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4/27/2015
IM Board Review 2015
Timir Paul, MD, PhD, MPH, FACC, FSCAI
Peripheral Arterial Disease
Lower Extremity Question
Based on the epidemiologic studies, which of the following risk factor has the highest risk for developing lower extremity PAD
1. diabetes
2. smoking
3. hypertension
4. hypercholesterolemia
5. hyperhomocysteinemia
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Case • 60 year female with CKD (GFR 27), diabetes, uncontrolled HTN, diastolic HF, presents for routine f/u. She c/o leg numbness.
• Denies any rest or exertional leg pain, fatigue
• No ulcer, gangrene, discoloration or cold foot
What do you do next?
What do you do next?
1. Proceed with CTA or MRA
2. ABI
3. Exercise ABI
4. Get more history and thorough PE
5. Aggressive risk factor modification
Screening for Asymptomatic
Patient With PAD
Class I indication:
Age ≥50 years with a history of smoking or
diabetes
or
Age ≥65 years
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Question
• A 65 yr male with h/o HTN, HLP and former smoker c/o bilateral thigh pain on walking and relieves at rest. He noticed this stable sx for last 1 yr. Currently taking HCTZ and rosuvastatin. BP 138/70, HR 68/min. No femoral bruits. Deep tendon reflexes are symmetric and normal at knees and ankles. Pedal pulses are 1+ B/L. Resting ABI 0.92 both legs.
Question
• Which of the following is the most appropriate test?
• A. CTA of B/L lower extremities
• B. MRI of lumber spine
• C. Segmental lower extremity pressures
• D. Exercise ABI
• E. Angiogram Patient With Intermittent Claudication
• ABI is the first test to diagnose symptomatic and asymptomatic PAD (class I) • If resting ABI is normal but clinical suspicion is high exercise ABI is recommended (class I) If ABI > 1.4, TBI is indicated
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Question
• A 71 yr male reports of both thighs and calves pain. ABI 0.68 in left and 0.75 in right ankle. There is no ulcer or gangrene. His sx improved slightly with exercise and intensive lifestyle modification. He also c/o dyspnea on exertion and mild b/l leg edema. He is taking ASA 325 mg daily
• What is the next step
1. Start cilostazol
2. Duplex lower extremity US
3. 2 D echo
4. Start statin
5. Add plavix
Contraindications to Cilostazol
 patients with symptoms of CHF
 Low EF
.
Pletal® (cilostazol) Package Insert. Rockville, Md: Otsuka America Pharmaceutical, Inc; 1999.
PAD
Clinical Presentations
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PAD ~ CAD
CAD
PAD
•
•
•
•
•
•
•
•
•
•
Non cardiac pain Atypical chest pain
Typical angina
UA/NSTEMI
STEMI
No leg pain
Atypical leg pain
Claudication
Critical limb ischemia
Acute limb ischemia
Clinical Presentations
Asymptomatic: Without obvious symptomatic complaint (but
usually with a functional impairment). This diagnosis should only
be made if the patient is physically active.
Exertional Pain
“Atypical” leg pain: Lower extremity discomfort that is exertional
but that does not consistently resolve with rest, consistently limit
exercise at a reproducible distance, or meet all “Rose
questionnaire” criteria.
Classic claudication: Lower extremity symptoms confined to the
muscles with a consistent (reproducible) onset with exercise and
relief with rest. Yet it has poor sensitivity and specificity for
identifying patients with PAD
Clinical Presentations
Rest Pain
Critical limb lschemia:
- Ischemic rest pain
- Ulceration/ non-healing wound
- Gangrene
Acute limb ischemia: The five “P”s, defined by the clinical
symptoms and signs that suggest potential limb jeopardy:
 Pain
 Pulselessness
 Pallor
 Paresthesias
 Paralysis (& polar, as a sixth “P”).
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Clinical Presentations of PAD
~15%
Classic (Typical) Claudication
50%
Asymptomatic
~33%
Atypical Leg Pain
(functionally limited)
1%‐2%
Critical Limb Ischemia
Diagnosis of PAD
 Diagnostic tools
•
Non-invasive Functional Studies
– Ankle-Brachial Index (ABI)
- Toe-Brachial Index (TBI), and Segmental Pressures
– Pulse Volume Recording (PVR)
•
•
Non-invasive imaging studies
–Arterial Duplex ultrasound, MR Angiography,
CT Angiography
Invasive imaging
– Angiography (gold standard)
Interpreting the Ankle‐Brachial Index
ABI
1.00–1.4
Interpretation
Normal
0.91–0.99
Borderline
0.41–0.90
Mild-to-moderate disease
≤0.40
Severe disease
>1.40
Noncompressible
ABI is 95% sensitive and 99% specific for PAD
Rooke et al, circulation 2011
Hirsch AT, et al. J Am Coll Cardiol. 2006;47:e1‐e192. Figure 6.
