Episodes Archives - Cardionerds

The following question refers to Section 8.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by University of Southern California cardiology fellow and CardioNerds FIT Trialist Dr. Michael Francke, and then by expert faculty Dr. Prateeti Khazanie.

Dr. Khazanie is an associate professor and advanced heart failure and transplant Cardiologist at the University of Colorado. Dr. Khazanie is an author on the 2022 ACC/AHA/HFSA HF Guidelines, the 2021 HFSA Universal Definition of Heart Failure, and multiple scientific statements.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

You are taking care of a 34-year-old man with chronic systolic heart failure from NICM with LVEF 20% s/p CRT-D. The patient was admitted 1 week prior with acute decompensated heart failure. Despite intravenous diuretics the patient developed acute kidney injury, and ultimately placed on intravenous inotropes on which he now seems dependent. He has been following up with an advanced heart failure specialist as an outpatient and has been undergoing evaluation for heart transplantation, which was subsequently completed in the hospital.

His exam is notable for an elevated JVP, a III/VI holosystolic murmur, and warm extremities with bilateral 1+ edema. His most recent TTE shows LVEF 20%, moderate MR, moderate-severe TR and estimated RVSP 34 mmHg. His most recent laboratory data shows Na 131 mmol/L, Cr 1.2 mg/dL, and lactate 1.6 mmol/L. Pulmonary artery catheter shows RA 7 mmHg, PA 36/15 mmHg, PCWP 12 mmHg, CI 2.4 L/min/m2 and SVR 1150 dynes*sec/cm5.

The patient was presented at transplant selection committee and approved for listing for orthotopic heart transplant. What is the most appropriate next step in the management of this patient?

A

Refer patient for transcatheter edge-to-edge repair for MR

B

Continue IV inotropes as a bridge-to-transplant

C

Refer patient for tricuspid valve replacement

D

Initiate 1.5L fluid restriction

Explanation

The correct answer is B – continue IV inotropes as a bridge-to-transplant.

Positive inotropic agents may improve hemodynamic status, but have not been shown to improve survival in patients with HF. These agents may help HF patients who are refractory to other therapies and are suffering consequences from end-organ-hypoperfusion.

Our patient is admitted with worsening advanced heart failure requiring intravenous inotropic support. He has been appropriately evaluated and approved for heart transplant. He has demonstrated the requirement of continuous inotropic support to maintain perfusion. In patients such as this with advanced (stage D) HF refractory to GDMT and device therapy who are eligible for and awaiting MCS or cardiac transplantation, continuous intravenous inotropic support is reasonable as “bridge therapy” (Class 2a, LOE B-NR).

Continuous IV inotropes also have a Class 2b indication (LOE B-NR) in select patients with stage D HF despite optimal GDMT and device therapy who are ineligible for either MCS or cardiac transplantation, as palliative therapy for symptom control and improvement in functional status.

Conversely, long-term use of either continuous or intermittent intravenous inotropic agents, for reasons other than palliative care or as a bridge to advanced therapies, is potentially harmful (Class 3: Harm, LOE B-R).

As of yet there is lack of clear evidence suggesting the benefit of one inotrope over another. To minimize adverse effects, the lowest possible dose of inotropes should be used, although the potential for development of tachyphylaxis should be acknowledged and the choice/dose of agent may need to be changed over time for longer periods of use. In addition, the ongoing need for inotropic support and the possibility of discontinuation should be regularly assessed.

Although guidelines give a Class 2a recommendation for transcatheter edge-to-edge MV repair in patients with reduced EF and severe MR with persistent symptoms despite GDMT, this patient’s MR was graded as moderate on his most recent TTE and as such, he would not be an appropriate candidate for TEER.

Although guidelines give a Class 1 recommendation for multidisciplinary management of patients with HF and VHD, as well as referral for consideration of intervention in patients with refractory TR, there are currently no guideline recommendations supporting surgical TVR in advanced HF patients with TR.

Although fluid restriction has been associated with modest improvements in hyponatremia in patients with advanced HF, the clinical benefits of this therapy remain uncertain and as such was given a Class 2b recommendation in the clinical guidelines.

Main Takeaway

Continuous intravenous inotropic support can be considered in patients with advanced heart failure refractory to GDMT who are awaiting durable MCS or heart transplant as “bridge therapy” (Class 2a) or for palliative therapy in patients with advanced HF who are ineligible for MCS/transplant (Class 2b), but is potentially harmful for long-term use for reasons beyond palliation or bridge to advanced therapies (class 3 recommendation).

Guideline Loc.

Section 8.3

Table 20

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The CardioNerds and Pulm PEEPs have joined forces to co-produce this important episode, delving into the management of decompensated right ventricular failure in pulmonary arterial hypertension. Joining us for this informative discussion are Pulm PEEPs co-founders, Dr. David Furfaro and Dr. Kristina Montemayor, along with Dr. Leonid Mirson (Internal Medicine Resident at Johns Hopkins Osler Medical Residency and Associate Editor of Pulm PEEPs), Dr. Bavya Varma (Internal Medicine Resident at Johns Hopkins, rising Cardiology Fellow at NYU, and CardioNerds Academy graduate), Dr. Mardi Gomberg-Maitland (Medical Director of the Pulmonary Hypertension Program at George Washington Hospital), and Dr. Rachel Damico (Pulmonologist and Associate Professor of Medicine at Johns Hopkins Hospital). Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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A 21-year-old woman with a past medical history notable for congenital heart disease (primum ASD and sinus venosus with multiple surgeries) complicated by severe PAH on home oxygen, sildenafil, ambrisentan, and subcutaneous treprostinil is presenting with palpitations, chest pain, and syncope. She presented as a transfer from an outside ED where she arrived in an unknown tachyarrhythmia and had undergone DCCV due to tachycardia into the 200s and hypotension. On arrival at our hospital, she denied SOB but did endorse nausea, leg swelling, and poor medication adherence. Her initial vitals were notable for a BP of 80/50, HR 110, RR 25, and saturating 91% on 5L O2.  On exam, she was uncomfortable appearing but mentating well. She had cool extremities with 1-2+ LE edema. Her JVP was 15cm H2O. She has an RV Heave and 2/6 systolic murmur. Her lungs were clear bilaterally. Her labs were notable for Cr 2.0, an anion gap metabolic acidosis (HCO3 = 11), elevated lactate (4.1), elevated troponin to 14,  and a pro-BNP of ~5000.  Her CBC was unremarkable. Her EKG demonstrated 2:1 atrial flutter at a rate of 130.

