ACCSAP

Question 1

Clinical & lab features of mycocarditis?

Answer 1

History of fever, cough, myalgia (URI sx)

Hypotension (low output), congestion (pulmonary edema), cool extremities, low urinary output, lactic acidosis, elevated LFTS >> cardiogenic shock

Labs might show: Elevated troponin, high BNP, leukocytosis, AKI, transaminitis

EKG: NSVT, VT, PVCs, ST changes

Question 2

Viral pathogens implicated in myocarditis?

Answer 2

Parvovirus (B19) and HHV-6. Previously most common pathogens were adenovirus and coxasakie viruses

Question 3

Diagnosis of myocarditis?

Answer 3

Usually made with endomyocardial biopsy which shows lymphocytic infiltration and myocyte necrosis. It can also help exlcude other causes like giant cell arteritis, sarcoidosis and eosinophillic myocarditis

Question 4

CMR findings in myocarditis?

Answer 4

Edema in T2 weighted image

Presence of early gladolinum enhancement

Abnormal late gladolinum enhacement with rim-like uptake in septum or subepicardial patchy distribution in lateral walls

Question 5

Treatment of fulminant myocarditis?

Answer 5

These patients are in low output failure with decreased forward flow and pulmonary congestion. Decreased forward flow can lead to multi-organ failure (liver, kidneys, brain etc).

Initially treat with dobutamine/milrinone plus diuretic such as furosemide. If still hypotensive could consider adding levophed. However, if no impovement these patients would require mechanical support either with ECMO or percutaneous LV assist device.

Note: High dose steroids can be used in checkpoint induced myocarditis, eosinophillic myocarditis, sarcoidosis, giant cell myocarditis seen on biopsy. However, acute stabilization is important.

Question 6

Indications for right heart catheterization?

Answer 6

Consider when patient has following:

• Concern for acute decompensated heart failure but there is ambiguity whether its lung or heart disease
• When effective therapy has not improved clinical outcomes, for example worsening AKI in light of optimal treatment
• When physical examination is not accurate or difficult to assess volume status

Question 7

Indications for CRT in HFreF?

Answer 7

LVEF less than or equal to 35% with

Sinus rhythm and LBBB with QRS >150 and NYHA class II-IV

CRT improves mortality, decreases hospitalizations in these patients.

Question 8

Treatment of secondary MR in HFrEF patients?

Answer 8

In HFrEF we should first optimize GDMT and if indicated do CRT (In MIRACLE trial, CRT improved LV dimensions and caused reduction in MR)

If there is still severe MR present from HFrEF, we should consider transcatheter edge to edge mitral valve repair (TMVR) (COAPT trial showed TVMR reduced mortality and hospitalizations; 29.1% vs 46.1% and 35.8% vs 67.9% respectively in patients with moderate to severe secondary MR and LVEF 20-50% with NYHA Class II-IV symptoms despite GDMT and/or CRT)

Surgical treatment has limited evidence and is not usually recommended.

Question 9

Features and treatment of low output heart failure?

Answer 9

Hypotension

Cool extremities

AMS

Low urine output

Congestive symptoms (dyspnea)

Treatment involves ionotropic support with milrinone or dobutamine. Note: Initiation of vasoactive agents like phenylephrine or vasopressin can increase SVR in cardiogenic shock and would be contraindicated

Question 10

EKG findings of amyloidosis?

Answer 10

Low voltage QRS complexes out or proportion to LV wall thickness.

Criteria for limb leads include

Criteria for precordial leads include

Pseudoinfarct patterns: Mostly in anterior leads (q waves, poor R wave progression) or inferior leads (q waves)

Question 11

Echocardiographic findings of amyloidosis?

Answer 11

Biatrial enlargement

Biventricular increased wall thickness

Apical sparing pattern with a 2:1 ratio on strain assessment “classic cherry on top with severely diminished basal strain”

Question 12

Diagnosis of cardiac amyloidosis?

Answer 12

If pre-test probability is high based on EKG and echo findings we should obtain:

PYP scan and urine and srum assessment of serum kappa/lambda free light chain ratio for plasma cell dyscrasias

Note: PYP scans can be falsely positive in patients with light chain amyloidosis and thus a diagnosis of transtherytin amyloidosis cannot be made without assessment of plasma cell dyscrasias.

Question 13

Theophyllline & Heart failure?

