ABFM Board Review, questions and
answers graded A+
Acute Coronary Syndrome (ACS) - Acute coronary syndrome Unstable angina (UA) Non-ST-elevation
myocardial infarction (NSTEMI) ST-elevation myocardial infarction (STEMI) Etiology: reduced
myocardial perfusion Reduced O2 supply (more common) Increased O2 demand
Acute Coronary Syndrome Other - Spasm at site of atherosclerotic plaque Normal coronary arteries
with spasm Prinzmetal's angina; transient ST elevation associated Arterial inflammation Kawasaki
disease Cocaine-induced Treat with NTG and CCB; avoid β-blocker
Acute Coronary Syndrome NSTEMI and UA - Both can cause ST-segment depression or prominent T-
wave inversion
2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary
Syndromes-Ischemia-guided strategy - Ischemia-guided strategy (lower risk patients, preference for
low intervention) 1. Aspirin (non-enteric coated, chewable) 2. P2Y12 inhibitor (clopidogrel,
ticagrelor) 3. Anticoagulation (heparin)
2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary
Syndromes-Early invasive strategy - Early invasive strategy (higher risk patients) 1. Aspirin (non-
enteric coated, chewable) 2. P2Y12 inhibitor (clopidogrel, ticagrelor) 3. Anticoagulation (heparin) 4.
Consider glycoprotein IIb/IIIa receptor blockers [Tirofiban (Aggrastat), Eptifibatide (Integrilin),
Abciximab (ReoPro)] before invasive treatment
2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary
Syndromes-Invasive - Recommends initial invasive strategy in patients with the following
characteristics: • Recurrent symptoms or ischemia despite adequate medical therapy • Previous PCI
or CABG, unless prior coronary angiography data indicate that no further revascularization is feasible
• High risk as categorized by clinical findings: • Heart failure • Serious ventricular arrhythmias
2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary
Syndromes-Invasive - Recommends initial invasive strategy in patients with the following
characteristics: Noninvasive test findings: Significant LV dysfunction with EF <0.40 Large anterior or
multiple perfusion defects or wall motion abnormalities on echocardiography High-risk Duke
treadmill score < -11 High-risk TIMI or GRACE scores Markedly elevated troponin levels
,Management of STEMI - Reperfusion as quickly as possible, ideally within 12 hours, assuming no
contraindications. Percutaneous coronary intervention (PCI) is preferred. Fibrinolytic therapy is
indicated: if onset of symptoms plus time to transport to a PCI-capable hospital is more than 12
hours if time from first medical contact at the non-PCI capable hospital to device time at PCI-capable
hospital is more than 2 hours
Dual antiplatelet therapy (DAPT)and Stent. BMS and DES-How long ACS, How long stable CAD - In
patients with ACS treated with BMS or DES implantation, DAPT should be given for at least 12
months. After one year, may stop P2Y12 inhibitor but continue aspirin indefinitely. If stents placed
for stable coronary artery disease (scheduled catheterization rather than ACS) • After BMS
implantation, DAPT for at least 1 month• After DES implantation, DAPT for at least 6 months
Coronary artery bypass graft (CABG)-when - Improved survival for: Left main coronary artery stenosis
3-vessel disease with abnormal left ventricular function (LVEF <50%) 2- or 3-vessel disease with
>75% stenosis of the proximal left anterior descending artery (LAD) Patients with diabetes have
better 8-year survival with CABG than with PTCA After CABG, DAPT for >1 year to reduce risk of graft
occlusionAcutely: If coronary anatomy is not suitable for PCI
2013 ACC/AHA Cholesterol Treatment Guidelines-4 groups - 1. Individuals with clinical ASCVD
2. With primary elevations of LDL-C > 190 mg/dL
3. 40-75 yrs with diabetes and LDL-C 70-189
4. Without clinical ASCVD or diabetes, age 40-75, LDL-C 70-189, and estimated 10-year ASCVD risk
>7.5%[Note: USPSTF uses threshold of 10% 10-year risk
Statin Intensity vs. Statin Benefit Group - 1. Individuals with clinical ASCVD
Age < 75: High-intensity
Age > 75: Moderate-intensity
2. With primary elevations of LDL-C > 190 mg/dL
High-intensity
3. 40-75 yrs with diabetes and LDL-C 70-189
Estimated 10-y ASCVD risk > 7.5%: High-intensity
Estimated 10-y ASCVD risk < 7.5%: Moderate-intensity
4. Without clinical ASCVD or diabetes, age 40-75, LDL-C 70-189 and estimated 10-year ASCVD risk of
7.5% or higher
Moderate-to-high intensity
,Statin Intensity -
HFrEF: Physiologic basis of treatment - Low cardiac output triggers neurohormonal activation, which
ultimately results in premature apoptosis of cardiac myocytes
1. Preload reduction Diuretics, nitrates
2. Afterload reduction ACEI, ARB, hydralazine, nitrates
3. Sympathetic blockade ß-blockers
4. Aldosterone-antagonist therapy Spironolactone, eplerenone
HFrEF mortality reduction - ACEI/ARB,Beta Blocker, Spironolactone, hydralazine,ARNI
Aldosterone antagonists in heart failure - Reduce mortality and improve ejection fraction
Appropriate if GFR >30mL/min and K+ < 4.5 mEq/dL Avoid concomitant NSAIDs and COX-2 inhibitors
Spironolactone (but not eplerenone) can cause breast tenderness and gynecomastia
SGLT2 inhibitors for heart failure - Both empagliflozin and dapagliflozin decrease all-cause mortality,
CV death, and HF hospitalization in patients with HFrEF, regardless of presence or absence of type 2
diabetes. SGLT2 inhibitors trigger osmotic diuresis and natriuresis, decrease arterial pressure and
stiffness, may reduce preload Indications: HFrEF with or without diabetes NYHA class II-IV HF
Administered in conjunction with background of GDMT for HF Caution if eGFR <30 mL/min
(dapagliflozin) or <20 mL/min (empagliflozin)
Good and bad drugs for HF - Digoxin and furosemide improve symptoms and reduce hospitalizations
in systolic HF. Furosemide may decrease mortality. Digoxin does not decrease mortality. Verapamil
and diltiazem, due to their negative inotropic effect, are associated with worsening heart failure and
an increased risk of adverse cardiovascular events.