Diagnosing RV failure in patients with PH:

RV dysfunction and RV failure are two separate entities. RV dysfunction can be measured on echocardiography, but RV failure can be thought of as a clinical syndrome where there is evidence of RV dysfunction and elevated right sided filling pressures.

RV failure is a spectrum and can present with a range of manifestations from evidence of R sided volume overload and markers of organ dysfunction, all the way to frank cardiogenic shock. Most patients with RV failure are not in overt shock.

One of the first signs of impending shock in patients with RV failure is the development of new or worsening hypoxemia. Patients with decompensated RV failure approaching shock often do not present with symptoms classic for LV low flow state. Instead, hypoxia 2/2 VQ mismatching may be the first sign and they can be otherwise well appearing. Particularly because patients with PH tend to be younger, they can often appear compensated until they rapidly decompensate.

Causes of decompensation for patients with RV dysfunction and PH:

Iatrogenesis (inadvertent cessation of pulmonary vasodilators by providers, surgery if providers are not familiar with risks of anesthesia), non-adherence to pulmonary vasodilators (either due to affordability issues or other reasons), infections, arrhythmias (particularly atrial arrhythmias), and progression of underlying disease.

Patients with atrial arrhythmias (atrial flutter or atrial fibrillation) and pulmonary hypertension do not tolerate the loss of the atrial kick well as it contributes a significant amount to their RV filling and impacts their cardiac output. It is often difficult to determine if the atrial arrhythmia is a cause or effect of decompensated RV failure, but its presence is associated with a worse prognosis. Efforts should be made to re-establish normal sinus rhythm in patients with decompensated RV failure and atrial arrhythmias. 

A patient’s home PH medications should never be stopped for any reason upon admission unless on the basis of recommendations by a pulmonary hypertension provider as this is often a cause of decompensation inpatient

Interpreting findings on echocardiogram: 

Echo is a useful screening tool. When interpreting evidence of RV dysfunction, it is important to look at the global picture and not just one measurement.

RVSP, though commonly reported, may be of limited value when evaluating for decompensation. It’s a function of blood pressure, heart rate, and cardiac output. RVSP may even decline as shock worsens.

TAPSE is useful as a marker of RV dysfunction if it is reduced, but it is difficult to follow over time and only gives information about cardiac function around the annulus; it may be normal even when apical RV function is depressed. RV fractional area of change may be more useful for global RV function. It is important to pay attention to the RV size overall, the degree of TR, and the presence of effusion all of which are associated with RV dysfunction.

­Tips regarding the interpretation of invasive hemodynamics:

Cardiac output by thermodilution is the standard way to calculate PVR. Despite the degree of TR that is typically present, it is thought to be a better representation of cardiac output than the estimated Fick calculation.  

Our experts agree that routine monitoring of invasive hemodynamics for acute decompensated RV failure is likely not helpful and has significant risks. A good external volume exam or CVP off a central venous catheter + central venous saturation will likely be all you need to navigate a patient with shock secondary to RV failure. A right heart catheterization (should be only done under fluoroscopy for patients with large RVs) may be helpful if the etiology of shock is unclear. 

Management of decompensated RV failure in patients with pulmonary hypertension

Managing preload is of utmost importance, perhaps the most important tenant of management of decompensated RV failure.  The overwhelming majority of patients with PH and decompensation are volume overloaded, it is exceptionally rare that someone would be dry. Furthermore, the myth that the RV is “preload responsive” is only true in the setting of acute RV injury (eg. RV infarction) and not so in patients with acute on chronic RV dysfunction. It is important to optimize preload in someone in decompensated RV failure and it is safe to do this more rapidly than traditionally taught. Exact goals varied between our experts, but anywhere from 2-4L net negative per day is reasonable especially if the patient is hemodynamically tolerating the fluid removal. If the patient is not responding to diuretics, hemodialysis with ultrafiltration may be necessary to optimize the patient.

Afterload is the next tenant of management. Optimizing the following parameters will reduce the patient’s pulmonary vascular resistance and reduce afterload to the right ventricle.

— Avoiding hypoxic pulmonary vasoconstriction, liberalize the patient’s O2 goal 

— Avoid permissive hypercapnia and academia in this patient population

— Do not withhold a patient’s pulmonary vasodilator until discussion with the PH team. If stopped inadvertently, restart this medication immediately. For patients with malfunctioning pumps, there is a phone number on the back that you can call for rapid troubleshooting. Sildanefil can be given IV if a patient is NPO. 

— Inhaled nitric oxide can improve oxygenation and reduce afterload  

— Intubation and mechanical ventilation greatly increase PVR and are poorly tolerated. Exacting care must be taken to titrate PEEP and tidal volume, and avoid intubation when possible.

— Starting a new systemic pulmonary vasodilator in decompensated RV failure may be considered under close guidance from the pulmonary hypertension team

Management of atrial arrhythmias:

As above, patients with severe pulmonary hypertension do not tolerate loss of sinus rhythm well. If they are decompensated, every effort should be made to re-establish normal sinus rhythm. 

