heart failure case study studocu

• © 2023

Managing Heart Failure in Primary Care: A Case Study Approach

• K. Melissa Smith Hayes   ORCID: https://orcid.org/0000-0001-8731-4325 0 ,
• Nicole R. Dellise 1

Assistant Professor, Vanderbilt University School of Nursing, Nashville, USA

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Director, Structural Heart Program, Director, Center for Advanced Heart Failure Therapy, Centennial Heart, Nashville, USA

Includes a comprehensive review of physical exam findings and common diagnostic testing used to diagnosis heart failure

Reviews best practice for transitioning the heart failure patient from hospital to home

Offers many didactical case studies

Provides a clear and concise overview of the management of heart failure for primary care clinicians

Offers “Practice Pearls” for the primary care provider treating heart failure

Discusses goals of care and end of life considerations for patients with heart failure

Addresses special heart failure considerations in the management and treatment of common diagnoses seen in primary care

Reflects current heart failure treatment guidelines outlined by AHA/HFSA

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Table of contents (19 chapters)

Front matter, pathophysiology of heart failure, heart failure across the population, comprehensive heart failure history.

• Leah A. Carr, Lisa D. Rathman, Roy S. Small

Physical Exam for Presence and Severity of Heart Failure

• Jessica B. Williams, Donna Harmon, JoAnn Lindenfeld

The Cardiology Referral for Heart Failure: Work-up and Expectations

• Kaushik Amancherla, Lisa Mendes

Heart Failure with Reduced Ejection Fraction

• Terri L. Allison, Beth Towery Davidson

Heart Failure with Preserved Ejection Fraction

• Anupam A. Kumar, Deepak K. Gupta

Transitions of Care and Self-Care Strategies for the Heart Failure Patient

• Kelly D. Stamp, Marilyn A. Prasun

Goals of Care for the Heart Failure Patient

• Christine M. Hallman, Krista R. Dobbie

Atrial Fibrillation and Heart Failure

• Tara U. Mudd

Cardiorenal Syndrome, Chronic Kidney Disease, Anemia, and Heart Failure

• Michelle Mason Parker, Mark Wigger

Diabetes and Heart Failure

• Angelina Anthamatten

Chronic Obstructive Pulmonary Disease, Obstructive Sleep Apnea, and Heart Failure

• J. Travis Dunlap, Melissa Glassford, Leslie W. Hopkins

Pulmonary Hypertension in Heart Failure

• Douglas J. Pearce

Liver Disease and Heart Failure

• Mary Lauren Pfieffer, Julie Hannah
• Heart failure
• Ejection Fraction
• Co-morbidity
• End of life
• Transitional care
• Diagnostics
• Case studies

K. Melissa Smith Hayes

Nicole R. Dellise

Book Title : Managing Heart Failure in Primary Care: A Case Study Approach

Editors : K. Melissa Smith Hayes, Nicole R. Dellise

DOI : https://doi.org/10.1007/978-3-031-20193-6

Publisher : Springer Cham

eBook Packages : Medicine , Medicine (R0)

Copyright Information : The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2023

Softcover ISBN : 978-3-031-20192-9 Published: 30 March 2023

eBook ISBN : 978-3-031-20193-6 Published: 29 March 2023

Edition Number : 1

Number of Pages : XIX, 328

Number of Illustrations : 10 b/w illustrations, 10 illustrations in colour

Topics : Nursing , Cardiology , Pharmacology/Toxicology

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Chapter 5:  10 Real Cases on Acute Heart Failure Syndrome: Diagnosis, Management, and Follow-Up

Swathi Roy; Gayathri Kamalakkannan

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Case 1: Diagnosis and Management of New-Onset Heart Failure With Reduced Ejection Fraction

A 54-year-old woman presented to the telemetry floor with shortness of breath (SOB) for 4 months that progressed to an extent that she was unable to perform daily activities. She also used 3 pillows to sleep and often woke up from sleep due to difficulty catching her breath. Her medical history included hypertension, dyslipidemia, diabetes mellitus, and history of triple bypass surgery 4 years ago. Her current home medications included aspirin, atorvastatin, amlodipine, and metformin. No significant social or family history was noted. Her vital signs were stable. Physical examination showed bilateral diffuse crackles in lungs, elevated jugular venous pressure, and 2+ pitting lower extremity edema. ECG showed normal sinus rhythm with left ventricular hypertrophy. Chest x-ray showed vascular congestion. Laboratory results showed a pro-B-type natriuretic peptide (pro-BNP) level of 874 pg/mL and troponin level of 0.22 ng/mL. Thyroid panel was normal. An echocardiogram demonstrated systolic dysfunction, mild mitral regurgitation, a dilated left atrium, and an ejection fraction (EF) of 33%. How would you manage this case?

In this case, a patient with known history of coronary artery disease presented with worsening of shortness of breath with lower extremity edema and jugular venous distension along with crackles in the lung. The sign and symptoms along with labs and imaging findings point to diagnosis of heart failure with reduced EF (HFrEF). She should be treated with diuretics and guideline-directed medical therapy for congestive heart failure (CHF). Telemetry monitoring for arrythmia should be performed, especially with structural heart disease. Electrolyte and urine output monitoring should be continued.

