MRI OF THE HEART EVALUATING FUNCTION AND MORPHOLOGY: END LV DIASTOLE AND END LV SYSTOLE
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Demographics
50 y.o. Female
50 y.o. Female
Caption
■ Right Heart: The right ventricle is mildly dilated in size with mildly reduced systolic function. The right atrium is mildly dilated in size.
■ Left Ventricle: The left ventricle is moderately dilated in size. Prominent trabeculation of the LV apex but no criteria fulfilling LV non-compaction.
■ LVEF = 24%
■ RVEF = 31%
■ Left Ventricle: The left ventricle is moderately dilated in size. Prominent trabeculation of the LV apex but no criteria fulfilling LV non-compaction.
■ LVEF = 24%
■ RVEF = 31%
Plane
Decubitus
Modality
MR - T2 weighted
ACR Codes
5.7
Figure Part
1
(
This image was
added on 2024-01-30
)
Quiz
case
Post MVC Cervical Disc Herniation, Lumbar Discopathy and Comorbidity of Severe Dilated Cardiomyopathy with LVEF of 25% and RVEF of 31%
History
The patient is a 50-year-old female who was allegedly involved in a work-related-MVC while in the employ of the first student in her job capacity of bus Monitor. She reports having worked for such employer for 6 years. She has lost time from work since 7/19/2023 to the present time.
She reports that on 07/19/2023 she was sitting on a school bus that was stopped on the freeway. A truck traveling at speed stuck the back of the bus and pushed in the safety door. She was transported to St. Joseph Hospital where she was examined, no radiographs were performed, she was prescribed Ibuprofen and a muscle relaxant. During the MVC she recalls sitting in a seat looking toward the windshield. There was no headrest, and she struck the back of her head against the seat. She had immediate headaches. The patient is not on any blood thinning medications. Patient has no weakness or numbness in her extremities.
PERTINENT PAST MEDICAL HISTORY:
The patient was in an MVC, (fender bender), while on the job in 2021. She reports losing 2 weeks from work and made a full recovery.
She does have diabetes and takes Escitalopram 10mg and Trulicity.
She had a hysterectomy in 2022. Reports when she was 8 years old she had the DIP of the 5th digit of the left hand amputated when it was caught in a door.
The patient denies work episodes, other vehicular accidents or slips, falls, athletic episodes where an injury was sustained. She denies rheumatoid arthritis, diabetes, kidney disease, tuberculosis, hearing loss, kidney stones, headaches, gout, seizures, asthma, ulcers, loss of sight, anemia, thyroid disease, stroke or any fractures. She has had a hysterectomy in the past. She has history of CTS.
May of 2023:
The patient presented to the ER in May of 2023 with multiple complaints.
• Shortness of breath: It is becoming progressively worse over the past several days. It is somewhat associated with exertion it is worse at night. She denies any frank cough she denies any chest pain she denies any fevers chills. She does report she smoked for 25 years about half a pack a day but she has no history of asthma nor COPD. She denies any leg swelling. She denies any recent surgeries she denies any recent travel. She has no history of ACS. She has not recently had COVID nor flu. She reports she feels like she is wheezing she tried someone else's inhaler but that did not seem to improve her symptoms she feels like her symptoms are getting progressively worse.
• She also reports a left-sided neck pain. This is been ongoing for approximately 1 year she feels like it is getting worse. It does not radiate she did not have any numbness nor tingling. She cannot recall any injuries. It is located over the left lateral aspect of the neck and is worse with movement.
September 2023:
• The patient presented to the emergency department complaining of shortness of breath and nonproductive cough. Patient states that she had symptoms for the past 2 weeks. Patient states that this feels similar to when she had pneumonia in the past. Patient states been taking inhaler, with minimal relief. Patient denies any sick contacts. Patient denies any active chest pain. Patient denies abdominal pain, nausea or vomiting. October 2023:
• The patient presents to the emergency department with shortness of breath and nonproductive cough. Patient states that she had symptoms for the past 2 weeks. Patient states that this feels similar to when she had pneumonia in the past. Patient states been taking inhaler, with minimal relief. Patient denies any sick contacts. Patient denies any active chest pain. Patient denies abdominal pain, nausea or vomiting. October 2023 – Cardiology Consult:
• The patient was admitted to hospital for dyspnea and treated for acute systolic heart failure exacerbation.