Management of RV perfusion:

Unlike the LV, the RV is perfused during BOTH systole and diastole. Maintaining effective coronary perfusion to the RV is essential in RV failure. For this reason, the systemic systolic pressure (as well as the mean arterial pressure) should be kept high enough to ensure that the RV is able to perfuse. There is no great body of evidence as to which pressor works best. Norepinephrine, vasopressin, and even phenylephrine are all reasonable choices to maintain appropriate perfusing blood pressure. 

Inotropy:

Patients in shock and RV failure do not always require inotropes, but if they do it’s often a sign of a grim prognosis. Either dobutamine or milrinone is reasonable, but the negative effects of these drugs (arrhythmias, tachycardia, and systemic hypotension) may limit their uses. 

Mechanical circulatory support:

Limited options are available. Balloon pumps and Impella devices have limited roles except in expert centers, and ECMO remains the standard of care. ECMO (either V-V or V-A) may have utility as a bridge to recovery if a reversible cause is identified, or a bridge to transplant if the patient is on the transplant list. 

Goals of care:

The prognosis of a patient admitted to the ICU with acute on chronic decompensated RV failure is guarded, with very high mortality rates even if not in shock

It is important for the patient’s longitudinal pulmonary hypertension provider to discuss the prognosis and goals of care ahead of time but this is not always possible. If they are admitted, early discussions regarding code status and prognosis are essential. It may be helpful to bring in the patient’s longitudinal pulmonary hypertension doctor into these discussions if possible. 

The following question refers to Section 4.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Dr. Maryam Barkhordarian, answered first by medicine resident CardioNerds Academy House Chief Dr. Ahmed Ghoneem, and then by expert faculty Dr. Kim Williams.

Dr. Williams is Chief of the Division of Cardiology and is Professor of Medicine and Cardiology at Rush University Medical Center. He has served as President of ASNC, Chairman of the Board of the Association of Black Cardiologists (ABC, 2008-2010), and President of the American College of Cardiology (ACC, 2015-2016).

The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Mr. O is a 48-year-old man with a past medical history significant for obesity (BMI is 42kg/m2), hypertension, type 2 diabetes mellitus, and hypercholesterolemia. His calculated ASCVD risk score today is 18.8%. You counsel him on the importance of weight loss in the context of CVD risk reduction. Which of the following weight loss recommendations is appropriate?

A

Maintaining a weight loss of at least 25% from baseline is required to influence blood pressure, cholesterol, and glycemic control. 

B

Hypocaloric diets lead to short term weight loss, but a healthy diet should be maintained over time to reduce CVD risk.

C

Liraglutide can be used to induce weight loss, as an alternative to diet and exercise.

D

Bariatric surgery is effective for weight loss but has no ASCVD risk reduction benefit.

Explanation

The correct answer is B. Energy restriction is the cornerstone of management of obesity. All the different types of hypocaloric diets achieve similar short-term weight loss, but these effects tend to diminish by 12 months. It is a class I recommendation to maintain a healthy diet over time to achieve CVD risk reduction. The Mediterranean diet is an example of a diet that can have persistent CV benefit beyond the 12 months.

Choice A is incorrect because maintaining even a moderate weight loss of 5 – 10% from baseline has favorable effects on risk factors including blood pressure, cholesterol, and glycemic control, as well as on premature all-cause mortality.

Choice C is incorrect because medications approved as aids to weight loss (such as liraglutide, orlistat and naltrexone/bupropion) may be used in addition to lifestyle measures to achieve weight loss and maintenance; they are not alternatives to a healthy lifestyle. Meta-analysis of medication-assisted weight loss found favorable effects on BP, glycemic control, and ASCVD mortality.

Choice D is incorrect because patients undergoing bariatric surgery had over 50% lower risks of total ASCVD and cancer mortality compared with people of similar weight who did not have surgery. Bariatric surgery should be considered for obese high-risk individuals when lifestyle change does not result in maintained weight loss (Class IIa). The ACC/AHA guidelines focused primarily on lifestyle interventions for obesity and had no specific recommendations for bariatric surgery or medication-assisted weight loss.

Main Takeaway

Weight reduction (even as low as 5-10% from baseline) and long-term maintenance of a healthy diet are recommended to improve the CVD risk profile of overweight and obese people. Medication and/or bariatric surgery may have a useful adjunctive role in some patients.

Guideline Loc.

Section 4.3.3

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The following question refers to Section 7.6 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by premedical student and CardioNerds Intern Pacey Wetstein, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Chief Dr. Teodora Donisan, and then by expert faculty Dr. Nancy Sweitzer.

Dr. Sweitzer is Professor of Medicine, Vice Chair of Clinical Research for the Department of Medicine, and Director of Clinical Research for the Division of Cardiology at Washington University School of Medicine. She is the editor-in-chief of Circulation: Heart Failure. Dr. Sweitzer is a faculty mentor for this Decipher the HF Guidelines series.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Ms. Smith is a 56-year-old woman following up in the cardiology clinic for a history of heart failure with reduced ejection fraction. Two years ago, she was diagnosed with non-ischemic cardiomyopathy with a left ventricular ejection fraction (LVEF) of 30%. Over time, she was initiated and optimized on guideline directed medical therapy. She is currently on Carvedilol 12.5 mg BID, Sacubitril/Valsartan 49/51 mg BID, Spironolactone 25 mg daily, Empagliflozin 10 mg daily, and Furosemide PRN for weight gain.

On today’s visit, her BP is 110/80 mmHg, and her HR is 67 bpm. Labs show a creatinine of 0.9 mg/dL, potassium of 5.1 mEq/L, NT-proBNP of 150 ng/L, and a HbA1c of 5.8%. Follow up transthoracic echocardiogram showed an improvement in LVEF to 55%. What are the most appropriate therapy recommendations for Ms. Smith?

