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A myocardial infarction MI , also known as a heart attack , occurs when blood flow decreases or stops to a part of the heart , causing damage to the heart muscle. Most MIs occur due to coronary artery disease. Treatment of an MI is time-critical. Worldwide, about Myocardial infarction MI refers to tissue death infarction of the heart muscle myocardium caused by ischaemia, that is lack of oxygen delivery to myocardial tissue. It is a type of acute coronary syndrome , which describes a sudden or short-term change in symptoms related to blood flow to the heart. The phrase "heart attack" is often used non-specifically to refer to myocardial infarction.

The pathologic features depend on the interval of time elapsed from onset of MI and death and from the extent of haemorrhage between the pericardium and the myocardial wall. The myocardial wall shows interruption or fissuring. The myocardial changes include coagulative necrosis with or without reperfusion pattern, according to the administered treatments. Cardiac arrhythmias are common in patients with STEMI and occur most frequently early after the development of symptoms.

Cardiogenic shock may be mimicked by aortic dissection and haemorrhagic shock. Severe MR with cardiogenic shock has a poor prognosis. Pericarditis occurs in transmural STEMI involving the full thickness of the myocardial wall to the epicardium.

Patients with pericarditis have larger infarcts, lower ejection fraction and higher incidence of congestive heart failure. Bleeding complications are higher in women than in men. Rare intracranial and gastrointestinal haemorrhages have also been reported.

The contribution of the pathologic study should add information to the clinical data and should match new sensitive diagnostic markers. National Center for Biotechnology InformationU. Journal List Heart v. Published online Apr Author information Article notes Copyright and License information Disclaimer. F PratiInterventional Cardiology, S. Giovanni Hospital, Roma, Italy.

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Keywords: myocardial infarction, pathology, reperfusion. This article has been cited by other articles in PMC. Open in a separate window.

Coronary arteries In reperfused MI the culprit lesion is expected to be patent: it may show ulceration with haemorrhagic invasion of the core or mural thrombus layered over the plaque ulceration.

Heart rupture The main risk factors for heart rupture include longstanding hypertension, female sex, advanced age, and no history of prior infarction. Left ventricular aneurysm Aneurysm after STEMI usually occurs in the left anterior wall, in association with left anterior descending occlusion and a wide infarcted area.

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Ventricular pseudoaneurysm Ventricular pseudoaneurysm is a rare complication. Arrhythmias Cardiac arrhythmias are common in patients with STEMI and occur most frequently early after the development of symptoms.

Pericarditis Pericarditis occurs in transmural STEMI involving the full thickness of the myocardial wall to the epicardium. References 1.

Clinical Pathology - CVS1-Myocardial Infarction Microscopy Tutorial.

Circulation - Int J Cardiol - Pathologic basis of disease. Elsevier Saunders, The potential adverse effects of habitual use of Catha edulis khat. Expert Opin Drug Saf 4 - Myocardial infarction after aspirin treatment, and Kounis syndrome.

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J R Soc Med 98 Coronary vasospasm due to hypercholinergic crisis: an example of normal coronary arteriogram and myocardial infarction. Eur Heart J 1 - Experimental reevaluation of myocardial ondulations in the early histological diagnosis of myocardial infarct.

Arch Inst Cardiol Mex 49 - Heart 82 - Circulation 97 - Am J Cardiol 68 36BB. Reffelmann T, Kloner R A.

Dating myocardial infarction histologically

Heart 87 - A serial intravascular ultrasound study. JAMA - Acute cardiogenic pulmonary edema. Relevance of multivessel disease, conduction abnormalities and silent ischemia. Int J Cardiol Clin Cardiol 15 - Time course of cytokine and extracellular matrix protein up-regulation in myocardial infarcts at 4hs.

B The confocal microscopic observation of early 4hs myocardial infarction showed a large area of TnC depletion in green the TnC reaction. In the group of early infarction approximately hours from the onset of ischemic symptoms and signs margination of PMN leukocytes that include neutrophils and monocytes was detectable in vessels at the periphery of the necrotic zone along with infiltration of these elements into the ischemic issue.

A crowd of PMN was visible along a line between infiltrated and non-infiltrated necrotic myocardium in large areas of necrosis. Immunohistochemistry confirmed the nature of the inflammatory cells. Time course of cytokines and extracellular matrix protein up-regulation in myocardial infarcts at hs.

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D CD15 reaction after 6 hrs, after 8 hrs, after 10 hrs, and 12 hrs. Semi-quantitative evaluation and statistical analysis of the immunohistochemical findings and gradation of the immunohistochemical reaction in the heart samples.