Answer 13

Theophylline relaxes bronchial smooth muscle and decreases airway resistence but increases heart rate and causes atrial tachyarrythmias. This can lead to acute decompensation of chronic heart failure.

Question 14

NSAIDs and heart failure?

Answer 14

NSAIDs decrease prostaglandins and therefore, decrease blood flow to the kidneys which leads to ADH and RAAS activation. This leads to water and sodium retention and edema. It also causes diuretic resistence and increased systemic vascular resistence.

NSAIDs such as ibuprofen should be avoided in heart failure

Question 15

Amlodipine and heart failure?

Answer 15

PRAISE-2 trial showed no benefit of amlodipine with regards to CV death and hospitalization. It’s use lead to increased peripheral edema and pulmonary edema. It’s use should be avoided in HF patients with reduced ejection fraction.

Question 16

How is PCWP measured?

Answer 16

The pulmonary artery occlusion pressure (PAOP; pulmonary capillary wedge pressure [PCWP] or pulmonary artery wedge pressure [PAWP]) estimates the left atrial pressure.

The PAOP tracing is obtained by inflating the balloon at the distal tip of the catheter. The balloon obstructs blood flow through a branch of the pulmonary artery. This creates a static column of blood between the catheter tip and the left atrium. Pressure at both ends of the column equilibrates, after which the pressure at the distal end of the catheter is equal to the pressure of the left atrium]. Thus, PAOP is a reflection of left atrial pressure.

Question 17

PCWP and LVEDP?

Answer 17

PCWP usually estimates the left ventricular end-diastolic pressure (ie, left ventricular preload) if there is no obstruction to flow between the left atrium and left ventricle and the compliance of the left ventricle is normal. Importantly, it does not directly measure the left ventricular end-diastolic volume, capillary hydrostatic pressure, or transmural pressures. Thus, the PCWP may not reliably indicate left ventricular preload when compliance of the left ventricle is abnormal (eg, large myocardial infarction or in cardiac tamponade).

Question 18

Normal PCWP?

Answer 18

Normal wedge pressures vary from 6 to 15 mmHg, with a mean of 9 mmHg

Question 19

PCWP tracing segments?

Answer 19

Physiologically, the PCWP tracing has similar components to the right atrial waveform with three positive and two negative deflections:

●The a wave reflects contraction in atrial systole, while the x descent reflects the fall in left atrial pressure that follows.

●The c wave, reflecting the closure of the mitral valve, is often not seen.

●The v wave represents both ventricular systole and passive atrial filling in atrial diastole.

●The y descent reflects the fall in left atrial pressure following opening of the mitral valve and the initiation of passive filling of the left ventricle.

Question 20

Large a waves in PCWP?

Answer 20

Increased amplitude of the a wave can be seen with increased resistance to left ventricular filling of any cause. Potential causes include:

Mitral stenosis

Left ventricular systolic dysfunction

Left ventricular diastolic dysfunction

Left ventricular volume overload

Myocardial ischemia or infarction with decreased left ventricular compliance

Question 21

Large v waves of PCWP tracing?

Answer 21

Large v waves - Increased amplitude of the v wave in the PAOP tracing may represent mitral regurgitation (MR)

Question 22

LV non compaction is characterized by?

Answer 22

Left ventricular noncompaction (LVNC) is a distinct phenotype characterized by prominent LV trabeculae and deep intertrabecular recesses

Question 23

LV non compaction morphological features?

Answer 23

An altered myocardial wall with prominent trabeculae and deep intertrabecular recesses, resulting in thickened myocardium with two layers consisting of noncompacted myocardium and a thin compacted layer of myocardium

Continuity between the LV cavity and the deep intertrabecular recesses, which are filled with blood from the ventricular cavity without evidence of communication to the epicardial coronary artery system.

Question 24

Genetic of LV non compaction?

Answer 24

LVNC can be either sporadic or familial.

Autosomal dominant inheritance is more common than X-linked inheritance or autosomal recessive inheritance.

In patients with LVNC, mutations have been reported primarily in genes coding for sarcomeric, cytoskeletal, Z-line, and mitochondrial proteins.

Sarcomere (TTN and MYH7)

Alpha-dystrobrevin (DTNA)

Tafazzin gene

Question 25

Major complications of LV non compaction?

Answer 25

The major complications of LVNC are HF, atrial and ventricular arrhythmias, sudden cardiac arrest, and thromboembolic events, including stroke

Question 26

Echocardiographic diagnostic criteria of LV non compaction?