A

Discontinue spironolactone

B

Discontinue empagliflozin

C

Decrease the dose of carvedilol

D

Continue current therapy

The correct answer is D – continue current therapy.

The patient described above was initially diagnosed with HFrEF and experienced significant symptomatic improvement with GDMT, so she now has heart failure with improved ejection fraction (HFimpEF). In patients with HFimpEF after treatment, GDMT should be continued to prevent relapse of HF and LV dysfunction, even in patients who may become asymptomatic (Class 1, LOE B-R). Although symptoms, functional capacity, LVEF and reverse remodeling can improve with GDMT, structural abnormalities of the LV and its function do not fully normalize, causing symptoms and biomarker changes to persist or recur if treatment is deescalated. Improvements in EF do not always reflect sustained recovery; rather, they signify remission.

Of note, HF relapse can be defined by at least 1 of the following:

o   A drop in the EF by >10% and to < 50%

o   An increase in LVEDV by >10% and to higher than the normal range

o   A 2-fold rise in NT-proBNP concentration and to > 400 ng/L

o   Clinical evidence of HF on examination

Choice A is incorrect as it would be incorrect to discontinue spironolactone. A potassium of 5.1 is still within the acceptable limit in a patient who has been on Spironolactone for two years, and this medication is an important part of GDMT for HFrEF.

Despite the improvement in Hb A1c, empagliflozin should be continued for heart failure with improved ejection fraction, as it is part of routine GDMT of HFrEF even in the absence of diabetes. Choice B is thus incorrect.

Similarly, carvedilol should be continued at the same dose as the patient’s heart rate is within the desired range. Furthermore, all GDMT should be continued in patients with HFimpEF, as emphasized above. Choice C is therefore also incorrect.

In patients with HFimpEF after treatment, GDMT should be continued to prevent relapse of HF and LV dysfunction, even in patients who may become asymptomatic. (Class 1, LOE B-R).

Section 7.6.2

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CardioNerds Co-Founder, Dr. Amit Goyal, along with Series Co-Chairs, Dr. Yoav Karpenshif and Dr. Eunice Dugan, and episode Lead, Dr. Sean Dikdan, had the opportunity to expand their knowledge on the topic of ventricular tachycardia and electrical storm from esteemed faculty expert, Dr. Janice Chyou. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian.

Electrical storm (ES) is a life-threatening arrhythmia syndrome. It is characterized by frequently occurring bouts of unstable cardiac arrythmias. It typically occurs in patients with susceptible substrate, either myocardial scar or a genetic predisposition. The adrenergic input of the sympathetic nervous system can perpetuate arrythmia. In the acute setting, identifying reversible triggers, such as ischemia, electrolyte imbalances, and heart failure, is important. Treatment is complex and varies based on previous treatments received and the presence of intra-cardiac devices. Many options are available to treat ES, including medications, intubation and sedation, procedures and surgeries targeting the autonomic nervous system, and catheter ablation to modulate the myocardial substrate. A multidisciplinary team of cardiologists, intensivists, electrophysiologists, surgeons, and more are necessary to manage this complex disease.

The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Pearls • Notes • References • Production Team

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Simple diagram of the classic “triad” of ES (see reference 10).

Treatment algorithm provided by the 2017 AHA/ACC/HRS guidelines (see reference 1).

1. Define electrical storm.

Electrical storm (ES), also called “arrhythmic storm” or “VT storm” refers to a state of cardiac instability associated with 3 or more episodes of VF, sustained VT, or appropriate ICD shocks within 24 hours. Sustained VT refers to 30 seconds of VT or hemodynamically unstable VT requiring termination in < 30 seconds. Incessant VT refers to continued, sustained hemodynamically stable VT that lasts longer than one hour. VT is incessant or recurrent when it recurs promptly despite repeated intervention for termination.1,2

In patients with ICDs for secondary prevention, ES is estimated to occur in 10-28% of patients.3–5 This incidence is much lower in patients who have ICDs implanted for primary prevention in whom the incidence has been estimated as low as 4% at 20 months of follow up.6 ES occurs at similar rates in patients with ischemic or non-ischemic cardiomyopathy.7

ES is associated with a poor prognosis and high cardiovascular mortality. The three-month mortality in patients with an episode of ES has been estimated at up to 18 times higher than in patients without any VT.6 Risk factors for the development of ES include male sex, advanced age, low left ventricular ejection fraction, use of class 1A antiarrhythmic drugs, and the presence of cardiovascular comorbidities.8,9

2. Evaluate the cause of VT storm (e.g., evaluation for ischemia, sarcoidosis , etc)

The classic triad of ES is a trigger, a substrate susceptible to ES, and autonomic input perpetuating the storm.10 Potential triggers are varied and typically include myocardial ischemia, decompensated heart failure, electrolyte abnormalities, hypoxia, drug-related arrhythmogenicity, and thyrotoxicosis.4,11 A clear trigger is often not found (only 13% of the time by some estimates).12 Searching for a trigger should not delay management decisions in the acute setting.

Structural heart disease unrelated to ischemia such as congenital heart disease and infiltrative cardiomyopathies can serve as the substrate for ES. Conditions related to genetic causes such as long QT syndrome or catecholaminergic polymorphic VT may be a rare etiology. These conditions represent an electrophysiologic substrate as opposed to a structural substrate.13

3. Choose an initial management strategy for patients with electrical storm in the CCU.

Treatment of ES is complex. The initial steps in management involve resuscitation, pharmacotherapy, device interrogation and reprogramming, and sedation. ACLS should be used in patients with pulseless VT or VF.

Patients with and without cardioverter-defibrillators may be treated differently. Defibrillations from an implanted device accentuate sympathetic tone and may perpetuate further arrhythmia.

