Acute Coronary Syndrome Subject


AcuteCoronary Syndrome


AcuteCoronary Syndrome

Accordingto the research conducted in the health sector, millions of patientsvisit hospital emergency departments yearly complaining of chestpain. More than two million patients get admitted to most hospitalsdue to chest pains, but research has revealed that only a quarter ofthem are identified or diagnosed with coronary heart disease. Acutecoronary syndrome (ACS) details on the spectrum of clinicalpresentations starting from the STEMI (ST-segment elevationmyocardial infarction) to other presentations stated on NSTEMI(non–ST-segment elevation myocardial infarction) or in other casesfrom unstable angina. The primary objective of managing the acutecoronary syndrome patient and victims is to control their cardiacischemic event and in return reduce unnecessary risk to them. Thisresearch gives details of a 58-year-old man who visits an emergencydepartment complaining of chest pain. His blood pressure was ratedhigh (180/96), high pulse rate above normal (98/minute) but the bodytemperature was identified to be standard or regular (37.8 °C).The signs showed the existence of a partial or complete thrombosisrelated to infarct artery (Bhatia et al., 2012).

Bya close diagnosis of a patient, the standard clinical descriptors maymake decisions and draw a conclusion for having observed the chestpain, the electrocardiogram with biochemical markers of themyocardial injury that may happen after or during an ischemic acuteepisode. A primary cause of ACS is the Atherosclerosis which mayoccur mostly from the disruption of those previous non-severelesions. Most of those patients of ACS who visits the emergencydepartment, complaints of some of the following issues:


II.Pain which may be described as squeezing or pressure and mayradiate to the neck, chest, jaw, back, either arm or upper abdomenamong other areas.

III.Exertional dyspnea which fortitude in pain or resting.

IV.The sympathetic discharge which leads to Diaphoresis.

V.Vagal simulations leading to Nausea.

VI.Decreased exercise rate or tolerance (Mezzaroma et al., 2011).

However,some of the physical findings analyzed from this man communicatedsome message since were on an exceptional case. When compared withthe normal case, range, and a conclusion could be identified asfollows.


2.Extra-cardiac vascular disease.

3.Hypertension: ventricular dysfunction as a result of myocardialischemia, infarction or valvular dysfunction.

4.Distention on the venous jugular.

5.Left heart failure signs such as pulmonary edema.

6.Cardiogenic shock due to cool, clammy skin diaphoresis.

7.Systolic murmur due to dynamic obstruction on left outflowventricular tract.

Someof the potential complications related to the acute coronary syndromeinclude the pulmonary edema (ischemia) and the myocardial infections(papillary muscle rupture) on the ventricular septum and the leftventricular free wall (ZouggariY et al., 2013).

TheESC (European Society of Cardiology) in 2012 released guidelines onhow to manage non-ST-segment elevation. Some of the components ofthose guidelines include the use of Can Rapid risk stratification ofUnstable angina patients that Suppress Adverse Outcomes with Early(CRUSADE) and a better strategy for implementing the guidelines ofAHA/ACC. In emergency set up, one of the most important tests ofangina is the electrocardiography, and some of the angina episodeschanges that can be identified at this stage include the following:

i.)Elevations of Transient ST-segment.

ii.) The dynamic T-wave changes including the normalizations, inversionsor the hyper- acute changes.

iii.) The ST depressions which may be down-sloping or horizontal.

Theguidelines of ACC/AHA (American College of Cardiology/American HeartAssociation) play a significant role in helping patients withcoronary disorders. These guidelines state that all patients withchest pain or any other syndromes related to acute coronary syndromes(ACS), must have 12-lead electrocardiography performed within thefirst 10 minutes of their arrival at the emergency department (BhatiaV et al., 2012).The results should be directed to the relevant facility or sectionfor further analysis hence since both the Cardiac markers andElectrocardiogram were pending, no conclusions could be drawn untilthe pending results were available.

Thehealing process of infarcted myocardium

Impairmentof acute blood flow on myocardium which occurs during the cardiacinfarction may have great consequences towards the surroundingregions of the heart. If doctors are unable to make early discoveryconcerning the obstruction of the blood vessel, those muscle cellsaffected by the lack of inadequate blood flow may die automatically.The identified problem has a significant impact to human because oncemyocardial tissue gets lost it can no longer be regenerated. Thepumping heart performance may remain impaired throughout thelifetime.

Inthe case of persistent on poor perfusion, many processes ofremodeling may occur mostly in those damaged parts of the myocardiumleading to the automatic replacement of those dead muscle tissue bythe scar tissue (ZouggariY et al., 2013).The process is frequently referred to as the healing even if theheart does not remain in the state of being intact after that. Inorders to prevent the heart from tearing, an optimum scar-forming andwound healing processes are therefore vital and paramount.

Whileinvestigating the damaged heart healing process, the researcherdiscovered the relevant information related to the roles played bythe immune system. Immediately after infarction, the white bloodcells move to protect the damaged muscle. Granulocytes are usuallythe fast to arrive and ensure the removal of the dead myocardialcells. At that moment, the immune system cells referred to as themacrophages get into the area. The researcher identified that thosemacrophages play a significant role towards the healing process.

Hundredsof proteins are expressed by those surviving myocardial cellsincluding the Reg3beta which acts as an attractant of macrophagesspecifically by promoting them more to get into the areas of thatdamaged myocardium (MezzaromaE et al., 2011).Over the research department, it was concluded that the reg3betaplays a significant role while regulating the wound healing. Adisturbed wound healing process could also be observed due to thereduced macrophage migration.

Instudying myocardial infarction, some of the myocardium dies along theprocess and get replaced by the scar tissue. The stage becomes thevulnerable period of the stability, and the formation of the scartissue plays a significant role towards the survival of the patientas a result of acute myocardial infarction (ObalD et al., 2012).While identifying out the vulnerable period, the scientists from MaxPlanck Institute of Lung and Heart Research discovered the reg3betagene which is far much useful in healing of those damaged tissues inheart.

Insummary, the reaction and response of organism towards the tissuedamages are well preserved and outlined throughout the evolutionperiod. However, there are specific characteristics which accompanythe cardiac healing. There are several hours which are usuallylimited where the rescue of viable myocardium occurs and this timewindow would be sufficiently large to influence healing of the scarand hence initiate inadequate therapy. Therefore, the support ofhealing mechanisms and their better understanding may help in thedevelopment of new therapeutic options.


ObalD, Keith R, Dai S,cDimova N, Kingery J, and Zheng YT (2012).Cardiomyocyte-restricted overexpression of extracellular superoxidedismutase increases nitric oxide bioavailability and reduces infarctsize after ischemia/reperfusion. Basic Res Cardiol. 107:305.

MezzaromaE, Toldo S, Farkas D, Seropian IM, Van Tassell BW and Salloum FN(2011). The inflammasome promotes adverse cardiac remodelingfollowing acute myocardial infarction in the mouse. Proc Natl AcadSci U S A. 2011 108:19725–30.

ZouggariY, Ait-Oufella H, Bonnin P, Simon T, Sage AP and Guerin C. B (2013)lymphocytes trigger monocyte mobilization and impair the heartfunction after acute myocardial infarction. Nat Med 19:1273–80.

BhatiaV, Parida AK, Pandey AK and Kaul U (2012). 12 lead ECG in thedetection of left main coronary artery occlusion during acutecoronary syndromes.&nbspIntJ Cardiol116:e83–4.