Answer 26

For diagnosis of LVNC using echocardiography, we use the Jenni criteria

The presence of all four of the following echocardiographic criteria are required for diagnosis:

• A thickened LV wall consisting of two layers: a thin compacted epicardial layer and a markedly thickened endocardial layer with numerous prominent trabeculations and deep recesses with a maximum ratio of noncompacted to compacted myocardium >2:1 at end-systole in the parasternal short-axis view.
• Color Doppler evidence of flow within the deep intertrabecular recesses.
• Prominent trabecular meshwork in the LV apex or midventricular segments of the inferior and lateral wall.
• Compacted wall thickness ≤8.1 mm. The criterion of maximal systolic compacta thickness of ≤8.1 mm was found to be very specific for myocardial thickening in LVNC compared to normal controls or patients with aortic stenosis

Question 27

Echocardiographic criteria of LV non compaction, where to measure?

Answer 27

Parasternal-short-axis echocardiographic end-systolic view of the left ventricle. The ratio of noncompacted myocardium (spanned by the red line [top section]) to compacted myocardium (spanned by the yellow line [bottom section]) is 3:1. Thickened left ventricular wall with a ratio ≥2:1 of non-compacted to compacted myocardium at end-systole and prominent trabecular meshwork in the LV apex or midventicle (along with color Doppler evidence of flow within the deep intertrabecular recesses) are the criteria for left ventricular noncompaction proposed by Jenni et al.

Question 28

Role of CMR in diagnosis of LV non compaction?

Answer 28

CMR is generally used to aid in the diagnosis of LVNC when echocardiographic findings are inconclusive.

In addition, since CMR provides morphologic information (including identification of fibrosis by late gadolinium enhancement (LGE) which may have prognostic implications)

NOTE: Presence of LGE on CMR indicative of fibrosis is the strongest predictor of worse outcomes.

Question 29

CMR criteria for aiding in diagnosis of LV non compaction?

Answer 29

A maximum end-diastolic noncompacted to compacted myocardial thickness ratio of >2.3

A trabeculated LV mass >20 percent of global LV mass

Question 30

Management of LV non compaction patients?

Answer 30

Exercise: (limit in patients with systolic dysfunction, arrhythmia, syncope history)

Test family members for genetics

Heart failure: Treat per guidelines

Anticoagulation: If indication present (atrial fibrillation, thrombus) anticoagulate. Also LVNC with LVEF <40 percent and/or atrial fibrillation who do not otherwise have an indication for anticoagulation.

ICD: Secondary prevention in those with sustained Vtach or SCD. Primary prevention in those with LVEF ≤35 percent and New York Heart Association (NYHA) class II to III HF

Question 31

Causes of HFpEF?

Answer 31

Coronary artery disease (MC)

Infiltrative/restrictive cardiomyopathy

Valvular heart disease

Percardial constriction

Question 32

In patients with HFpEF who present with worsening symptoms or decompensation?

Answer 32

We must assess for ACS/CAD. If patient has elevated troponin, EKG changes we should use TIMI score to guide whether patient needs invasive strategy (cath) vs ischemia guided approach (stress).

Note: Coronary artery disease is very common in patients with HFpEF and therefore both stable and ACS patients with preserved EF should get an ischemia evaluation.

Question 33

Role of ECG in heart failure?

Answer 33

ECG is a valuable tool in patients with heart failure

• Presence of Q waves can indicate underlying ischemia
• Presence of SVT/Atrial fibrillation/Atrial flutter can indicate tachycardia induced myopathy
• Low voltage QRS and pseudoinfarct pattern could indicate amyloidosis

Question 34

Clinical features of TTR amyloidosis?

Answer 34

Common in elderly black patients

Hypotension, dizziness, autonomic symptoms

Peripheral edema, volume overload, heart failure

Carpel tunnel syndrome

Question 35

Features of hereditary hemochromatosis?

Answer 35

Arthralgias

Diabetes

Hyperpigmentation

Elevated LFTs, cirrhosis

Cardiac: Restrictive or dilated cardiomyopathies. Low voltage QRS, atrial fibrillation

Question 36

Diagnosis of cardiac hemochromatosis?

Answer 36

CMR is the test of choice!

There are decreased myocardial signals on T2 weighted images

Note: Endomyocardial biopsy is not used for diagnosis given accuracy of CMR for hemochromatosis.