In the initial evaluation of patients who present with signs and symptoms of heart failure, pro-BNP level measurement may be used as both a diagnostic and prognostic tool. Based on left ventricular EF (LVEF), heart failure is classified into heart failure with preserved EF (HFpEF) if LVEF is >50%, HFrEF if LVEF is <40%, and heart failure with mid-range EF (HFmEF) if LVEF is 40% to 50%. All patients with symptomatic heart failure should be started on an angiotensin-converting enzyme (ACE) inhibitor (or angiotensin receptor blocker if ACE inhibitor is not tolerated) and β-blocker, as appropriate. In addition, in patients with New York Heart Association functional classes II through IV, an aldosterone antagonist should be prescribed. In African American patients, hydralazine and nitrates should be added. Recent recommendations also recommend starting an angiotensin receptor-neprilysin inhibitor (ARNI) in patients who are symptomatic on ACE inhibitors.

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5: Case Study #4- Heart Failure (HF)

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• Page ID 9899
• 5.1: Learning Objectives
• 5.2: Patient- Meryl Smith
• 5.3: In the Supermarket
• 5.4: Emergency Room
• 5.5: Day 0- Medical Ward
• 5.6: Day 1- Medical Ward
• 5.7: Day 2- Medical Ward
• 5.8: Day 3- Medical Ward

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This case study involves a 76 year old female named Mary Lou Poppins, who presented to the ED accompanied by her son. She called her son after having symptoms of shortness of breath and confusion. Her past medical history includes hypertension, hyperlipidemia, coronary artery disease, and she was an everyday smoker for 30 years. She reports her home medications are lisinopril, simvastatin, and baby aspirin. Her current lifestyle includes: being a widow of six years, she lives alone, she walks her dog everyday, she drives to her knitting group three days a week, she makes dinner for her grandchildren once a week, she attempts to eat healthy but admits to consuming salty and high fat foods, and she insists on being very independent.

Mary Lou Poppins initial vitals in the emergency department includes a blood pressure of 138/70, heart rate of 108. respiratory rate of 26, temperature 98.9 degrees fahrenheit, and oxygen saturation of 84%. Her initial assessment included alert and oriented to person and place, dyspnea, inspiratory crackles in bilateral lungs, and a cough with pink frothy sputum. Her labs and diagnostics resulted in a BNP of 740 pg/ml, an echocardiogram showing an ejection fraction of 35%, an ECG that read sinus tachycardia, and a chest x-ray that confirmed pulmonary edema.

The Emergency Department physician diagnosed Mary Lou Poppins with left-sided heart failure. The orders included: supplemental oxygen titrated to keep saturation >93%, furosemide IV, enoxaparin subq, and metoprolol PO. Nursing Interventions included: monitoring oxygen saturation, adjusting oxygen route and dosage according to orders, assessing mentation and confusion, obtaining IV access, reassessing vitals, administering medications, and keeping the head of the bed elevated greater than 45 degrees. She was admitted to the telemetry unit for further stabilization, fluid balance monitoring, and oxygen monitoring.

On day one of hospital admission, Mary Lou Poppins required 4L of oxygen via nasal cannula in order to maintain the goal saturation of >93%. Upon assessment, it was determined that she was oriented to person and place. Auscultation of the lungs revealed bilateral crackles throughout, requiring collaboration with respiratory therapy once in the morning, and once in the afternoon. Physical therapy worked with the patient, but she was only able to ambulate for 100 feet. During ambulation, the patient had a decrease of oxygen saturation and dyspnea, requiring her oxygen to be increased to 6L. At the end of the day, strict intake and output monitoring showed an intake of 1200 mL of fluids, with an urinary output of 2L.

On day two of admission, Mary Lou began demonstrating signs of improvement. She only required 2 L of oxygen via nasal cannula with diminished crackles heard upon auscultation. Morning weight showed a weight loss of 1.3 lbs and the patient was oriented to person, place, and sequence of events. During physical therapy, she was able to ambulate 300 feet without required increased oxygen support. Daily fluid intake was 1400 mL with a urinary output of 1900 mL.

On the third and final day of admission, Mary Lou was AOx4 and did not require any type of oxygen support. When physical therapy arrived, the patient was able to ambulate 500 feet, which was close to her pre-hospital status. When the doctor arrived, the patient informed him that she felt so much better and felt confident going home. The doctor placed orders for discharge.

Upon discharge and throughout the patient’s hospital stay, Mary Lou Poppins was educated regarding the disease process of heart failure; symptoms to monitor for and report to her doctor; the importance of daily monitoring of weight, blood pressure, and heart rate; and the importance of adhering to a diet and exercise regime. Education was also provided regarding her medications and the importance of strictly adhering to them in order to prevent exacerbations of heart failure. Smoking cessation was also included in her plan of care. The patient received an informational packet regarding her treatment plan, symptoms to monitor for, and when to call her physician. Upon discharge, the patient was instructed to schedule a follow up appointment with her cardiologist for continued management of her care.

The patient was put in contact with a home health agency to help manage her care. The home health nurse will help to reinforce the information provided to the patient, assess the patient’s home and modify it to meet her physical limitations, and help to create a plan to meet daily dietary and exercise requirements. Regular follow-up appointments were stressed to Mary Lou Poppins in order to assess the progression of her disease. It will be important to monitor her lab values to also assess her disease progression and for any potential side effects associated with her medications. Repeat echocardiograms will be necessary to monitor her ejection fraction; if it does not improve with the treatment plan, an implanted cardiac defibrillator may be necessary to prevent cardiac death.

Open-Ended Questions

• What were the clinical manifestations that Mary Lou Poppins presented with in the ED that suggested the new onset of CHF?
• What factors most likely contributed to the onset of CHF?
• What patient education should Mary Lou Poppins receive on discharge in regards to managing her CHF?

