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Sunday, 22 July 2012

Pathogenetic of Acute Coronary Syndrome

Acute Coronary Syndrome (ACS) is one of the clinical manifestations of Coronary Heart Disease (CHD) main result of the atherothrombotic process, in addition to ischemic stroke and peripheral arterial disease (PAD). Atherothrombotic is a chronic disease in a highly complex and multifactorial and interrelated.

Atherothrombotic consist of atherosclerosis and thrombosis. Atherosclerosis is the process of formation of plaques (atherosclerotic plaques) result from the accumulation of several materials such as lipid-filled macrophages (foam cells), massive extracellular lipid and fibrous plaque containing smooth muscle cells and collagen.
      Recent developments, describes the process of atherosclerosis is an inflammation / infection, which was initially characterized by the presence of early abnormalities in the endothelial layer, the formation of foam cells and fatty streaks, the formation of fibrous lesions cups and more, and the rupture of unstable atherosclerotic plaque.
    Many studies have shown that inflammation plays an important role in the process of atherosclerosis. On coronary heart disease, inflammation starting from the initial formation of plaque to plaque instability that ultimately results in plaque rupture and thrombosis in ACS.
       The atherosclerotic process (initiation, progression and complication in atherosclerotic plaques), gradually goes from a young age, is also said to be even since the age of the children had formed a line patches of fat (fatty streaks) in the surface layer of blood vessels, and slow-gradually in older age can develop into patches of sclerosis (plaques or crust on the blood vessels) so that the constriction and / or blockage of blood vessels. If the plaque was ruptured, torn or bleeding subendotel, start the process trombogenik, part or all of which clog the coronary arteries. At this moment appeared a variety of clinical presentations such as angina or myocardial infarction. The atherosclerotic process can be stable, but can also not stable or progressive. Consequences that can cause death is the process of atherosclerosis that is not stable / progressive who is also known as ACS  (pic 2)

Picture 2
        While thrombosis is the formation of blood clots found in the blood vessel or heart cavity. There are two types of thrombosis, ie arterial thrombosis (white thrombus) that is found in arteries, where the thrombus was found more platelets, and venous thrombosis (red thrombus) that is found in veins and contains more red blood cells and less platelets . Components that play a role in the process of thrombosis is a blood vessel wall, blood flow and blood of its own that includes platelets, coagulation system, fibrinolytic system, and the natural anticoagulant.
       Recent explain the pathogenesis of ACS is caused by obstruction and thrombotic occlusion of coronary arteries, which is caused by a vulnerable atherosclerotic plaque erosion, fissure, or rupture. The main cause of ACS is triggered by erosion, fissure, or rupture of atherosclerotic plaques is due to the presence of the condition of unstable atherosclerotic plaques (vulnerable atherosclerotic plaques) with the characteristic; large lipid core, thin fibrous cups, and plaque shoulder (shoulder region of the plague) is full with the activity of inflammatory cells such as T lymphocytes and other (pic3). 
Picture 3
       Thick plaque that can be seen by the percentage of narrowing of the coronary vessels in coronary angiography examination does not mean anything as long as the plaque is in stable condition. In other words, the risk of rupture of the atherosclerotic plaque is not determined by the amount of plaque (the degree of narrowing) but by susceptibility (vulnerability) plaques. Erosion, fissure, or rupture of atherosclerotic plaque (which already exist in the coronary artery wall) released vasoactive substances (collagen, lipid core, macrophages and tissue factor) into the bloodstream, stimulating aggregation and adhesion of platelets and fibrin formation, the process of forming a thrombus or thrombosis . Formed thrombus can lead to total or subtotal coronary occlusion. Severe coronary occlusion caused by erosion or rupture in a relatively small atherosclerotic plaque will lead to unstable angina pectoris and does not lead to tissue death. Thrombus usually transient / unstable and cause temporary occlusion that lasts between 10-20 minutes   
      When the occlusion causing tissue death but can be overcome by collateral or a rapid lysis of thrombus (spontaneous or by the action of thrombolysis) will arise NSTEMI (no damage, all myocardial layers). Thrombus that occurred more persistent and lasts up to more than 1 hour. When the occlusion is not settled and the overall  compensated  by collateral having a layer of myocardial necrosis (Q-wave infarction), or also known as STEMI. Formed thrombus is fixed and persistent causes myocardial perfusion stopped suddenly which lasted more than 1 hour and cause transmural myocardial necrosis. Now more and more clearly believed that thrombosis is a fundamental mechanism of the ACS, thrombosis of coronary arteries is mainly caused by the rupture of vulnerable atherosclerotic plaques due to fibrous protective cups that had a thin, cracked and broken. Fibrous layer of the cups are not static, but they are always remodeling due to metabolic activities, endothelial dysfunction, the role of inflammatory cells, extracellular matrix interference or extra-cellular matrix (ECM) due to the activity of matrix  metalloproteinase-s (MMPs), which inhibits the formation of collagen and activity of inflammatory cytokines.
         Recent developments, explain and specify that the inflammatory process plays an important role is crucial in poto-biological process of ACS, in which plaque vulnerability is largely determined by the inflammatory process. Inflammation can be local (on the plaque itself) and can be systemic. Inflammation can also disrupt the homeostatic balance. In the state of inflammation are elevated concentrations of fibrinogen and plasminogen activator inhibitor in the circulation. Inflammation can also cause blood vessels due to vasospasm in hampered blood flow.
    Vasoconstriction of the coronary arteries also had a role in the pathogenesis of ACS. Vasoconstriction occurs in response to mild endothelial dysfunction near the lesion or in response to the disruption of the plaque from the lesion itself. Endothelial function regulate vascular tone by releasing relaxing factors are nitric oxide (NO) is known as the endothelium Derived Relaxing Factor (EDRF), prostacyclin, and contraction factors such as endothelin-1, thromboxane A2, prostaglandin H2. On endothelial dysfunction, the contraction factor is more dominant than the relaxation factor. On the plaque disruption that had occurred vasocontriction dependent platelet mediated by serotonin and thromboxane A2, and thrombin-dependent vasoconstriction presumably due to direct interaction between these substances in vascular smooth muscle cells.
       Association of Specialists in Cardiovascular Indonesia Governance Guidelines on Acute Coronary Syndrome Without ST-elevation (2004) does so on the pathogenesis of ACS, there are roughly five causes are not mutually exclusive. In other words, the causes are not mutually exclusive, some patients had more than two causes.
1. Occlusive thrombus on a plaque that is not already there
2. Dynamic obstruction (coronary spasm or vasoconstriction)
3. Progressive mechanical obstruction
4. Inflammation and or infection
5. Factors or circumstances trigger