Question 37

Treatment for hereditary hemochromatosis?

Answer 37

Iron chelation therapy

Phlebotomy

Question 38

ACE-I, ARBs and Bradykinin?

Answer 38

ACE-I inhibit kinase which breaks down bradykinin. Therefore, low kinase leads to higher levels of bradykinin and cough. ARBs do not inhibit kinase and therefore, bradykinin levels decrease.

ACE-I also increase the levels of substance P

Question 39

Entresto and BNP levels?

Answer 39

Sacubitril is a neprilysin inhibitor. Neprilysin degrades naturitic peptides and so BNP levels increase with Sacubitril use.

Question 40

Entresto vs Ace/ARBs?

Answer 40

Entresto is first line therapy for patient with HFrEF and symptoms. For patients who cannot take Entresto, we use ACEI as second line therapy.

Question 41

Features of fulminant myocarditis?

Answer 41

Young patient

Hypotension, cool and pale skin

Bibasalar crackles, pulmonary and peripheral edema

ST elevations, elevated troponin, low voltage QRS due to edema in myocardium

Reduced EF

Question 42

Causes of fulminant mycocarditis?

Answer 42

Conditions associated with fulminant myocarditis include lymphocytic myocarditis (autoimmune, toxic, or infectious), giant cell myocarditis, acute necrotizing eosinophilic myocarditis, immune checkpoint inhibitor myocarditis, and, more rarely, cardiac sarcoidosis.

Question 43

Indications for endomyocardial biopsy?

Answer 43

Endomyocardial biopsy (EMB) is recommended if there is:

New onset of unexplained heart failure (HF) of <2 weeks’ duration associated with hemodynamic compromise;

Unexplained new-onset HF between 2 weeks’ and 3 months’ duration that is associated with a dilated left ventricle and new bradyarrhythmia, new ventricular arrhythmias, or a failure to respond to standard care within 1-2 weeks of diagnosis; and

HF that is rapidly progressing when there is a high suspicion that the cause can only be confirmed by histology.

Note: EMB is important to rule out giant cell and eosinophillic myocarditis both of which can respond to immunosuppression

Question 44

Differential diagnosis of acute heart failure in young patients?

Answer 44

The differential diagnosis of acute HF in young people includes cardiac sarcoidosis, myocarditis (due to giant cell, eosinophilic, or lymphocytic myocarditis), coronary artery disease (possibly with a spontaneous coronary artery dissection), peripartum cardiomyopathy, and takotsubo cardiomyopathy.

Question 45

Pressure volume loop curve?

Answer 45

Question 46

Contractility in pressure volume curve?

Answer 46

The end-systolic pressure–volume relationship (ESPVR) describes the maximum possible tension (pressure) than can be generated for any given end-diastolic volume (EDV). Contractility is described by the slope of this line.

Question 47

Cardiovascular effects of checkpoint inhibitors?

Answer 47

Cardiovascular adverse events with ICIs may range from myocarditis and resultant heart failure to potentially serious arrhythmias. Although myocarditis may be completely reversible, mortality is up to 50% in fulminant cases. Symptoms range from dyspnea to cardiogenic shock. Troponin and B-type natriuretic peptide may be elevated. ECG may show conduction abnormalities and echocardiography may show reduced LVEF.

Endomyocardial biopsy reveals interstitial inflammation with lymphocytes

Question 48

Risk factors for peripartum cardiomyopathy?

Answer 48

African american race

Gestation hypertension

Advanced maternal age

Multiparity

Preclampsia

Question 49

Symptoms of peripartum cardiomyopathy?

Answer 49

Fatigue

Dyspnea

Hypoxemia

Pulmonary edema, rales

Wheezing

Question 50

Diagnosis of peripartum cardiomyopathy?

Answer 50

Usually diagnosed in the last month of pregnancy up to 5 months after pregnancy

LVEF < 45% without focal wall motion abnormalities

Note: Biventricular decreased systolic function is also common

Question 51

Features of acute transplant rejection?

Answer 51

Shortness of breath, other symptoms of heart failure

MC early echocardiographic finding is diastolic dysfunction

Arrhythmias such as PACs

Question 52

Diagnosis of acute cellular rejection?

Answer 52

Best test is endomyocardial biopsy

Note: Coronay allograft vasculopathy usually occurs after 1 year

Question 53

Benefits of CRT in heart failure patients?

