ACS - Unstable Angina Flashcards
What is UA?
MI at rest/minimal exertion in the absence of acute cardiomyocyte necrosis
Risk factors for UA
- diabetes mellitus
- hyperlipidaemia
- hypertension
- metabolic syndrome
- renal impairment
- peripheral arterial disease
- Hx of IHD
- obesity
- age
- smoking
- cocaine use
- physical inactivity
- Fx
Aetiology of UA
- CAD
- MOST COMMON= coronary artery narrowing caused by a thrombus that develops on a disrupted atherosclerotic plaque and is usually non-occlusive
-OR, intense vasospasm of coronary artery (variant or Prinzmetal’s angina) due to vascular smooth muscle or endothelial dysfunction
Pathophysiology of UA
- the initiating lesion in CAD is a fissure in the vessel endothelial lining over an underlying cholesterol plaque, which results ina loss in the integrity of the plaque cap.
- thin fibrous cap, high lipid content, few smooth muscle cells, high proportion of macrophages and monocytes
- fissure/plaque rupture leads to exposure of subendothelial matrix elements (collagen), stimulating platelet activation and thrombus formation
- tissue factor release activates the coagulation cascade- fibrin formation
- if occlusive thrombus = STEMI unless area is richly collateralised
- not occlusive thrombus = UA or NSTEMI
- arterial inflammation, related to infection, may cause plaque destabilisation, rupture and ACS
- activated macrophages and T-cells at the plauqe increase enzyme expression (metalloproteinase) = thinnning and disruption of the plaque = ACS
- myocardial supply and demand mismatch may cause ichaemia without significant CAD:
- increased myocardial oxygen requirements such as fever/tachycardia/thyrotoxicosis
- reduced coronary blood flow- hypotension
- reduced myocardial oxygen delivery- anaemia or hypoxaemia
Case Histories of UA
1) A 65-year-old man, who smokes and has a history of hypertension and peripheral vascular disease, now presents with increasing frequency and severity of chest discomfort over the past week. He reports that he previously had chest pain after walking 100 metres, but now is unable to walk more than 50 metres without developing symptoms. The pain radiates from his chest to the left side of the neck and is only eased after increasing periods of rest.
2) A 45-year-old woman with type 1 diabetes (diagnosed when she was a teenager) presents to the accident and emergency department with abdominal pain, nausea, and shortness of breath that woke her up from sleep.
Other presentations:
Unstable angina may present without chest pain or with atypical or non-specific symptoms, especially in younger and older populations; female patients; or in the presence of diabetes, dementia, and renal failure, epigastric pain, syncope. Atypical symptoms include dyspnoea, indigestion, dizziness, syncope (usually related to severe pain), sweating, and weakness.
Diagnosis of UA
- resting 12 lead ECG within 10 mins of first medical contact
- order high sensitivity troponin (within 60 mins)- 0/1 hour algorithm, chest x-ray, FBC (thrombocytopenia), U&E, creatinine- egfr, LFTs, blood glucose, CRP (rule out other causes- pneumonia)
- CKD may increase troponin
- A diagnosis should be made by cardiologist
- symptoms suggestive of MI
- no ST-elevation, maybe ST-depression, transient ST-segment elevation, or T-wave inversion
- no troponin elevation
- signs of left ventricular failure
- aortic dissection (radial-radial delay)
-diagnosis confirmed by further imaging- invasive coronary angiography (if -Tn, function stress testing, coronary CTA
ECG- v7-v9 may detect left circumflex artery occlusion (on back)
- medication that may affect treatment of UA:
- anticoagulants
- antiplatelet drugs
- recent use of phosphodiesterase inhibitors (sildenafil, vardenafil, tadalafil).
- known hypersensitivity to aspirin
-antiplatelet and anticoagulant therapy
Investigations list for UA
- ECG
- hs-cTn
- chest x-ray
- FBC
- U & E , creatinine
- LFTs
- blood glucose
- CRP
Consider:
- echocardiogram (assess left ventricular systolic function)
- invasive coronary angiography
- functional stress testing
- coronary CT angiography
Other differentials for UA
- stable angina (pain only on exertion/stress, not worsening over time)
- prinzmetal (variant or vasospastic) angina
- NSTEMI
- STEMI
- congestive heart failure
- chest wall pain
- pericarditis
- myocarditis
- aortic dissection (tearing chest pain, unequal pulses)
- pulmonary embolism
- pleuritis
- pneumothorax
- perforated abdominal viscus
Management of UA
- single loading dose of aspirin ASAP (HAS-BLED score- assess risk of bleeding)
- glyceryl trinitrate- pain relief
- morphine
- anti-emetic - ondansetron, metoclopramide, cyclizine
-GRACE score for ACS prognosis
- dual antiplatelet therapy with aspirin
- P2Y12 inhibitor- prasugrel, ticagrelor, clopidogrel
Consider:
- anticoagulation
- fondaparinux, heparin
- invasive - coronary angiography, revascularisation
- FST, imaging
- manage hyperglycaemia
Post-stabilisation
- anti-anginal medication- bisoprolol, carvedilol, verapamil
- glyceryl trinitrate
- continue dial antiplatelet therapy- aspirin and prasugrel/ticagrelor/clopidogrel
Consider:
- ACE inhibitor or angiotensin-II receptor antagonist- enalapril, ramipril, lisinopril, valsartan, iosartan, candesartan
- statin - atorvastatin, rosuvastatin
- aldosterone antagonist- eplerenone, spironolactone
-CDV risks modification
Complications of UA
- bleeding
- thrombocytopenia- heparin induced, glycoprotein IIb/a induced,
- congestive heart failure
- ventricular arrhythmias-