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Treatment of PAD
Options
• Exercise
• Medical Therapy
• Revascularization
–
–
–
–
–
Percutaneous Transluminal Angioplasty (PTA)
Stents
Atherectomy
Thrombolytics
Vascular surgery
Goals of Therapy for Patients With PAD
Limb outcomes
• Improve ability to walk
– Increase in peak walking distance
– Improvement in quality‐of‐
life (QoL)
• Prevention of progression to CLI and amputation
Cardiovascular
morbidity and mortality
outcomes
• Decrease in morbidity from non‐fatal MI and stroke
• Decrease in CV mortality from fatal MI and stroke
Non‐pharmacologic Therapy for Intermittent Claudication
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Supervised Exercise Rehabilitation
Class I indication:
Supervised exercise training program is
recommended as an initial treatment modality for
patients with intermittent claudication and pre‐requisite for revascularization
Pharmacotherapy for Claudication
• Cilostazol
–Cilostazol increase walking distance to 100‐
150% and is a class I recommendation –Cilostazol is contraindicated in HF patients
• Pentoxifylline (do not answer)
Pharmacologic Effects of Cilostazol
• Platelets aggregation inhibitor
• Antithrombotic
• Vasodilation
• Increase blood flow
• Increase HDL (10%)
• Decrease TG (15%)
• Inhibition of vascular smooth muscle cell proliferation (in vitro)
Drug Class Phosphodiesterase III inhibitor Dosing 50‐100 mg bid
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Medications for Patients With PAD
Therapeutic Goal
Drug
To Reduce
Ischemic
Events
To Improve
Claudication
Symptoms
Aspirin/Clopidogrel
Yes
No
Cilostazol
No
Yes
Treatment to Improve Cardiovascular Outcomes
PAD is CAD equivalent
• Risk factors modification is a class I indication
• The same ATP III/JNC goal for
‐ Blood pressure ‐ Cholesterol • Smoking cessation
• Hba1C < 7.0
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Drug Therapy
• Aspirin (75 mg to 325 mg) • Plavix is an alternative • Not both ‐ Blockers Are Effective and Not
Contraindicated in PAD
Radack K. Arch Intern Med. 1991;151:1769.
Non Drug Therapy
• Supervised exercise program and rehabilitation in all symptomatic PAD patients
• Angioplasty or Surgery – If medical therapy fails
– Rest pain
– Poorly healing ulcer
For acute limb ischemia‐
Start heparin and interventional cardiology consultation for embolectomy or arterial thrombolysis/PTA
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Asymptomatic PAD Revascularization
• Class III
• Revascularization (endovascular or surgical) is not indicated as prophylactic therapy in an asymptomatic patient with lower extremity PAD Renal Artery Stenosis (RAS)
Diagnosis of RAS
Class I indications:
1. Resistant, accelerated and malignant hypertension
2. New azotemia or worsening renal function after administration of ACEI/ARB
3. Sudden unexplained pulmonary edema
4. Unexplained atrophic kidney or discrepancy in size between 2 kidneys > 1.5 cm
5. HTN before age 30 or severe HTN after age 55 years
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Diagnostic modalities
Class I
Duplex ultrasound
CT angiogram
MRA Renal angiogram is the gold standard
Indications for Revascularization
Class I:
Percutaneous revascularization is indicated for patients with significant RAS and recurrent unexplained heart failure or sudden unexplained pulmonary edema
Class IIa
Percutaneous revascularization is reasonable for patients with hemodynamically significant RAS and unstable angina
Indications for Revascularization
Hypertension:
Preservation of renal function
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Diseases of Aorta
Questions A 62 yr old male with family h/o AAA presents for routine f/u examination. He is a past smoker. BP is 138/82 with HCTZ. Which one of the following is a correct statement.
1. Screen for lipids
2. US Screen for AAA
3. US screen for AAA when he will be 65
4. Goal BP is <130/80
5. Do nothing as he is asymptomatic
Questions • Which of the following are indications for infrarenal AAA repair?
1. Diameter > 5.5 cm
2. Expansion rate greater than 1 cm/yr
3. Inflammatory or infectious etiology
4. Recurrent atheroembolism
5. All of the above
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Question
A 68 yr male with HTN, DLP, current smoker and family h/o of AAA. He had an US done 2 yrs ago that did not reveal AAA.