Nursing Case Studies by and for Student Nurses Copyright © by jaimehannans is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License , except where otherwise noted.

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Heart Failure Center Patient Cases

HOME | HF CENTER HOME | FAQ | ABOUT

Heart Failure: Ask the Expert – Patient Cases

Welcome to the GCVI HF Center’s Ask the Expert – Patient Cases channel! On this channel you will have access to multiple heart failure patient cases published by leading ACC experts. We also encourage you to engage and consult with ACC global experts on cases specific to your practice. Ask the Expert through the online portal below!

Engage with ACC global experts!

Heart Failure Patient Case Quizzes

• Unrecognized HFpEF in a Type 2 DM Patient – Reducing CV and HF Risk
• Untreated HFrEF/Ischemic Cardiomyopathy in Type 2 DM – How to Optimize Medical Therapy to Improve Heart Failure Outcomes
• Restrictive Cardiomyopathies Series: Advanced HF Therapies in ATTR Cardiac Amyloidosis (Certified Patient Case Study)
• ECG of the Month: Variable QRS Morphologies in Heart Failure 
• Untreated HFrEF/Ischemic Cardiomyopathy in Type 2 DM
• Unrecognized HFpEF in a Type 2 DM Patient

Regional Patient Case Quizzes Select your region to view available courses.

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Case 4 – A 79-Year-Old Man with Congestive Heart Failure Due to Restrictive Cardiomyopathy

Sumaia mustafa.

1 Instituto do Coração (InCor) HC-FMUSP, São Paulo, SP – Brasil

Alice Tatsuko Yamada

Fabio mitsuo lima.

2 Grupo Fleury Medicina e Saúde, São Paulo, SP – Brasil

Valdemir Melechco Carvalho

Vera demarchi aiello, jussara bianchi castelli.

JAP, a 79-year-old male and retired metalworker, born in Várzea Alegre (Ceará, Brazil) and residing in São Paulo was admitted to the hospital in October 2013 due to decompensated heart failure.

The patient was referred 1 year before to InCor with a history of progressive dyspnea triggered by less than ordinary activities, lower-extremity edema, and abdominal enlargement. He sought medical care due to the abdominal enlargement, which was diagnosed as an ascites. He denied chest pain, hospitalization due to myocardial infarction or stroke, hypertension, dyslipidemia, and diabetes.

The patient was a previous smoker and had stopped smoking at the age of 37 years. He was also an alcoholic and reported drinking alcohol for the last time 1 year before.

He was referred to InCor for treatment of heart failure.

An echocardiogram revealed an increased thickness in the septum (17 mm) and free left ventricular wall (15 mm), and a left ventricular ejection fraction of 26%.

The patient reported daily use of enalapril 10 mg, spironolactone 25 mg, furosemide 80 mg, omeprazole 40 mg, and ferrous sulfate (40 mg Fe) three tablets.

On March 12, 2013, his physical examination showed a weight of 55 kg, height of 1.75 m, body mass index (BMI) of 18 kg/m 2 , heart rate of 60 bpm, blood pressure of 90 X 50 mm Hg, and the presence of a hepatojugular reflux. There were no signs of jugular venous hypertension, and the pulmonary and cardiac auscultations were normal. He had ascites, and his liver was palpable 5 cm below the right costal margin. Peripheral pulses were palpable, and a ++/4+ edema was observed.

An ECG (February 23, 2012) had shown a sinus rhythm, heart rate of 52 bpm, PR interval of 192 ms, QRS duration of 106 ms, indirect signs of right atrial overload (wide variability in QRS amplitude between V1 and V2), and left atrial overload (prolonged and notched P waves), low QRS voltage in the frontal plane with an indeterminate axis, an electrically inactive area in the anteroseptal region and secondary changes in ventricular repolarization ( Figure 1 ).

ECG: sinus bradycardia, low-voltage QRS complexes in the frontal plane, indirect signs of right atrial overload (small QRS complexes in V1 and wide QRS complexes in V2), left atrial overload, electrically inactive area in the anteroseptal region.

A chest x-ray showed cardiomegaly.

Laboratory tests performed on April 20, 2012, had shown the following results: hemoglobin 13.1 g/dL, hematocrit 40%, mean corpuscular volume (MCV) 87 fL, leukocytes 9,230/mm 3 (banded neutrophils 1%, segmented neutrophils 35%, eosinophils 20%, basophils 1%, lymphocytes 33%, and monocytes 10%), platelets 222,000 /mm 3 , cholesterol 207 mg/dL, HDL-cholesterol 54 mg/dL, LDL-cholesterol 138 mg/dL, triglycerides 77 mg/dL, creatine phosphokinase (CPK) 77 U/L, blood glucose 88 mg/dL, urea 80 mg/dL, creatinine 1.2 mg/dL (glomerular filtration rate ≥ 60 mL/min/1.73 m 2 ), sodium 131 mEq/L, potassium 6.3 mEq/L, aspartate aminotransferase (AST) 22 U/L, alanine aminotransferase (ALT) 34 U/L, uric acid 6.3 mg/dL, TSH 1.24 µUI/mL, free T4 1.36 ng/dL, prostate-specific antigen (PSA) 1.24 ng/mL. On urinalysis, urine specific gravity was 1.007, pH 5.5, the sediment was normal, and there were no abnormal elements.

