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Coronary Artery Disease (Chronic Stable Angina (Treatment (General…
Coronary Artery Disease
- Also: atherosclerotic heart disease or ischemic heart disease.
- most common cause of cardiovascular morbidity and mortality
- insufficient perfusion of the coronary arteries from an abnormal narrowing of the vessels, leading to insufficient oxygen delivery to the myocardial tissue.
- M:F=2:1
- peak incidence of symptomatic IHD is age 50-60 (men) and 60-70 (women)
Risk Factors and Markers
- Non-Modifiable Risk Factors:
Age (males > 45, females > 55), Male, postmenopausal female, Family history of of pre- mature CAD (males < 55, females < 65)*
- Modifiable Risk Factors:
Hyperlipidemia*, HTN*, DM*, Cigarette smoking*, Psychosocial stress, Obesity, Sedentary lifestyle, Heavy alcohol intake
-* Major risk factor
- hypertension, peripheral arterial disease,
- Markers of Disease:
Elevated lipoprotein(a), Hyperhomocysteinemia,
Elevated high-sensitivity C-reactive protein, Coronary artery calcification, Carotid IMT/plaque, Ankle-brachial index
Chronic Stable Angina
- symptom complex resulting from an imbalance between oxygen supply and demand in the myocardium
-
Signs and Symptoms
- typical:
(1)retrosternal chest pain, radiating to left (±right) shoulder/ arm/ neck/ jaw
(2) precipitated by the “3 Es”: exertion, emotion, eating;
(3) brief duration, lasting <10-15 min and typically relieved by rest and nitrates
- atypical/probable angina (meets 2 of the above); non-cardiac chest pain (meets < 1 of the above)
- Levine’s sign: clutching fist over sternum when describing chest pain
Diagnosis
- history & physical exam
- labs: Hb, fasting glucose, fasting lipid profile
- ECG: ST segment depression, CXR, echo, stress testing
Treatment
General
- lifestyle modification
- risk factor reduction (eg, smoking, cholesterol, hypertension). Hormone replacement therapy is not protective in postmenopausal women.
- treatment of risk factors: statins, antihypertensives
- acute symptoms with ASA, O2, IV nitroglycerin, and IV morphine, and consider IV β-blockers.
- Treat chronic symptoms with nitrates, ASA, and β-blockers; CCBs are second-line agents for symptomatic control only.
- ASA and β-blockers have been shown to have a mortality benefit
- Second-line anti-anginal drugs:
Ivabradine, Nicorandil, Ranolazine
- Invasive:
Percutaneous coronary intervention
Coronary artery bypass grafting
- Antiplatelet Therapy: Aspirin, clopidogrel when ASA contraindicated
- Nitrates: Glyceryl trinitrate
decrease preload (venous dilatation) and afterload (arteriolar dilatation), and increase coronary perfusion
- Beta-blocker: Atenolol, Bisoprolol, Metoprolol
increase coronary perfusion and decrease demand (HR, contractility) and BP
- Calcium channel blockers: Verapamil, Diltiazem, Amlodipine
increase coronary perfusion and decrease demand (HR, contractility) and BP
verapamil/diltiazem with β-blockers may cause symptomatic sinus bradycardia or AV block
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SYNDROME X
- typical symptoms of angina but normal angiogram
- more common in women than in men.
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Acute Coronary Syndromes
- clinical syndromes caused by plaque disruption or vasospasm that leads to acute myocardial ischemia
- includes the spectrum of UA, NSTEMI, and STEMI
STEMI
S&S
- acute-onset substernal chest pain, commonly described as a pressure or tightness that can radiate to the left arm, neck, or jaw.
- diaphoresis, shortness of breath, light- headedness, anxiety, nausea/vomiting, and syncope.
- ST-segment elevations and cardiac enzyme release secondary to prolonged cardiac ischemia and necrosis.
- The best predictor of survival is left ventricular EF.
Diagnosis
- ECG: ST-segment elevations or new LBBB. ST-segment depressions and dominant R waves in leads V1–V2 can also be reciprocal change indicating posterior wall infarct.
- Cardiac enzymes: Troponin I is the most sensitive and specific cardiac enzyme; CK-MB and the CK-MB/total CK ratio (CK index) are also regularly checked. Both troponin I and CK-MB can take up to 6 hours to rise following the onset of chest pain
ST-segment abnormalities
- elevation in leads II, III, and aVF: inferior MI involving the RCA/PDA and LCA
- elevation in leads V1–V4 usually indicates an anterior MI
involving the LAD
- elevation in leads I, aVL, and V5–V6 points to a lateral MI
involving the LCA.
- depression in leads V1–V2 (anterior leads) can be indicative of an acute transmural infarct in the posterior wall. Obtain posterior ECG leads V7–V9 to assess for ST-segment elevations.
trEatmEnt
- ASA, β-blockers, clopidogrel, morphine, nitrates, and O2.
- If the patient is in heart failure or in cardiogenic shock, do not give β-blockers; instead, give ACEIs provided that the patient is not hypotensive
- angiography and PCI should be performed
- If PCI cannot be performed within 90 minutes, there are no contraindications to thrombolysis (eg, a history of hemorrhagic stroke or recent ischemic stroke, severe heart failure, or cardiogenic shock), and the patient presents within 3 hours of chest pain onset, thrombolysis with tPA, re- teplase, or streptokinase should be performed instead of PCI.
- Long-term treatment includes ASA, ACEIs, β-blockers, high-dose statins, and clopidogrel (if PCI was performed). Modify risk factors with dietary changes, exercise, and tobacco cessation.
- Indications for CABG:
unable to perform PCI (diffuse disease)
left main coronary artery disease
triple-vessel disease
Depressed ventricular function
ComPliCations
- Arrhythmia is the most common
- Less common: reinfarction, left ventricular wall rupture, VSD, pericarditis, papillary muscle rupture, left ventricular aneurysm or pseudoaneurysm, and mural thrombi.
- Dressler’s syndrome, an autoimmune process occurring 2–10 weeks post-MI, presents with fever, pericarditis, pleural effusion, leukocytosis, and ↑ ESR
- First day: Heart failure.
- 2–4 days: Arrhythmia, pericarditis.
- 5–10 days: Left ventricular wall rupture, papillary muscle rupture
- Weeks to months: Ventricular aneurysm
Unstable Angina/NSTEMI
- clinically defined by any of the following:
accelerating pattern of pain: increased frequency, increased duration, decreased threshold of exertion, decreased response to treatment
angina at rest, new-onset angina
angina post-MI or post-procedure (e.g. percutaneous coronary intervention [PCI], coronary artery bypass grafting [CABG])
- NSTEMI indicates myocardial necrosis marked by elevations in troponin I and CK-MB without ST-segment elevations seen on ECG.
Diagnosis
- Unstable angina is not associated with elevated cardiac markers, but ST changes may be seen on ECG.
- NSTEMI is diagnosed by serial cardiac enzymes and ECG
Treatment
- acute symptoms with ASA, O2, IV nitroglycerin, and IV morphine, and consider IV β-blockers.
- Patients with chest pain refractory to medical therapy, a TIMI score of ≥ 3, a troponin elevation, or ST changes > 1 mm should be given IV heparin and scheduled for angiography and possible revascularization (percutaneous coronary intervention [PCI] or CABG).
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