When is the next US should be performed for f/u
1. 1 yr
2. 3 yrs
3. 5 yrs
4. No further US
5. Any time between 70‐75 yrs
Abdominal Aortic Aneurysms (AAA)
Signs and Symptoms ‐ AAA
• Pain‐ abdomen, back, flank
• Pulsatile abdominal mass
• Physical examination lacks sensitivity (69% for <5 cm) • Livedo‐ atheroembolism
–
–
–
–
–
Blue or gangrenous toes
Livedo reticularis
Elevated serum creatinine
Eosinophilia
Accelerated HTN
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Screening high risk population
AAA Surveillance
Size (cm) 3.0‐3.4
3.5‐3.9
4‐4.9
>5
Surveillance interval
3 yrs
1 yr
6 months
3 months
• If AAA 4‐5.4 US every 6‐12 months
• For smaller AAA every 2‐3 yrs
AAA‐ indications for surgery
1. Diameter > 5.5 cm
2. Expansion rate greater than 1 cm/yr
3. Inflammatory or infectious etiology
4. Recurrent atheroembolism
5. Symptomatic
6. Ruptured or contained rupture
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Thoracic Aortic Aneurysm Risk Factors of Thoracic AA
•
•
•
•
Hypertension, tobacco, atherosclerosis
Famililal
Congenital‐ bicuspid aortic valve
Infectious and Inflammatory
– Syphilis, TA, GCA, Behcet, Ankylosing spondylosis
• Connective tissue disease
– EDS, Marfan, Turner’s
Trauma‐ sudden deceleration
Ascending Aortic Aneurysm
Surveillance Aneurysm 3.5‐ 4.4 cm
Annual CT or MR
Aneurysm 4.5‐ 5.4 cm
Semi‐annual CT or MR
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Medical Management of TAA
• Control hypertension
First : beta‐blockers
2nd : vasodilator
Other risk factors modification
Indications for Thoracic AA Surgery Ascending aortic diameter >= 5.5 cm
Exceptions:
‐ Expansion rate greater than 0.5 cm/yr
‐ Infectious etiology ‐ Traumatic origin
‐ Symptomatic
‐ Bicuspid aortic valve, Marfan, Turner, Ehlers‐Danlos, familial
thoracic aortic aneurysm and dissection (>4.0‐5.5 cm)
‐ Patients undergoing aortic valve repair or replacement and who
have an ascending aorta or aortic root > 4.5 cm
Acute Aortic Dissection
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Acute Aortic Syndromes
• Aortic dissection (classic)
• Intramural hematoma (IMH)
• Penetrating atherosclerotic ulcer (PAU) Question
A 64‐year‐old man presents with the sudden onset of tearing chest pain. On presentation, he has a heart rate of 130 beats/min with a systolic blood pressure of 80 mm Hg. A bedside TEE demonstrates the presence of a proximal aortic dissection. A pericardial effusion with partial diastolic collapse of the right ventricle is also present. Significant respiratory variation is noted across mitral and tricuspid Doppler inflows. Appropriate treatment is
1. Immediate percutaneous pericardiocentesis to relieve the tamponade, followed by surgery to replace the ascending aorta
2. Proceed immediately to the operating room
3. Emergency angiography to define coronary anatomy, followed by surgery
4. Intra‐aortic balloon pump to stabilize the hemodynamics, followed by surgery
Question
A 60‐year‐old hypertensive man presents with tearing back pain. MRI confirms the presence of a descending thoracic dissection originating beyond the left subclavian artery. Appropriate initial treatment includes
1. Immediate surgery to replace the descending aorta
2. Intravenous nitroprusside followed by immediate surgery
3. Intravenous nitroprusside alone; surgery for persistent pain, or for involvement of renal or mesenteric arteries
4. Intravenous beta‐blockade and nitroprusside; surgery for persistent pain, or for involvement of renal or mesenteric arteries
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Question
• Which of the following has the lowest mortality?
• 1. Type A dissection treated medically
• 2. Type A dissection treated surgically
• 3. Type B dissection treated medically
• 4. Type B dissection treated surgically
Questions
63 yr male admitted for symptomatic repair of 5.6 cm of AAA. He has h/o DM, dyslipidemia and family h/o MI in brother at age 58. BP is borderline controlled with ACE and HCTZ. what is the next appropriate step?
1. Proceed with surgery
2. Nuclear stress test
3. Exercise stress test
4. Titrate up BP meds 5. Transfer patient to ICU and start nitroprusside
Question
• 58 yr male with h/o CAD presents with severe chest pain radiating to back. BP 185/100, HR 100/min. A decrescendo murmur was heard on the precordium. What you should do next:
1. Stat surgery consult
2. EKG and troponin
3. IV nitroprusside
4. BB and IV nitroprusside
5. CT with contrast
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Question
58 yr male with h/o CAD presents with tearing chest pain radiating to back. BP 100/60 in right arm and 140/70 in left arm, HR 100/min. CXR showed widened mediastinum
What you should do next:
1. EKG and troponin
2. Surgery consultation
3. BB and IV nitroprusside
4. Emergent CT with contrast
5. 3 and 4
Types of Dissection
Stanford classification
• Ascending aortic dissection – Type A
• All others dissections – Type B
Acute Aortic Dissection Clinical Presentation
‐ Chest pain radiating to back – CHF
– Shock
– Syncope
– CVA ( focal neurologic deficits) – Paraplegia
– Acute arterial occlusion – HTN, AR, pulse deficits/ differential BP
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Dissecting Ascending Aortic Aneurysm
Type A Dissection
•
•
•
•
•
•
Chest pain radiating to back
Acute AR murmur and HF
Widened mediastinum
Blood pressure differential between arms
Cardiac tamponade
Evidence of thromboembolism or dissection of branch arteries (stroke, MI )
• This is an emergency
• Treatment is surgery
• In what other conditions you see wide mediastinum?