• Noted on Echo: Severely reduced LVEF 25%. The patient has had intermittent shortness of breath which was worse the days leading up to this presentation. She thought it was related to black mold, environmental exposure in her home. She has had intermittent lower extremity edema. On presentation she was started on furosemide and has had improvement in her dyspnea. She denies chest pain at rest or with exertion. She has not had near syncope or syncope. Rare palpitations.
• In the past she has had EKG with non-specific T-wave abnormalities in V1-V6 significant for possible anterolateral ischemia:
• Diagnosed as NYHA class III heart failure based on symptoms. Acute systolic heart failure due to mixed ischemic and non-ischemic dilated cardiomyopathy
• Patient treated based on guidelines, acutely with furosemide and long-term with guideline directed medical therapy
• Patient high-risk for sudden cardiac death so has been given a life vest
She has a strong family history of cardiomyopathy and multiple first-degree relatives with cardiomyopathies and early coronary disease. Her 26-year-old son died suddenly from a cardiomyopathy.
• Current Facility-Administered Medications:
o atorvastatin (Lipitor) tablet 10 mg, 10 mg, oral
o dapagliflozin propanediol (Farxiga) tablet 10 mg, 10 mg, oral
o furosemide (Lasix) injection 20 mg, 20 mg, intravenous, Daily
o magnesium oxide (Mag-Ox) tablet 400 mg, 400 mg, oral, BID with meals, ondansetron (Zofran) injection 4 mg, 4 mg, intravenous
Review of Systems:
The patient has loss of sleep only obtaining 5 hours of sleep in an 8 hour timeframe due to pain and discomfort. This results in daytime fatigue. She has weakness of the right upper extremity, neck and back. The patient denies areas of interest in the following categories: HEENT, Respiration, Cardiac, GI, GU, Vascular, Other Musculoskeletal, Other neurologic, Hematologic, Endocrine, Skin and Psychiatric.
The patient presented to the ER in May of 2023 with multiple complaints.
• Shortness of breath: It is becoming progressively worse over the past several days. It is somewhat associated with exertion it is worse at night. She denies any frank cough she denies any chest pain she denies any fevers chills. She does report she smoked for 25 years about half a pack a day but she has no history of asthma nor COPD. She denies any leg swelling. She denies any recent surgeries she denies any recent travel. She has no history of ACS. She has not recently had COVID nor flu. She reports she feels like she is wheezing she tried someone else's inhaler but that did not seem to improve her symptoms she feels like her symptoms are getting progressively worse.
• She also reports a left-sided neck pain. This is been ongoing for approximately 1 year she feels like it is getting worse. It does not radiate she did not have any numbness nor tingling. She cannot recall any injuries. It is located over the left lateral aspect of the neck and is worse with movement.
September 2023:
• The patient presented to the emergency department complaining of shortness of breath and nonproductive cough. Patient states that she had symptoms for the past 2 weeks. Patient states that this feels similar to when she had pneumonia in the past. Patient states been taking inhaler, with minimal relief. Patient denies any sick contacts. Patient denies any active chest pain. Patient denies abdominal pain, nausea or vomiting. October 2023:
• The patient presents to the emergency department with shortness of breath and nonproductive cough. Patient states that she had symptoms for the past 2 weeks. Patient states that this feels similar to when she had pneumonia in the past. Patient states been taking inhaler, with minimal relief. Patient denies any sick contacts. Patient denies any active chest pain. Patient denies abdominal pain, nausea or vomiting. October 2023 – Cardiology Consult:
• The patient was admitted to hospital for dyspnea and treated for acute systolic heart failure exacerbation.
• Noted on Echo: Severely reduced LVEF 25%. The patient has had intermittent shortness of breath which was worse the days leading up to this presentation. She thought it was related to black mold, environmental exposure in her home. She has had intermittent lower extremity edema. On presentation she was started on furosemide and has had improvement in her dyspnea. She denies chest pain at rest or with exertion. She has not had near syncope or syncope. Rare palpitations.
