and a canalicular tract from endocardium to pericardium, through which color-Doppler examination suggested blood crossing the myocardial wall. A cardiac magnetic resonance imaging further reinforced the possibility of contained LVFWR.

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Full-Size and Partially Truncated Cardiac Troponin Complexes in the Blood of Patients with Acute Myocardial Infarction

Clinical Chemistry ◽

10.1373/clinchem.2018.301127 ◽

2019 ◽

Vol 65 (7) ◽

pp. 882-892 ◽

Cited By ~ 13

Author(s):

Alexandra V Vylegzhanina ◽

Alexander E Kogan ◽

Ivan A Katrukha ◽

Ekaterina V Koshkina ◽

Anastasia V Bereznikova ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Troponin I ◽

Troponin T ◽

Gel Filtration ◽

Free Form ◽

Plasma Samples ◽

Full Size ◽

Troponin Complex ◽

Almost All

AbstractBACKGROUNDThe measurement of cardiac isoforms of troponin I (cTnI) and troponin T (cTnT) is widely used for the diagnosis of acute myocardial infarction (AMI). However, there are conflicting data regarding what forms of cTnI and cTnT are present in the blood of AMI patients. We investigated cTnI and cTnT as components of troponin complexes in the blood of AMI patients.METHODSGel filtration techniques, sandwich fluoroimmunoassays, and Western blotting were used.RESULTSPlasma samples from patients with AMI contained the following troponin complexes: (a) a cTnI-cTnT-TnC complex (ITC) composed of full-size cTnT of 37 kDa or its 29-kDa fragment and full-size cTnI of 29 kDa or its 27-kDa fragments; (b) ITC with lower molecular weight (LMW-ITC) in which cTnT was truncated to the 14-kDa C-terminal fragments; and (c) a binary cTnI-cTnC complex composed of truncated cTnI of approximately 14 kDa. During the progression of the disease, the amount of ITC in AMI samples decreased, whereas the amounts of LMW-ITC and short 16- to 20-kDa cTnT central fragments increased. Almost all full-size cTnT and a 29-kDa cTnT fragment in AMI plasma samples were the components of ITC. No free full-size cTnT was found in AMI plasma samples. Only 16- to 27-kDa central fragments of cTnT were present in a free form in patient blood.CONCLUSIONSA ternary troponin complex exists in 2 forms in the blood of patients with AMI: full-size ITC and LMW-ITC. The binary cTnI-cTnC complex and free cTnT fragments are also present in patient blood.

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