Anthrax
Acute Aortic Dissection Medical management
• Pain control
• Hypertensive patients
– IV beta‐blocker (caution with acute AI)
– or labetalol
Normotensive Patients:
IV beta blocker
BP goal: SBP 100‐120 mm Hg
Diagnostics
• CT scan with contrast or MRA • TEE for critically ill patients who cannot move from a monitored setting
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Type B Aortic Dissections
• Uncomplicated Type B dissections usually treated medically
• Beta blockers and nitroprusside for acute dissections
• Long term BB for all patients
• Surgery
– If pain persists ‐ If major aortic vessels (renal arteries) are involved
Other Diseases of Aorta
• Aortic atheroma
• Penetrating aortic ulcer
• Intramural Hemotoma
– Crescent like thickening of aortic wall
– Absence of dissection flap
• Marfan syndrome
– Aortic root dilatation
– MVP
• Takayasu’s arteritis
Intramural Hemotoma
• Intramural hematoma is a variant of aortic dissection
• Type B is common
• Risk factors, signs & symptoms and management of acute IMH are the same as for aortic dissection
• No intimal flap by TEE
• Relatively smooth luminal surface
• False negative aortogram
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Takayasu’s Arteritis
• Young adult women from Japan and other parts of Asia
• Areas of focal stenosis in multiple major arteries
• The mainstay of therapy is corticosteroids
• Large vessels bypass and angioplasty/stenting is often required
Coarctation of Aorta
Coarctation of Aorta
Aortopathy/Association
• Aortic medial Changes
• Bicuspid aortic valve
• 5 fold increase in intracranial aneurysm in patient with coarctation
• Often associated with Turners Syndrome
• Usually occurs just distal to left subclavian artery
• BP differential between upper and lower extremities
• Collaterals: subclavian, axillary, internal mammary, scapular, intercostal
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Physical exam
•
•
•
•
•
•
Delayed femoral pulses
Systolic murmur LSE → con nuous
Collateral murmurs
4th sound with LVH and hypertension
Loud A2 if hypertension
Ejection click ± systolic murmur with bicuspid aortic valve
Diagnostic Imaging
• CXR
– Figure “3” sign – aortic knob
– Rib notching from enlarged intercostal arteries
• Echo – Doppler
• CT, MRI / MRA
• Angiogram
Indications for Intervention
• Peak to peak gradient > 20 mmHg
• Peak to peak gradient < 20 mmHg in presence of imaging evidence of significant coarctation
with radiological evidence of significant collateral flow
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Pericardial and Myocardial Diseases
Question
A 68‐year‐old man develops recurrent chest discomfort 5 days after an anterior myocardial infarction. The pain is sharp and radiating toward both clavicles. He is afebrile and there is no pericardial friction rub on physical exam. BP 132/70, HR 110. EKG showed diffuse ST elevations. CXR showed pleural effusion. He in on 325 mg aspirin, statin, plavix, metoprolol and lisinopril. Question
The most appropriate therapy for this patient is
– High dose aspirin
– Indomethacin and Colchicine – Indomethacin
– Corticosteroids
– Nitro drip and morphine PRN
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Dressler’s Syndrome
Post‐cardiac injury syndrome
• Fever, pericarditis, pleuritis
(typically a low grade fever and a pericardial friction rub)
• Occurs in the first few days to several weeks following MI or heart surgery
• Incidence: 6‐25% • Treat with high‐dose aspirin/NSAIDs
Question
A 45 yr female presents for evaluation of left sided pleuritic type chest pain for last 2 weeks. No relation to exertion or rest but worse when supine and got better transiently on leaning forward. The pain got better with acetaminophen. Reports that she had low grade fever for the last 1 week but no cough. She was treated for acute pericarditis 1 year ago with ibuporfen and her symptom was resolved in few days. Currently she is taking acetaminophen intermittently. Temp 100F, HR 105/min, BP 140/88. No JVD, wheezing. EKG showed sinus tachycardia without and ST changes. Question
Which of the following is the most appropriate management?
A.
B.
C.
D.
E.
