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A 64-year-old man is evaluated in the office 7 days after discharge from the hospital for non–ST- elevation myocardial infarction. He was treated with percutaneous coronary intervention using a radial artery approach. Right femoral artery access was initially attempted, but the catheter guidewire could not be passed. During the procedure, an abdominal aortogram was obtained (shown). He has not had any symptoms of claudication. Medical history is significant for hyperlipidemia. He is a current smoker with a 40-pack-year history. Medications are low-dose aspirin, ticagrelor, metoprolol, and atorvastatin.

On physical examination, vital signs are stable. The right femoral pulse is faint, and a bruit is heard over the right femoral artery. No foot or toe ulceration is noted.
A. Cilostazol
B. Cardiac rehabilitation
C. Endovascular iliac stenting
D. Vorapaxar
Treat asymptomatic lower extremity peripheral artery disease.
In this patient with asymptomatic peripheral artery disease (PAD) and acute coronary syndrome treated with percutaneous coronary intervention, the most appropriate next step in management is cardiac rehabilitation. Cardiac rehabilitation is indicated in all patients after hospitalization for acute coronary syndrome and percutaneous coronary intervention. In some patients, exercise can provoke symptoms of intermittent claudication; however, the presence of PAD is not a contraindication to cardiac rehabilitation.
Cilostazol, a phosphodiesterase inhibitor with antiplatelet and vasodilatory properties, is not indicated in patients without claudication, such as this one. There is no evidence that cilostazol prevents progression of disease or improves outcomes in asymptomatic patients with PAD.
This patient's iliac artery stenosis could be treated safely and effectively with an endovascular approach; however, endovascular treatment of PAD is not recommended in asymptomatic patients. There is no empiric evidence that endovascular intervention prevents disease progression to intermittent claudication or critical limb ischemia.
Vorapaxar inhibits thrombin-induced and thrombin receptor agonist peptide–induced platelet aggregation. Vorapaxar reversibly inhibits protease-activated receptor-1, although its long half-life makes it effectively irreversible. It does not appear to affect coagulation parameters, nor does it inhibit platelet aggregation due to adenosine diphosphate, collagen, or thromboxane mimetic activities.
Vorapaxar has been shown to reduce hospitalizations for acute limb ischemia in patients with symptomatic PAD, an effect that was mostly driven by patients who experienced lower extremity bypass graft thrombosis. When added to standard antiplatelet therapy, vorapaxar was also associated with a significant increase in major bleeding. In this patient with asymptomatic PAD, the benefits of adding vorapaxar to standard therapy are uncertain.
Asymptomatic lower extremity peripheral artery disease is managed with aggressive risk factor modification; cilostazol and surgical intervention do not affect progression of disease or prevent acute limb ischemia.
Foley TR, Waldo SW, Armstrong EJ. Medical therapy in peripheral artery disease and critical limb ischemia. Curr Treat Options Cardiovasc Med. 2016;18:42. PMID: 27181397 doi:10.1007/s11936-016- 0464-8
Copyright 2018, American College of Physicians.
A 78-year-old woman is evaluated during follow-up of nonischemic heart failure with reduced ejection fraction diagnosed 6 months ago. She has New York Heart Association functional class III symptoms. She is receiving optimal guideline-directed medical therapy consisting of valsartan- sacubitril, carvedilol, spironolactone, and furosemide.
On physical examination, blood pressure is 104/62 mm Hg and pulse rate is 58/min. A grade 2/6 holosystolic murmur is heard at the apex, and a grade 1/6 crescendo-decrescendo systolic murmur is heard at the base. There is no jugular venous distention or peripheral edema.
ECG shows sinus rhythm and left bundle branch block with QRS duration of 155 ms. Echocardiogram shows an ejection fraction of 30%, left ventricular end-systolic dimension of 53 mm, mild to moderate mitral regurgitation, and mild aortic stenosis.
A. Cardiac resynchronization therapy
B. Ivabradine
C. Mitral valve clip placement
D. Transcatheter aortic valve implantation
Treat heart failure with cardiac resynchronization therapy.
Cardiac resynchronization therapy (CRT) (Option A) is the most appropriate treatment. This patient with heart failure with reduced ejection fraction is on optimal guideline-directed medical therapy. CRT is indicated in patients with a left ventricular ejection fraction (LVEF) of 35% or less, New York Heart Association (NYHA) functional class II to IV symptoms despite guideline-directed medical therapy, sinus rhythm, and left bundle branch block with a QRS complex of 150 ms or longer (class 1 recommendation). In such patients, CRT is associated with improved LVEF, reduced symptoms, and improved survival rates. Many patients who meet the indication for CRT also meet indications for implantable cardioverter-defibrillator (ICD) therapy. ICD therapy reduces mortality in patients with NYHA class I to III heart failure symptoms and LVEF less than 35% on optimal medical therapy. This patient meets the criteria for ICD placement, but she may experience substantial improvement in ejection fraction with CRT and may not require or benefit from ICD insertion.
In patients with LVEF of 35% or less who are in sinus rhythm with a heart rate of at least 70/min and taking maximally tolerated doses of a β-blocker, the sinoatrial node modulator ivabradine (Option B) reduces heart failure–associated hospitalizations and the combined end point of mortality and heart failure hospitalization. Ivabradine is not indicated in this patient with a heart rate of 58/min.
The mitral valve clip (Option C) is designed to approximate mitral valve leaflets and reduce mitral regurgitation. Mitral valve clip placement is reasonable for patients with severe secondary mitral regurgitation with heart failure symptoms and a left ventricular end-systolic dimension less than 70 mm and pulmonary artery pressure less than 70 mm Hg. CRT is more likely to improve symptoms and is the most appropriate step for this patient before considering a mitral valve clip.
Transcatheter aortic valve implantation (TAVI) (Option D) is usually reserved for patients with symptomatic severe aortic stenosis. Factors that increase procedural risk include reduced ejection fraction, another reason not to proceed with TAVI in this patient.
Cardiac resynchronization therapy is indicated for patients with ejection fraction of 35% or less with left bundle branch block, QRS duration of 150 ms or greater, and New York Heart Association functional class II to IV symptoms despite guideline-directed medical therapy.
Wu A. Heart failure. Ann Intern Med. 2018;168:ITC81-ITC96. PMID: 29868816
Copyright 2019, American College of Physicians.