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Acute Coronary Syndromes

Acute coronary syndromes have been a major hemodynamic insult to a person's homeostat balance in the normal physiological systems. The main pathophysiologic rational is impaired blood supply to the heart in relation to increased oxygen demand, through vasospasm of coronary vessels or thrombosis in any coronary arteries. It is unquestionably established that atherosclerosis is the leading etiology behind coronary syndromes. Acute coronary syndromes include:

1. Acute myocardial infarction

2. Non-Q wave myocardial infarction

3. Acute exacerbation of angina pectoris

4. Unstable angina pectoris

5. Sudden cardiac death

Acute coronary syndromes, are a group of complex coronary artery disease resulting from accumulation of various high risk factors. It is a process of summation of diverse epidemiological risk factors, pathological risk factors and biochemical risk factors. 

Epidemiological Risk Factors

1. Cigarette smoking

2. Hypertension

3. Hyperlipidemia

4. Coronary prone personality

5. Obesity

6. Diabetes Mellitus 

Pathological Risk Factors

1. Atherosclerosis

2. Platelet Activation

3. Endothelial Dysfunction 

Biochemical Risk Factors

1. Total cholesterol >240 mg/dL

2. HDL <35 mg/dL

3. Hyperhomocystinemia

4. Hemochromatosis

Vascular endothelial has a very important and regulating role in normal biological rhythm of the vessel. It has a central regulatory role in maintaining biological functions of the cardiovascular system. Acute coronary syndromes may also be a result of chronic inflammatory reaction of the vascular endothelium. Vascular dysfunction is the term which includes deviation.

Endothelial dysfunction affects the cardiovascular system in following manner

1. Decreases vasodilator function through oxygen derived free radicals which degrade vasomotor functions through EDRF (Endothelial Derived Relaxing Factor which works through cGMP activation)

2. Releases growth factors and promotes proliferation of vascular smooth muscle cells

3. Releases inflammatory cytokinins like tumor necrosis factor, interleukins, gamma interferons.

4. Increases chemotactic effects of macrophages

5. Activation of platelets

6. Development of LDL oxidation with the help of oxygen derived free radicals

7. Promotion of vascular cell adhesion molecule-l(VCAM-1)

8. Promotes neovascularization 

Pathogenesis of Coronary Syndromes

Higher risk factors responsible for acute coronary syndromes

Oxidative stress & Release of oxidative free radicals

Activation of platelets

Atherosclerotic plaque rupture

Blockage of blood vessels with thrombosis

Impaired blood supply in the coronary artery

Acute Coronary syndromes 

Thrombogenic Risk Factors

Local factors

Type of plaque disruption (erosed, ulcerated)

Severity of stenosis

Accompanied structure

Nature of the wall of residual thrombosis


Systemic Factors

Infections (C pneumoniae, CMV, H. Pyroli)


Fibrinogen and coagulation factors and contents

Cholesterol lipoprotein (a)

With the inflammation of the endothelium, there is release of thromboxane, prostaglandin and

their metabolites in response to ADP induced platelet aggregation, which favors atherosclerotic plaque. This atherosclerotic plaque may have EKG and clinical manifestations of ischemia. Thromboxane A2, stimulates phospholipase C through platelet proteins Gq-a and GB-7, they in turn alters physiological balances by elevating intracellular Ca+2 and further facilitation the actions of Protein Kinase C and Thromboxane A2. All these events enhances activation of fibrogen receptors (GP lib-Ilia), fibrogen binding and platelet aggregation.

Clinical Features

Almost more than half of the patients usually have prior history of major strenuous physical activities, sudden outburst of emotional stress or medical or surgical illness. The usual time of presentation is early in the morning (When higher sympathetic activities present, which may favor thrombosis). The chest pain is of very severe, deep visceral in character (worst pain which has been ever felt). It can be a heavy feeling, squeezing, crushing or pressing in nature. Pain is usually limited to central chest and/or near the epigastrium with radiation to the arms. rarely, it may radiate to the abdomen, back or jaw. There may be certain associations of nausea, vomiting or anxiety or in unusual circumstances of sudden loss of consciousness, acute confusional state or a sensation of profound heaviness. Physical examination related to increased sympathetic activity, signs of ventricular dysfunctions, decreases intensity of heart sounds, gallop rhythm are also present.

Laboratory Examination

In the ER, complete blood counts, chemistry, EKG and chest X-ray should be taken. In acute MI less than 4 to 8 hours of presentation, serum cardiac markers (CK-MBs, Cardiac specific troponin T, Cardiac specific troponin I) are very important. However, they are nonspecific.

Cardiac Imaging: In clinical practice, two dimensional echocardiography is the most commonly performed investigation for the acute coronary syndromes. Abnormalities of the valve movement is very common feature in echocardiography. Echocardiography is very useful investigation to distinguish previous right ventricular infarction, ventricular aneurysm, pericardial effusion and ventricular thrombosis. Myocardial imaging study with thallium 201 or tech 99m sestamibi have pivotal roles to differentiate old infarction.

EKG Stress Testing: EKG Stress testing is very useful when properly ordered. In acute severe myocardial infarction, stress test is never indicated. It may be planned after stabilization. Definite indications of EKG stress testing include:

AMI with atypical presentations in men or postmenopausal women

Assessment with previous history of CHD

Evaluation of exercise induced cardiac arrhythmia



Large MI within 3 days

Catastrophic emergencies like aortic dissection/rupture

Severe aortic stenosis

Severe uncontrolled hypertension

Uncompensated heart failure

Unstable arrhythmia

Severe left ventricular outflow obstruction

Recent or active cerebral ischemia

Radionuclide stress testing has been evaluated in specific circumstances. Although, it is not indicated in AMI. In presence of contraindications, stress testing increases mortality several times.



It has been proved that effective prehospital emergency care and initial evaluation in ER is very crucial in the management of acute coronary syndromes. Thrombolysis is the treatment of choice in acute myocardial infarction. The following guidelines for the thrombolytic or non-thrombolytic management strategy, should be followed.

ST elevation of >0.1 mV in at least 2 leads


Left Bundle Branch Block

Ischemic chest pain syndrome of >20 minutes duration


Present:  Thrombolytic therapy        Absent: Non thrombolytic therapy


There are different types of treatment approaches offered. Thrombolysis is the preferred strategy. Interventional thrombolysis is also indicated in selected highly beneficial patients. However, controversies exist for the preference of treatment modality. It is accepted that treatment choice should be made according to the circumstances, and facilities available.

The first use of thrombolytic therapy was reported by Flether and his colleagues in 1958. One major drawback of early clinical trials was questionable efficacy of the treatment. In 1969, Chazov administered intracoronary streptokinase in Soviet Union, and now it is since last two decades, reperfusion is the major and important part of management strategy for Acute Myocardial Infarction.


The proportion of patients presenting with AMI are eligible for thrombolytic therapy has varied in reports because of eligibility criteria. Eligibility is based on the admission ECG and time

window criteria or on the discharge diagnosis of myocardial infarction Patients with ineligibility for thrombolysis be considered for PTCA

Criteria for Initiating Thrombolysis

Chest pain consistent with angina

ECG Changes: (1) ST >1 mm, 2 contiguous limb leads (2) ST 2mm, 2 contiguous precordial leads

New left bundle branch block

Absence of contraindications