Myocardial Infarction

C. Kate Meier DVM, DACVM (Cardiology) , Mark A. Oyama DVM, DACVIM (Cardiology) , in Pocket-size Animal Disquisitional Care Medicine, 2009

INTRODUCTION

Myocardial infarction is the end consequence of either acute or chronic myocardial ischemia. Myocardial ischemia differs slightly from myocardial hypoxia in that ischemia results in a stasis of waste products of cellular metabolism in addition to a lack of oxygen commitment, leading to cellular damage above and across that from hypoxemia. one Myocardial infarction is a pathologic diagnosis and, depending on whether it is acute or chronic, is characterized by loss of normal cardiac myocyte structure (i.east., myocytolysis, coagulative necrosis, inflammatory cell infiltration, and fibrosis). Myocardial infarction has a host of causes and is a leading crusade of cardiovascular disease and death in humans.ii The vast majority of myocardial infarction in people stems from coronary avenue affliction and atherosclerosis, both of which are relatively uncommon in the veterinary patient population. In dogs, collateral circulation of the coronary arterial supply is relatively all-encompassing,1 then the probability of irreversible myocardial ischemia from any one coronary arterial occlusion may be lower in this species.

The clinical manifestations of myocardial ischemia and infarction in veterinary patients tin can range from nonspecific symptoms to severe life-threatening arrhythmias and congestive middle failure. Thus, clinical suspicion of myocardial infarction should atomic number 82 to aggressive management and supportive care. Prognosis depends on the severity of clinical signs, presence of concurrent disease, and response to initial therapy.

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Myocardial Infarction

Ruben Bunag , in xPharm: The Comprehensive Pharmacology Reference, 2007

Nomenclature

Myocardial infarction is classified co-ordinate to the region of the center afflicted, which depends on the major coronary artery that is occluded. Thus, the nomenclature includes: (ane) left ventricular anterior, which is commonly due to occlusion of the left anterior descending coronary avenue; (two) left ventricular inferior and posterior, which is usually due to right coronary artery or circumflex coronary avenue apoplexy; (3) left ventricular lateral, which is usually due to circumflex coronary artery occlusion; and (4) right ventricular, which is associated with involvement of a variety of coronary arteries Antman and Braunwald (2001).

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K

MELVYN KOBY Yard.D. , ... FRED F. FERRI M.D. , in Geriatric Clinical Advisor, 2007

DEFINITION

Astute coronary syndromes are manifestations of ischemic eye disease and represent a wide clinical spectrum that includes unstable angina/non-ST pinnacle MI and ST-elevation MI.

1.

Myocardial infarction is characterized by necrosis resulting from an insufficient supply of oxygenated blood to an area of the eye. According to the articulation European Social club of Cardiology/American College of Cardiology, either one of the following criteria for acute evolving or recent MI satisfies the diagnosis:

a.

Typical rise and gradual fall (troponin) or more rapid ascent and fall (CK-MB) of biochemical markers of myocardial necrosis with at least 1 of the following:

i.

Ischemic symptoms

two.

Evolution of pathologic Q waves on ECG

3.

ECG changes indicative of ischemia (ST-segment elevation or depression)

iv.

Coronary artery intervention (e.g., coronary angioplasty)

b.

Pathologic findings of astute MI

2.

ST peak MI: area of ischemic necrosis that penetrates the entire thickness of the ventricular wall and results in ST-segment elevation.

iii.

Unstable angina: coronary arterial plaque rupture with fragmentation and distal arterial embolization resulting in myocardial necrosis. Usually occurs without ST elevation and is thus termed not-ST elevation MI.

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Antiphospholipid Syndrome in Systemic Autoimmune Diseases

Ricard Cervera , ... Joan C. Reverter , in Handbook of Systemic Autoimmune Diseases, 2017

half-dozen.5.2 Myocardial Infarctions

Myocardial infarction (MI) was seen in 5.5% of patients course the Euro-Phospholipid grouping and it was the outset clinical manifestation for two.8% of them [i]. Indeed, some studies point out a relation betwixt a faster atherosclerosis evolution and the presence of aPL, particularly in SLE patients [56]. However, reports of aPL in patients with MI take yielded alien results. While some authors reported that aCL are mutual in young, postinfarction patients and should be regarded as markers for recurrent cardiovascular events [57], other investigators could not confirm this finding [58].