Once a patient is stabilized, more advanced therapies involving autonomic modulation or catheter ablation (CA) can be utilized. In the patient with ischemia, emergent revascularization should be pursued. The need for mechanical circulatory support (MCS) should be determined. Inotropes and many vasopressors are sympathetic agonists and may worsen the arrhythmia by accentuating adrenergic tone, and so the benefits of improved hemodynamics need to be weighed against the risk of worsening electrical instability.

Initial pharmacotherapy in ES includes an antiarrhythmic drug and a beta blocker. Typically loading the patient with IV amiodarone and administering a non-selective beta blocker like propranolol is done. This combination has been shown in ES patients to have superior freedom of arrhythmia compared to using metoprolol.14 Propranolol’s superiority may also be due to its ability to cross the blood-brain barrier. Lidocaine has improved efficacy in ischemic VT.15,16 Procainamide has been shown to be useful in patients with hemodynamically stable VT.17

4. Identify predisposing conditions that should be managed to help treat electrical storm such as ischemia and AHF.

Identifying and managing specific triggers is an important initial step in the management of ES. Hypoxia on vital signs or evidence of decompensated HF on exam (with JVD, edema, crackles on auscultation) can implicate volume overload; this can be managed with diuresis.

Ischemic ECG changes on the 12-lead ECG when the patient’s ventricular arrhythmia is broken, can suggest myocardial ischemia. If ischemia is believed to be the trigger, urgent revascularization should be pursued while resuscitation is underway.

Blood work should include screening for electrolyte abnormalities and thyroid disease. Carefully screening the patient’s medication list and checking a digoxin level  (when appropriate) can help detect drug-induced arrhythmia.

Once out of the acute setting, genetic testing may be important in patients without structural disease for determining an etiology. Idiopathic VT, Brugada syndrome, long QT syndrome, short QT syndrome, early repolarization syndrome, catecholaminergic polymorphic VT, arrhythmogenic right ventricular cardiomyopathy, and cardiac sarcoidosis are potential etiologies that may be related to ES.10

5. Recognize when to use general anesthesia to aid in the stabilization of electrical storm and incessant VT.

Intubation and deep sedation are immediate next steps to minimize the sympathetic drive contributing to the arrhythmia. This treatment is very effective at terminating arrythmia and preventing immediate recurrence.18,19 This step is used in the acute setting for ES that persists despite pharmacotherapy. Note that propofol is a negative inotrope with the potential to worsen heart failure in decompensated patients and precipitate shock.

In addition to breaking the sympathetic cycle that drives this pathophysiology, sedation mitigates some of the psychological stress that repeated ICD shocks can cause in patients.20

6. Describe considerations specific to patients with implanted ICDs.

If a patient with an ICD presents with ES, the device should be interrogated. It is important to confirm the shocks are appropriate. Inappropriate shocks can occur in up to 40% of patients with an ICD; causes may include atrial arrythmia, oversensing, and lead fracture.21,22 Inappropriate ICD shocks are associated with a worse outcome.

Overdrive pacing is a possible therapy to prevent ES. If the ES is hemodynamically stable, then the ICD therapies may be disabled manually or with the use of a magnet.

If anti-tachycardia pacing (ATP) treats the ventricular arrythmia effectively, adjusting these settings and increasing the use of ATP can mitigate unnecessary shocks in the future.23

7. Understand the role of catheter ablation in the management of electrical storm.

Research has shown an excellent response of ES to catheter ablation (CA). CA has a class 1 indication in patients with ES due to anti-arrhythmic drug refractory VA in both ischemic and nonischemic cardiomyopathy.2

Treatment of an initial episode of ES with CA has shown a reduction in all-cause mortality compared to other modalities.24 At nearly 1-2 years of follow up, nearly 90% of patients with ES that undergo CA are free from further ES, and roughly two-thirds of these patients are free from any ventricular arrythmia (VA) recurrence.25,26

CA is also relatively safe in this setting, with procedure-related mortality estimated to be less than 1%.27 Rapid transfer to an experienced catheter ablation capable facility is important in all critically ill patients with ES.

8. Consider when it may be appropriate to use mechanical support such as IABP, pVAD and ECMO.

Mechanical circulatory support (MCS) may be necessary to maintain adequate perfusion when the patient is suffering from cardiogenic shock due to unstable arrhythmia.

Patients with high risk for hemodynamic decompensation during CA can be preemptively supported with MCS. This practice has been shown to improve mortality compared to rescue or no MCS. 28,29 The PAAINESD score may be useful in identifying high risk patients. This score assigns numerical values to the following risk factors: pulmonary disease, age over 60 years, general anesthesia, ischemic cardiomyopathy, NYHA class III or IV, LV EF < 25%, VT storm, and diabetes mellitus. 2,28

An intra-aortic balloon pump may be sufficient but requires the patient to have enough adequate forward flow to generate a pulse. Extracorporeal membrane oxygenation (ECMO) has been studied and shows good long-term outcomes.29 Guidelines have a IIa recommendation for hemodynamic support with ECMO or a temporary LVAD during CA in select patients. 2

9. Discuss other strategies such as sympathectomies (stellate ganglion block vs. surgical), stereotactic radio ablation, and transplant for refractory cases.

There are several therapies available to treat ES that specifically target the autonomic nervous system (ANS).30 While sedation is used for this purpose acutely, other interventions seek to mitigate sympathetic activity in the subacute or chronic setting. These include stellate ganglion blockade (SGB), thoracic epidural anesthesia (TEA), cardiac sympathetic denervation (CSD), and renal artery sympathetic denervation (RSD).

