Acute Coronary Syndromes

Acute coronary syndromes (ACS) refers to a spectrum of acute clinical manifestations of coronary artery disease. The hallmark of ACS is the presence of myocardial ischaemia caused by an abrupt reduction of coronary blood flow. Myocardial ischemia is the term we use when the heart muscle is starved of essential nutrient and this commonly leads to symptoms of chest pain (called angina).

Coronary Artery Disease (CAD) and its manifestations

CAD is due to a process called coronary atherosclerosis, which is an accumulation of fatty deposits in the coronary artery wall. As coronary atherosclerosis progresses, this leads to gradual narrowing of the coronary arteries that are responsible for supplying nutrient to the muscle of the heart. Although the exact mechanism is unknown, certain risk factors in a person increase the likelihood of atherosclerosis. These include smoking, diabetes mellitus, high blood pressure, high cholesterol and strong family history of premature CAD.

Once the narrowing in the arteries becomes critical, the amount of blood may not be able to meet the demand of the heart muscle. When angina occurs only on exertion, it is due to a stable narrowing (plaque) which only gives rise to symptoms when the demand exceeded what the narrowed artery can supply. This is called stable angina. It is promptly relieved by rest which reduce the demand of the heart muscle or by medications to dilate the narrowed artery, so as to increase the blood supply to the heart muscle.

In contrast, ACS is due to sudden disruption of the lining of the narrowing within the artery wall (called plaque rupture) and subsequent clot (thrombus) formation on the site, leading to sudden complete or near complete blockade of the coronary artery. This can lead to worsening of angina or death of portion of heart muscle (i.e. heart attack/myocardial infarction). Without treatment, a high proportion of patients with ACS may subsequently develop further heart attacks or even death.

In ACS patients, adequate control of risk factors is vital in order to prevent future events and complications.

Cholesterol, blood pressure and sugar levels will be checked while in hospital and appropriate medications initiated when necessary.

The patient’s heart function will also be assessed during coronary angiography or by echocardiography while in the ward before discharged. If there is significant damage to the heart muscle which resulted in impaired heart function, medications like beta-blockers and angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB) will be added in the hospital. If there is no contraindication, as these medications have been proven to prolong life in patients with poor heart function after a heart attack.

In patients with severely damaged heart muscle and who did not improve despite adequate treatment, an automated implantable cardiac defibrillator (AICD) may be required to reduce the risk of sudden cardiac death.

ACS consists of 3 conditions which can cause angina and can be further differentiated based on electrocardiogram (ECG) and blood tests (cardiac markers imply damage of the heart muscle). The clinical presentation and prognosis of ACS depend on the degree of narrowing of the artery caused by the thrombus after the plaque rupture.

1. Unstable angina – worsening of pervious narrowing after plaque rupture but not completely occluded. There is worsening of angina (more frequent angina, angina with lesser exertion, angina at rest or recent onset angina). As there is no heart muscle damage resulting in cell death, cardiac markers would not be elevated.
   
   
2. Non-ST elevation myocardial infarction (NSTEMI or partial heart attack) – partial or transient complete occlusion of the artery after plaque rupture. There is evidence of muscle damage on blood tests resulting in elevation of cardiac markers but there is no characteristic ST segment elevation on ECG.
   
   
3. ST elevation myocardial infarction (STEMI or full heart attack) – Complete and persistent occlusion of artery after plaque rupture. There is evidence of muscle damage with elevation of cardiac markers in blood test with characteristic ST segment elevation on ECG.
   
   

The goal of treatment for patients with ACS is to reduce or prevent further thrombus formation at the site of plaque rupture and relief of ischaemia by reducing the demand of heart muscle or increase the blood supply by unblocking the artery blockage.

1. Unstable angina and NSTEMI
   The presentation and prognosis of unstable angina and NSTEMI are similar and therefore the treatment for both is the same. The only difference is that in NSTEMI, there is damage of a portion of heart muscle with abnormal increased levels of cardiac markers detected in the blood.
   