Aspirin Ibuprofen
Colchicine
Colchicine and aspirin
Prednisone
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Common Causes
– Idiopathic is the commonest
– viral infections: ‐
‐
‐
‐
‐Coxsackie A and B (highly cardiotropic) are the most common viral cause of pericarditis and myocarditis
Uremia Myocardial infarction (acute, post) Medications (hydralazine, procainamide, INH)
Radiation
Acute Pericarditis
Diagnostic Clues
• Chest pain‐ pleuritic; worse by lying supine, relieved by sitting and leaning forward
• Pericardial friction rub
• Pathognomic for pericarditis
• EKG : most important clue
• Troponin and CK‐MB may be elevated in myopericarditis
• An extensive initial evaluation is not warranted in uncomplicated patients because of low diagnostic yield
Evaluation of Acute Pericarditis
• Pericarditis is a clinical and electrocardiographic diagnosis
• Pericardial effusion on echo neither confirms nor excludes the diagnosis
• Do not need an echo to diagnose acute pericarditis
• A normal echo does not rule out pericarditis
• Pericardiocentesis with subsequent pericardial fluid analysis should be reserved for cardiac tamponade, suspected purulent, tuberculous or neoplastic pericarditis
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Acute Pericarditis
Treatment
– NSAIDs (Indomethacin 75‐225 mg daily, Ibuprofen 400‐800 mg tid‐qid) for 1 month
– Colchicine 0.6 mg bid for 3 months
– ASA 650‐800 mg q 6‐8 hrs (2 to 4 g/day) preferred in pericarditis with MI
– Corticosteroids are symptomatically effective, but preferably avoided. Use for short term only in refractory cases of relapsing pericarditis
ESC Guidelines for Management of Pericardial Diseases
• First episode of Acute Pericarditis:
NSAIDs Class I
NSAIDs + Colchicine Class IIa
Eur Heart J 2005
Recurrent /Relapsing idiopathic Pericarditis – Colchicine (0.6 mg BID) should be started with 1st episode of recurrent pericarditis (6 months)
– NSAIDs for 1 month – Prednisone are occasionally effective – Steroid dependency requiring gradual tapering over 3‐12 months
– Pericardiectomy may be helpful in drug refractory recurrent pericarditis
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ESC Guidelines for Management of Pericardial Diseases
• Recurrent Pericarditis:
NSAIDs + Colchicine Class I
Pericardial Effusion
Pericardial Tamponade
Etiology
• Includes all causes of pericarditis
• Hypothyroidism
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Pericardial Effusion
Benign Tamponade
• Normal JVP
• No Pulsus
• Elevated JVP
• Pulsus paradoxus
• Prominent X descent
Signs and Symptoms of Tamponade
Signs
ECG
• Electrical alternans
• Diffuse low voltage
• S tachycardia
• S. Tachycardia • Hypotension or narrow PP
• Decrease urine output
• ± pericardial rub
• Elevated JVP
• Prominent x descent
• Attenuated y descent
• Pulsus paradoxus
Pulsus alternans
Severe Cardiomyopathy
Tamponade
2‐D Echo/doppler findings
•
•
•
•
•
Pericardial effusion
Diastolic collapse of RV and RA
Dilated IVC (IVC plethora, 97% sensitivity, 99% PPV)
Abnormal ventricular septal motion
Increased respiratory variation of the mitral and tricuspid flow velocities
• Reduced chamber size
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Pericardiocentesis
• Do
For tamponade or If need to make a diagnosis
• Don’t Do
If there is any suggestion of aortic dissection
Question
• A 67 yr male s/p CABG 5 years ago. He presents with increasing DOE for the last 4‐5 months. Exam showed JVP 10 cm, pedal edema and hepatomegaly.
• EKG and CXR‐ unremarkable
Question
• Most likely diagnosis
1. Tamponade
2. Restrictive cardiomyopathy
3. Constrictive pericarditis
4. Ischemic cardiomyopathy
5. Effusive constrictive pericarditis
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Question
• A 54 yr male presents for evaluation of fatigue. She also reports of intermittent LE edema for the last 4 months. She had past medical h/o breast cancer 10 yrs ago, treated with surgery, radiation and chemo. Has h/o hypertension, but no diabetes. • Physical exam shows HR 75, BP 110/70. JVP distends with inspiration. Carotid pulses are full and brisk. Heart sounds revealed S4.
• Labs
• BUN/Cr: 18/0.8, albumin 4.5, Hb 14.0
• ECG ‐ unremarkable
Question
• Echo showed normal RV and LV systolic function with EF 60%. A small LV cavity with normal wall thickness, diastolic dysfunction without respiratory variation. Valves are normal. • What is the diagnosis
• 1. Hypertrophic cardiomyopathy
• 2. Restrictive CMP
• 3. Constrictive pericarditis
• 4. Hypertensive CMP
• 5. Chemo induced CMP
Constrictive Pericarditis
Etiologies
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Presenting Symptoms
• CHF (fatigue, DOE) •
•
•
•
•
Chest pain GI symptoms
Tamponade
Arrhythmia Liver disease 67%
8%
6%
5%
4%
4%
Presenting Signs
• Mostly RV failure symptoms
Elevated JVP
88%
Peripheral edema
Hepatomegaly
64%
53%
Pericardial Knock
47%
Ascites
37%
Kussmaul’s
21%
Pulsus Paradoxus
19%
Constrictive Pericarditis
Diagnostic Tests
•
•
•
•
•
•
Chest X‐ray
Computed tomography
Echocardiography
Magnetic Resonance Imaging
Cardiac Catheterization
Surgical Exploration
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CXR and CT
Pericardial calcification
Pericardial Thickening
>2 mm Thickness
MRI is the most sensitive to measure pericardial thickness
