Angina - Coronary Artery Disease:

Patients usually present with symptoms that may suggest underlying coronary artery disease. Chest pain reflecting such a cause is referred to as “angina”. It is usually a tight sensation, exertion related, often localised to the centre of chest, but can radiate as a band like sensation across the chest. Frequently it can spread or radiate to the throat or down one or more arms.

The process by which angina occurs relates to insufficient blood flow reaching a section of heart muscle. This pathological process is referred to as “myocardial ischaemia”. For most patients this is due to a progressive narrowing within an artery that restricts blood flow. Under resting circumstances there is usually enough blood flow.  But when the demands of the heart are increased, usually with exertion or heightened emotion, the normal increase in blood supply cannot match the increased demand.

Narrowing of coronary vessels usually occur as a result from progressive damage to the inner lining of the artery (called the intima). Risk factors (see later) are all culprits in damaging the intima and result in abnormal proliferation of smooth muscle cells within the wall. Initially this growth is outside the vessel, but eventually the increased bulk tends to grow into the vessel itself, restricting flow. Effective risk factor treatment over a period of time can fortunately reverse this process. In a significant minority of patients without known risk factors, coronary artery disease can still develop. Certain groups are at greater risk of developing coronary disease. This especially applies to the Asian population, where the risk of coronary disease is 4x higher, and can present in younger patients.

Age is an important concern, as the diagnosis of disease is often dismissed in younger patients, despite classical symptoms. Also, in younger adults, angina can occur despite the absence of coronary narrowings. Occasionally, a layer of heart muscle can loop over a coronary artery, causing compression and resulting in angina. This is called a muscle bridge and is generally not a severe condition but can cause debilitating symptoms.

Less commonly, young patients can experience angina despite having normal or near normal coronary arteries due to anomalous coronary arteries. In this case, the origins of the left or right coronary arteries come from the opposite side of the aorta, and cross in front of the heart to supply the heart muscle. This results in the coronary artery being compressed, causing symptoms. The significance of any anomalous connection or muscle bridging can be determined by a functional myocardial ischaemic test (such as a stress echocardiogram or myocardial perfusion scan). Usually, such cases are managed with medication.

Investigation of cardiac sounding chest pain is described under the “Cardiac Investigations”. Essentially tests would be either a functional test (such as an exercise test, or nuclear scan, or stress echocardiogram), or by direct assessment of the coronary arteries (with coronary CT angiography or cardiac catheterization). Exercise testing is frequently performed as it is the least invasive test. Selection of the most appropriate test may depend on the description of symptoms and the patient’s mobility.

Unstable Angina:
What separates stable angina, from unstable angina or a heart attack (myocardial infarction) is if the bulky narrowing (called a plaque) ruptures. This is a serious condition and requires urgent hospitalization. Factors that may cause this include weakening of the wall of the plaque. If this occurs then the blood coagulation system is activated using the clotting system and platelets. This will further narrow the vessel as clot builds up. In unstable angina, the vessel does not entirely block off, but restricts blood flow so much that even under resting conditions, angina and ischaemia can occur. If enough blood supply exists, no permanent heart muscle damage may occur. Unstable angina can be characterised by symptoms that are: new in onset (never occurred previously), or increasing in frequency or duration, or occurring at rest.

Treatment should be prompt to stabilize the plaque. This includes medication to thin the blood with aspirin and clopidogrel (to counteract the platelets), low molecular heparin (to counteract the clotting system) and beta-blockers to reduce the hearts work. In the majority of patients an invasive strategy would subsequently be adopted to visualize the coronary arteries (cardiac catheterization) and potentially unblock them with a stent or balloon angioplasty. Full risk factor modification usually with cholesterol reduction is necessary.

Non ST segment Myocardial Infarction (NSTEMI):
This is a condition a little like the process of unstable angina mentioned earlier, except that the heart muscle blood supply was impaired long enough to have damaged a small amount of heart muscle; akin to a partial heart attack. Although technically it is a type of heart attack, it is more of a warning of future heart muscle damage. The diagnosis is clinical, usually with a typical story of chest pain. The ECG is often abnormal, but without the classical changes seen in a proper myocardial infarction (hence the term: “non ST segment”). Evidence of heart muscle damage is evidenced by measuring chemicals called “troponins” that are released into the blood stream from damaged heart muscle cells. In some ways, it should be regarded as a “partial heart attack” or a “threatened heart attack”.

The diagnosis of this is important as the treatment strategy usually involves urgent coronary angiography. This is because a significant proportion of patients will progress to a full blown myocardial infarction subsequently (within 6 weeks). If angiography reveals significant coronary narrowing, then intervention usually with balloon angioplasty and stenting is customary.

Myocardial Infarction:
In this case the plaque has ruptured and clot has formed, but the vessel has become occluded. As there is no blood supply to affected muscle, then permanent damage “infarction” may occur if not treated. Very urgent hospitalization is necessary to unblock the vessel to prevent or minimize the damage. Depending on the hospital facilities either a “clot busting” drug (so called thrombolysis) is given to dissolve the clot, or emergency angioplasty with a stent can be inserted. The latter is referred to as primary angioplasty, where the vessel is reopened by inflating a balloon over the clot area and expanding a premounted coil (stent – see later) to open the vessel.

Following acute intervention, the mainstay of management includes aggressive risk factor modification (usually lifelong with statins), aspirin (lifelong) and clopidogrel (the latter for at least one year).

Patients often complain about the vast number of medications that are prescribed after an attack. For the most part these drugs are not designed to improve symptoms, but more to protect the heart against future damage. It can be regarded almost as an “insurance policy” to prevent future events. In addition to aspirin and clopidogrel, these drugs include beta blockers and ACE inhibitors.

Close attention is also made to determine a patient’s prognosis after an event to identify patients at high risk of complications. This usually includes an echocardiogram and an exercise test.

Complications following myocardial infarction include electrical disturbances with malignant rhythm disturbances. These can be treated with drugs, but sometimes necessitate a defibrillator (see ICD under “Arrhythmia”). Occasionally very slow rhythms can supervene that may necessitate a temporary or even a permanent pacemaker.

After discharge patients are encouraged to return back to normal activity. Patients should not drive a car for 6 weeks. In addition all hospitals offer a cardiac rehabilitation programme too. This involves a series of talks, advice and an exercise programme. If patients participate actively in this programme, it confers additional cardiac protection (as powerful as some of the medication).