• In the past she has had EKG with non-specific T-wave abnormalities in V1-V6 significant for possible anterolateral ischemia:
• Diagnosed as NYHA class III heart failure based on symptoms. Acute systolic heart failure due to mixed ischemic and non-ischemic dilated cardiomyopathy
• Patient treated based on guidelines, acutely with furosemide and long-term with guideline directed medical therapy
• Patient high-risk for sudden cardiac death so has been given a life vest
She has a strong family history of cardiomyopathy and multiple first-degree relatives with cardiomyopathies and early coronary disease. Her 26-year-old son died suddenly from a cardiomyopathy.
• Current Facility-Administered Medications:
o atorvastatin (Lipitor) tablet 10 mg, 10 mg, oral
o dapagliflozin propanediol (Farxiga) tablet 10 mg, 10 mg, oral
o furosemide (Lasix) injection 20 mg, 20 mg, intravenous, Daily
o magnesium oxide (Mag-Ox) tablet 400 mg, 400 mg, oral, BID with meals, ondansetron (Zofran) injection 4 mg, 4 mg, intravenous
Review of Systems:
The patient has loss of sleep only obtaining 5 hours of sleep in an 8 hour timeframe due to pain and discomfort. This results in daytime fatigue. She has weakness of the right upper extremity, neck and back. The patient denies areas of interest in the following categories: HEENT, Respiration, Cardiac, GI, GU, Vascular, Other Musculoskeletal, Other neurologic, Hematologic, Endocrine, Skin and Psychiatric.
Exam
On the initial visit to the Doctor of Chiropractic the following was recorded: The patient is 5’1” and weighs 170 pounds. Blood pressure of the left arm and the seated position is 134/84 mmHg.
Ranges of motion were measured by Dual Inclinometry. Findings were compared to “normal” from The AMA Guides to the Evaluation of Permanent Impairment 5th Edition. Active range of motion of the cervical spine revealed flexion to be accomplished to 13°/50°, left rotation to 20°/80°, right rotation to 25°/80°, left lateral bending to 14°/45°, right lateral bending to 12°/45° and extension to 9°/60°. She reports neck pain with all ranges of motion. The bicep and triceps reflexes were graded 2/4 bilaterally. Active range of motion of the shoulders revealed the right shoulder could be elevated to 90° with report of right shoulder pain. The left shoulder could be fully elevated. Neer’s testing revealed the right shoulder could be elevated to 90° with report of right shoulder pain. The Hawkins-Kennedy and supraspinatus procedures were positive on the right side. Muscle strengths of the upper extremities revealed a weakness of the proximal muscles of the right shoulder. She also demonstrated a weakness of the right supraspinatus muscle graded 4/5. Cervical compression testing revealed neck pain radiating down the right upper extremity with tingling in the right hand. Grip strength was tested using a Jamar dynamometer. The right hand tested to 35 pounds and the left hand tested to 45 pounds. She is left hand dominant. Active range of motion of the thoracic spine revealed flexion to be accomplished to 4°/30° with report of right mid and lower back pain.
Postural evaluation revealed a low left shoulder and even hips. Muscle spasm was noted in the thoracic and lumbar regions paraspinally. Active range of motion of the lumbar spine revealed flexion to be accomplished to 18°/60°, left lateral bending to 9°/25°, right lateral bending to 4°/25° and extension to 3°/25°. She reported lower back pain with these ranges of motion. The subpatellar and Achilles reflexes were graded 2/4 bilaterally. She was able to arise onto her toes in the static position. She demonstrated right ankle dorsiflexion weakness on the right side. She was able to perform a partial squat with report of lower back pain. He was able to arise onto his toes and heels in the static position. She was able to perform a partial squat with report of lower back pain. The straight leg raise could be accomplished to 40° on the right side with report of right lower back pain. The straight leg raise on the left side could be performed to 35° with report of lower back pain extending down the right lower extremity to the ankle. Muscle strengths of the lower extremities revealed a weakness of the right quadricep and right extensor hallucis each graded 4/5. Percussion and posterior to anterior compression of the spine produced report of pain over the mid dorsal and lower back regions.
Hypomobility was noted at C2-6, T1-4 T7-10, T12-L5, sacrum base, and bilateral Ilium. Muscle spasm was noted over the cervicothoracic and lumbar regions paraspinally. Pain/tenderness, asymmetry/misalignment, abnormal range of motion, and tissue/tone changes were associated with the areas of hypomobility.