Normal pericardial thickening does not exclude constrictive pericarditis (pericardial thickening may be normal in 20% of cases)
Prominent Y descent in RAP
Constrictive Pericarditis
Treatment of Constrictive Pericarditis
• Cautious diuretics • Acute /transient Effusive Constrictive Pericarditis can be treated with aggressive anti‐inflammatory
• Pericardiectomy is the most effective treatment for chronic constriction
• Surgical mortality from pericardiectomy is approximately 6‐19%
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Summary Constrictive Pericarditis
•
•
•
•
•
•
Respiratory Variation in diastolic filling Increased ventricular interdependence
Ventricular discordance
Hepatic vein flow reversals with expiration
BNP is not markedly elevated
LA is not markedly elevated
Myocardial Diseases
Restrictive Cardiomyopathy
Causes
Myocardial
Noninfiltrative diseases
‐idiopathic
‐familiar
‐scleroderma
Infiltrative
– Amyloidosis
– Sarcoidosis
– Hemochromatosis
– Glycogen storage diseases
Endomyocardial
–
–
–
–
–
–
endomyocardial fibrosis
hypereosinophilic synd
carcinoid anthracycline toxicity
Radiation metastatic cancer
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Restrictive Cardiomyopathy
signs and symptoms
•
•
•
•
•
•
•
Edema
Elevated JVP
Dyspnea
Rapid X and Y descents
Ascites
Hepatomegaly
Low output symptoms
Atrial arrhythmias are frequent
Right sided heart failure is more severe than left HF
Cause specific Echo findings
Restrictive cardiomyopathy
• Amyloid heart disease – Thickened myocardium/septum (refractile on Echo)
– Pericardial effusion
– Thickened regurgitant valves
Endomyocardial fibrosis
 Apical thrombus without underlying apical
akinesis
 Mitral regurgitation
Amyloid vs LVH
ECG: Amyloid low voltage Treatment
Restrictive Cardiomyopathy
• Treatment directed to underlying disease (e.g. amyloidosis)
• Diuretics for symptomatic relief
• Pacemaker for conduction abnormalities
• B‐blockers should be avoided because elevated HR frequently maintains cardiac output
• Avoid digoxin and CCB in amyloid because they bind to amyloid protein and increase risk of toxicity
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Treatment
Restrictive Cardiomyopathy
• Heart transplantation is the only proven therapy for severe restrictive CMP
• Corticosteroids and cytotoxic drugs are appropriate during early stages of eosinophilic
endocarditis
• Endomyocardial fibrosis can be surgically resected and the mitral valve can be replaced
Constriction vs Restriction
• Both have similar presentations and clinical examination
• It is important to differentiate restrictive cardiomyopathy from constrictive pericarditis
• Treatment is different
• Rarely, restrictive CMP and constrictive pericarditis coexist , particularly in radiation induced heart disease
Dip and Plateau
Is this diagnostic for constriction?
Abrupt cessation of diastolic filling
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Constriction vs Restriction
Restrictive CMP
Constriction
Similar Hemodynamics
High/Equalization of diastolic pressures
Dip and Plateau/Square Root
Constriction vs Restriction
Hemodynamic Criteria
Criteria •
•
•
•
•
•
Constriction
LVEDP‐ RVEDP
RVSP
RVEDP/RVSP
Ventricular Elevated filling P
Dip and Plateau
< 5
<50
>0.3
Discordance
+ +
Restriction
>5
>50
<0.3
Concordance
+
+
Wood P. AJC, 1961; Yu et al. Circ 1953
Constriction vs Restriction
Constriction Restriction
• Atrium not markedly dilated
markedly dilated
• Pul HTN
• BNP
mild > mild and common
not markedly elevated
markedly elevated
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LV‐RV Pressure Relationship
Ventricular Interdependence
Restrictive CMP
Constriction
Think “ Constriction”
• When there is heart failure (esp RHF) out of proportion to myocardial or valve findings
• When there is a h/o prior chest radiation: breast cancer, lung cancer, hodgkins
• When there is a h/o prior cardiac surgery
• When there is h/o TB, RA and LFTs abnormalities
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Take home message
Constriction vs Restriction
• Differentiate restriction by
– Enlarged atrium, moderate pulmonary HTN (PA pressure > 50), moderately elevated BNP compared to constriction
– Interventricular concordance in restriction and discordance in constriction
Hypertrophic Cardiomyopathy
Question
An asymptomatic 20 yr male wants to play soccer. Routine P/E reveals systolic murmur and brisk carotid upstroke. Echo showed 17 mm thick interventricular septum.
Which one was is true?
1. Can play soccer
2. Can do bowling
3. Start BB
4. Repeat echo in 6 months
5. Genetic screen for first degree relatives
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Questions
35 yr female has progressive dyspnea and angina for the last 4 months. There is a 2/6 late peaking systolic murmur that increases in intensity with valsalva. Echo showed EF 65%, SAM, septum 2.3 cm, gradient 30 mm Hg
What is the next best step?
1. Beta blocker
2. Septal ablation
3. Surgical myomectomy 4. ICD
5. Nothing as gradient is low
Questions
34 yr female with h/o syncope presents with dyspnea. Echo showed LVH with a gradient of 25 mm Hg. Exercise stress by modified Bruce protocol showed no EKG changes. Baseline BP was 128/76 and at 5 min of exercise BP was 110/74.