Answer 53

RT has been shown to improve ventricular contractile function, reverse ventricular remodeling, improve LVEF, and reduce secondary mitral regurgitation. It can also improve blood pressure, allowing titration of neurohormonal antagonists that may have additional benefits.

Question 54

Indications for CRT placement?

Answer 54

Cardiac resynchronization therapy (CRT) is indicated for patients who have an LVEF ≤35%, sinus rhythm, left bundle branch block (LBBB) with a QRS duration of ≥150 msec, and New York Heart Association (NYHA) class II or III symptoms or ambulatory class IV symptoms on guideline-directed medical therapy

Question 55

Types of chemotherapy related cardiac dysfunction [CRCD]:

Answer 55

Type I CRCD is well studied and understood. It is most commonly associated with anthracyclines (i.e., doxorubicin) and generally results in myocyte destruction and clinical heart failure. This is at least in part a result of iron-based oxygen free radicals that pose an oxidative stress on the cardiac myocytes, ultimately leading to myocyte necrosis.

Type II dysfunction, as seen with trastuzumab (monoclonal antibody against the human epidermal growth factor receptor 2 molecule), is often associated with loss of myocardial contractility but is less likely to be associated with myocyte death. As a result, it is much more likely to be reversible when compared with type I CRCD. Trastuzumab-related cardiac dysfunction has been shown to respond to drug cessation and usual medical therapies for heart failure with reduced ejection fraction (HFrEF; i.e., angiotensin-converting enzyme inhibitors, beta-blockers) in contrast to type I CRCD, which tends to be permanent

Question 56

Mortality of HFpEF vs HFrEF?

Answer 56

Multiple studies have shown that mortality is similar for both types

Question 57

Evaluation of new onset heart failure?

Answer 57

Coronary angiography should be considered in the evaluation of new onset heart failure to rule of ischemic etiology. This is especially true in older patients (low concern for myocarditis) who have risk factors for CAD.

Patients with risk factors and high pre-test probability should undergo coronary angiography. (Stress testing is appropriate for those without risk factors and not high pre-test probability)

Question 58

BNP and HFpEF?

Answer 58

Normal BNP values (≤100 pg/mL) may be seen in a large percentage of patients with heart failure with preserved ejection fraction (HFpEF). Thus, a normal BNP cannot be used to rule out heart failure (HF) in patients with normal LVEF.

Note: In a single-center cohort study of patients with HFpEF confirmed by elevated pulmonary capillary wedge pressure on right heart catheterization, about 30% of symptomatic outpatients had normal BNP despite high prevalence of HF symptoms and signs, including exertional dyspnea, orthopnea, elevated jugular venous pressure, and lower extremity edema.

Question 59

Causes of low BNP?

Answer 59

Female sex

Young age

Obesity

Question 60

Patient presents with diaphoresis, hypotension, cool extremities and pulmonary edema has the following M-mode tracing

Answer 60

The M-mode tracing of the mitral valve shows fluttering of the anterior leaflet of the mitral valve due to the turbulent jet of aortic insufficiency (the echocardiographic correlate of the Austin-Flint murmur). Preclosure of the mitral valve is another sign of rapidly rising left ventricular end-diastolic pressure, and the echocardiographic M-mode may show that the mitral valve is closed prior to onset of the QRS.

Question 61

Treatment of acute AR in hemodynamically unstable patients?

Answer 61

The treatment of acute aortic regurgitation is surgical replacement of the valve. Hemodynamic support with extracorporeal membrane oxygenation and percutaneous left ventricular assist devices may be required, but immediate surgery is the best option.

Question 62

Intra-aortic balloon pump and acute AR?

Answer 62

Intra-aortic balloon pump is contraindicated in aortic regurgitation because it inflates in diastole and worsens the regurgitation.

Question 63

IABP placement ?

Answer 63

IABP is a balloon inflated and deflated with helium.

It is introduced via femoral approach and sits in the proximal descending arota (1-2 mm below the left subclavian and above the renal arteries)

Once placed we require heparin anticoagulation

Question 64

IABP mechanism of action?

Answer 64

Balloon inflates during diastole > Increased diastolic pressure and retrograde flow > Since coronary arteries perfuse in diastole this increases coronary perfusion and also systemic BP

Balloon deflates during isovolumeric contraction > As the balloon deflates before the opening of the aortic valve, it creates a suction force which then decreased afterload and less pressure during isovolumetric contraction to open the aortic valve > decreased afterload and workload of the heart > increased cardiac output

Question 65

Contrindications to IABP?