A new echocardiographic assessment on April 20, 2012, had shown an aortic diameter of 32 mm, left atrium of 52 mm, septal and posterior left ventricular wall thickness of 15 mm, diastolic/systolic left ventricular diameters of 46/40 mm, and left ventricular ejection fraction of 28%. Both ventricles had diffuse and marked hypokinesia. The valves were normal and the pulmonary artery systolic pressure was estimated at 32 mmHg ( Figure 2 ).

Echocardiogram - a) Four-chamber view: marked enlargement of the left and right atria; b) parasternal long-axis view: enlarged left atrium, left ventricular wall thickening, normal cavity.

A 24-hour electrocardiographic (Holter) monitoring on April 19, 2012, showed a baseline sinus rhythm with a lowest rate of 46 bpm and greatest rate of 97 bpm; 48 isolated, polymorphic, and paired ventricular extrasystoles; 137 atrial extrasystoles; and an episode of atrial tachycardia over three beats with a frequency of 98 bpm. There were no atrioventricular or intraventricular blocks interfering with the conduction of the stimulus.

The patient was transferred from the pacemaker clinic to the general cardiopathy clinic.

During a clinic appointment on January 22, 2013, the patient was asymptomatic and reported the use of enalapril 10 mg, spironolactone 25 mg, furosemide 60 mg, and carvedilol 12.5 mg. His physical examination was normal.

The main diagnostic hypotheses were hypertrophic or restrictive cardiomyopathy.

A testicular ultrasound (September 09, 2013) was normal, except for cystic formations in the right inguinal canal. An abdominal ultrasonography (September 10, 2013) showed substantial ascites and hepatic cysts with internal septations, and no signs of portal hypertension.

After presenting an increase in dyspnea with the development of paroxysmal nocturnal dyspnea, worsening ascites and lower-extremity edema, and paresthesia on hands and feet, the patient was admitted to the hospital.

On physical examination (October 19, 2013) he was oriented and eupneic, with a heart rate of 69 bpm, blood pressure of 80 X 60 mmHg, a normal pulmonary auscultation, cardiac auscultation with arrhythmia and no murmurs, substantial ascites, and edema and hyperemia of the lower extremities.

A chest x-ray (October 21, 2013) showed cardiomegaly and interstitial lung infiltrates; the lateral incidence showed the right ventricle markedly enlarged ( Figures 3 and ​ and4 4 ).

Chest x-ray (October 21, 2013), posteroanterior (PA) view: pulmonary interstitial infiltrates and cardiomegaly.

Chest x-ray (October 21, 2013) in lateral view: right ventricle markedly enlarged.

On ECG, the patient presented atrial flutter with variable atrioventricular block, indirect signs of right atrial overload (Peñaloza-Tranchesi sign), heart rate of 61 bpm, low QRS voltage in the frontal plane, intraventricular conduction impairment, left ventricular overload, and secondary changes in ventricular repolarization ( Figure 5 ).

ECG: Atrial flutter, impaired intraventricular conduction, left ventricular overload.

Laboratory tests on October 19, 2013, showed the following results: hemoglobin 13.5 g/dL, hematocrit 42%, leukocytes 7,230/mm 3 (neutrophils 66%, eosinophils 12%, lymphocytes 13%, monocytes 9%), platelets 232,000 /mm 3 , urea 193 mg/dL, creatinine 2.03 m/dL (glomerular filtration rate of 34 mL/min/1,73 m 2 ), sodium 133 mEq/L, potassium 3.9 mEq/L, C-reactive protein (CRP) 18.1 mg/L, vitamin B12 360 pg/mL, folic acid 8.35 ng/mL, total bilirubin 0.75 mg/dL, direct bilirubin 0.37 mg/dL, AST 24 U/L, ALT 16 U/L, gamma-glutamyl transferase (gamma GT) 241 U/L, alkaline phosphatase 166 U/L, iron 71 µg/dL, ferritin 62.9 ng/mL, prothrombin time (PT, INR) 0.95, activated partial thromboplastin time (aPTT, rel) 0.95, ionic calcium 1.09 mmol/L, chloride 89 mEq/L, and arterial lactate 15 mg/dL. Urinalysis showed urine specific gravity of 1.020, pH 5.5, proteinuria 0.25 g/L, epithelial cells 4,000/mL, leukocytes 2,000/mL, erythrocytes 3,000/mL, and hyaline casts 27,250/mL.

Another echocardiogram performed on October 21, 2013, showed a left atrial diameter of 56 mm, septal thickness of 18 mm, posterior wall thickness of 13 mm, left ventricle (diastole/systole) with 46/40 mm, left ventricular ejection fraction of 28%, pulmonary artery systolic pressure estimated at 45 mmHg, marked left ventricular and moderate right ventricular dysfunction, and moderate tricuspid insufficiency.

An ultrasound of the kidneys and urinary tract (October 24, 2013) showed that the left kidney measured 9.6 cm, and the right kidney measured 9 cm and had simple cortical cysts.

Serum protein electrophoresis was normal, and a urinary electrophoresis did not detect proteins. Measurement of serum beta 2-microglobulin was 7 mg/mL (limit for individuals above the age of 60 years = 2.6 mg/mL).

A biopsy of the cheek mucosa (October 23, 2013) showed deposits of amyloid substance in the deep chorion and in the adjacent adipose tissue.

Stool microscopy (October 25, 2013) was positive for Blastocystis hominis and Entamoeba coli .

A paracentesis drained 3,500 mL of a yellowish fluid with normal cellularity.