INDICES:
The patient completed a Revised Oswestry Low Back Pain Disability Questionnaire on 07/20/2023 and scored 70%. The patient completed a Neck Disability Index Questionnaire on 07/20/2023 and scored 54%. The patient completed a Rivermead Post Concussion Symptoms Questionnaire and scored 3 in the RPQ-3 category and scored 23 in the RPQ-13 category. DISABILITY: The patient has a temporary total disability relative to the MVC of 07/19/2023.
The patient completed a Revised Oswestry Low Back Pain Disability Questionnaire on 07/20/2023 and scored 70%. The patient completed a Neck Disability Index Questionnaire on 07/20/2023 and scored 54%. The patient completed a Rivermead Post Concussion Symptoms Questionnaire and scored 3 in the RPQ-3 category and scored 23 in the RPQ-13 category. DISABILITY: The patient has a temporary total disability relative to the MVC of 07/19/2023.
Findings
MRI LUMBAR SPINE – Performed in August 2023.
• Anterior spurring is/bulging is noted at the T11-12 and L4-5 levels. L4-5: There is a diffuse disc bulge of the annulus fibrosus with faint central annular tear measuring less than 2 mm in AP dimension which encroaches upon the anterior surface of the thecal sac. No significant foraminal stenosis is evident.
• L5-S1: There is a diffuse disc bulge of the annulus fibrosus with faint central annular tear measuring less than 2 mm in AP dimension which encroaches upon the anterior epidural fat. No significant foraminal stenosis is evident.
MRI RIGHT SHOULDER – Performed in August 2023:
• A LABRAL TEAR IS NOTED, BEST SEEN ANTERIORLY ON THE AXIAL IMAGES. THERE IS TENDINOPATHY OF THE LONG HEAD OF THE BICEPS TENDON.
• THERE IS ABNORMAL SIGNAL AT THE RIGHT SUPRASPINOUS TENDON COMPATIBLE PARTIAL/INTRASUBSTANCE TEAR. THERE IS A MINIMAL AMOUNT OF FLUID WITHIN THE SUBACROMIAL-SUBDELTOID BURSA COMPATIBLE WITH MICROPERFORATION OF THE ROTATOR CUFF.
• THERE ARE NO FOCAL BONY CONTUSIONS.
MRI CERVICAL SPINE –
• C3-4: THERE IS A CENTRAL DISC HERNIATION PROTRUSION OF THE TYPE MEASURING LESS THAN 2 MM IN AP DIMENSION WHICH ENCROACHES UPON THE ANTERIOR SUBARACHNOID SPACE. NO SIGNIFICANT FORAMINAL STENOSIS IS EVIDENT.
• C4-5: THERE IS A BROAD-BASED CENTRAL DISC HERNIATION OF THE PROTRUSION TYPE MEASURING APPROXIMATELY 2 MM IN AP DIMENSION WHICH ENCROACHES UPON THE ANTERIOR SUBARACHNOID SPACE. NO SIGNIFICANT FORAMINAL STENOSIS IS EVIDENT.
• C5-6: THERE IS A BROAD-BASED CENTRAL DISC HERNIATION OF THE PROTRUSION TYPE MEASURING APPROXIMATELY 3 MM IN GREATEST AP DIMENSION WITH SLIGHT ASYMMETRY TO THE LEFT WHICH PARTIALLY EFFACES THE ANTERIOR/LEFT ANTERIOR SUBARACHNOID SPACE. BORDERLINE CENTRAL CANAL STENOSIS IS NOTED. NO SIGNIFICANT FORAMINAL STENOSIS IS EVIDENT.
• C6-7: THERE IS A RIGHT PARACENTRAL DISC HERNIATION OF THE PROTRUSION TYPE MEASURING APPROXIMATELY 2 MM IN AP DIMENSION WHICH ENCROACHES UPON THE RIGHT ANTERIOR SUBARACHNOID SPACE. NO SIGNIFICANTFORAMINAL STENOSIS IS EVIDENT.
• September 2023 Plain Film Chest Radiography:
o FINDINGS/IMPRESSION: Unchanged cardiac and mediastinal contours. No focal consolidation, pleural effusion, or pneumothorax. Bones without acute findings.
● CTA Chest October 2023:
● FINDINGS:
○ Pulmonary arteries: Contrast bolus is optimal. No central segmental or subsegmental
○ pulmonary artery filling defects identified.