Percutaneous SBG involves an injection of anesthetic directly into the stellate ganglia with or without ultrasound guidance. This is a temporizing measure that can be performed in the acute or subacute setting. It has shown complete suppression of VA in 50% of patients for the subsequent 48 hours.31

TEA involves the percutaneous administration of a local anesthetic directly into the thoracic epidural space. This is also a temporary treatment best used as a bridge to definitive treatment, such as CA or surgical denervation. In ES patients with a failed CA TEA can reduce VA up to 80% in most patients.32

CSD is a surgical measure that offers a more permanent solution. It can be useful in refractory ES that has not responded to multiple treatments. CSD has achieved 80% event-free survival up to 2 years.33 Guidelines recommend CSD in ES when beta-blockade, anti-arrhythmic drugs, and CA are deemed ineffective with a class IIb recommendation.1

RSD functions similarly but has the added benefit of being non-surgical and directly reducing catecholamine secretion.

Cardiac transplantation would be indicated in a patient that has unrelenting ES despite these aggressive measures. Patients with MCS and life-threatening arrhythmias qualify as status 1 for OHT.34 Whereas VT/VF without MCS by itself would qualify a patient as status 2.

The following question refers to Sections 3.3 and 3.4 of the 2021 ESC CV Prevention Guidelines.

The question is asked by CardioNerds Academy Intern student Dr. Adriana Mares, answered first by Brigham & Women’s medicine resident & Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Allison Bailey.

Dr. Bailey is an advanced heart failure and transplant cardiologist at Centennial Heart. She is the editor-in-chief of the American College of Cardiology’s Extended Learning (ACCEL) editorial board and was a member of the writing group for the 2018 American Lipid Guidelines. 

The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Ms. Priya Clampsia is a 58-year-old never-smoker with a history of hypertension. Her BMI is 29 kg/m2. She also mentions having pre-eclampsia during her pregnancy many years ago. She describes a predominately sedentary lifestyle and works as a receptionist. You see her in the clinic to discuss routine preventive care. Her most recent lipid panel results were LDL of 101 mg/dL, HDL of 45 mg/dL, and triglycerides of 190 mg/dL. What additional step will provide valuable information regarding her CVD risk profile?

A

Send additional lab workup including C-reactive protein and lipoprotein (a)

B

Measure her waist circumference

C

Assess her work stress

D

Ask her about history of preterm birth

E

B, C, and D

Explanation

The correct answer is E – measuring her waist circumference, assessing her occupational stress, and obtaining history about adverse pregnancy outcomes including preterm birth all add valuable information for CVD risk stratification.

BMI is easily measured and can be used to define categories of body weight. However, body fat stores in visceral tissue carry higher risk than subcutaneous fat and therefore, waist circumference can be a simple way to measure global and abdominal fat. When waist circumference is ≥102 cm in men and ≥88 cm in women, weight reduction is advised. While these WHO thresholds are widely accepted in Europe, it is important to note that different cut-offs may be appropriate in different ethnic groups.

Work stress is important to ascertain as well because there is preliminary evidence of the detrimental impact of worse stress on ASCVD health, independent of conventional risk factors and their treatment. Work stress is determined by job strain (i.e., the combination of high demands and low control at work) and effort-reward imbalance.

Pre-eclampsia is associated with increase in CVD risk by factor of 1.5-2.7 compared with all women. Both preterm (RR 1.6) and still birth (RR 1.5) are also associated with a moderate increase in CVD risk. Taking a thorough pregnancy history is important in determining future cardiovascular risk in women. The ESC guidelines give a Class IIb (LOE B) recommendation that in women with history of premature or stillbirth, periodic screening for hypertension and DM may be considered. Of note, the 2018 ACC/AHA guidelines include preeclampsia and premature menopause (occurring at age <40 years) as risk-enhancing factors for statin therapy but state that the mechanism or cause of preterm birth is often unknown, so it is difficult to include it as a risk-enhancing factor.

Choice A (sending additional lab workup including CRP and LPa) is incorrect. The ESC guidelines do not recommend using routine circulating biomarkers as they do not improve risk prediction and publication bias distorts the evidence (Class III, LOE B). While some biomarkers like lipoprotein (a) are promising, further work is still needed. Conversely, the 2019 ACC/AHA guidelines do include, if measured, elevated high-sensitivity C-reactive protein (≥2mg/L) and elevated Lp(a) (>50mg/dL or >125nmol/L) and elevated apoB (≥130 mg/dL) as risk-enhancing factors. Specific indications for measuring Lp(a) include family history of premature ASCVD and specific indications for measuring apoB include triglyceride ≥200mg/dL.

Main Takeaway

The ESC guidelines do not recommend routine measurement of additional circulating and urine biomarkers as further data and research is still needed in this area; however, there are specific situations in which these biomarkers may be warranted.

Guideline Loc.

Section 3.3.7, 3.3.9, 3.3.10, 3.4.12

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The following question refers to Sections 7.3.2, 7.3.8, and 7.6.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by Palisades Medical Center medicine resident & CardioNerds Intern Dr. Maryam Barkhordarian, answered first by Hopkins Bayview medicine resident & CardioNerds Academy Fellow Dr. Ty Sweeny, and then by expert faculty Dr. Robert Mentz.

Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz is a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Ms. Betty Blocker is a 60-year-old woman with a history of alcohol-related dilated cardiomyopathy who presents for follow up. She has been working hard to improve her health and is glad to report that she has just reached her 5-year sobriety milestone. Her current medications include metoprolol succinate 100mg daily, sacubitril-valsartan 97-103mg BID, spironolactone 25mg daily, and empagliflozin 10mg daily. She is asymptomatic at rest and up to moderate exercise, including chasing her grandchildren around the yard. A recent transthoracic echocardiogram shows recovered LVEF from previously 35% now to 60%. Ms. Blocker does not love taking so many medications and asks about discontinuing her metoprolol. Which of the following is the most appropriate response to Ms. Blocker’s request?