During hospitalization, the patient received daily intravenous furosemide 60 mg, carvedilol 25 mg, hydrochlorothiazide 100 mg, hydralazine 75 mg, isosorbide 80 mg, aspirin 100 mg, spironolactone 25 mg, and enoxaparin 40 mg. The patient also received oxacillin 2 g/day for 7 days initially, and later vancomycin, meropenem and teicoplanin, and piperacillin/tazobactam.

A new chest x-ray (November 08, 2013) showed cardiomegaly and an interstitial pulmonary infiltrate suggestive of pulmonary congestion ( Figure 6 ).

Chest x-ray (November 08, 2013): pulmonary interstitial infiltrates suggestive of pulmonary congestion and cardiomegaly.

During a new paracentesis (November 11, 2013), the aspirated fluid was bloody, and the patient presented hypotension and decreased consciousness, progressing to cardiac arrest with pulseless electrical activity, which was reverted. This was followed by ventricular tachycardia, cardioverted with 200 J.

New tests (November 11, 2013 - morning) showed the following results: hemoglobin 11.9 g/dL, hematocrit 36%, leukocytes 7,780/mm 3 (neutrophils 83%, eosinophils 2%, lymphocytes 9%, and monocytes 6%), platelets 188,000 /mm 3 , urea 301 mg/dL, creatinine 4.14 mg/dL, sodium 125 mEq/L, potassium 4.4 mEq/L, CRP 97.06 mg/L. On venous blood gas analysis, pH was 7.33, bicarbonate 19.9 mmol/L, and base excess (-) 5.4 mmol/L. Additional tests performed on the same day (November 11, 2013 – 5:44 pm) showed hemoglobin of 6.3 g/dL, sodium of 123 mEq/L, potassium of 5.4 mEq/L, venous lactate of 93 mg/dL, PT (INR) of 3.2 and aPTT (rel) of 1.98.

Later during the day, the patient progressed with shock refractory to high doses of dobutamine (20 µg/kg/min ) and norepinephrine (1.2 µg/kg/min), followed by cardiac arrest with pulseless electrical activity that recovered but was followed by a new irreversible cardiac arrest with pulseless electrical activity during intra-aortic balloon placement (November 11, 2013 – 6:30 pm).

Clinical Aspects

The patient JAB, a 79-year-old previous smoker and alcoholic man residing in São Paulo, attended an outpatient clinic at InCor due to heart failure which worsened progressively since 2012, requiring hospitalization for treatment.

Heart failure is a systemic and complex clinical syndrome, defined as a cardiac dysfunction that causes the blood supply to be insufficient to meet tissular metabolic demands, in the presence of a normal venous return, or which only meets the demands with high filling pressure 1 .

Prevalence studies estimate that 23 million individuals worldwide have heart failure and that 2 million new cases are diagnosed annually. According to DATASUS information, Brazil has about 2 million individuals with heart failure and 240,000 new cases diagnosed annually 2 .

The main causes of heart failure are hypertension, coronary artery disease, Chagas disease, cardiomyopathies, endocrinopathies, toxins, and drugs, among others 1 . The cardinal manifestations of heart failure are dyspnea and fatigue, and may include exercise intolerance, fluid retention, and pulmonary and systemic congestion 3 . The patient in this case presented with progressive dyspnea triggered by less than ordinary activities, lower-extremity edema, and ascites, which characterized him as class III according to the New York Heart Association (NYHA) classification.

On complementary tests, the echocardiogram showed marked left ventricular hypertrophy with some degree of asymmetry, and reduced ejection fraction. Cardiac hypertrophy is often associated with hypertension or hypertrophic cardiomyopathy, but both present with normal or increased ECG voltage. Therefore, the findings of ventricular hypertrophy associated with decreased ECG voltage in the absence of pericardial effusion are exclusive of infiltrative cardiomyopathies, a group of cardiac disorders within the restrictive cardiomyopathies 4 .

Restrictive cardiomyopathy may occur with a wide variety of systemic diseases. Some restrictive cardiomyopathies are rare in clinical practice and may present initially with heart failure. This type of cardiomyopathy is characterized by filling restriction, with reduced diastolic volume in one or both ventricles, normal or close to normal systolic function, and ventricular wall thickening. It may be idiopathic or associated with other diseases, such as amyloidosis, endomyocardial disease with or without eosinophilia, sarcoidosis, and hemochromatosis, among others 5 . In this case, the presence of amyloid deposits in the cheek mucosa biopsy indicated a diagnosis of amyloidosis, and the increase in serum beta-2 microglobulin reflected a worse prognosis 5 .

Amyloidosis is characterized by deposits of amyloid protein in different organs and tissues. These deposits may be responsible for different types of clinical presentation, with a spectrum that ranges from lack of symptoms to sequential organic dysfunction culminating with death 6 .

Cardiac amyloidosis is caused by amyloid deposits around cardiac fibers, and can be identified by a left ventricular wall thickening exceeding 12 mm in the absence of hypertension with at least one of the following characteristics: conduction disorder and low voltage complexes on the ECG, restrictive cardiomyopathy, low cardiac output, isolate atrial involvement (as commonly seen in elderly individuals) or diffuse involvement affecting the ventricles. In the latter situation, it can cause heart failure with a poor prognosis 4 , 7 .