Western blot analysis. These two chronological groups are homogenous and the described morphological changes were classified when clinical data coherently supported the microscopic chronological modification. Our data show that some investigated parameters, such as CD15, IL, MCP-1, have a significantly different expression in the groups being studied very early and older infarction. Monocyte chemotactic protein MCP -1, expressed by the main inflammatory and stromal cells, such as endothelial cells, mediates the recruitment of mononuclear cells, modulates monocyte and lymphocyte phenotype and regulates fibrous tissue deposition and angiogenesis.

Its expression is upregulated after proinflammatory stimuli and tissue injury [ 19 ]. Neutrophils are major players in inflammation and are known to express all components of the IL It is well known that the response of the myocardium to ischemic insult can be divided into overlapping phases: the inflammatory phase, the proliferative phase and the maturation phase.

Sudden induction of ischemia triggers a series of events that culminate in the death of ischemic cardiomyocytes; the necrotic muscle elicits an inflammatory cascade that serves to clear the infarct from dead cells and matrix debris, and ultimately results in the healing and replacement of the damaged tissue with scarring [ 320 ]. The pathological pictures of the later stages i. In the inflammatory phase, immediately following myocardial ischemia, chemokines and cytokines are induced in the infarct and marked leukocyte infiltration is noted.

Neutrophils and macrophages clear the wound from dead cells and matrix debris. If, on one hand, the pathophysiological mechanisms underlying the very early phase of myocardial response to ischemia are well known [ 35 ], on the other hand, the weakest part of the available morphological evidence to date appears to be right in this phase when cellular reaction is not yet histologically detectable.

The finding of IL, MCP-1 expressions in the cardiac specimens of early infarction confirm a considerable amount of existing data that show the role of humoral cytokines and inducible chemokines, complement, and toll-like receptors and cellular monocytes, macrophages, dendritic cells, T cells, mast cells, platelets, endothelial cells mediators in the initial healing phases following cardiomyocytes death [ 461724 - 31 ].

Myocardial infarction

Activation of cytokine cascades in the infarcted myocardium was established in numerous studies. In experimental models of myocardial infarction, the induction and release of the pro-inflammatory cytokines are regularly described [ 1617 ].

The multifunctional, overlapping and often contradictory effects of the cytokines have hindered understanding of their functional role in cardiac injury and repair. Many authors have attempted to assess the histological age of MI, classifying the chronological phenomena into phases using histochemical methods only. The first attempts were established by White et al.

An attempt to define early infarct necrosis was afterwards performed by Lodge-Patch [ 33 ] who focused on the character of the cellular exudate as the most valuable feature in estimating the age of a young infarct. The results constitute important findings concerning morphological changes and chronological organization of myocardial infarct. Nuclear changes in muscle fibers, necrosis and phagocytosis of muscle, interstitial edema, neutrophils and polimorphonuclears infiltration were found to be a typical pattern at a time of hours from the onset of acute symptoms [ 33 ].

These findings suggested that the age of a cardiac infarct could be told from its histological appearances. However, myocardial infarcts could not be accurately dated before hours from the onset. The lesion is unrelated to ischemia. Its presence in acute coronary syndromes is probably due to catecholamines released within the myocardium as a reflex response [ 35 ] to regional asynergy of the infarcted or perinfarcted zone, a hypothesis that is supported by the abolishment of contraction bands and ventricular fibrillation with beta-blocking agents in experimental myocardial infarction and in reperfusion necrosis [ 36 ].

Contrary to the general opinion that excess catecholamines produce cardiotoxicity mainly through binding to adrenoceptors, there is increasing evidence that catecholamine-induced deleterious actions may also occur through oxidative mechanisms [ 3738 ], which undoubtedly occur during myocardial reperfusion after ischemia [ 17 ]. Interstitial edema and wavy fibers have been also described [ 39 ] in very early infarct but these findings are very unspecific [ 21 ]. Consequently, despite several attempts, no suitable histological criteria have materialized into forensic practice.

The histological age determination of myocardial infarction is an important task of forensic medicine and requires thorough knowledge of the general and specific pathology of myocardial infarction. So, we need to investigate the pathology of myocardial infarction as a cause of sudden cardiovascular death. Sometimes, we need to judge the medical practice in the cases of in-hospital myocardial infarction among patients who were treated for other diseases and to determine the causal relationship with myocardial infarction as cause of death.

In the very near future, proteomics may help clinicians and pathologists to better understand mechanisms related to cardiac repair and remodeling and provide targets for future therapies. ET and VF conceived of the study, participated in its design and coordination and helped to draft the manuscript. MN and IR carried out the histological and immunohistochemical studies and drafted the manuscript.

