Abstract 18987: Wavefront Progression of Necrosis During Myocardial Infarction Revisited: The Wave Expands From Endo to Epi as Well as From Center to Lateral Borders

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Rebeca Lorca ◽  
Marta Jimenez-Blanco ◽  
Jose Manuel García-Ruiz ◽  
Gonzalo Pizarro ◽  
Rodrigo Fernández-Jiménez ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Occlusion ◽  
Myocardial Necrosis ◽  
Short Axis Slice ◽  
Relative Mass ◽  
Control Group ◽  
Lateral Extension ◽  
Lateral Direction ◽  
Acute Coronary Occlusion

Background and purpose: The widely accepted wavefront theory of myocardial necrosis during acute coronary occlusion describes its progression as a wavefront from endo towards epicardium. The lateral affection of the myocardium would be predetermined by the location of the coronary occlusion. At the time this phenomenon was firstly described, advanced imaging technology was not available. Current cardiac magnetic resonance (CMR) is able to accurately characterize the necrosis progression in vivo. Methods: A total of 220 patients with reperfused anterior STEMI (METOCARD-CNIC trial population) were studied. All the patients underwent cine, T2-weighted and late gadolinium enhancement CMR at day 5-7 after STEMI. Endo- and epicardial contours of each LV short axis slice was traced, and each one was divided by 100 cords for analysis. Infarct size was characterized in its 2 dimensions: lateral (defined as the percentage of cords with enhancement in every slice) and transmural extension (percentage of enhancement within each cord, nested in the lateral extension). All slices were weighed according to their relative mass. We compared these parameters between the cardioprotected metoprolol group and the control group. Results: A strong lineal correlation between transmural and lateral infarct extension was observed (r: 0.88, p<0.001). We found that despite the edema lateral extension was larger than the IS lateral extension, this difference decreased as the transmurality affection increased. Finally, the infarct reduction exerted by metoprolol was derived from both the transmural and lateral extensions of IS. Conclusions: The transmural and lateral extension of necrosis after myocardial infarction are directly correlated. A proven cardioprotective therapy prevented the necrosis progression in both dimensions. These findings cannot be explained by the classical wavefront theory, suggesting that the necrotic wavefront progresses also in the lateral direction.

Abstract 19100: Transmural and Lateral Remodeling of the Post-infarction Scar Tissue: Serial Cardiac Magnetic Resonance Imaging Study From the Metocard-Cnic Trial

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Marta Jimenez-Blanco ◽  
Rebeca Lorca ◽  
Jose Manuel García-Ruiz ◽  
Gonzalo Pizarro ◽  
Rodrigo Fernández-Jiménez ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Imaging Study ◽  
Short Axis Slice ◽  
Myocardial Scar ◽  
Spatial Behavior ◽  
Surrounding Tissue ◽  
Relative Mass ◽  
Short Axis ◽  
Lateral Extension

Background: The remodeling process that occurs following an acute myocardial infarction produces changes in the myocardial scar and the surrounding tissue. The spatial evolution of the scar has not been yet characterized using MRI. Purpose: To describe the spatial behavior of myocardial scar on its transmural and lateral dimensions following an acute myocardial infarction. Methods: A total of 220 patients with acutely reperfused anterior STEMI (METOCARD-CNIC trial population) were studied. All the patients underwent cardiac MRI at day 7 and 6 months after presentation. The spatial distribution of the scar was analyzed using short axis late gadolinium enhancement images. Endo and epicardial contours of each LV short axis slice was traced, and each one was divided by 100 cords for analysis (Figure 1A). The lateral extension was defined as the percentage of cords with enhancement in every slice, and the transmural extension as the percentage of enhancement within each cord, nested in the lateral extension (Figure 1B). All slices were weighed according to their relative mass. Data were compared by paired t test. Results: Six months after STEMI, myocardial scar was smaller in both dimensions (Figure 1C). Mean ± SEM lateral scar, as a percentage of cords affected, at 7 days and 6 months were, respectively, 27.9 ± 1.1 and 22.2 ± 1.0 (p < 0.001). Transmurality also decreased significantly, mean percentage at day 7 was 46.8 ± 1.5 and at 6 months 35.4 ± 1.4 (p < 0.001). All these changes were accompanied by an increase in LV end-diastolic volume (171.47 ± 2.5 and 190.61 ± 2.9 (p < 0.001)). Conclusions: The myocardial scar remodeling process following a STEMI includes a reduction in both its transmural and lateral extensions.

