Warung Bebas

Thursday, 26 July 2012

How to Prevent Coronary Heart Disease

No old motto better than "Prevention is better than cure". This goes for anyone, especially in people who have high risk factors.
Priority of prevention, performed mainly on:
a. Patients with CHD, peripheral arterial disease, and cerebrovascular atherosclerosis.
b. Patients without symptoms but considered high risk because of:

- Many risk factors and the magnitude of the 10-year risk ≥ 5% (or by more than 60 years of age) to have a fatal cardiovascular disease.
- The increase of one component of risk factors: cholesterol ≥ 8 mmol / l (320 mg / dl), low density lipoprotein (LDL) cholesterol ≥ 6 mmol / l (240 mg / dl), BP ≥ 180/110 mmHg.
- Patients with diabetes type 2 and type 1 with microalbuminuria.
c. Close family, with:
- Patients with atherosclerotic cardiovascular disease earlier
- Patients with high risk but without symptoms.
d. People who regularly perform a clinical examination.

1. Guidelines for Primary Prevention of Cardiovascular Disease and Stroke
     It has been a lot of evidence that suggests that CHD can be prevented, and research for this continues. From the results of long-term prospective study, showed that people with low risk factors have a smaller risk for developing CHD and stroke.
    ACC / AHA recommends directions for prevention of cardiovascular disease risk factors determined from the existing
a. Risk factors:
 Search for risk factors -> Destination: adults know the extent and importance of risk factors checked routinely.
Recommendation: Examination of risk factors should begin at the age of 20 years. Family history of CHD should be routinely monitored. Smoking, diet, alcohol, physical activity should be evaluated regularly. Blood pressure, body mass index, waist circumference, should be examined interval of 2 years. Cholesterol checks and blood sugar levels must still be monitored as well.

b. Estimation of risk factors in general -> All adults over the age of 40 should know their risk factors for CHD disease. Objectives: reducing the risk factors as much as possible.
Recommendation: Every 5 years (or more if there are changes in risk factors), particularly those with ≥ 40 years of age or a person with more than 2 risk factors, should be able to identify the risk factors based on a count of 10-year risk factor. Risk factor is smoking seen in blood pressure, cholesterol checks, blood sugar levels, age, gender, and diabetes. Patients with diabetes or a 10-year risk> 20% is considered as CHD patients (CHD risk equivalent).

Intervention efforts by non-pharmacologic and various pharmacologic and clinical trials show a beneficial thing.
a. Smoking:
-> Stop total. Not exposed, the environment smokers.
b. Blood Pressure Control
-> Destinations TD <140/90 mm Hg; <130/80 in renal impairment or heart failure, or <130/80 mm Hg in diabetes.
c. Diet
-> Objective: Eat a healthy diet.
d. Giving Aspirin
-> Objective: Low-dose aspirin in patients with high cardiovascular risk (in particular patients with a 10-year risk of cardiovascular events ≥ 10%).
e. Lipid arrangements in the Body
-> Primary goal: LDL - C <160 mg / dl if ≤ 1 risk factor, LDL-C <130 mg / dl if they have ≥ 2 risk factors and CHD risk 20%, or LDL-C <100 mg / dl if ≥ 2 risk factors and 10% had CHD risk ≥ 20% or if the patient is also affected by diabetes.
-> Secondary Objectives (if LDL-C is a prime target): if triglycerides> 200 mg / dl, and then used non-HDL-C as the second goal; non HDL-C <190 mg / dl to ≤ 1 risk factor; non -HDL-C <160 mg / dl to ≤ 2 risk factors and CHD risk ≤ 10 years at 20%, non-HDL-C <130 mg / dl for diabetes or with ≥ 2 risk factors and risk of CHD 10 years> 20 %.
-> Target else therapy: triglycerides> 150 mg / dl; HDL-C <40mg/dl in men and <50 mg / dl in women.
f. Physical Activity
-> Objective: at least 30 minutes of physical activity or physical activity of moderate intensity every day within 1 week.
g. Weight regulation
-> Objective: Achieve danmempertahankan weight (BMI 18.5 to 24.9 kg/m2). When BMI ≥ 25 kg/m2, waist circumference ≤ 40 inches in men and ≤ 35 inches in women.
h. Management of Diabetes
-> Objective: fasting blood sugar levels (<110 mg / dl) and HbA1c (<7%).
i. Chronic Atrial Fibrillation
-> Objective: Achieving sinus rhythm or chronic atrial fibrillation if it appears, the anticoagulant
with INR 2.0 to 3.0 (target 2.5).

