Acute Coronary Syndrome

Introduction and Facts

Acute Coronary Syndrome (ACS) is a major cardiovascular problem because it causes high hospitalization rates and high mortality rates. Much progress has been made through research and therefore management guidelines are needed to summarize existing research.

Pathophysiology

Most ACS is an acute manifestation of a torn or ruptured coronary atheromatous plaque. This is related to changes in plaque composition and thinning of the fibrous cap that covers the plaque. This event will be followed by the process of platelet aggregation and activation of the coagulation pathway. A thrombus rich in platelets (white thrombus) is formed. This thrombus will block the coronary arteries, either totally or partially; or become microemboli that occlude more distal coronary vessels. In addition, there is the release of vasoactive substances that cause vasoconstriction, which exacerbates coronary blood flow disorders. Reduced coronary blood flow causes myocardial ischemia. The oxygen supply is stopped for approximately 20 minutes causing the myocardium to undergo necrosis (myocardial infarction).

Myocardial infarction is not always caused by complete occlusion of a coronary artery. Subtotal obstruction accompanied by dynamic vasoconstriction can cause ischemia and necrosis of heart muscle tissue (myocardial). The consequences of ischemia, in addition to necrosis, are impaired myocardial contractility due to hibernating and stunning processes (after ischemia is gone), dysrhythmias and ventricular remodeling (changes in ventricular shape, size and function). Some ACS patients do not experience plaque tearing as described above. They have ACS due to dynamic obstruction due to local spasm of the epicardial coronary arteries (Prinzmetal's angina). Coronary artery narrowing, without spasm or thrombus, may result from plaque progression or restenosis after Percutaneous Coronary Intervention (IKP). Several extrinsic factors, such as fever, anemia, thyrotoxicosis, hypotension, tachycardia, can trigger ACS in patients who already have atherosclerotic plaques.

Clinical Symptoms and Complications

Patients with myocardial ischemia may complain of typical chest pain (typical angina) or atypical (equivalent angina).

The typical complaint of angina is a feeling of pressure/heaviness in the retrosternal area, radiating to the left arm, neck, jaw, interscapular area, shoulder, or epigastrium. These complaints can last intermittent / several minutes or persistent (> 20 minutes). Complaints of typical angina are often accompanied by accompanying complaints such as diaphoresis, nausea/vomiting, abdominal pain, shortness of breath, and syncope.

Common presentations of atypical angina include pain in the area where typical angina propagates, a sense of indigestion, unexplained shortness of breath, or sudden unexplained weakness. This atypical complaint is more common in young patients (25-40 years) or the elderly (>75 years), women, people with diabetes, chronic kidney failure, or dementia.

The diagnosis of ACS becomes stronger if the complaint is found in patients with the following characteristics:

1. Men

2. Known to have non-coronary atherosclerotic disease (peripheral / carotid artery disease)

3. Known to have CHD on the basis of having experienced a myocardial infarction, coronary bypass surgery, or IKP

4. Having risk factors: age, hypertension, smoking, dyslipidemia, diabetes mellitus, family history of early CHD, classified as high risk, moderate risk, low risk according to the NCEP (National Cholesterol Education Program)

Diagnosis

By integrating the information obtained from the history, physical examination, electrocardiogram, cardiac marker tests, and chest radiographs, the initial diagnosis of patients with chest pain complaints can be grouped as follows: non-cardiac, Stable Angina, Possible ACS, and Definitive ACS

Physical examination. Physical examination is performed to identify the precipitating factors of ischemia, complications of ischemia, comorbidities and to rule out differential diagnosis. Acute mitral valve regurgitation, triple heart sound (S3), soft wet rhonchi and hypotension should always be examined to identify ischemic complications. The presence of signs of acute mitral valve regurgitation, hypotension, diaphoresis, fine wet crackles or pulmonary edema raises the suspicion of ACS.

Electrocardiogram examination. All patients with chest pain or other complaints suggestive of ischemia should undergo a 12-lead ECG as soon as possible on arrival in the emergency room. In addition, leads V3R and V4R, and V7-V9 should be recorded in all patients with ECG changes suggestive of inferior wall ischemia. Meanwhile, leads V7-V9 should also be recorded in all angina patients who have a nondiagnostic baseline ECG. Wherever possible, the ECG recording is made within 10 minutes of the patient's arrival in the emergency room. The ECG should be repeated every time the angina recurs.