Answer 65

Aortic regurgitation

Aortic dissection/aneursym

Severe PAD

Sepsis

Coagulopathy & contraindication to anticoagulation

Question 66

Indications of IABP use?

Answer 66

1. Failure to come off bypass/wean off bypass
2. Cardiogenic shock from severe acute MR/VSD awaiting surgery
3. High risk PCI
4. Cardiogenic shock/acute systolic heart failure

Question 67

Physical exam AS vs HOCM?

Answer 67

The degree of obstruction in oHCM, and therefore the intensity of the murmur, is dependent on preload. When preload is decreased (as with Valsalva maneuver), there is less volume flowing through the narrowed outflow tract, and therefore more obstruction, leading to an increase in murmur intensity.

Question 68

Features of acute severe MR?

Answer 68

Hypotension > cool/clammy/pale

Pulmonary congestion > hypoxia, SOB

No or faint murmur due to equalization of LA and LV pressures

Question 69

EF and LVOT VTI in acute severe MR?

Answer 69

EF is usually = SV/EDV x 100

SV = EDV - ESV (ESV decreased due to retrograde flow and EDV increases due to more blood moving in from higher preload, so both cause increased SV)

In acute severe MR, there is increased preload and therefore, increased SV which causes high EF and hyperdynamic precordium

However, LVOT VTI is decreased due to less forward flow

Question 70

Role of ARNi in HFrEF?

Answer 70

In patients with chronic, symptomatic, New York Heart Association (NYHA) class II or III HFrEF who tolerate an angiotensin-converting enzyme inhibitor or angiotensin-receptor blocker, replacement by an angiotensin receptor–neprilysin inhibitor (ARNI) is recommended to further reduce morbidity and mortality.

Question 71

Ivabradine indication in HFrEF?

Answer 71

Ivabradine can be beneficial to reduce heart failure hospitalization for patients with symptomatic (NYHA class II-III) stable chronic HFrEF (LVEF ≤35%) who are receiving guideline-directed medical therapy, including a beta-blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of ≥70 bpm at rest (class IIa indication).

Question 72

Role of ultrafiltration for fluid removal in HF patients?

Answer 72

Plasma ultrafiltration for fluid removal in patients with heart failure was associated with more adverse events than diuretic therapy in the AVOID-HF (Aquapheresis versus Intravenous Diuretics and Hospitalization for Heart Failure) and CARRESS-HF (Cardiorenal Rescue Study in Acute Decompensated Heart Failure) trials.

Question 73

Chemotherapy induced cardiomyopathy, monitoring?

Answer 73

CIMP occurs in 8% of patients who received an anthracycline with cyclophosphamide, but increases to 27% with the addition of trastuzumab. Patients will often develop asymptomatic LV dysfunction prior to developing symptomatic signs of heart failure. Unlike anthracyclines, CIMP due to trastuzumab is not related to a cumulative dose and does not appear to cause myocyte death. LV dysfunction can be reversible with treatment discontinuation, including the ability to rechallenge patients after recovery.

Echocardiography to assess LVEF is mandatory to establish a baseline for serial monitoring of cardiac function when using a chemotherapeutic agent known to be associated with LV dysfunction. It is important to obtain precise measurements of LVEF using the biplane method of discs with the use of ultrasonic contrast to aid in endocardial border definition and volume calculations. Three-dimensional echocardiography may also be valuable because it is considered the most accurate LVEF measurement by echocardiography. CIMP is usually defined as a reduction in LVEF of ≥10% in asymptomatic patients or ≥5% in symptomatic patients.

Cardiac biomarkers (troponin and B-type natriuretic peptides [BNP]) can be used to monitor for the development of cardiac dysfunction. Reduction in left ventricular ejection fraction (LVEF) can be a late phenomenon in chemotherapy-induced cardiomyopathy (CIMP), and troponin and BNP may provide incremental value in identifying patients at a higher risk for developing CIMP. This may be particularly useful for patients receiving trastuzumab, as left ventricular (LV) dysfunction is often asymptomatic.

Question 74

Treatment of atrial fibrillation in heart failure patients that have failed rate control strategy?

Answer 74

If a chronic heart failure patient has atrial fibrillation with RVR and treated with cardioversion with restoration to NSR, we need a rhythm control strategy.

