Acute Coronary Syndromes and dyslipidemia

Question 1

ACS intro

Answer 1

Spectrum of clinical syndromes caused by plaque disruption or vasospasm that leads to acute myocardial ischemia

Question 2

Unstable angina/NSTEMI

Answer 2

unstable angina is defined as CP that is new onset, is accelerating (occurs with less exertion, lasts longer, or is less responsive to meds), or occurs at rest. It is distinguished from stable angina by patient history.

It signals presence of impending infarct based on plaque instability.

In contrast, NSTEMI indicates myocardial necrosis marked by elevations of troponin I and CK-MB without ST elevations on ECG

Question 3

Diagnosis of unstable angina/NSTEMI

Answer 3

1) Patients should be risk stratified according to the Thrombolysis in MI study criteria to determine likelihood of adverse cardiac events (TIMI)
2) Unstable angina is not associated with elevated cardiac enzymes, but ST changes may be seen on ECG
3) NSTEMI is diagnosed by serial cardiac enzymes and ECG

Question 4

Treatment of unstable angina/NSTEMI

Answer 4

1) Acute treatment of symptoms is the same as that for stable angina and consists of clopidogrel, unfractionated heparin, or enoxaprin
2) Patients with CP refractory to medical therapy, a TIMI of 3 or higher, a troponin elevation, or ST changes more than 1mm should be given IV heparin and scheduled for angio and possible revascularization (PCI or CABG)

Question 5

TIMI risk score for unstable angina/NSTEMI

Answer 5

score is 0-7. Higher risk is 3 or more. They benefit from enoxaprin (vs unfractionated heparin), gp2b3a inhibitors and early angio

Each is 1 point:

1) 65 yo or more
2) 3 or more cardiac risk factors (premature FHx, DM, smoking, HTN, high cholesterol)
3) Known CAD (stenosis over 50%)
4) ASA use in past 7d
5) Severe angina (2 or more episodes within 24h)
6) ST deviation of 0.5mm or more
7) Positive cardiac marker

Question 6

STEMI

Answer 6

Defined as ST segment elevations and cardiac enzyme release secondary to prolonged cardiac ischemia and necrosis

Question 7

History and physical for STEMI

Answer 7

1) Presents with acute-onset substernal chest pain, commonly described as a pressure or tightness that can radiate to the L arm, neck, or jaw
2) Associated symptoms may include diaphoresis, SOB, lightheadedness, anxiety, n/v, and syncope
3) Physical exam may reveal arrhythmias, hypotension (cardiogenic shock), evidence of new CHF
4) The best predictor of survival is LV EF

Question 8

Diagnosis of STEMI

Answer 8

1) ECG will show ST segment elevations or new LBBB. ST-depressions and dominant R waves in V1-V2 can also be reciprocal change indicating posterior wall infarct
2) Sequence of ECG changes: Peaked T waves then ST elevation then Q waves then T inversion then ST normalization then T wave normalization over several hours to days
3) Cardiac enzymes: Troponin I is the most sensitive and specific. CK-MB and CK-MB/total CK ratio (CK index) are also regularly checked. Both Trop I and CK-MB can take up to 6h to rise following the onset of CP

Question 9

ECG abnormalities in STEMI

Answer 9

1) ST elevation in leads II, III, aVF = inferior MI involving RCA/PDA and LCA. Obtain right sided ECG to look for ST elevations in the RV
2) ST elevation in leads V1-V4 usually indicated anterior wall MI involving LAD and diagonal branches
3) ST elevation in leads I, aVL and V5-V6 points to lateral MI involving LCA
4) ST elevation in leads V1-V2 (anterior leads) can be indicative of acute transmural infarct in the posterior wall. Obtain posterior ECG leads V7-V9 to assess for ST elevations there.

Question 10

Treatment of STEMI

Answer 10

1) 6 key meds should be considered: ASA, B-blockers, Clopidogrel, Morphine, Nitrates, O2
2) If patient is in HF or in cardiogenic shock, do not give B-blockers; instead give ACEIs provided they are not hypotensive
3) Emergent angio and PCI should be performed. If possible, the patient should undergo PCI for the lesion thought to be responsible for the STEMI
4) If PCI cannot be performed within 90 minutes, there are no contraindications to thrombolysis (cardiogenic shock, recent stroke, severe HF) and the patient presents within 3 h of CP onset, thrombolysis with tPA, reteplase or streptokinase should be performed instead of PCI
5) PCI should be attempted immediately for the lesion thought to be responsible for STEMI; the patient is a candidate for CABG afterward
6) Long term treatment includes ASA, ACEIs, B-blockers, high dose statins, and clopidogrel (If PCI was performed). Modify risk factors with diet, exercise, and tobacco cessation