   Reducing and preventing formation of thrombus
   
   After the plaque ruptured in the artery, platelet plays a vital role in initiating the clot. If there is no contraindication, you will be given 2 types of antiplatelet agents to prevent further platelet deposition at the ruptured plaque. These 2 agents are also required when there is intention to perform coronary stenting (see below). Anti-coagulation (heparins) will also be given to dissolve the clot that has formed on the ruptured plaque. This is usually given as injection under the skin (subcutaneously) or occasionally as an infusion into a vein (intravenously). Please see Table 1 for various combinations of antiplatelet agents and anti-coagulation. Both antiplatelet and anticoagulation agents have been proven to reduce heart attack and death in patients with ACS.
   
   Reducing demand and improving supply
   
   At the beginning of your admission, you may be required to continuously rest in bed to reduce the demand of your heart until your condition become more stable. Oxygen will be given to improve oxygenation of the blood, thus increasing the oxygen supply to the heart. Medications like beta-blockers will be prescribed to slow down the heart rate, which reduces the demand of the heart muscle, while nitrates (IV or oral) dilate the artery to improve the blood supply to the heart muscle.
   
   The most effective method to improve blood supply, however, is to unblock the artery, which can be done by either coronary angioplasty (inserting stents via the wrist or groin) or CABG, especially in  patients with extensive or high risk blockages. (Figure 4 – TIMI risk score) In high risk patients, a coronary angiography is suggested to be performed within 24 hours to check the number and severity of the blocked coronary artery. Your doctor who performs the coronary angiography will advise you what the best treatment option is. In general, coronary stenting can be performed safely in patients with 1 or 2 blocked arteries but in patients with all 3 blocked arteries (especially patients with diabetes mellitus) CABG may be a better option.
   
   
2. STEMI

The treatment of STEMI is completely different from unstable angina and NSTEMI, in terms of urgency and treatment options. In STEMI, the artery is completely occluded by thrombus and the heart muscle supplied by that artery will be irreversibly damaged if not opened within 6 to 12 hours. The longer the artery remains occluded the more extensive the damage to the heart muscle and the speed of treatment in STEMI is therefore crucial.

There are 2 treatment options for STEMI – powerful clot buster (thrombolysis) or coronary stenting (primary angioplasty). Although intravenous thrombolysis is easy and fast, the success rate of opening the artery in STEMI is only 50 to 60%. It also carries the inherent risk of bleeding complications, especially intracranial haemorrhage, which is usually fatal. In NHCS, all patients with STEMI are considered for primary angioplasty if there is no contraindicated. The occluded artery is usually opened successfully in 90% of patients by inserting a stent at the site of ruptured plaque. Primary angioplasty in large centers and experienced operators has been shown to improve outcomes compared to intravenous thrombolysis. However, primary angioplasty for patients with STEMI needs to be performed immediately, preferably within 60 to 90 minutes of admission to ED, in order to achieve maximum benefit.

While in ED, patient will be given loading doses of 2 antiplatelet agents. Once the informed consent for primary angioplasty is given, the patient is transferred to cardiac catherisation laboratory where the primary angioplasty team members will immediately perform coronary angiography and stenting if appropriate. Occasionally stenting may not be required or possible and in some cases urgent coronary artery bypass surgery is necessary. 

After the procedure (usually 60 to 90 minutes depending on the complexity of the lesions) the patient will be admitted to coronary care unit (CCU) for monitoring of heart rhythm and blood pressure.  Patients with STEMI may develop life threatening rhythm and complications after heart attack. Early detection and treatment of these complications saves lives.

Similar to unstable angina and NSTEMI, medications to decrease the demand of heart muscle (beta-blocker) and improve blood supply to heart muscle (nitrates) will be given.

Eating Well Guide for Acute Coronary Syndrome (ACS) [Video]