Our patient, who was not hypertensive, presented low voltage complexes on the ECG, which were more prominent in the frontal plane, an electrically inactive area in the anteroseptal region, and diffuse changes in ventricular repolarization. This pattern can be found in some diseases in addition to infiltrative cardiomyopathies, such as decompensated hypothyroidism, pericardial effusion, chronic obstructive pulmonary disease, and obesity. Other electrocardiographic information, such as the pattern of infarction, can be found with or without obstructive coronary atherosclerotic disease by deposition of substances in the microcirculation and small intramyocardial arteries 8 .

Amyloidosis may be classified as primary, secondary, or hereditary. Primary amyloidosis, in which AL is the primarily involved protein, may be further subdivided into idiopathic (localized forms) or associated with multiple myeloma or other plasma cell dyscrasias (systemic forms) 9 .

Multiple myeloma is a neoplastic disorder of plasma cells that affects individuals with an average age of 70 years at diagnosis. Some characteristics of the patient in this case could suggest multiple myeloma: age, male gender, renal failure, and cylindruria. However, other important clinical parameters were absent, such as hypercalcemia, anemia, and bone disease. Also, the Bence-Jones protein, which is present in up to 75% of the cases, was not detected on urinary electrophoresis 10 .

The secondary type of amyloidosis results from deposits of AA protein and frequently arises as a complication of infectious or inflammatory processes, such as rheumatoid arthritis (the most common cause), tuberculosis, systemic lupus erythematosus, inflammatory bowel disease, syphilis, or even neoplastic diseases. Pro-inflammatory cytokines, which are present in these disorders, stimulate the hepatic production of serum A amyloid 11 .

Finally, the hereditary type of the disease has an autosomal dominant transmission and may involve several types of amyloid proteins, such as the AA protein in some groups of patients with familial Mediterranean fever, and the ATTR protein (derived from the transthyretin or prealbumin) in familial amyloid polyneuropathy 12 .

As for the treatment, measures to control symptoms related to diastolic heart failure, such as volume control, should be implemented. Diuretics and vasodilators should be administered with caution since the cardiac output in these patients is greatly dependent on increased venous pressures. Specific treatment should be directed to the etiology of the amyloidosis 13 .

After an evaluation in the clinic on January, 2013, the patient received medications that are proven to modify the rates of hospitalization and mortality in heart failure with reduced ejection fraction (beta-blockers, angiotensin-converting enzyme inhibitors, aldosterone antagonist), and symptom-relieving agents (diuretics) 14 . The patient was receiving enalapril 10 mg, spironolactone 25 mg, furosemide 60 mg, and carvedilol 12.5 mg.

After 8 months, due to the decompensated heart failure and hypotension, the patient returned to the emergency room and required hospitalization. The use of conventional therapy for heart failure often worsens the progression of amyloidosis. Therefore, cardiac amyloidosis should be suspected when the patient’s clinical condition worsens in response to conventional treatment, particularly in individuals older than 50 years. The therapy is exclusively symptomatic and should not include digitalis, beta-blockers, angiotensin-converting enzyme inhibitors, or calcium channel antagonists, since some studies have shown an increased sensitivity to these drugs which can lead to hypotension and intensification of conduction disorders 15 .

Therefore, the decompensation of the patient’s heart failure with deterioration of the ascites culminated in two paracenteses, with the last paracentesis probably accompanied by a puncture accident due to the appearance of bloody fluid, decrease in red blood count, and hypovolemic shock associated with cardiogenic shock, culminating in a mixed refractory shock and cardiac arrest with pulseless electrical activity (Dr. Sumaia Mustafa, Dr. Alice Tatsuko Yamada).

Diagnostic hypotheses:

• Heart failure due to restrictive cardiomyopathy (probably cardiac amyloidosis associated with multiple myeloma);
• Decompensated heart failure;
• Cause of death: mixed shock (hypovolemic + cardiogenic) with cardiac arrest with pulseless electrical activity (Dr. Sumaia Mustafa, Dr. Alice Tatsuko Yamada) .

The heart weighed 680 g and was increased in volume due to moderate cavity dilation and wall thickening in all four chambers ( Figure 7 ). The myocardium had an increased consistency. The endocardium of the atria, in particular, was finely granular and brown-yellowish in appearance. There were no significant changes in the valves, and the coronary arteries were armed without significant obstruction of their lumen.

Gross Section of the heart base showing biatrial enlargement and thickening of the cardiac walls. Note the granular aspect of the right atrial endocardium (area demarcated with an ellipse).

Histological examination of the myocardium showed extracellular deposits of amorphous and eosinophilic material promoting atrophy of the contractile cells. These deposits stained positive with Congo red when observed under polarized light ( Figures 8 and ​ and9). 9 ). This same material was present in the interstitium of the cheek mucosa evaluated by biopsy ( Figure 10 ) according to data from the clinical history. Deposits were also observed in the tunica media of muscular arteries in both lungs ( Figure 11 ) and in the renal hilum.

Photomicrography of the ventricular myocardium showing atrophic cardiomyocytes due to deposits of amorphous eosinophilic material in the interstitium. Hematoxylin and eosin staining (20x objective magnification).

Photomicrography of myocardial tissue obtained under polarized light. Note the greenish material that corresponds to amyloid substance stained by Congo red (5x objective magnification).

Biopsy of the cheek mucosa performed approximately 1 month before death. Note that the mucosal chorion reacts positively to Congo red (photomicrography obtained under conventional microscopy with a 10x objective magnification).

Photomicrography of a peripheral muscular pulmonary artery showing areas of positivity for deposits of amyloid in the arterial wall (Congo red staining photographed under conventional microscopy, 5x objective magnification).