2. Secondary Prevention of Coronary Heart Disease
Secondary prevention in individuals suffering from CHD has been proven, is an attempt to prevent recurrent CHD was no longer
a. Smoke
-> Objective: Stop the total, are not exposed to environmental smoke
b. Blood Pressure Control
-> Objective: BP <140/90 mmHg or <130/80 mmHg in patients with diabetes or chronic kidney disease
c. Lipid Management
-> Goal: LDL-C <100 mg / dl If Triglserid ≥ 200 mg / dl, non-HDL-C should be <130 mg / dl
d. Physical activity
-> Objective: 30 minutes, 7 days a week (at least 5 days per week)
e. Weight regulation
-> Objective: BMI: 18.5 to 24.9 kg/m2. Waist circumference: men <40 inches, women <35 inches.
f. Management of Diabetes
-> Objective: HbA1c <7%
Antiplatelet drug use / Anticoagulants: Aspirin, clopidogrel, warfarin as indicated.
Use of Renin-Angiotensin-Aldosterone System Blockers: replace with ARB if intolerant.
The use of Beta-Blockers: unless there are contraindications.
Influenza vaccination in patients with cardiovascular disorders.

Secondary prevention is very necessary to remember:

- Individuals who have ever been, or has been proven to suffer from coronary heart disease, heart disease tend to have longer, more likely than those who had never hurt the heart.
- The process of atherosclerosis is the underlying CHD, it can affect other organs of blood vessels in the brain that lead to cerebrovascular disease (stroke), the aorta or carotid arteries, peripheral arteries, etc.. Therefore, secondary prevention for CHD may also be the primary prevention of atherosclerotic disease to others.
Secondary prevention has not been fully received attention (underutilized) of medical practitioners, as reported by WHO in 2004, particularly in countries with per capita income, low and medium.

Wednesday, 25 July 2012

Treatments and Theraphy of Coronary Heart Disease

The goal of treatment are:
a. Improve prognosis by preventing myocardial infarction and death. Efforts is how to reduce the occurrence of acute thrombotic and left ventricular dysfunction. This goal can be achieved by lifestyle modification or pharmacologic interventions that will:

(i) subtracting the progressive plaque
(ii) stabilize the plaque, by reducing inflammation and improving endothelial function, and finally
(iii) to prevent thrombosis or endothelial dysfunction in the event of plaque rupture.
Drugs used: antithrombotic drugs: a low-dose aspirin, ADP receptor antagonists (thienopyridin) that clopidogrel and ticlopidine; cholesterol-lowering drugs (statins), ACE-Inhibitors: Beta-blockers: Calcium channel blockers (CCBs).
b. To cope with symptoms and ischemia: the drug used. Nitric working short and long term, beta-blockers, CCBs.

General Procedures
       To patients suffering from CHD and their families, need to be briefed about the course of the disease and the choice of drugs available. Patients should be reassured that most cases of angina can be improved with medication and lifestyle modifications so that the quality of life better. Comorbid disorders such as hypertension, diabetes, dyslipidemia, etc..
CHD treatments, consisting of pharmacological treatment and myocardial revascularization. Keep in mind that none of the above nature cure. In other words it is necessary lifestyle modifications and addressing the causes that disease progression can be slowed.