What is the next best step
1. Beta blocker
2. Pacemaker
3. BIV pacemaker
4. ICD
5. Myomectomy
Hypertrophic Cardiomyopathy
• Autosomal dominant (50%)
• Echo screening of all first‐degree relatives of patients with HCM
• Syncope, sudden cardiac death (after vigorous exercise)
• Chest pain, dyspnea, arrhythmias
• Exam
– Bifid pulse
–
–
–
–
Usually no radiation to carotids/carotid ‐brisk
Early systolic murmur increases with standing and valsalva
Murmur decreases with handshake and sitting
Risk of SCD in HCM ~ 1% annually
Pulsus bisferiens? Aortic regurgitation
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EKG and Echo findings of HOCM
• Q waves that mimic MI
• Deep T inversions in precordial leads in apical HOCM
• Echocardiography
Systolic anterior motion of MV (SAM) Asymmetrical septal hypertrophy MR
HOCM vs AS
HOCM
AS
•
•
•
•
•
•
•
•
•
•
•
•
Pulsus parvus et tardus
Usually present
Single sustained
Present
May be present
Murmur
•
•
•
•
•
Decrease murmur
Decrease mummur
Decrease murmur
Increase or no change
Increase Carotid pulse‐ Bifid pulse Carotid radiation – none
Apex beat‐ tripple ripple
Ejection sound‐ none
AR‐ none
Murmur
–
–
–
–
–
Valsalva‐ ↑
Squatting to standing‐ ↑
Hand gripping‐ ↓
Amyl nitrate‐ ↑
Post PVC ↑
Hemodynamics
• Aortic pressure tracing:
Spike and dome pattern‐ a rapid rise and
fall followed by a plateau
Post –PVC
HOCM – Decreased pulse‐pressure
AS ‐
Increased pulse ‐pressure
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AS vs HOCM
Post PVC beat
AS
HOCM
Differentiating features: 1. Aortic Upstroke
2. Pulse pressure
3. Contour‐ Spike and dome
HOCM vs Athlete’s Heart
Echo
HOCM
• LV diastolic cavity (LVEDD) < 45 mm Athlete’s Heart
• LV diastolic cavity > 55 mm
• Marked LA enlargement
• No LA enlargement
• SAM and MR usually present
• Absent
HOCM‐ High risk of SCD
Major RF
• Prior cardiac arrest or
• Sustained Ventricular Tachycardia/V fib
• Family h/o SCD Minor RF
• Recent unexplained syncope (>=2 episodes in yr)
• NSVT
• Blunted or hypotensive BP response during exercise
• Massive ventricular wall thickness >3 cm
•
•
•
•
Age < 30 yrs at diagnosis
Familial form Significant outflow tract gradient > 50 Malignant genotype
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Who needs ICD
• Risk factors 0
1
2+ Prior SCD
Sustained VT Recommendation
Reassurance
Individualize
ICD (recommend)
ICD
ICD
Drug Treatment
•
•
•
•
•
Beta –blockers
Calcium channel blockers
Disopyramide
Avoid digoxin, ACEI and other vasodilators
Avoid diuretics
Non drug therapy
• Septal ablation or surgery for symptomatic patients despite maximal medical therapy
• Myomectomy (gold standard)
• ICD needed for patients at high risk of SCD
– VT or NSVT on holter
– Family h/o sudden cardiac death
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Indications for Surgery or Septal Ablation
• Angina, dyspnea and/or syncope resulting in significant impairment in quality of life
• Symptoms persists despite appropriate medical therapy • LVOT obstruction (>50 mm Hg)
HOCM
• Endocarditis prophylaxis ?
No
Discussion
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Myocarditis
Clinical Presentations
• Acute myocarditis
• Fulminant myocarditis
– Dramatic acute heart failure with cardiogenic shock in the absence of other etiologies
– Hemodynamic compromise, rapid onset of sx (usually within 2 weeks)
– Need high dose vasopressor or even a VAD
• Giant cell myocarditis
– Heart failure with a progressive, relentless, downhill course
– Biopsy showed multinucleated giant cells without granulomas
– Ventricular arrhythmias are common
• Chronic active myocarditis
Diagnostic tests
– Echo
– Cardiac MRI
• Delayed enhancement on T1‐weighted images
• Endomyocardial Biopsy
– In fulminant and giant cell myocarditis (Class I) – Otherwise EMB is a Class IIb
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Therapeutic Approaches
• Medical Treatment
–
–
–
–
Conventional / supportive treatment Specific treatment/ interferon
Immuno‐suppressants
Immuno‐modulating therapy
• Mechanical Circulatory Support
– IABP
– Ventricular assist device
– Indicated in Fulminant Myocarditis
• Heart Transplantation
Take Home Message
• Myocardial biopsy is not routinely indicated in patients with suspected myocarditis
• In general, there should be low threshold for biopsy:
‐ Suspicion of giant cell myocarditis
‐ Rapidly deteriorating myocarditis
‐ Fulminant myocarditis
• Patients with fulminant myocarditis have an excellent long term prognosis
• Patients with giant cell myocarditis have an extremely poor prognosis with median survival 6 months
Take Home Message
• Immunosuppressive therapy has not been shown to improve outcomes and should be reserved for patients with giant cell myocarditis or clinical deterioration despite standard therapy
• Steroids is indicated in hypersensitivity myocarditis
• Temporary mechanical support/devices may be life‐saving especially in fulminant myocarditis
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Question
• A 45 yr female with HTN and CKD presents with dyspnea and decreased urine output. She was given IV diuretics and her sx improved. However, her renal function deteriorates with BUN 80 and Cr 5.1. On hospital day 4 her BP 85/45, HR 120. No JVD. Heart sound diminished. TTE showed right atrial collapse, moderate sized effusion and respiratory variation across the mitral valve, IVC decrease with respiration. Question
Next step of management
1. Urgent pericardiocentesis
2. IV hydration
3. Immediate dialysis
4. Continue diuresis
5. Repeat TTE in next day
Question
• A 35 yr male presented with low grade fever, cough and pleuritic chest pain. ECG showed diffuse ST elevation. A TTE showed large pericardial effusion. He was treated with ibuprofen. He returns a month later for f/u. He denies any chest pain but he notes B/L ankle swelling. ECG normal. A repeat TTE shows resolved pericardial effusion but new findings consistent with constriction.