β-blockers in heart failure - Metoprolol succinate 12.5 - 25 mg daily 200 mg daily Carvedilol 3.125 mg
twice daily 50 mg twice daily Bisoprolol 1.25 mg daily 10 mg daily Use with caution or not at all:
Hemodynamic instability Heart block or bradycardia Severe asthma or COPD - 2nd generation β-
blockers are cardioselective (β1 ); selectivity diminishes at higher doses
HFpEF treatment - Careful decrease in heart rate, using ß-blocker (or nondihydropyridine CCB) is
appropriate. If rapid atrial fibrillation/flutter is present, digoxin is indicated for rate control. Larger
doses of ß-blocker or non-dihydropyridine CCB may have excessive negative inotropic effect. Limited
data to support use of aldosterone antagonists in HFpEF.
, Mobitz Type I Second Degree AV Block (Wenckebach) - The PR interval progressively lengthens until
a P wave fails to conduct and a beat is "dropped." • Almost always represents disease of the AV
node. May be seen in athletically fit individuals, especially during sleep.• In the acute setting, inferior
wall ischemia is likely. Inferior wall is supplied by RCA, which also supplies the AV node. Anterior wall
is supplied by the left coronary artery, which supplies the His-Purkinje system. • Treatment: the
rhythm itself generally does not require treatment; the underlying cause may
Mobitz type II second degree block - • Intermittently non-conducted P waves not preceded by PR
prolongation and not followed by PR shortening • Usually disease of the distal conduction system,
below the AV node (His-Purkinje system) • May progress to third degree AV block • Treatment:
permanent pacemaker
One way to think about AV blocks - Lump together: 1 st degree AV block Mobitz type I second-
degree AV block These are less significant
Mobitz type II second-degree AV block Third degree AV block These are (much) more significant and
typically require intervention, such as a pacemaker
Narrow Complex Tachycardia Treatment - Options to quickly slow AV conduction include: Vagal
maneuvers: Valsalva, unilateral carotid massage IV adenosine: 6 mg bolus; follow with 12 mg if
ineffective IV ß-blocker: metoprolol 5 mg IV diltiazem: 15-30 mg bolus • Ventricular response in sinus
tachycardia and atrial flutter gradually slows; ventricular response in AVNRT abruptly converts to
sinus rhythm. • Digoxin also slows AV conduction, but because it requires loading over hours, it is
not quickly effective.
SVT: Long-term therapy - "Pill in the pocket" for prn use Diltiazem 120 mg or propranolol 80 mg or
flecainide 3 mg per kg Typically use the medication that converted the rhythm Diltiazem 240-360 mg
daily Verapamil 240-480 mg daily Metoprolol 25-200 mg daily Flecainide 50-300 mg daily Catheter
ablation (radiofrequency or cryoablation) 95% effective, expensive Inadvertent heart block risk < 5%
Multifocal Atrial Tachycardia - Irregular narrow-complex rhythm with three or more P waves of
variable morphology. • Differences from wandering atrial pacemaker: significantly increased rate
and almost invariably associated with severe pulmonary disease. • Treatment: verapamil, diltiazem,
metoprolol.
Atrial fibrillation: rate control - Outcomes equivalent to rhythm control - AFFIRM study (2002) • Non-
dihydropyridine CCBs, particularly diltiazem, do not affect the β2 receptors in the lung so can be
used in COPD. • β-blockers provide the most effective control of heart rate in AF, both at rest and
during exercise so generally are tried first. 2nd generation β-blockers (metoprolol, carvedilol,
bisoprolol) are β1 -selective so can be considered in patient with COPD, though the selectivity is lost
at higher doses. Propranolol is a nonselective β-blocker. • Digoxin is no longer recommended for
monotherapy but can be added to βblocker or CCB.