A

Since the patient is asymptomatic, metoprolol can be stopped without risk

B

Stopping metoprolol increases this patient’s risk of worsening cardiomyopathy regardless of current LVEF or symptoms

C

Because the LVEF is now >50%, the patient is now classified as having HFpEF and beta-blockade is no longer indicated; metoprolol can be safely discontinued

D

Metoprolol should be continued, but it is safe to discontinue either ARNi or spironolactone

Explanation

The correct answer is B – stopping metoprolol would increase her risk of worsening cardiomyopathy.

Heart failure tends to be a chronically sympathetic state. The use of beta-blockers (specifically bisoprolol, metoprolol succinate, and carvedilol) targets this excess adrenergic output and has been shown to reduce the risk of death in patients with HFrEF. Beyond their mortality benefit, beta-blockers can improve LVEF, lessen the symptoms of HF, and improve clinical status. Therefore, in patients with HFrEF, with current or previous symptoms, use of 1 of the 3 beta blockers proven to reduce mortality (e.g., bisoprolol, carvedilol, sustained-release metoprolol succinate) is recommended to reduce mortality and hospitalizations (Class 1, LOE A). Beta-blockers in this setting provide a high economic value.

Table 14 of the guidelines provides recommendations for target doses for GDMT medications. Specifically for beta blockers, those targets are 25-50mg twice daily for carvedilol (or 80mg once daily for the continuous release formulation), 200mg once daily for metoprolol succinate, and 10mg once daily for bisoprolol.

While we should be cognizant of pill-burden and other barriers to our patients’ quality of life, we must counsel them about the risks of discontinuing any element of guideline directed medical therapy (GDMT). The 2022 heart failure guidelines recommend the long-term use of beta blockers for patients diagnosed with HFrEF, even if symptoms improve (Option A). Conversely, long-term treatment should also be maintained even if symptoms do not improve to reduce the risk of major cardiovascular events. Importantly, the abrupt withdrawal of beta blockers can lead to clinical deterioration.

Our patient here has heart failure with improved ejection fraction (HFimpEF) defined as having a previous LVEF ≤ 40% and a ≥ 10-point increase from baseline with a follow-up measurement of LVEF > 40%. HFimpEF is distinct from HFpEF and was proposed in the “Universal Definition and Classification of Heart Failure” by Bozkurt et al published in JCF 2021 in order to distinguish those who benefit from continued GDMT. Accordingly, in patients with HFimpEF after treatment, GDMT should be continued to prevent relapse of HF and LV dysfunction, even in patients who may become asymptomatic (Class 1, LOE B-R). While GDMT may improve symptoms, functional capacity, LVEF, and reverse remodeling in patients with HFrEF, these favorable changes do not reflect full and sustained recovery but rather remission with susceptibility to worsening with GDMT withdrawal. Therefore, stopping any element of her GDMT (BB, ARNi, or MRA) would be incorrect (Options A, C, D).

Main Takeaway

In patients with HFrEF who experience improvement in heart failure symptoms and cardiac function on GDMT (develop HFimpEF), it is important to continue optimizing GDMT to prevent relapse, even if asymptomatic.

Guideline Loc.

Section 7.3.2

Section 7.3.8, Table 14
Section 7.6.2

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CardioNerds (Drs. Amit Goyal and Dan Ambinder) join Dr. Mina Fares, Dr. Johannes Bergehr, and Dr. Christina Peter from Cambridge University Hospitals in the UK. They discuss a case involving a man man in his 40’s presented with progressive heart failure symptoms. He has extensive background cardiac history including prior episodes of myocarditis and complete heart block status post permanent pacemaker implantation. Ultimately a diagnosis of Danon disease is made. Dr. Sharon Wilson provides the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, Hirsh Elhence.

“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.

CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ).

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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A man in his 40s with a history of cardiac issues, including prior myocarditis and complete heart block, presented with progressive heart failure symptoms. Extensive cardiac investigations were conducted, revealing dilated left ventricle, mild to moderate left ventricular systolic dysfunction, normal coronaries, infero-lateral late gadolinium enhancement on cardiac MRI, and low-level uptake on PET-CT. Differential diagnosis included worsening underlying cardiomyopathy, recurrent myocarditis, tachycardia-related cardiomyopathy, pacemaker-induced LV dysfunction, and sarcoidosis. The patient’s condition improved with heart failure medications, and cardiac MRI showed a mildly dilated left ventricle with moderate systolic dysfunction and active inflammation in the anterior wall. Further evaluation indicated a family history of hereditary cardiomyopathy, and the patient exhibited phenotypic features such as early-onset heart disease, arrhythmias, family history of cardiomyopathy, learning problems, intellectual disability, and mild proximal myopathy. Genetic testing confirmed a LAMP2 mutation, leading to the diagnosis of Danon disease.

The following question refers to Section 3.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Hirsh Elhence, answered first by Mayo Clinic Fellow Dr. Teodora Donisan, and then by expert faculty Dr. Eugene Yang.

Dr. Yang is professor of medicine of the University of Washington where he is medical director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and chair of the ACC Prevention of CVD Section.

The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Please choose the CORRECT statement from the ones below.

A

CAC scoring can be considered to improve ASCVD risk classification around treatment decision thresholds.

B

Patients with type 1 or type 2 diabetes are considered very high CV risk, regardless of comorbidities and other risk factors.

C

CKD does not increase the cardiovascular risk in the absence of other risk factors.

D

Men and women older than 65 years old are at high cardiovascular risk.

Explanation

Option A is correct. Coronary artery calcium (CAC) scoring can reclassify CVD risk upwards and downwards in addition to conventional risk factors and may thus be considered in men and women with calculated risks around decision thresholds (Class IIb, Level B). If CAC is detected, its extent should be compared with what would be expected for a patient of the same sex and age. CAC scoring does not provide direct information on total plaque burden or stenosis severity and can be low or even zero in middle-aged patients with soft non-calcified plaque.