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Question
What is the next step 1. Obtain cardiac MRI to better assess the pericardium
2. Start a course of colchicine
3. Obtain RHC and LHC
4. Obtain TEE and surgical consultation
5. Reassure the patient and f/u in 3 months for worsening symptoms
Question
• A 72 yr female with no cardiac disease or malignancy presents to clinic with fatigue, lower extremity swelling and SOB. On exam she is pale, lethargic with dry skin. BP 95/60 and HR 60. 3+ edema in LE. ECG showed low voltage with electrical alternans. Echo showed large pericardial effusion.
Question
What is the next step of management
1. Pericardiocentesis
2. Start IV diuresis
3. Check TSH 4. Right and left heart cath
5. Cardiac MRI to assess pericardium and
r/o infiltrative diseases. 49
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Question
• A 65 yr male with cardiomyopathy; EF of 25‐
30%, presents for follow‐up. BP 144/ 88. He is taking carvedilol 6.25 bid, lisinopril 10 mg daily, rosuvastatin, asa and lasix. He is doing well and currently asymptomatic. But he still feels fatigue and exercise tolerance is not adequate. He wants to improve his exercise tolerance. What is the next best recommendation.
Question
• 1. Add spironolactone
• 2. Start outpatient continuous dobutamine
infusion
• 3. Enroll in exercise training program
• 4. Add digoxin • 5. Increase the dose of lisinopril to adequately control BP. Question
• A 30 yr female presented to urgent care with 3 days of fever and SOB. She was diagnosed with viral infection and was sent home. Now she presents for routing follow up 3 months later. On exam she appears healthy and without symptoms. BP 100/60, HR 70, RR 12. No JVD but apical displacement noted. Echo showed EF 35% with dilated heart, no other abnormality.
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Which is next best recommendation
•
•
•
•
•
1. Start ACEI, BB, diuretics 2. Repeat echo in 6 months and f/u sx
3. Start ACEI and BB
4. Start ACEI, BB and steroids
5. She is well compensated, no need any meds
Question • Which of the following conditions is not associated with elevated right ventricular diastolic pressures with a deep and plateau pattern.
• 1. Acute RV infarction
• 2. Massive PE
• 3. Cardiac tamponade
• 4. Restrictive cardiomyopathy
• 5. Constrictive pericarditis
Question
Which abnormal LV filling pattern is least likely to benefit from BB therapy?
1. Impaired relaxation
2. Grade II diastolic dysfunction
3. Restrictive filling pattern
4. None of the above
5. 2 and 3 51
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Question
• 70 yr old male presents with new exertional dyspnea, orthopnea and leg edema. No CP. No h/o HTN, DM or smoking. BP is 110/65, HR 62. Elevated JVP, lungs clear, distant heart sound with quite precordium. EKG showed low voltage QRS. CXR‐ normal size heart, pulmonary congestion. Echo showed normal EF, normal cavity size with moderately concentric LVH, a small pericardial effusion. Coronary angiography showed mild diffuse non‐obstructive CAD.
Which of the following is the next best step
1. Start coreg 3.125 bid and lisinopril 2.5 daily
2. Start aspirin, statin, low dose bb and ACE
3. order serum and urine immunoelectrophoresis
4. If symptoms persists bring back to cath lab for ergonovine challenge to look for spasm
5. Start low dose coreg, lisinopril and aldosterone
Question
• 81 yr female presents to ER with severe SOB at rest. H/o long standing HTN. Recent Echo showed EF 60%, LVH and pseudonormal pattern of diastolic filling
• BP 182/ 62
• HR 106, irregularly irregular
• Respiration 30 per min
• Cr 1.5, trop < 0.01, ECG: Afib
• CXR: pulmonary congestion
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What is the next most appropriate step in management
•
•
•
•
•
1. control BP
2. diuresis
3. control HR
4. TEE with DC cardioversion
5. all of the above
Questions
Summary
Tamponade
• Physical findings
– sinus tachycardia
– elevated jugular venous pressure
– pulsus paradoxus
– Hypotension
• Electrocardiogram – sinus tachycardia
– low voltage
– electrical alternans
• Echocardiographic – a large effusion with a swinging heart – RA collapse; early RV diastolic collapse
– reciprocal changes in right and left ventricular volumes with respiration
– respiratory flow variation across the AV valves is the most specific finding
– IVC plethora is very sensitive
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