Article IX - Unstable Angina – How to Stabilize it?

“Is it a heart attack?” a newly admitted forty years old banker asked me and I replied in negative. His tenses face mellowed down and started wearing a smile. “Then it must be an episode of angina!” he concluded. My shaking head in negative perplexed the patient. “This is a stage in between the two, it is neither stable angina nor is it a heart attack but some thing between the two,” I explained. When angina becomes more frequent and brought on by milder exertion or starts occurring at rest without any exertion, it is called unstable angina. This disease forms the main bulk of admissions to a cardiology unit and coronary care unit. Unstable angina has to be taken very seriously as an episode of unstable angina may lead to heart attack or death. Inspite of aggressive medical therapy 30 days rate of death and myocardial infarction approximates 9.1 percent. This has resulted in employing several therapeutic agents and strategies in the treatment of unstable angina. We now understand that the heterogeneity in presentation and clinical course followed by unstable angina is due to heterogeneity in causation.

“What causes unstable angina?” he asked. Last decade witnessed strides of advances in our understanding of the causation of unstable angina. “Unstable angina develops due to rupture and fissuring of the blockage called plaque which leads to activation and aggregation of blood particles called platelets producing a clot and blocking the vessel hence reducing blood supply to heart muscle,” I updated his knowledge. A blockage/plaque is composed of a core made of lipid and has a fibrous cap. If the core is hard the chances of rupture are slim, on the other hand if its soft it can fissure and expose the inside sticky material. When lipid core increases beyond 40%, the plaque becomes soft and liable to fissure and rupture. The cap made of fibrous tissues may be thin or thick. This cap covering the plaque may rupture at shoulders more easily. Plaque cap usually gives way at lateral margins where it is attached to more normal intima. Blood enters the plaque and clot is formed due to thrombogeneity of exposed subendothelial tissue. The thrombus can extend into the lumen of coronary artery and propagate distally.

“How does a stable blockage become unstable?” asked Hameed. The factors that may come into play before a plaque/blockage ruptures are like increase in blood pressure, heart rate, and blood viscocity. External factors that exert mechanized stress on the plaque and lead to eventual rupture includes increased vasomotor tone, and disruption of nutrient vessels.

“What are the new advances in treatment?” he changed the topic from causes to treatment. “Well, the culprit is blockage in the vessel and the ideal treatment would be to restore blood supply by opening the vessel,” I replied and quickly added, “but opening of blockage may not be always possible, practical or feasible.” In the last two decades unstable angina was treated conservatively as wait and watch policy. Recently angioplasty has been advocated in patients with unstable angina resistant to conservative therapy or in preference to medical treatment. It is an effective revascularization procedure but is associated with a higher risk of complications including heart attack, emergency surgery, repeat angioplasty and in-hospital death, when performed in patients with unstable angina as compared to those with stable angina. Coronary angioplasty is an option to consider in the management of patients with unstable angina when the coronary anatomy is suitable, preferably as a semielective procedure after initial pharmacologic stabilization or more urgently in patients who have refractory symptoms of unstable angina.

Despite the fact that the world has advanced so much, not all acute coronary care units have enough facilities for complex intervention, so majority of patients with unstable angina are treated conservatively. The data supports the current policy of initially treating, the patient with unstable angina at the closes medical facility, rather than sending them to medical centers with advanced facilities. Patient with on going ischemia or hemodynamic instability can be transferred from noninvasive facility to invasive facility for specialized treatment.

Furthermore, angioplasty or surgical revascularization procedures are expertise dependent and are not available round the clock. Supporters of invasive approach argue that early angiography has several benefits like early identification of blockages which need urgent bypass surgery e.g left main coronary artery disease. It offers early identification of normal coronary arteries, hence excluding coronary disease so preventing risk of prolonged antiplatelet or antithrombin therapy. It has the potential cost saving effect in terms of decreased hospital stay.

One study suggested a long term benefit by reducing death and heart attack in invasive group, but the intervention in this group was either selective or was performed a few days to weeks later, allowing the patients to be stabilised. However other studies have failed to show any benefit in patients treated invasively as opposed to those treated conser-vatively in terms of death and heart attack.

“What if a patient does not want to have angiography, cannot afford angiography or a hospital does not have facilities for the procedure?” he was determined to learn every thing about unstable angina. Addition of aspirin, clopidogrel and intravenous Heparin to conventional angina treatment has improved clinical outcome. Newer strategies have been developed to improve the unstable angina treatment. Platelet function can be inhibited by various drugs to variable degree for variable duration. SAccordingly various drugs are used for multiple purposes in different clinical situations. Newer agents, by blocking IIb IIIa receptors are more effective as they block the common pathway receptor and lead to complete inhibition of platelet aggregation. Theraphy in the form of heparin plus oral aspirin is the current mode of treatment for patients hospitalized with unstable Angina.

Low molecular weight Heparin are prepared from fractionation of standard Heparin – several preparations of Low molecular weight Heparin exist e.g. Nadroparin, Deltaparin, Panaparin, Enoxaprin etc. A number of studies have documented that Low molecular weight Heparin adds a significant clinical benefit to that of aspirin in the treatment of acute unstable angina. However, it is not clear whether Low molecular weight Heparin offer better outcome. Many studies have concluded that Low Molecular Weight Heparin have a definite role in the management of unstable angina.

Unstable angina is a medical emergency. It needs prompt and accurate diagnosis and institution of treatment. Coronary angioplasty should be offered to patients with continued chest pain, haemodynamic instability, worsening of ECG or resistance to treatment. All patients should be treated with antianginal drugs plus heparin and antiplatelets agents.

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Ref: Heal Thy Heart written by Prof: Dr. Muhammad Hafizullah