Angina Pectoris and Unstable Angina

Angina pectoris is a complex of symptoms seen in coronary heart disease that results from the mismatch between myocardial oxygen supply and demand. It can be further classified into

• Classic angina
• Angina equivalent
• Variant angina
• Unstable angina

Generally it is characterized by paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort (variously described as constricting, squeezing, choking, or knifelike) caused by transient (15 seconds to 15 minutes) myocardial ischemia that falls short of inducing the cellular necrosis that defines infarction¹

  Both genetic and environmental risk factors play a role in the development of coronary artery disease and therefore angina. The identification of these factors is vital as intervention can lead to disease prevention or to modification of the course of the disease. Important risk factors are tabled below^4,5,6 

 The most common cause of stable angina pectoris is stenosis by an atherosclerotic plaque of the proximal segments of the left anterior descending, right or circumflex coronary arteries.²

The macroscopic plaque/occlusion renders the heart vulnerable to further ischemia whenever there is increased demand from events such as physical activity, emotional excitement, or any other cause of increased cardiac workload. Typical angina pectoris is usually relieved by rest or nitroglycerine, a strong vasodilator. Although the coronary arteries are usually maximally dilated by intrinsic regulatory influences, nitroglycerine also decreases cardiac work by dilating the peripheral vasculature. In particular instances, local vasospasm may contribute to the imbalance between supply and demand.^{2, 3}

 Coronary artery stenosis and thrombosis, the causes of angina and myocardial infarction are mostly caused by atherosclerosis. The plaques are composed of free lipid within the intima associated with smooth muscle cell and macrophage proliferation, fibrosis and hyperplasia of the overlying endothelium. the blood flow and/or contraction of the arterial wall results in shearing forces that cause fissures or rupture of the atherosclerotic plaque resulting in exposure of  thrombogenic material within the plaque and the formation of platelet thrombi. These may form emboli which move into the distant coronary arteries and cause thrombotic occlusion or they may resolve.

Despite re-endothelialisation, lesions may progress and stenose the arteries or artery. These events result in the clinical picture or spectrum that may begin as stable angina but move on to become chronic, unstable or in the setting of myonecrosis, frank myocardial infarction. This progression is seen in over 10-15% of untreated cases of stable angina.^1,2,3

Angina spontaneously remits in 1/3 of patients. It is associated with a mortality rate of up to 4% per year depending on the number of vessels affected. Unstable angina has a higher mortality of 15% within one year if untreated.

Typical angina is an exercise related, pressing precordial chest pain radiating to the jaw and left arm that is alleviated by nitrates. it is often worse when exercising in cold air. Sometimes it is experienced as breathlessness (transient left ventricular dysfunction) rather than pain. It may come on when lying down at night (decubitus angina caused by increased venous return in incipient heat failure) or at rest(fixed artheromatous disease or coronary artery spasm).^1,2

In engaging the patient with suspected angina pectoris a detailed and accurate clinical history is of paramount importance. Physical examination may show evidence of coronary artery disease, this may include an evaluation of  blood pressure, evidence of abnormal lipid metabolism such as tendon xanthomas or xanthelesma, fundoscopic changes reflecting long-standing hypertension or diabetes mellitus, or evidence of peripheral vascular disease such as abnormal pulses.. Aortic stenosis commonly seen in angina should be excluded and the presence of a new mitral regurgitation murmur during chest pain may signal extensive ischemia. Generally however the clinical picture over and beyond that described in the clinical history section above is usually unremarkable⁷.

The focus of general and specific investigations in this early setting is aimed at evaluating risk factors and exploring their modifiability.

• ECG
  • The ECG is often unremarkable but it may show evidence of ischemia or prior myocardial infarction.
  • Furthermore the ECG may be rendered unreliable by the presence of Bundle branch block, Wolff-Parkinson-White syndrome or intraventricular conduction delay
• Exercise stress testing

• Total cholesterol: Frequently elevated
• HDL cholesterol: Frequently reduced
• LDL cholesterol: Frequently elevated
• CRP: Elevation between 3-10 may indicate increased risk for CAD^{7,8, 9}.