Bone marrow histological examination showed hypercellularity of moderate degree for the patient's age, and no signs of monoclonal proliferation. Immunohistochemical reactions for immunoglobulin kappa and lambda light chains were inconclusive, and CD138 labeling showed no proliferation of plasma cells.

Autopsy findings included a 4-cm hepatic cyst in the right lobe lined with flat cells without atypia, and retention cysts in the right kidney. The right adrenal weighed 44 g and was increased in volume and completely calcified. The histological examination showed only calcification and was inconclusive for the possibility of prior malignancy.

There was a voluminous serosanguinous ascites and a serous pericardial effusion. We found no visceral or abdominal vessel injury resulting from the paracentesis and the amount of bloody material in the ascitic fluid was small.

Histologically, there were signs of congestive heart failure in the lungs and liver (Dr. Vera Demarchi Aiello) .

Diagnoses: Cardiovascular amyloidosis;

Congestive heart failure;

Calcified nodule in the right adrenal gland (Dr. Vera Demarchi Aiello).

Mass spectrometry

Mass spectrometry gathers all qualities to establish an unequivocal diagnosis of amyloidosis since it has a high sensitivity and ability to identify the proteins through sequencing 16 . Therefore, we adopted an approach based on shotgun proteomics to identify the amyloid deposits in the sample.

Sections of heart tissue containing amyloid deposits (confirmed by staining with Congo red) fixed in formalin and embedded in paraffin were dissected and the proteins were then extracted with Liquid Tissue® MS Protein Prep Kit (Expression Pathology) according to the manufacturer's protocol. After digestion with trypsin, the resulting peptides were analyzed by high-resolution liquid chromatography-mass spectrometry using the mass spectrometer Q-Exactive (Thermo Fisher Scientific). The acquisitions of spectral data were carried out using the DDA (date dependent analysis) mode with a selection of the 10 most abundant ions for sequencing by HCD (Higher-energy collisional dissociation). The data were processed with the software MaxQuant. The proteomic analysis was performed in triplicate.

The processed data generated lists of proteins representing the protein content of the sample. In total, 25 possible amyloid proteins were investigated in these lists in order to determine the identity of the deposited substance. There were 15 peptides belonging to transthyretin that together covered 76.2% of the full sequence of the protein.

To confirm the result, we also evaluated the abundance of different peptides present in the sample. Among the 25 most abundant peptides, three belonged to transthyretin (ALGISPFHEHAEVVFTANDSGPR, TSESGELHGLTTEEEFVEGIYK, and GSPAINVAVHVFR). The others were assigned to actin, myosin, desmin, and myoglobin, confirming the identity of the amyloid protein (Dr. Fabio Mitsuo Lima and Dr. Valdemir Melechco Carvalho- Fleury Group).

Cardiovascular amyloidosis due to deposition of transthyretin (Dr. Vera Demarchi Aiello, Dr. Jussara Bianchi Castelli, Dr. Fabio Mitsuo Lima and Dr. Valdemir Melechco Carvalho) .

This case demonstrates how important it is in amyloidosis to investigate the deposited substance. Amyloidosis is a generic name to describe a group of diseases characterized by extracellular deposits of different substances in different organs. These substances are fibrillar proteins that become insoluble with changes in their spatial conformation. More than 20 types of proteins have been described in these deposits 16 . From an anatomopathological perspective, the deposits can be characterized by immunohistochemical reactions, but with some restrictions as described below. The cardiovascular system is most often affected by the AL protein (deposits of light-chain immunoglobulin), senile, and familial forms 17 , 18 .

The pathologist may identify neoplastic proliferation of plasmocytes producing the deposited immunoglobulins by bone marrow examination labeled for these cells. In tissue preparations, the pathologist may demonstrate by immunohistochemistry if the deposited substance is one of these immunoglobulins. Some authors recommend a biopsy of other organs before the endomyocardial biopsy to confirm the diagnosis and identify the type of amyloid 19 . In this case, immunohistochemical labeling was not helpful in establishing the diagnosis, because it was inconclusive to the type of protein deposited.

Although there are reports in the literature of identification of transthyretin in tissues by immunohistochemical reactions, this was not possible in this case. However, with mass spectrometry analysis, we identified that the deposited protein was transthyretin, which is usually present in senile and familial forms of amyloidosis. In this patient, the familial form was less likely due to the exclusive involvement of heart and blood vessels. However, only a genetic research and evaluation of other members of the family could exclude it completely.

Another point that deserves discussion in this case is the laboratory report of high levels of immunoglobulin E. We could assume that this referred to the deposited protein, but the diagnostic methods performed to complement the autopsy revealed that this was not the case.

Dr. Vera Demarchi Aiello and Dr. Jussara Bianchi Castelli (Pathology Laboratory, InCor, FMUSP).

Heart Failure; Cardiomyopathy, Restrictive; Ascites; Cardiomegaly; Heart Arrest.

Editor da Seção: Alfredo José Mansur ( rb.psu.rocni@rusnamja )

Editores Associados: Desidério Favarato ( rb.psu.rocni@otaravaflcd )

Vera Demarchi Aiello ( rb.psu.rocni@arevpna )

New study shows effect of socio-economic factors—housing, food, neighborhood—to predict diabetic patients’ risk of heart failure

A recent study by  Case Western Reserve University  used national data from U.S. military veterans with diabetes to validate and modify a widely accepted model used to predict the risk of heart failure in diabetic patients.