In the first four causes, the imbalance of oxygen occurs primarily due to a myocardial oxygen supply is reduced, while the fifth is the cause of the imbalance is mainly due to increased myocardial oxygen demand, usually accompanied by a state of persistent lack of oxygen supply.

A. Thrombus is not occlusive, to the existing plaque
The most common cause of ACS is a decrease in myocardial perfusion due to coronary artery narrowing as a result of the existing thrombus in the atherosclerotic plaque is torn / broken and usually not until the clog. Myicroemboli (small emboli) of platelet aggregation and components of plaque rupture, which resulted in the distal small infarcts, the cause of the release of markers of myocardial damage in many patients.

B. Dynamic obstruction
A rather rare cause of obstruction is dynamic, which may be caused by continuous focal spasm in a coronary artery segment epicardium (Prinzmetal angina). Hypercontractility spasm is caused by vascular smooth muscle and / or due to endothelial dysfunction. Dynamic coronary obstruction can also be caused by abnormal constriction of the blood vessels smaller.

C. Progressive mechanical obstruction
The third cause of ACS is a narrowing of the great but not because of spasm or thrombus. This occurs in some patients with progressive atherosclerosis or with re-stenosis after percutaneous coronary intervention (PCI).
D. Inflammation and / or infection
The fourth is the cause of inflammation, caused by / associated with the infection, which may cause narrowing of the arteries, plaque destabilization, rupture and thrombogenesys. Macrophages and T lymphocytes on a wall plaque increase the expression of enzymes such as metalloproteinase, which can lead to thinning and plaque rupture, so the next can result in ACS.
E. Factors or circumstances trigger
The fifth is the cause of ACS is a secondary result of conditions beyond the originator of the coronary arteries. In these patients there is cause a narrowing of the coronary arteries resulting in myocardial perfusion limited, and they typically suffer from chronic stable angina. ACS of this type because of:
• Increased myocardial oxygen demand, such as fever, tachycardia, and thyrotoxicosys
• Reduction in coronary blood flow
• Reduction in myocardial oxygen supply, such as anemia and hypoxemia.
The fifth cause of ACS in the above are not fully stand alone and a lot of overlap. In other words, each person has more than one cause and interrelated.

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