Check heart markers. Creatinine kinase-MB (CK-MB) or troponin I/T is a marker of cardiac myocyte necrosis and is a marker for the diagnosis of myocardial infarction. Troponin I/T as a marker of cardiac necrosis has a higher sensitivity and specificity than CK-MB. An increase in cardiac markers only indicates the presence of myocyte necrosis, but cannot be used to determine the cause of the myocyte necrosis (coronary/noncoronary causes). Troponin I/T can also be increased due to noncoronary cardiac abnormalities such as tachyarrhythmias, cardiac trauma, heart failure, left ventricular hypertrophy, myocarditis/pericarditis.

Laboratory examination. Laboratory data, in addition to cardiac markers, that must be collected in the emergency room are routine blood tests, current blood sugar, electrolyte status, blood coagulation, kidney function tests, and lipid panels. Laboratory tests should not delay ACS therapy.

Chest X-ray examination. Given that the patient is not allowed to leave the emergency room for examination purposes, a chest radiograph should be performed in the emergency room using a portable device. The purpose of the examination is to make a differential diagnosis, identify complications and comorbidities.

Based on the history, physical examination, electrocardiogram (ECG) examination, and examination of cardiac markers, Acute Coronary Syndrome is divided into:

1. ST segment elevation myocardial infarction (STEMI: ST segment elevation myocardial infarction)

2. Myocardial infarction with non ST segment elevation (NSTEMI: non ST segment elevation myocardial infarction)

3. Unstable angina pectoris (STEAM: unstable angina pectoris)

Management and Care

The treatment for acute coronary syndrome (ACS) includes several strategies, which are based on the severity and type of ACS (e.g., ST-elevation myocardial infarction [STEMI] or non-ST-elevation myocardial infarction [NSTEMI]).

• Oxygen Therapy: Recommended for patients with hypoxemia (oxygen saturation <90%). Routine oxygen therapy is not recommended for those with normal oxygen levels .
• Nitrates: Sublingual nitrates may be administered to relieve ischemic chest pain. However, they should be used with caution, especially in patients with hypotension or recent use of phosphodiesterase inhibitors .
• Pain Relief: Intravenous opioids like morphine are used to relieve severe chest pain, though they may slow the absorption of oral medications .
• Beta-Blockers: Intravenous beta-blockers, such as metoprolol, are recommended for patients undergoing primary percutaneous coronary intervention (PCI) if there are no signs of acute heart failure and systolic blood pressure is above 120 mmHg .
• Antithrombotic Therapy:
• Antiplatelet Therapy: Aspirin is started with a loading dose, followed by a maintenance dose. P2Y12 inhibitors such as clopidogrel, prasugrel, or ticagrelor are recommended, particularly for patients undergoing PCI .
• Anticoagulation: Unfractionated heparin (UFH), enoxaparin, or fondaparinux may be used for anticoagulation in the acute phase of ACS .
• Reperfusion Therapy (PCI or Fibrinolysis): Primary PCI is the preferred reperfusion strategy for STEMI patients, provided it can be performed within 120 minutes of diagnosis. If not feasible, fibrinolysis is recommended .
• Fibrinolytic Therapy: Fibrinolysis should be initiated in STEMI patients who cannot undergo PCI within the recommended time window. Agents like tenecteplase or alteplase are used .

Reference:

1. Perhimpunan Dokter Spesialis Kardiovaskuler Indonesia. Pedoman tatalaksana sindrom koroner akut. [Internet]. [Cited 27/8/2021]. Available from: https://inaheart.org/wp-content/uploads/2021/07/Pedoman_tatalaksana_Sindrom_Koroner_Akut_2015.pdf
2. European Society of Cardiology (ESC). 2023 ESC Guidelines for the management of acute coronary syndromes. European Heart Journal. 2023;00:1-107. DOI: https://doi.org/10.1093/eurheartj/ehad191