Radioisotope imaging-this can increase the specificity of stress testing by evaluating myocardial function and flow. It can be used in conjunction with treadmill or pharmacologic stress testing¹⁰.

• Stress echocardiography-this two dimensional echocardiography is an alternative to radioisotope scanning in detection of myocardial insufficiency⁷.
• Cardiac imaging via CT or MRI-both seem to confer high sensitivity and are under evaluation⁷
• Coronary angiography and revascularization(in intervention section)- A catheter is passed into the coronary arteries themselves via the femoral (thigh) artery and the aorta. Contrast is then injected into the arteries and an xray taken. Exact areas of narrowing (due to plaques) can then be identified. The main use of angiography is in assessing patients who are being considered for revascularization procedures. Angioplasty can be performed at the same time by the placement of stents (metallic tubes which hold the narrowed area open) ^{11, 12}.

General Treatment: this involves addressing the risk factors and counselling the patient to: cease cigarette smoking; lose excess weight; achieve good diabetes control.

Medical Treatment: includes preventative therapy, symptomatic therapy, and interventions.

Preventative therapy:

• Aspirin: reduces the risk of adverse events (myocardial infarction) by reducing the coagulability of the blood.
• Statins (eg. simvastatin): these drugs decrease the amount of cholesterol in the blood and increase the percentage of good fats (HDL- high density lipoproteins).

Symptomatic Relief:

• Vasodilators (Nitrates, Beta Blockers and Calcium channel blockers) all help to prevent attacks of angina. The nitrates ( eg. GTN-glyceryl trinitrate) are particularly effective at relieving the pain of an attack.
• Heparin - in the case of unstable angina: use either in intravenous form or as low molecular weight heparin (subcutaneous).
• Analgesia: In the case of unstable angina morphine and metoclopramide may be given.
• Newer drugs such as the Potassium channel agonist Nicorandel and the Nitric Oxide modulator Perhexiline are being used in cases of angina which are not sufficiently controlled with more traditional regimes.
• The use of Spinal Cord Stimulation is currently being investigated for treatment of chest pain in patients with Angina.

Interventions:

• Coronary angioplasty: Percutaneous transluminal coronary angioplasty (PTCA) is a technique whereby a catheter is introduced into the coronary arteries by way of the femoral artery. When an area of stenosis (narrowing) is detected on angiography, it can then be stretched open by the introduction of a "balloon" which is inflated by the cardiologist. Once this has been achieved, a decision on whether to place a stent is made. A stent is a metallic mesh tube which then holds the stretched portion of the artery open, preventing re-stenosis. In general, patients with single discrete stenoses are good candidates for PTCA. In stable angina which is well controlled by medication, angioplasty may confer better symptomatic control but is of uncertain prognostic benefit.
• Revascularization should be considered in patients who have limiting angina despite medications or high-risk features on clinical history, stress testing, or catheterization. Patients who have multivessel CAD, proximal left anterior descending or left main CAD, reduced LV function, or a large ischemic burden as found by stress testing should be referred for revascularization. Five-year rates of MI and death are similar between PCI and CABG ^7,11, although CABG generally yields more complete revascularization and more complete resolution of symptoms. Recent data favor CABG in high-risk patients who have reduced ejection fraction and diabetes^7,12. The choice of drug-eluting stents over bare metal stents is associated with lower rates of restenosis, reduced angina, and fewer repeat revascularizations ^7,13,14 .

Coronary Artery Bypass Grafting (CABG): This is a surgical procedure where a donor blood vessel from another site in the body is used to bypass area of stenosis. CABG confers significant symptomatic and prognostic benefits in patients with severe triple vessel disease (areas of stenosis in all three coronary arteries). Wherever possible the LIMA (left internal mammary artery) is used to supply blood to the coronary circulation downstream from the stenosis. Grafts using the saphenous vein (from the leg) are still frequently used. Newer minimally invasive techniques using laparoscopic (keyhole) technology are currently being developed.

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