Dating myocardial infarction histology

Added: Jonpaul Thompson - Date: 05.09.2021 01:43 - Views: 25270 - Clicks: 3162

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Learn More. Ischemic heart disease is one of the leading causes of morbidity and death worldwide. Consequently, myocardial infarctions are often encountered in clinical and forensic autopsies, and diagnosis can be challenging, especially in the absence of an acute coronary occlusion. Precise histopathological identification and timing of myocardial infarction in humans often remains uncertain while it can be of crucial importance, especially in a forensic setting when third person involvement or medical responsibilities are in question.

A proper post-mortem diagnosis requires not only up-to-date knowledge of the ischemic coronary and myocardial pathology, but also a correct interpretation of such findings in relation to the clinical scenario of the deceased. For these reasons, it is important for pathologists to be familiar with the different clinically defined types of myocardial infarction and to discriminate myocardial infarction from other forms of myocardial injury.

This article reviews present knowledge and post-mortem diagnostic methods, including post-mortem imaging, to reveal the different types of myocardial injury and the clinical-pathological correlations with currently defined types of myocardial infarction. Acute ischemic heart syndromes, which are acute myocardial infarction MIvarious types of Dating myocardial infarction histology angina and sudden coronary death, are the prevailing acute life-threatening diseases with high mortality rates.

They occur not only in the Western World but also in industrialized developing countries [ 12 ]. Consequently, a diagnosis of MI or sudden coronary death is often considered in situations of clinical or forensic autopsy. Coronary artery disease CADwhich underlies most cases of MI, and also the ischemic myocardial pathology in different stages of injury and repair have been studied extensively to improve post-mortem diagnosis. Ancillary techniques to visualize ischemic injury have been developed or are now under investigation for improvement [ 3 — 5 ].

Recent developments are non- or minimally invasive post-mortem imaging techniques to detect coronary occlusion and ischemic injury in order to serve as an adjunct to, or even to replace, cardiac autopsy with pd ischemic death [ 67 ].

These novel post-mortem approaches presently attract much interest; autopsy rates tend to decrease gradually in many countries [ 8 ]. However, in some situations, these diagnostic modalities alone may prove inadequate or insufficient to explain a clinical suspicion of myocardial ischemia. Examples are the sudden coronary deaths without thrombus, the cases of peri-procedural myocardial ischemia after therapeutic coronary interventions in which early myocardial ischemia cannot be detected yet or the non-coronary causes of ischemia. Finally, in some cases, also types of myocardial injury other than ischemic should be considered.

This is reflected in the current clinical classification of MI, which discriminates five types with differences in etiological background, pathogenic mechanisms and evolving treatment strategies [ 9 ]. In this article, we review the present knowledge and post-mortem diagnostic methods to reveal MI at autopsy, how it should be discriminated from other forms of myocardial injury, and in particular, how pathology should be interpreted in relation to currently defined clinical types of MI.

Clinical diagnosis of MI Dating myocardial infarction histology based on the presence of elevated cardiac troponin levels, in combination with prolonged chest pain, ECG recordings or regional wall motion abnormalities indicative of recent onset ischemia or angiographic detection of a coronary thrombus. Type 1 MI is the result of acute coronary artery atherothrombosis.

Type 2 MI are infarctions that result from myocardial oxygen supply-demand imbalance and are not due to acute coronary plaque disruption and thrombosis. MI type 2 includes also relatively rare non-atherosclerotic coronary diseases such as spontaneous dissection or embolization. Nevertheless, it should be noted that stable not thrombosed coronary plaques are commonly present in patients with type 2 MI. Patients who present with clinical symptoms that are highly suspicious of MI in combination with new ECG changes or are in ventricular fibrillation VFbut who die before cardiac biomarkers of ischemia can be identified, are deated as type 3 MI.

MI diagnosed by a ificant rise of biomarkers related to percutaneous coronary revascularization procedures are deated as type 4 MI. They can be temporally related to the procedure within 48 h leading to critical myocardial flow reduction, but may also Dating myocardial infarction histology due to acute complications of a device such as in-stent thrombosis, coronary dissection or the late stent complications such as restenosis and late onset thrombosis. Similarly, type 5 MI is due to ischemic injury associated with coronary artery bypass grafting CABG within 48 h of the procedure.

It can be procedure-related, or related to low-flow, poor run-off or reperfusion damage. In clinical guidelines, a distinction is made between myocardial injurywhich encompasses any form of acute myocardial damage or destruction, and MI, resulting from myocardial ischemia only [ 9 ]. Evidently, MI is a form of myocardial injury, and both entities share the presence of raised serum levels of cardiac troponin cTn in a patient.

In order to discriminate clinically a MI from other types of myocardial injury, additional criteria such as angina symptoms and characteristic ECG changes are needed. For example, differential diagnosis of myocarditis is not always presented by clinical settings and this differentiation may arise from pathological standpoint [ 11 ]. The most frequent cause of acute myocardial ischemia is atherothrombotic occlusion of a coronary artery [ 312 ]. This implies that in cases of sudden death, acute coronary occlusion can explain arrhythmic death [ 3 ]. The underlying pathology of mural or occlusive coronary thrombosis is variable and can be due to plaque ruptureserosions or, less frequently, protruding calcified nodules.