The model, called the WATCH-DM score, is used to predict the likelihood of heart failure in diabetes patients within five years.

But because it overlooks the influence of social determinants of health‚ such as housing, food and a patient’s neighborhood, the researchers used a social deprivation index (SDI), a multi-component summary score, to adjust the WATCH-DM score. 

The SDI, introduced by the  Robert Graham Center,  a group of clinical researchers, can quantify the level of disadvantage in particular areas using food, housing, transportation and community conditions. Prior research demonstrated this score is directly proportional to the level of health disparities observed in communities.

The study identified about 1 million U.S. veterans with type 2 diabetes without heart failure treated as outpatients at Veterans Affairs medical sites nationally in 2010.

Researchers used patient zip codes to obtain their SDI, which was then entered into the risk calculator to determine how likely they would be hospitalized for heart failure within five years.   

While the hospitalization rate for heart failure for the whole cohort of more than 1 million patients was 5.39%, this incidence varied from 3% (in the least socially deprived) to 11% (in the most deprived). 

Researchers found that, depending on the patients’ other clinical information, adding the SDI into the risk-prediction model could even double the probability of that patient developing heart failure in the next five years.

The team of investigators then optimized the WATCH-DM score for each SDI group using a statistical correction factor and improved its predictive accuracy across the whole range of the social determinants of health. 

“We found that adding the SDI enhanced the WATCH-DM score’s ability to forecast risk,” said Salil Deo, an associate professor in the  Department of Surgery at Case Western Reserve School of Medicine, who led the study. “These results highlight the necessity of including social determinants of health in any future clinical risk prediction algorithms. This will increase their accuracy, which will benefit patients by improving their health outcomes.”

View the calculator. 

“We hope our study encourages healthcare providers to adopt a wholistic approach when treating patients in the future,” Deo said. “Understanding and quantifying social inequity is likely the first step we can take toward trying to ensure that it does not affect the health of our patients.” 

For more information, contact Patty Zamora at [email protected] .

Wegovy Helps Those With Both Diabetes, Heart Failure: Study

By Robin Foster HealthDay Reporter

TUESDAY, April 9, 2024 (HealthDay News) -- For people struggling with both diabetes and a common type of heart failure, the weight-loss drug Wegovy may do more for their health than help them shed pounds, new research suggests.

In the study, published Saturday in the New England Journal of Medicine , researchers reported that the drug helped people with type 2 diabetes who also had obesity-related "heart failure with preserved ejection-fraction," on several fronts.

This condition happens when the heart pumps normally, but the organ is too stiff to fill properly.

“I think the answer from the trial clearly suggests that, while weight loss is likely an important factor, it cannot explain everything,” study co-author Dr. Mikhail Kosiborod , a cardiologist and vice president of research at St. Luke’s Health System in Kansas City, Mo., told CNN .

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“I think that’s incredibly exciting because first of all, these patients are really difficult to treat and there are a lot more of them every day,” Kosiborod said. “And until recently, we had very little to offer them, so if we know it actually modifies the disease process, we have something really effective -- and by the way, really well-tolerated as well -- and that’s, of course, great news for patients and great news for doctors taking care of patients.”

People with obesity-related heart failure tend to tire easily and have trouble breathing, and those who also have type 2 diabetes have a more severe form than those who don’t have the blood sugar disease.

The researchers who conducted this latest study -- which was funded by drug maker Novo Nordisk -- also published a study last fall that found that Wegovy delivered significant benefits to people without diabetes who had obesity-related heart failure. However, the team wanted to see whether the drug would work as well in people who also had diabetes.

Wegovy was first approved in 2021 to treat obesity. Just last month, the U.S. Food and Drug Administration also approved Wegovy to reduce the risk of cardiovascular death, heart attack and stroke in obese/overweight adults with heart disease. This latest study offers up fresh evidence that Wegovy’s benefits extend to people with diabetes.

For the study, the researchers randomly assigned 616 people who had type 2 diabetes and heart failure with preserved ejection-fraction into two groups. The participants came from 108 sites in 16 countries, and all had a body-mass index of 30 or more. One group got Wegovy, and the other group got a placebo.

The participants who got Wegovy started at a lower dose and worked their way to a 2.4 milligram dose once a week. Researchers followed both groups for a year.

Patients who got Wegovy had much better outcomes, with more weight loss and a bigger reduction in heart failure-related symptoms and physical limitations. They also could walk farther over the course of six minutes   and showed improvements in biomarkers for inflammation.

There were 55 serious adverse events reported in the group that took Wegovy and 88 in the placebo group. Six people died in the Wegovy group, compared with 10 in the placebo group. One death in the Wegovy group and four in the placebo group were related to heart issues.

The findings of this trial, along with the one published last year, suggest Wegovy works for a broad population of people, Kosiborod said.

Kosiborod, who presented the research Saturday at the American College of Cardiology annual meeting in Atlanta, added that he thinks the study opens up the possibility of treating heart failure by treating obesity.

“Obesity, it is a lot more than weight. It’s a systemic cardiometabolic condition that causes all kinds of bad things, and treating obesity involves weight loss, but it means a lot more than that,” he said. “We have to target it, and I think future standards of care for this type of heart failure will improve, and without a doubt in my mind, it’s going to include obesity management.”

More information

Drugs.com has more on weight-loss drugs .

SOURCES: New England Journal of Medicine , April 6, 2024; CNN

Copyright © 2024 HealthDay . All rights reserved.

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