Pharmacologic treatment
* Low-dose aspirin
From various studies have clearly shown that aspirin is still the main drug for the prevention of thrombosis. Meta-analysis showed that a dose of 75-150 mg equal effectiveness compared with larger doses. Therefore, aspirin is recommended in all patients with CHD were given unless contraindicated encountered. In addition to aspirin is also recommended that given the long-term side effects but it should be noted gastrointestinal irritation and bleeding, and allergies. Cardioaspirin provide a more minimal side effects other than aspirin.
* Inhibits platelet aggregation
Thienopyridine Clopidogrel and ticlopidine are antagonists of ADP and inhibits platelet aggregation. Clopidogrel is more indicated in patients with resistance or intolerance to aspirin.
AHA / ACC guidelines update the 2006 include a combination of aspirin and clopidogrel should be given to patients with PCI with stent implantation, over 1 month for bare metal stent, 3 months for sirolimus eluting stent and 6 months for paclitaxel-eluting stent.
* Cholesterol-lowering drugs
Treatment with statin use to reduce risk in both primary prevention and secondary prevention. Various studies have shown that statins can reduce complications by 39% (Heart Protection Study), Ascott-LLA atorvastatin for primary prevention of CHD in post-hypertension.
Than as a cholesterol-lowering statins, also have other mechanisms (pleiotropic effect) which can act as an anti-inflammatory, anti-thrombotic etc.. Provision of atorvastatin 40 mg one week prior to PCI may reduce myocardial damage due to the action. Target reduction in LDL cholesterol is <100 mg / dl and in high risk patients, DM, CHD patients is recommended lowering LDL cholesterol <70 mg / dl.
* ACE-Inhibitor/ARB
The role of ACE-I as secondary prevention for Cardioprotection in patients with CHD has been demonstrated from various studies, among others., HOPE study, etc. EUROPA study. If intolerance to ACE-I may be replaced by the ARB.
* Nitrate is generally recommended, because nitrate has an effect so venodilator myocardial preload and left ventricular end volume and thus decreases myocardial oxygen consumption also decreases. Nitrates also dilate blood vessels of normal and atherosclerotic experiencing. Raise collateral blood flow, and inhibits platelet aggregation. When an attack of angina does not respond to short-term nitrate, then be wary of myocardial infarction. Drug side effects are headaches, and flushing.
* Beta blockers 
Beta Blockers are also a standard drug. Beta blockers block the effects of catecholamines on the circulation and Beta-1 receptors which can cause a decrease in myocardial oxygen consumption. Beta blockers do with the provision of a target heart rate 50-60 per minute. The most important  contraindication to beta blocker administration is history of bronchial asthma, and acute left ventricular dysfunction.
* Calcium antagonists 
 have the effect of vasodilatation. Calcium antagonists can reduce complaints in patients who had received nitrates or beta blockers; but it is also useful in patients whoose contraindications to the use of Beta blockers. Calcium antagonists is not recommended if there is a decrease in left ventricular function or conduction disturbances atrioventricular. 

Treatment recommendations to improve the prognosis of patients with unstable angina according to the ESC 2006 as follows.:
1. Giving aspirin 75 mg per day in all patients without specific contraindications (ex. active gastric bleeding, aspirin allergy, or a history of aspirin intolerance) (level of evidence A).
2. Statin treatment for all patients with coronary heart disease (evidence level A).
3. The provision of ACE inhibitors in patients with an indication of the provision of ACE inhibitors, such as hypertension, left ventricular dysfunction, history of myocardial infarction with left ventricular dysfunction, or diabetes (level of evidence A).
4. Provision of oral beta-blockers in patients with heart failure or myocardial infarction who had received (evidence level A).

Myocardial revascularization
      There are two ways that have proven good revascularization in stable CHD is caused by atherosclerotic coronary revascularization act of surgery, coronary bypass surgery (coronary artery bypass surgery = CABG) and percutaneous intervention (PCI = percutneous coronary intervention).
Lately, both methods have progressed rapidly in the introduction of action, off pump with minimally invasive surgery and drug eluting stent (DES). Revascularization goal is to improve survival or prevent infarction or for relief of symptoms. Where the action is chosen, depending on the risk and patient complaints.
Indications for Revascularization
In general, patients who have indications for coronary arteriography and actions performed catheterization showed narrowing of the coronary arteries is a potential candidate for myocardial revascularization action. In addition, the act of revascularization performed on the patient, if:
a. Treatment failed to control the patient's complaints.
b. Non-invasive test results indicate a risk of infarction.
c. Found a high risk for the incidence and mortality.
d. Patients prefer the intervention compared with usual treatment and fully understand the risks of the treatment given to them.

Actions CABG Surgery
Surgery is better to do than with medication, in the circumstances:
a. Significant stenosis (≥ 50%) in the left main (LM).
b. Significant stenosis (≥ 70%) in the region proximal to the 3 major coronary arteries.
c. Significant stenosis in two main areas, including coronary artery stenosis is high enough levels in the proximal region of the left anterior descending coronary artery.