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Kawasaki Disease

C. Reuter , ... S. Shulman , in The Centre in Rheumatic, Autoimmune and Inflammatory Diseases, 2017

7.ii Myocardial Infarction

Myocardial infarction is the most common cause of death in KD. In a Japanese study of 195 cases, myocardial infarction normally occurred in the showtime year after onset of disease, although one-quaternary of patients had a myocardial infarction more than than a twelvemonth after resolution of the acute phase of KD. The first myocardial infarction was fatal in 22% of patients and asymptomatic in 37% [225]. Of those patients who survived a first infarct, 16% had a second myocardial infarct [225]. Nevertheless, another study of threescore patients with myocardial infarction due to KD constitute a 30-year survival rate of 63% with worse outcomes occurring in patients with poor postinfarction left ventricular ejection fractions (LVEF) [226]. Unfortunately, chest hurting complaints with myocardial infarction primarily occur but in older children. As a result, patients with a history of KD and significant coronary abnormalities should be evaluated immediately if they develop dyspnea, lethargy, inconsolable crying, significant abdominal hurting, or airsickness without clear viral syndrome, diaphoresis, or syncope [225]. Patients with giant (>8   mm or z  >   10) coronary aneurysms are at greatest risk for having infarcts, specially related to thrombi and/or to stenotic areas side by side to a giant aneurysm. Near fatal infarctions are the result of obstruction of the left primary coronary artery or both the right coronary and left anterior descending coronary arteries. Approximately half of the KD survivors of astute myocardial infarction had one or more than complications, including ventricular dysfunction, mitral regurgitation, and arrhythmias [225]. As with adults, when diagnosed with an acute coronary thrombosis, prompt fibrinolytic therapy should be attempted at a tertiary intendance heart [7,227], but the degree of reversibility of coronary thrombosis in children with KD may be less than that in adults with atherosclerotic disease. Belatedly cardiac sequelae of KD sometimes practice non manifest until adulthood [228].

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Cardiovascular Diseases

Mark Rishniw , in The Cat, 2012

Myocardial Infarction

Myocardial infarction has been documented on necropsy in cats with HCM. 23 Still, more than recently, cardiologists accept recognized what appears to be myocardial infarction in cats without evidence of HCM. Often, these patients have no clinical signs associated with the lesion, which is identified by echocardiography. Affected cats are often older and commonly have other diseases, such as chronic kidney disease. Echocardiographic features include regional thinning of the left ventricular wall or interventricular septum associated with regional dyskinesia or hypokinesia of the affected wall segment. Compensatory eccentric hypertrophy can occasionally occur if the afflicted region is large. The etiology is ordinarily unknown, and currently no pathologic testify exists in the veterinarian literature to support this antemortem observation. Moreover, no treatment exists to specifically address such presumptive myocardial injury.

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Inflammatory Response During Myocardial Infarction

Joaquim B. Oliveira , ... Andrei C. Sposito , in Advances in Clinical Chemistry, 2018

i Introduction

Myocardial infarction (MI) follows the occlusion of a coronary artery by a thrombus generated over a ruptured atherosclerotic plaque [i]. This outcome triggers a wave front end of jail cell death, which determines the release of endogenous molecules from necrotic cells to the extracellular infinite [2–4]. These molecules, namely, danger-associated molecular patterns (DAMPs), bespeak danger to surrounding cardiomyocytes through pattern recognition receptors (PRRs), sparking an intense inflammatory response [5].

At a first glance, inflammation plays a role in clearing the myocardium from cellular droppings and recruiting inflammatory cells to the injury site. This consequence set up the grounds to the subsequent, overlapping phase of cardiac healing. Nonetheless, to benefit cardiac recovery the extend of the inflammatory response is tightly regulated past a wide range of molecular effectors, such every bit cytokines and chemokines, with remarkable immunomodulatory properties [2–4]. In fact, dysregulated, temporally prolonged, or spatially extended inflammation leads to death of feasible cardiomyocytes, enhanced matrix degradation and extend fibrosis [half dozen].

The inflammatory phase securely contributes to the recovery of cardiac function subsequently an ischemic insult. This has led to an increasing interest in pharmacological strategies to modulate this response and possibly benefit clinical outcomes [7]. Indeed, very recently the CANTOS Trial showed that inhibiting specific cytokines is a promising target for improving cardiovascular outcomes [viii]. Not less importantly, MI triggers a systemic inflammatory response, which contributes to atherosclerotic plaque instability and recurrence of cardiovascular events [9–xi].

This chapter reviews the cardinal events of the inflammatory, repair, and remodeling stage following MI. The mechanisms involved in the progression of atherosclerosis through inflammation after an ischemic insult will also exist explored. Our aim is to provide the fundamentals for farther comprehension of the promising immunomodulatory therapeutic strategies for MI and bring light to the fascinating complication of the postal service-MI events.

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Small RNA Delivery for In Situ Tissue Regeneration

N.J. Kim , ... S.J. Lee , in In Situ Tissue Regeneration, 2016

Cardiac Tissue Regeneration

Myocardial infarction is a leading crusade of death in the globe [115]. It has been demonstrated that miRNAs play important roles during different forms of heart diseases. Hullinger et al. showed that inhibition of miR-fifteen family unit could amend cardiomyocytes resistant to hypoxia-induced prison cell death [116]. Systemic delivery of anti-miR-xv   dose dependently repressed miR-xv family in both murine and porcine cardiac tissues. The results showed that anti-miR targeting to miR-15 family in mice reduced infarct size and enhanced cardiac part in response to ischemic injury. Very recently, Eulalio et al. selected miRNAs (I-miR-590 aIhsa-miR-199a) to promote jail cell cycle reentry of adult cardiomyocytes ex vivo and to promote cardiomyocyte proliferation in both neonatal and adult animals [117]. After myocardial infarction in mice, these miRNAs stimulated marked cardiac regeneration and nigh complete recovery of cardiac functional parameters (Fig. 7.half dozen).