Also, intraplaque haemorrhages contribute to the acute flow reduction in these instances [ 14 — 16 ]. It is important to note that there can be a considerable time interval between the onset of plaque disruption and the evolving critical stenosis or occlusion by thrombus. And also the onset of necrosis in the heart and the clinical manifestation of symptoms of MI are not always around the same time [ 1718 ]. It is not rare to find even organized thrombi or ificant myocardial necrosis at autopsy in a patient with acute onset of ischemic symptoms [ 1819 ].

At autopsy, the main coronary arteries and large branches such as diagonal and obtuse marginal are examined by transversely sectioning at 3-mm intervals to identify thrombus and critical stenosis. For reliable interpretation, heavily calcified arteries are decalcified prior to cross sectioning.

The most severely affected sections can be sampled for histology [ 3 ]. Accuracy can be improved by a visual aid, similar to that in Fig. Ideally, gross assessments should be confirmed by histology, taking the internal elastic lamina as the original lumen size. This approach has a good inter-observer reproducibility in high-degree lesions [ 21 ]. However, lumen shape may affect the interpretation of stenosis, with pathologists overestimating the stenosis caused by slit-like lumens, and underestimating concentric and eccentric stenosis [ 22 ]. Geometric remodelling of the artery contributes importantly to the rate of lumen stenosis.

Arteries are dynamic organs, in which compensatory expansive enlargement in association with Dating myocardial infarction histology plaques Dating myocardial infarction histology constrictive shrinkage in stable collagen-rich plaques is known as positive and negative remodelling respectively [ 23 ].

Many of these stenoses have stable tissue composition of fibrous tissue and calcifications but without thrombus [ 25 ]. In these instances, microscopy of malperfused territories of the myocardium can be a helpful adjunct in diagnosis. Clinically, these infarctions are diagnosed as type 2 MI.

However, in some cases, mural thrombus can be identified histologically, which implies a reclassification to type 1 MI. The evidence described so far relates to atherosclerotic CAD. Coronary artery segments with different degrees of atherosclerotic stenosis. Coronary artery spasm CAS is defined as an intense constriction of the vascular wall, which causes total or subtotal occlusion of the coronary arteries. The presence of an area of regional infarction in the myocardium could point towards spasm in the artery when no other explanation for the infarction is provided.

It can affect either the epicardial arteries, as initially proposed by Prinzmetal et al. The most frequent pathologic substrate of CAS is atherosclerotic CAD, but it has also rarely been reported in normal vessels [ 27 ]. Imaging tools such as computerized tomographic angiography CTAintravascular ultrasound IVUS and optical coherence tomography OCT show that the coronary artery segments where spasm is inducible are typically characterized by diffuse intimal and medial thickening with low lipid or calcium content, negative remodelling and small luminal area [ 2829 ].

These features are in line with the hypothesis that vascular smooth muscle cell hyper-reactivity is a pathophysiological substrate for spasm [ 30 ]. Clinically, the combination of severe CAD and spasm is associated with adverse prognosis [ 31 ]. At autopsy, there are no distinctive gross or histologic hallmarks of CAS; thus, the possible morphologic substrates associated with an increased risk of spasm must be searched for, as well as microscopic evidence of ischemia.

Drugs cocaine, amphetamine and derivatives, androgenic anabolic steroids, chemotherapyphysical and mental stress and release of vasoconstrictor agents by activated platelets mural thrombus are considered precipitating factors of spasm [ 32 — 35 ]. Small vessel diseases SVD can occur without obvious structural changes of the heart. It is particularly seen in hypertrophic and dilated hearts, preferentially in the subendocardial areas of the myocardium. SVD is also a common feature in diabetic hearts and hearts of patients with longstanding hypertension, but structural changes such as some vascular wall thickening, if present, are difficult to interpret in practice and subject to interpretation bias.

It is important to note that in all these instances, myocardial areas with reduced flow due to concomitant epicardial large vessel coronary stenosis are most vulnerable. In transplanted heartsSVD can be caused by widespread small vessel stenosis due to cardiac allograft vasculopathy [ 40 ].

Microvascular coronary embolization with thromboembolic materials distal to a thrombosed epicardial plaque can be found at autopsy in patients who died of MI [ 163941 ] and occur nowadays even more frequently in acute MI patients who are treated with primary percutaneous coronary intervention PCI for acutely thrombosed plaques. In clinical studies, such emboli are an uncommon cause of acute MI, although they may result in microinfarctions occurring scattered through the myocardium. In later stages, they may leave small areas of replacement fibrosis.

Moreover, microvascular embolization can occur in patients with atrial fibrillation, prosthetic heart valves, infective endocarditis or cardiac myxoma.

Progressive stenosis or acute thrombotic occlusion of a coronary artery can be treated by means of PCI in order to prolong life, to relieve symptoms, or minimize myocardial necrosis. At present, nearly all PCI procedures involve implantation of a metal stent or more recently, bioresorbable scaffolds BRS. Stent-related complications, which are thrombosis and fibrocellular restenosis, have reduced ificantly over the past years, mainly due to widespread application of drug-eluting stents DES [ 42 ].

Acute stent thrombosis is very rare and may occur due to stent malposition, dissection, long or angulated stented segments, or sometimes due to hypersensitivity reactions. Moreover, fibrocellular restenosis remains a problem in the still large group of patients, worldwide treated with non-coated bare metal stents BMS. A more recently described long-term complication is the occurrence of in-stent neoatherosclerosis.

Dating myocardial infarction histology

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