Question 11

Indications for CABG

Answer 11

they are “UnLimiTeD”

Unable to perform PCI (diffuse disease)
L main coronary artery disease
Triple vessel disease
Depressed ventricular function

Question 12

Complications of STEMI

Answer 12

1) Arrhythmia is the most common complication following acute MI; lethal arrhythmia is the most frequent cause of death
2) Less common complications include reinfarction, LV wall rupture, VSD, pericarditis, papillary muscle rupture (with mitral regurgitation), LV aneurysm or pseudoaneurysm, and mural thrombi
3) Dressler’s, an autoimmune process starting 2-10d post-MI, presents with fever, pericarditis, pleural effusion, leukocytosis, and high ESR
4) Timeline. Day 1 is HF. Day 2-4 is arrhythmia and pericarditis. 5-10 days is LV wall rupture (acute pericardial tamponade causing electrical alternans, pulseless electrical activity), papillary muscle rupture (severe MR). Weeks to months later for ventricular aneurysm (CHF, arrhythmia, persistent ST elevation, MR, thrombus formation)

Question 13

Dyslipidemia

Answer 13

Defined as total cholesterol above 200, LDL above 130, triglycerides above 150, and HDL below 40. All of these are risk factors for CAD.

Etiologies include obesity, DM, alcoholism, hypothyroidism, nephrotic syndrome, hepatic disease, Cushing’s syndrome, OCP use, high dose diuretic use, and familial hypercholesterolemia

Question 14

History and Physical for dyslipidemia

Answer 14

Most patients have no specific signs or symtpoms. Patients with extremely high TG or LDL levels may have xanthomas (eruptive nodules in the skin over the tendons), xanthelasmas (yellow fatty deposits in skin around eyes) and lipemia retinalis (creamy appearance of retinal vessels)

Question 15

Diagnosis of dyslipidemia

Answer 15

1) Conduct fasting lipid profile for patients 35 or older or in those 20 or above with CAD risk factors, and repeat every 5 years or sooner if lipid levels are elevated
2) Total serum cholesterol above 200 on 2 dif occasions is diagnostic for hypercholesterolemia
3) LDL above 130 or HDL below 40 is diagnostic of dyslipidemia even if total cholesterol is below 200

Question 16

Tx of dyslipidemia

Answer 16

1) Based on risk stratification
2) The first intervention should be 12w trial of diet and exercise in a patient with no known atherosclerotic vascular disease

Question 17

Risk stratification for dyslipidemia

Answer 17

1) If you have CAD or CAD risk equivalents. LDL should be below 100 or below 70. LDL to start lifestyle mods is 100. LDL to start drugs is 130.
2) 2 or more risk factors. LDL should be below 130. Consider lifestyle changes at 130. Drugs at 160
3) 0-1 risk factors. LDL should be below 160. Start lifestyle mods at 160 and drugs at 190.

Risks: Smoking, HTN, low HDL, FHx of premature CAD, age (men over 45, women over 55). HDL above 60 is a negative risk factor and removes 1 risk factor from total score.

CAD equivalents: symptomatic carotid artery disease, peripheral artery disease, AAA, diabetes

Question 18

HMG Co-A reductase inhibitors

Answer 18

Statins.

1) Mech: Inhibit the rate-limiting step in cholesterol synthesis.
2) Effects: Lower LDL. Lower TGs.
3) Side effects: Increased LFTs, myositis, warfarin potentiation

Question 19

Lipoprotein lipase stimulators

Answer 19

Fibrates like Gemfibrozil.

1) Mech: Increase lipoprotein lipase leading to increased VLDL and TG catabolism
2) Effects: Lower TGs, raise HDL
3) Side effects: GI upset, cholelithiasis, myositis, increased LFTs

Question 20

Cholesterol absorption inhibitors

Answer 20

Ezetimibe (Zetia)

1) Mech: Lower absorption of cholesterol at the small intestine brush border
2) Effects: Lowers LDL
3) Side effects: Diarrhea, abdominal pain. Can cause angioedema.

Question 21

Niacin

Answer 21

“Niaspan”

1) Mech: reduced fatty acid release from adipose tissue. Reduced hepatic synthesis of LDL.
2) Effects: Increased HDL. Lower LDL
3) Side effects: Skin flushing (can be prevented with ASA), parasthesias, pruritus, GI upset, increased LFTs

Question 22

Bile acid resins

Answer 22

Cholestyramine, colestipol, colesevelam

1) Mech: Bind intestinal bile acids, leading to reduced bile acid stores and increased catabolism of LDL from plasma
2) Effects: lowers LDL
3) Side effects: Constipation, GI upset, LFT abnormalities, myalgias. Can lower absorption of other drugs from the small intestine