Figure 7.6. (A) Schematic of in vivo experiments using synthetic miRNAs. n  =   eight per group. (B) EdU and α-actinin staining of rat hearts injected with miRNAs. Scale confined, ane   mm (top), 100   μm (bottom). (C) Percent of proliferating cells. (D) Confocal microscopy of rat hearts injected with hsa-miR-590-3p and hsa-miR-199a-3p. Scale bar, x   μm. (E) Schematic of in vivo experiments using AAV vectors. n  =   9 per group. (F) Mouse hearts transduced with AAV vectors. Scale bar, 1   mm. (Thousand) Ratio between center and body weight. (H) CM cross-sectional surface area. (I) Percentage of cells positive for H3S10ph. (J) Confocal microscopy of H3S10ph-stained mouse hearts transduced with AAV. Scale bar, 10   μm. All panels, mean   ±   SEM; ∗∗p  <   .01, ∗∗∗p  <   .001 relative to control.

 Reprinted from Eulalio A, Mano M, Dal Ferro Chiliad, Zentilin L, Sinagra One thousand, Zacchigna S, et al. Functional screening identifies miRNAs inducing cardiac regeneration. Nature 2012;492:376–81.

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Intendance of Surgical and Other Fragile Models

Andrea R. Slate , Rivka L. Shoulson , in The Laboratory Rat (Tertiary Edition), 2020

3 Myocardial Infarction

Myocardial infarction tin can be induced in rats by surgical ligation of the left inductive descending (LAD) coronary artery. Traditional models of large myocardial infarction to achieve subsequent heart failure areassociated with a depression rate of survival, approximately 50% at the fourth dimension of surgery and 35% at half dozen months in some studies ( Goldman and Raya, 1995). Refinements in technique have been described to improve perioperative survival and consistency of infarct size. These refinements include endotracheal intubation and ventilation, proper identification of the LAD, ligation 8   mm from the origin, avoiding surgical contact with the lungs, removal of air from the chest cavity prior to closure, and deflation of the lungs prior to extubation (Srikanth et al., 2009). These improved techniques issue in a model with an 87% survival rate at the time of surgery, no boosted deaths for the subsequent 90 days, and a consistent infarct size 21%   ±   iv% of the left ventricular wall.

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Arterial hypertension, angina pectoris, myocardial infarction and eye failure

Kevin M. O'Shaughnessy , in Clinical Pharmacology (Eleventh Edition), 2012

Cardiovascular uses:

Angina pectoris : β-occludent reduces cardiac work and oxygen consumption.

Hypertension : β-blockade reduces renin secretion and cardiac output; there is fiddling interference with homeostatic reflexes.

Cardiac tachyarrhythmias : β-occludent reduces drive to cardiac pacemakers: subsidiary backdrop (encounter Tabular array 25.i, p. 430) may also be relevant.

Myocardial infarction and β-adrenoceptor blockers : there are two modes of use that reduce acute mortality and forbid recurrence: the so-called 'cardioprotective' upshot.

•

Early on apply within half dozen   h (or at most 12   h) of onset (intravenously for 24   h then orally for 3–four   weeks). Do good has been demonstrated only for atenolol. Cardiac work is reduced, resulting in a reduction in infarct size past up to 25% and protection against cardiac rupture. Surprisingly, tachyarrhythmias are non less frequent, mayhap because the cardiac βii receptor is not blocked by atenolol. Maximum benefit is in the first 24–36   h, but mortality remains lower for upwards to 1   year. Contraindications to early on utilise include bradycardia (<   55 beats/min), hypotension (systolic <   90   mmHg) and left ventricular failure. A patient already taking a β-blocker may exist given additional doses.

•

Late employ for secondary prevention of another myocardial infarction. The drug is started between 4   days and 4   weeks afterwards the onset of the infarct and is connected for at least ii   years. 21

•

Option of drug. The agent should be a pure antagonist, i.e. without ISA.

Aortic dissection and after subarachnoid haemorrhage: by reducing force and speed of systolic ejection (contractility) and blood pressure.

Obstruction of ventricular outflow where sympathetic activity occurs in the presence of anatomical abnormalities, e.g. Fallot'due south tetralogy (cyanotic attacks): hypertrophic subaortic stenosis (angina); some cases of mitral valve illness.

Hepatic portal hypertension and oesophageal variceal bleeding: reduction of portal pressure (see p. 548).

Cardiac failure (run across too Ch. 25): there is now clear evidence from prospective trials that β-blockade is beneficial in terms of mortality for patients with all grades of moderate heart failure. Data back up the utilize of both non-selective (carvedilol, α-blocker too) and β1-selective (metoprolol and bisoprolol) agents. Survival benefit exceeds that provided by ACE inhibitors over placebo. The negative inotropic furnishings can even so be significant, then the starting dose is low (e.one thousand. bisoprolol 1.25   mg orally daily in the morn or carvedilol 3.125   mg twice daily, with food) and may exist tolerated simply with boosted antifailure therapy, e.thousand. diuretic.

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