In patients with structural heart disease such as heart failure with reduced ejection fraction we use amiodarone or dofelitide

Question 75

Cinical features of amyloidosis?

Answer 75

Heart failure (dyspnea, edema)

Peripheral neuropathy

Carpel tunnel syndrome

Lumbar spinal stenosis

Self-curing hypertension (hypertension not requiring pharm treatment)

EKG shows discordance between electrocardiogram voltage and echocardiographic wall thickness BUT IS PRESENT IN MINORITY OF PATIENTS

Question 76

Diagnosis of amyloidosis?

Answer 76

Nuclear scanning with technetium-labeled bone-avid tracers such as technetium-99m (Tc-99m) pyrophosphate (PYP; is specific for ATTR cardiac amyloidosis as a noninvasive alternative to myocardial biopsy.

Serum kappa and lambda light chain (AL) measurement and serum and urine protein immunofixation have supplanted serum protein electrophoresis for screening for AL amyloid. In cases of suspected cardiac amyloid with evidence of a monoclonal protein, consultation with hematology and a bone marrow biopsy may be helpful. Bone marrow biopsy is not indicated for ATTR amyloid.

Question 77

Iron therapy in heart failure patients?

Answer 77

IV iron therapy should be used when there is New York Heart Association (NYHA) functional class II or III heart failure and either one of the following criteria are met: 1) the ferritin level is <100 ng/mL; or 2) the ferritin level is between 100-299 ng/mL and the iron saturation is <20%. Treatment is recommended even if the patient has no anemia

Question 78

Oral iron & EPO therapy in heart failure patients?

Answer 78

IRON-5 (Short Term Oral Iron Supplementation in Systolic Heart Failure Patients Suffering From Iron Deficiency Anemia) and IRONOUT-HF (Oral Iron Repletion Effects on Oxygen Uptake in Heart Failure), were both negative for any clinical improvement or surrogate endpoint improvement with oral iron.

Studies using erythropoietin suggest harm, and its use is now a Class III recommendation in the 2017 ACC/AHA/HFSA focused update. In the RED-HF (Reduction in Events by Darbepoetin Alfa in Heart Failure) trial, a randomized double-blind study of 2,278 patients, there was no improvement in the primary endpoints of death or recurrent hospitalization, and there was an increase in both thromboembolic events and ischemic stroke

Question 79

Imaging features of pulmonary and cardiac sarcoidosis?

Answer 79

Pulmonary involvement as suggested by the chest X-ray with bilateral perihilar and right paratracheal lymphadenopathy (“lambda sign”)

Restrictive cardiomyopathy, conduction abnormalities, heart failure symptoms

Question 80

Diagnosis of cardiac sarcoidosis?

Answer 80

Echocardiography reveals thinning and akinesis of the basal interventricular septum.

BUT CMR or FDG-PET required for diagnosis

Cardiac magnetic resonance imaging, which usually shows midmyocardial and epicardial late gadolinium enhancement, particularly in the basal septum and basal lateral wall; T2 imaging can also detect active inflammation in some cases. Positron emission tomography with 18F-fluorodeoxyglucose (FDG-PET) can also confirm active inflammation in a pattern suggestive of sarcoid.

Question 81

Prophylactic therapy to prevent chemotherapy induced cardiomyopathy?

Answer 81

Cancer therapies including anthracyclines, human epidermal growth factor receptor-2 (HER2) antagonists, immune checkpoint inhibitors, and select tyrosine kinase inhibitors may be associated with the development of left ventricular (LV) dysfunction and have emerged as important etiologies of cardiomyopathy. Regular surveillance of LV function is important during treatment with cardiotoxic agents. LV dysfunction may be an indication for temporary or permanent interruption of cancer therapy.

A European Society of Cardiology (ESC) position paper proposes a prophylactic regimen including angiotensin-converting enzyme inhibitors/angiotensin-receptor blockers (ACEIs/ARBs) and beta-blockers if there are multiple cardiac risk factors.

The 2013 American College of Cardiology Foundation/American Heart Association (ACCF/AHA) Guideline for the Management of Patients With Heart Failure recommends the initiation of both beta-blockers and ACEI/ARB therapy once evidence of left ventricular dysfunction occurs.

The American Society of Echocardiography (ASE) defines chemotherapy cardiotoxicity as a drop in the LVEF of >10 percentage points or to a value of <53%.