scholarly journals Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction

2021 ◽  
Vol 33 ◽  
pp. 100767
Author(s):  
H. Pendell Meyers ◽  
Alexander Bracey ◽  
Daniel Lee ◽  
Andrew Lichtenheld ◽  
Wei J. Li ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Occlusion ◽  
Acute Coronary Occlusion ◽  
Criteria For Diagnosis

Mineralocorticoid Receptor Activation by Aldosterone or Corticosterone Induces Hypertension, Myocardial Infarction and Proteinuria

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 723-723
Author(s):  
Qing-Feng Tao ◽  
Diego Martinez vasquez ◽  
Ricardo Rocha ◽  
Gordon H Williams ◽  
Gail K Adler
Keyword(s):  
Myocardial Infarction ◽  
Drinking Water ◽  
Mineralocorticoid Receptor ◽  
Critical Role ◽  
Weight Ratio ◽  
Myocardial Necrosis ◽  
Receptor Activation ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

P165 Aldosterone through its interaction with the mineralocorticoid receptor (MR) plays a critical role in the development of hypertension and cardiovascular injury (CVI). Normally, MR is protected by 11β-hydroxysteroid dehydrogenase (11β-HSD) which inactivates glucocorticoids preventing their binding to MR. We hypothesis that if activation of MR by either aldosterone or glucocorticoids induces hypertension and CVI, then the inhibition of 11β-HSD with glycyrrhizin (GA), a natural inhibitor of 11β-HSD, should induce damage similar to that observed with aldosterone. Sprague-Dawley rats were uninephrectomized, and treated for 4 weeks with 1% NaCl (in drinking water) for the control group, 1% NaCl + aldosterone infusion (0.75 μg/h), or 1% NaCl + GA (3.5 g/l in drinking water). After 4 weeks, aldosterone and GA caused significant increases in blood pressure compared to control rats ([mean ± SEM] 211± 9, 205 ± 12, 120 ± 9 mmHg, respectively, p<0.001). Both aldosterone- and GA-treated rats had a significant increase in proteinuria (152.2 ± 8.7 and 107.7 ± 19.5 mg/d, respectively) versus controls (51.2 ± 9.5 mg/d). There was a significant increase (p<0.001) in heart to body weight ratio in the rats treated with aldosterone or GA compared with control (3.92 ± 0.10, 3.98 ± 0.88, and 3.24 ± 0.92 mg/g, respectively). Hearts of GA and aldosterone treated rats showed similar histological changes consisting of biventricular myocardial necrosis and fibrinoid necrosis of small coronary arteries and arterioles. These data suggests that in rodents activation of MR by either aldosterone or corticosterone leads to severe hypertension, vascular injury, proteinuria and myocardial infarction. Thus, 11β-HSD plays an important role in protecting the organism from injury.

Inhibition of nonexocytotic norepinephrine release by desipramine reduces myocardial infarction size

2006 ◽  
Vol 84 (11) ◽  
pp. 1185-1189 ◽  
Author(s):  
Doreen Richardt ◽  
Andreas Dendorfer ◽  
Ralph Tölg ◽  
Peter Dominiak ◽  
Gert Richardt
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Coronary Occlusion ◽  
Tricyclic Antidepressant ◽  
In Vivo Model ◽  
Norepinephrine Release ◽  
Area At Risk ◽  
Transport Direction

During myocardial ischemia, a substantial accumulation of norepinephrine occurs in the ischemic zone due to a local nonexocytotic release of norepinephrine. Norepinephrine release is driven by the neuronal monoamine transporter (NET), which reverses its usual transmembrane transport direction. We investigated whether this local accumulation of norepinephrine contributes to irreversible myocardial injury in an in vivo model of myocardial infarction. Male, anaesthetized Wistar rats were subjected to 30 min coronary occlusion and subsequent 120 min reperfusion. Five minutes prior to coronary occlusion, the NET inhibitor desipramine was administered intravenously. Infarct size (IS) was determined by TTC-staining and was related to the area at risk (AAR). The influence of desipramine on cardiac norepinephrine release was investigated in isolated perfused hearts with 30 min of regional ischemia. Norepinephrine was measured in the effluent from the hearts by HPLC and electrochemical detection. Desipramine (0.1–0.8 mg/kg) dose-dependently reduced infarct size (IS/AAR) from 0.54 to 0.21 and suppressed postischemic norepinephrine release from 245 to 108 pg/mL. In summary, the data indicate that nonexocytotic release of norepinephrine in myocardial ischemia exaggerates acute ischemic damage, because suppression of ischemia-induced release of norepinephrine by the tricyclic antidepressant desipramine effectively reduces infarct size in an in vivo model of myocardial ischemia.