PCI acts
        In the first act of percutaneous transluminal angioplasty is only performed on the blood vessels only, now it has grown more rapidly both because of the experience, equipment, especially stents and drug investigations. In patients with stable CHD with appropriate coronary anatomy of the PCI can be performed on one or more blood vessels (multi-vessel) with a good (successful PCI). The risk of death by about 0.3-1% of this action. Action PCI in patients with stable CHD compared with medical drugs, not add to survival and it is different than CABG.

Installation of Elective Stent and Drug-eluting stents (DES)
      Stenting can reduce restenosis and repeat PCI compared with balloon angioplasty actions. Currently available drug-coated stent (drug-eluting stent = DES) as serolimus, paclitaxel, etc.. Compared with bare-metal stents, the use of DES may reduce restenosis. RAVEL study showed restenosis can be reduced to 0%. Direct stenting (stent without balloon pre-dilatation with the first) is a feasible action in patients with coronary artery stenosis without calcification is a specific, single lesion, without angulation or severe turtoasitas. Direct action stenting can reduce the time the action / ischemic time, reduce radiation, the use of contrast, to reduce costs.

Primary Percutaneous Coronary Intervention actions (Primary PCI)
        Stable CHD patients had complications and had a heart attack (ACS), mortality is very high (> 90%). With advances in technology have now been able to do primary percutaneous coronary intervention (primary PCI) is a technique to remove thrombi and dilate the narrowed coronary arteries with balloon catheters and stent insertion is often done. This action can remove the blockage immediately, so that blood flow can be normal again, so the heart muscle damage can be avoided. Primary PCI is the treatment of acute cardiac infarction are best at this, because it can stop the attack of acute cardiac infarction and reduce mortality to below 2%.


Tuesday, 24 July 2012

How to Diagnose Coronary Heart Disease

The first step in the management of Coronary Heart Disease (CHD) is the designation of a definite diagnosis. Correct diagnosis is important, because if a diagnosis of CHD has been made, in which are likely to have the sense that people will be able to experience cardiac infarction or sudden death. Diagnosis is wrong always have bad consequences on quality of life of patients ..

In addition, their opportunities for employment, may be reduced. If this happens to older people, then they probably should have retired too early, to be repeatedly hospitalized to eat excessively or drugs of potential toxins for a long time. On the other hand, fatal consequences can occur when the presence of CHD is unknown or if the presence of other cardiovascular diseases that cause angina pectoris missed and go undetected.

Diagnostic Method
      Here, the most important diagnostic methods of CHD, either currently existing or in the foreseeable future, will potentially have a major role. Physicians should choose whatever checks that need to be made to the patient to achieve the accuracy
maximum diagnostic risks and costs to a minimum. Stages of the evaluation conducted in patients with angina pain:

Diagnostic Steps
1 Anamnesis
2. physical examination
3. laboratory
4. Photos of the chest
5. Non-invasive cardiac examination
- Resting ECG
- Test of physical exercise (treadmill)
- A combination of physical exercise testing imaging:
- Physical exercise testing echocardiography (Stress Eko)
- Physical exercise testing Myocardial Perfusion Scintigraphy
- Physical exercise testing pharmacologic Combination Imaging Technique
- Echocardiography break
- Monitoring ECG ambulatoir
- Non-invasive technique of determining the classification of the coronary and coronary anatomy:
- Computed Tomography
- Magnetic Resonanse arteriography
6. Invasive testing to determine coronary anatomy
- Coronary arteriography
- Intra-vascular ultrasound (IVUS)

        Any patient with chest pain needs to be done a thorough anamnesis, the determination of risk factors, physical examination and ECG. In patients with mild symptoms of angina pectoris, fairly non-invasive examination. When patients with severe complaints and takes action and the possibility of revascularization, the action was an indication of angiography.
        On the dubious circumstances to do the treadmill test. The treadmill test is more sensitive and specific compared with resting ECG and a test of choice for detecting patients with angina pectoris and the possibility of this examination the ingredients are easy and affordable cost. In certain circumstances, it is difficult to interpret the results of the treadmill as in patients with resting ECG abnormalities, among others.: LBBB, repolarization abnormalities, LVH and so on.
          Another alternative tests, which can be done is to echocardiography and non-invasive technique of determining coronary calcification and coronary anatomy, Computed Tomography, Magnetic Resonanse arteriography, the sensitivity and specificity is higher. In addition the test is also suitable for patients who can not do excercise, where the exercise test can be done by using drugs dipyridamole or dobutamine

Evaluate Algorithm of Patient with Angina

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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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