Option B is false. Not all patients with diabetes are very high risk by default.

·       Moderate risk: well controlled diabetes, <10 years duration, without evidence of target organ damage and no additional ASCVD risk factors.

·       High risk: patients not fulfilling the criteria above, without ASCVD and/or severe target organ damage.

·       Very high risk: diabetic patients with established ASCVD and/or severe target organ damage.

Severe target organ damage is defined by:

·       eGFR <45 mL/min/1.73 m2

·       eGFR 45-59 mL/min/1.73 m2 and microalbuminuria (albumin-to-creatinine ratio, ACR 30 -300 mg/g)

·       Proteinuria (ACR >300 mg/g)

·       Presence of microvascular disease in at least 3 different sites (e.g., microalbuminuria + retinopathy + neuropathy

Option C is false. CKD carries at least a high CVD risk even in the absence of diabetes or ASCVD.

·       Moderate CKD carries a high CVD risk:

o   eGFR 30−44 mL/min/1.73 m2 and ACR <30

o   eGFR 45−59 mL/min/1.73 m2 and ACR 30−300

o   eGFR ≥60 mL/min/1.73 m2 and ACR >300

·       Severe CKD carries a very high CVD risk:

o   eGFR<30 mL/min/1.73 m2

o   eGFR 30−44 mL/min/1.73 m2 and ACR >30

Option D is false. There is an age difference between men and women with regards to cardiovascular risk. Age is a major CVD risk driver, but age cutoffs should be used with flexibility.

·       Women < 50 years-old and men < 40 years old are usually at low 10-year CVD risk. It is still important to be aware of unfavorable modifiable risk factors that can sharply increase their lifetime CVD risk.

·       Women > 75 years-old and men > 65 years-old are usually at high 10-year CVD risk.

·       Only between the ages of 55 – 75 years in women and 40 – 65 years in men does the 10-year CVD risk vary around commonly used thresholds for intervention.

Of note:

·       In younger, apparently healthy patients, we also discuss lifetime CVD risk estimates since 10-year risk assessments often underestimate risk.

·       In an aging population, treatment decisions should take competing non-CVD risk into account.

·       In patients with established ASCVD we can discuss about residual CVD – defined as the risk estimated after initial lifestyle changes and risk factor treatment.

Main Takeaway

Estimating CVD risk is not only important in apparently healthy patients, but also in patients with diabetes, renal disease, established ASCVD, or older patients. This can provide information to allow shared decision making and personalized approach for our patients.

Guideline Loc.

Table 3, page 3237; Section 3.2.3., page 3243; Table 4, page 3244

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The following question refers to Section 7.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

The question is asked by New York Medical College medical student and CardioNerds Intern Akiva Rosenzveig, answered first by Lahey Hospital and Medical Center internal medicine resident and CardioNerds Academy House Faculty Leader Dr. Ahmed Ghoneem, and then by expert faculty Dr. Clyde Yancy.

Dr. Yancy is Professor of Medicine and Medical Social Sciences, Chief of Cardiology, and Vice Dean for Diversity and Inclusion at Northwestern University, and a member of the ACC/AHA Joint Committee on Clinical Practice Guidelines.

The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Ms. M is a 36-year-old G1P1 woman 6 months postpartum who was diagnosed with peripartum cardiomyopathy at the end of her pregnancy. She is presenting for a follow up visit today and notes that while her leg edema has resolved, she continues to have dyspnea when carrying her child up the stairs. She also describes significant difficulty sleeping, though denies orthopnea, and notes she is not participating in hobbies she had previously enjoyed. She is currently prescribed a regimen of sacubitril-valsartan, metoprolol succinate, spironolactone, and empagliflozin.  What are the next best steps?

A

Screen for depression

B

Counsel her to follow a strict low sodium diet with goal of < 1.5g Na daily

C

Recommend exercise therapy and refer to cardiac rehabilitation

D

A & C

Explanation

The correct answer is D – both A (screening for depression) and C (referring to cardiac rehabilitation) are appropriate at this time.

Choice A is correct. Depression is a risk factor for poor self-care, rehospitalization, and all-cause mortality among patients with HF. Interventions that focus on improving HF self-care have been reported

to be effective among patients with moderate/severe depression with reductions in hospitalization and mortality risk. Social isolation, frailty, and marginal health literacy have similarly been associated with poor HF self-care and worse outcomes in patients with HF. Therefore, in adults with HF, screening for depression, social isolation, frailty, and low health

literacy as risk factors for poor self-care is reasonable to improve management (Class 2a, LOE B-NR). 

Choice C is correct. In patients with HF, cardiac rehabilitation has a Class 2a recommendation (LOE B-NR) to improve functional capacity, exercise tolerance, and health-related QOL; exercise training (or regular physical activity) for those able to participate has a Class 1 recommendation (LOE A) to improve functional status, exercise performance, and QOL.

Choice B is incorrect. For patients with stage C HF, avoiding excessive sodium intake is reasonable to reduce congestive symptoms (Class 2a, LOE C-LD). However, strict sodium restriction does not have strong supportive data and is not recommended. There are ongoing studies to better understand the impact of sodium restriction on clinical outcomes and quality of life. The AHA currently recommends a reduction of sodium intake to <2300 mg/d for general cardiovascular health promotion; however, there are no trials to support this level of restriction in patients with HF.

Main Takeaway

Depression is a risk factor for poor HF self-care and worse outcomes in patients with heart failure and so it is reasonable to screen for depression in these patients. Exercise therapy and cardiac rehabilitation have been shown to improve outcomes in HF patients. While avoiding excess sodium intake is reasonable in HF patients to reduce congestive symptoms, there is no specific strict sodium level recommended.

Guideline Loc.

Section 7.1

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