○ Thyroid: Visualized portion unremarkable.
○ Lymph Nodes: There are few about 2 cm pathologically enlarged in the AP window and cutdown of the afternoon catheter.
○ Heart/Pericardium: Unremarkable. No pericardial effusion. no evidence of aortic aneurysm or dissection.
○ Mediastinum: Unremarkable.
○ Major Vasculature: Unremarkable.
○ Lungs/Airways/Pleura: Small bilateral pleural effusion and bibasal compressive atelectasis left greater than right. No pneumothorax identified. Major central lobar bronchi are patent.
○ Bones/Body Wall: Unremarkable.
○ Upper abdomen: Unremarkable.
● EKG: Sinus tachycardia, nonspecific T wave abnormality ● Echo: Mildly dilated left ventricle, global severely reduced LV systolic function, EF 25%, moderately reduced RV function ● LHC and RHC: There is severe left ventricular systolic dysfunction. EF around 20 to 25%. This is likely mixed ischemic/nonischemic cardiomyopathy because the degree of cardiomyopathy is out of proportion with the one-vessel CAD. One-vessel CAD with an occluded right coronary artery which is well collateralized via right to right and left-to-right collaterals. Guideline directed medical therapy for cardiomyopathy and CAD. ● November 2023: Cardiac MRI:
○ This study was protocoled to evaluate cardiac morphology and function only.
○ Morphology: ■ Right Heart: The right ventricle is mildly dilated in size with mildly reduced systolic function. The right atrium is mildly dilated in size.
■ Left Ventricle: The left ventricle is moderately dilated in size. Prominent trabeculation of the LV apex but no criteria fulfilling LV non-compaction.
■ Left Atrium: The left atrium is mildly dilated in size and measures 4.8cm in its maximal dimension.
■ Pericardium: Normal pericardium.
■ Ascending aorta at the level of the pulmonary artery bifurcation: (normal).
■ Descending aorta at the level of the pulmonary artery bifurcation: (normal)
■ Pulmonary artery at the level of the bifurcation: (normal)
■ Function:
■ LV end diastolic volume = 174 ml
■ LV end systolic volume = 131 ml
■ LV stroke volume = 42 ml
■ LVEF = 24%
■ RVEF = 31%
■ Wall Motion: The cine acquisitions demonstrate severe global systolic dysfunction of the left ventricle.
■ Cardiac Valves: This MRI was not protocoled to assess for significant valvular regurgitation or stenoses. However, mild mitral regurgitation noted.
■ Gadolinium Enhanced Images: Late gadolinium enhanced images demonstrate abnormal late gadolinium enhancement of the mid-septal walls, which is commonly seen in dilated cardiomyopathy. No evidence of myocardial infarction or inflltrative process.
• Anterior spurring is/bulging is noted at the T11-12 and L4-5 levels. L4-5: There is a diffuse disc bulge of the annulus fibrosus with faint central annular tear measuring less than 2 mm in AP dimension which encroaches upon the anterior surface of the thecal sac. No significant foraminal stenosis is evident.
• L5-S1: There is a diffuse disc bulge of the annulus fibrosus with faint central annular tear measuring less than 2 mm in AP dimension which encroaches upon the anterior epidural fat. No significant foraminal stenosis is evident.
MRI RIGHT SHOULDER – Performed in August 2023:
• A LABRAL TEAR IS NOTED, BEST SEEN ANTERIORLY ON THE AXIAL IMAGES. THERE IS TENDINOPATHY OF THE LONG HEAD OF THE BICEPS TENDON.
• THERE IS ABNORMAL SIGNAL AT THE RIGHT SUPRASPINOUS TENDON COMPATIBLE PARTIAL/INTRASUBSTANCE TEAR. THERE IS A MINIMAL AMOUNT OF FLUID WITHIN THE SUBACROMIAL-SUBDELTOID BURSA COMPATIBLE WITH MICROPERFORATION OF THE ROTATOR CUFF.
• THERE ARE NO FOCAL BONY CONTUSIONS.
MRI CERVICAL SPINE –
• C3-4: THERE IS A CENTRAL DISC HERNIATION PROTRUSION OF THE TYPE MEASURING LESS THAN 2 MM IN AP DIMENSION WHICH ENCROACHES UPON THE ANTERIOR SUBARACHNOID SPACE. NO SIGNIFICANT FORAMINAL STENOSIS IS EVIDENT.
