Acute coronary syndrome Flashcards
Most common clinical presentation of angina
Chest pain on exertion
Key factors contributing to progression of atheroma
Smoking Hypertension Hyperlipidemia Diabetes Obesity
Associated symptoms with angina
Dyspnea
Nausea
Diaphoresis
Faintness
Atheroma formation
- Damage to the arterial wall produces an inflammatory response and the development of atheromatous plaques.
- Exposure of the arterial endothelium to LDLs, the products of glycosylation associated with diabetes, vasoconstrictor hormones associated with hypertension, pro-inflammatory molecules from smoking, or excess adipose tissue results in the expression of adhesion molecules that allow leukocytes to stick to the arterial wall.
- Upon entry into the artery wall, blood monocytes begin to scavenge lipids and become foam cells.
- Macrophage foam cells release additional cytokines and effector molecules that stimulate smooth muscle cell migration from the arterial intima into the media, as well as smooth muscle cell proliferation.
- Initial fatty deposition of lipoprotein in the arterial intima develops into atherosclerotic plaques.
- Ischaemic symptoms may result from obstruction of blood flow due to atherosclerotic plaques or when a clot or vasospasm is superimposed on less severe plaques
At what occlusion % does angina typically occur
At >70% occlusion or coronary arteries
Precipitants of angina with fixed stenosis
mental and emotional stress, sexual activity, tachycardia from any cause, or the metabolic demands of fever, thyrotoxicosis, and hypoglycaemia
Types of angina
Stable: induced by activity, relieved by rest
Unstable: +frequency or severity, occurs on minimal exertion/at rest. ++Risk of MI
Prinzmetal: coronary artery spasm->at rest, STE that resolves once pain resolves
Risk factors for angina
Strong
advancing age smoking hypertension elevated LDL cholesterol isolated low HDL cholesterol diabetes inactivity obesity family history of premature ischaemic heart disease illicit drug use male sex
Investigations in angina
Resting ECG->normal
Hb
Fasting lipid profile
Fasting blood glucose
Others to consider: TSH->hypo(dyslipid, IHD)/hyper(+work load) HbA1C Stress ECG Angiography Stress echocardiograph
History and examination in angina
Angina pain syndrome description
Risk factors
Examination: associated cardiac, PAD, fundoscopy, bruits
Laboratory testing
Long term Management of stable angina
- Modify risk factors->beta blocker, statin, Anti-PLT, ACE-i
- Lifestyle->smoking cessation, exercise, diet
- Cardiac rehabilitation
- Consideration of revascularisation
- Management of acute symptoms
- Avoid precipitants
Pharmacological regime for angina risk modification
Aspirin 75-150mg OD
Metoprolol 25-100mg BD +/= Nifedipine (used if not controlled with b-blocker/verapamil) + Isosorbide mononitrate
Atorvastatin 80mg
Perindopril
Treatment of episodes of angina
Stop activity as soon as pain felt
Before taking medication lay down’GTN SL every 5 minutes. Max use 3 times
If persists >10minutes despite two doses, take a third and call the ambulance
Follow-up in angina
Assess risk factors, symptoms, complications, promote adherence to lifestyle/pharmacological
See every 4-6 months initially to help encourage smoking, weight, diet, activity
Patients not known to have diabetes mellitus should have a fasting blood glucose measurement every 3 years
Those with established diabetes mellitus should have HbA1c measured at least annually
A lipid profile should be obtained as clinically warranted to ascertain whether the goal of lowering LDL cholesterol by ≥50% is achieved and/or to check for compliance.
What is the single most important change people can make for cardiovascular health
Smoking cessation
Indications for referral in angina
Diagnostic uncertainty New angina of sudden onset Angina not controlled by drugs Refractory angina in those not suitable for CAG Previous CABG Positive stress test