scholarly journals Troponin T and Histological Characteristics of Rat Myocardial Infarction Induced by Isoproterenol

2007 ◽  
Vol 7 (3) ◽  
pp. 212-217 ◽  
Author(s):  
Sabaheta Hasić ◽  
Radivoj Jadrić ◽  
Emina Kiseljaković ◽  
Zakira Mornjaković ◽  
Mira Winterhalter-Jadrić
Keyword(s):  
Myocardial Infarction ◽  
Troponin T ◽  
Myocardial Necrosis ◽  
Control Group ◽  
High Dose ◽  
Male Adult ◽  
Histological Changes ◽  
Significant Difference ◽  
Intraperitoneal Dose ◽  
Histological Characteristics

In our investigation, we used short-time model of myocardial infarction of rats induced by high dose of isoproterenol (ISP). We investigated cardiac troponin T blood level (cTnT) and histological characteristics of rat myocardium. ISP, single, intraperitoneal dose 250 mg/kg was given to male, adult, Wistar rats (n=12). Rats were distributed depending on their body weight in subgroups: ISP I (BW 260-280g) and ISP II (BW 250-400g). Control group (n=9) was treated with intraperitoneal dose of 0,95% NaCl. Cardiac TnT was measured by electrochemiluminiscence (ECLA) sandwich immunoassay in rat serum 4 hours after ISP application. Rats’ hearts were dissected and examined by qualitative histological method (HE). Statistical significance was set at 0,05. There was significant difference in cTnT of ISP II (p=0,0001) vs. control and ISP I (p<0,05) vs. control. Significant difference was beetween ISP I and ISP II subgroups (p<0.001). The accent of histological changes of myocardium was on nuclei of cell. Cells showed acydophilic changes and nuclei disappearance as signs of coagulative necrosis development. Extensivity of histological changes were different beetween ISP I and ISP II subgroup. Used dose of ISP induced development of myocardial necrosis in rats. Suben-docardial portion of myocardium was more vulnerability than subepicardial portion. Rats of ISP II had more extensive histological changes than these in ISP I. Administered doses of ISP enabled cTnT utilization as a marker of myocardial necrosis.

scholarly journals Diagnosis of myocardial infarction at autopsy: AECVP reappraisal in the light of the current clinical classification

2019 ◽  
Vol 476 (2) ◽  
pp. 179-194 ◽  
Author(s):  
Katarzyna Michaud ◽  
◽  
Cristina Basso ◽  
Giulia d’Amati ◽  
Carla Giordano ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Injury ◽  
Coronary Occlusion ◽  
Diagnostic Methods ◽  
Myocardial Infarctions ◽  
Post Mortem ◽  
Acute Coronary Occlusion ◽  
Different Types ◽  
Third Person ◽  
Myocardial Pathology

Abstract 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.

Use of an Artificial Neural Network for Data Analysis in Clinical Decision-Making: The Diagnosis of Acute Coronary Occlusion

1990 ◽  
Vol 2 (4) ◽  
pp. 480-489 ◽  
Author(s):  
William G. Baxt
Keyword(s):  
Neural Network ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Artificial Neural Network ◽  
Coronary Occlusion ◽  
Clinical Decision Making ◽  
Clinical Decision ◽  
Acute Coronary Occlusion ◽  
Artificial Neural ◽  
Better Than

A nonlinear artificial neural network trained by backpropagation was applied to the diagnosis of acute myocardial infarction (coronary occlusion) in patients presenting to the emergency department with acute anterior chest pain. Three-hundred and fifty-six patients were retrospectively studied, of which 236 did not have acute myocardial infarction and 120 did have infarction. The network was trained on a randomly chosen set of half of the patients who had not sustained acute myocardial infarction and half of the patients who had sustained infarction. It was then tested on a set consisting of the remaining patients to which it had not been exposed. The network correctly identified 92% of the patients with acute myocardial infarction and 96% of the patients without infarction. When all patients with the electrocardiographic evidence of infarction were removed from the cohort, the network correctly identified 80% of the patients with infarction. This is substantially better than the performance reported for either physicians or any other analytical approach.

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