MDP participated in the design of the study and performed the statistical analysis. All authors read and approved the final manuscript. Authors want to thank Dr. Santina Cantatore for the technical support. National Center for Biotechnology InformationU.

Background

Journal List J Transl Med v. J Transl Med. Published online Jul 2. Author information Article notes Copyright and License information Disclaimer. Corresponding author. Emanuela Turillazzi: ti. Received Mar 31; Accepted Jun This article has been cited by other articles in PMC. Abstract Background Experimental and human studies have demonstrated that innate immune mechanisms and consequent inflammatory reaction play a critical role in cardiac response to ischemic injury.

Conclusions Essential markers i. Background From a clinical point of view, the term myocardial infarction MI can be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia. Open in a separate window. Figure 1. The time course of the inflammation, repair, and remodeling of the infarcted heart. Methods Clinical data and tissue specimens The clinical data and autopsy records of the autopsies performed at the Departments of Forensic Pathology of the University of Foggia and the University of Pisa Italy over the period - were evaluated, and 26 cases in which MI was indicated as cause of death were selected.

Dating Myocardial Infarction Histologically, debate iglesia ni cristo vs ang dating daan live, batman o retorno online dating, casey dating blog los angeles Short Sexy Description: free sex chat with countryconnectionsqatar.com full fun to girls/ No matter what Sculfor+dating city you live in, if you are visiting on business or seeking a personal tour guide, adding a beautiful shemale escort will make your time that much more pleasurable. Browse from a wide range of exotic Shemale Escort profiles Sculfor+dating and find a local beautiful playmates or companion to show you an amazing time / Myocardial infarction (MI) refers to tissue death of the heart muscle caused by ischaemia, that is lack of oxygen delivery to myocardial countryconnectionsqatar.com is a type of acute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart. Unlike the other type of acute coronary syndrome, unstable angina, a myocardial infarction occurs Causes: Usually coronary artery disease.

Western blot analysis Western blot analysis was performed. Statistical analysis A semi-quantitative evaluation of the immunohistochemical findings and gradation of the immunohistochemical reaction were described with an ordinal scale and the median value reported. Results Clinical data and histological results were compared to assemble the MI cases in chronological homogenous groups.

Figure 2. Figure 3. Table 1 Semi-quantitative evaluation and statistical analysis of the immunohistochemical findings and gradation of the immunohistochemical reaction in the heart samples. Figure 4. Foci of contraction band necrosis.

Oct 26,   The symptoms of acute myocardial infarction (MI) are chest pain, which may radiate to the arm or jaw, sweating, nausea, and chest tightness or pressure. The diagnosis rests on laboratory findings of myocardial necrosis, which causes leakage of myocardial enzymes, such as troponin, into the circulating blood. Apr 18,   The clinical diagnosis of myocardial infarction (MI) relies on symptoms, electrocardiographic findings, and biochemical markers (troponin, serum creatine kinase, creatine kinase?MB). 1,2 Acute ischaemic syndromes are now classified as unstable angina/non?ST?elevation MI (UA/NSTEMI) and acute ischaemic syndromes with ST?elevation Cited by: Israel+women+online+dating, free online canadian dating sites, dating sites for singles in mumbai , dating m1 helmet/

At immunohistochemistry loss of cellular antigen myoglobin and cardiac troponin is detectable earlier than the accumulation of plasma markers C5b-9 complex, fibronectin. General and intense eosinophilia of myofibers. Interstitial oedema. MCP-1 decrease as intensity in respect to the first hours. Pronounced necrosis of the infarcted areas; strong evidence of PMN margination with further leukocyte penetration of the infarct area. Strong immunopositivity to anti CD15 antibodies was observed.

Discussion Our data show that some investigated parameters, such as CD15, IL, MCP-1, have a significantly different expression in the groups being studied very early and older infarction. Competing interests The authors declare that they have no competing interests.

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Acknowledgement Authors want to thank Dr. Third universal definition of myocardial infarction. Systematic characterization of myocardial inflammation, repair, and remodeling in a mouse model of reperfused myocardial infarction.

J Histochem Cytochem. The immune system and cardiac repair. Pharmacol Res. Regulation of the inflammatory response in cardiac repair. Circ Res. Cardiovasc Res. World J Cardiol. Sudden cardiac death and myocardial ischemia indicators: a comparative study of four immunohistochemical markers.

Am J Forensic Med Pathol. Immunohistochemical detection of early myocardial infarction. The utility of C4d, C9, and troponin T immunohistochemistry in acute myocardial infarction.



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