• C4-5: THERE IS A BROAD-BASED CENTRAL DISC HERNIATION OF THE PROTRUSION TYPE MEASURING APPROXIMATELY 2 MM IN AP DIMENSION WHICH ENCROACHES UPON THE ANTERIOR SUBARACHNOID SPACE. NO SIGNIFICANT FORAMINAL STENOSIS IS EVIDENT.
• C5-6: THERE IS A BROAD-BASED CENTRAL DISC HERNIATION OF THE PROTRUSION TYPE MEASURING APPROXIMATELY 3 MM IN GREATEST AP DIMENSION WITH SLIGHT ASYMMETRY TO THE LEFT WHICH PARTIALLY EFFACES THE ANTERIOR/LEFT ANTERIOR SUBARACHNOID SPACE. BORDERLINE CENTRAL CANAL STENOSIS IS NOTED. NO SIGNIFICANT FORAMINAL STENOSIS IS EVIDENT.
• C6-7: THERE IS A RIGHT PARACENTRAL DISC HERNIATION OF THE PROTRUSION TYPE MEASURING APPROXIMATELY 2 MM IN AP DIMENSION WHICH ENCROACHES UPON THE RIGHT ANTERIOR SUBARACHNOID SPACE. NO SIGNIFICANTFORAMINAL STENOSIS IS EVIDENT.
• September 2023 Plain Film Chest Radiography:
o FINDINGS/IMPRESSION: Unchanged cardiac and mediastinal contours. No focal consolidation, pleural effusion, or pneumothorax. Bones without acute findings.
● CTA Chest October 2023:
● FINDINGS:
○ Pulmonary arteries: Contrast bolus is optimal. No central segmental or subsegmental
○ pulmonary artery filling defects identified.
○ Thyroid: Visualized portion unremarkable.
○ Lymph Nodes: There are few about 2 cm pathologically enlarged in the AP window and cutdown of the afternoon catheter.
○ Heart/Pericardium: Unremarkable. No pericardial effusion. no evidence of aortic aneurysm or dissection.
○ Mediastinum: Unremarkable.
○ Major Vasculature: Unremarkable.
○ Lungs/Airways/Pleura: Small bilateral pleural effusion and bibasal compressive atelectasis left greater than right. No pneumothorax identified. Major central lobar bronchi are patent.
○ Bones/Body Wall: Unremarkable.
○ Upper abdomen: Unremarkable.
● EKG: Sinus tachycardia, nonspecific T wave abnormality ● Echo: Mildly dilated left ventricle, global severely reduced LV systolic function, EF 25%, moderately reduced RV function ● LHC and RHC: There is severe left ventricular systolic dysfunction. EF around 20 to 25%. This is likely mixed ischemic/nonischemic cardiomyopathy because the degree of cardiomyopathy is out of proportion with the one-vessel CAD. One-vessel CAD with an occluded right coronary artery which is well collateralized via right to right and left-to-right collaterals. Guideline directed medical therapy for cardiomyopathy and CAD. ● November 2023: Cardiac MRI:
○ This study was protocoled to evaluate cardiac morphology and function only.
○ Morphology: ■ Right Heart: The right ventricle is mildly dilated in size with mildly reduced systolic function. The right atrium is mildly dilated in size.
■ Left Ventricle: The left ventricle is moderately dilated in size. Prominent trabeculation of the LV apex but no criteria fulfilling LV non-compaction.
■ Left Atrium: The left atrium is mildly dilated in size and measures 4.8cm in its maximal dimension.
■ Pericardium: Normal pericardium.
■ Ascending aorta at the level of the pulmonary artery bifurcation: (normal).
■ Descending aorta at the level of the pulmonary artery bifurcation: (normal)
■ Pulmonary artery at the level of the bifurcation: (normal)
■ Function:
■ LV end diastolic volume = 174 ml
■ LV end systolic volume = 131 ml
■ LV stroke volume = 42 ml
■ LVEF = 24%
■ RVEF = 31%
■ Wall Motion: The cine acquisitions demonstrate severe global systolic dysfunction of the left ventricle.
■ Cardiac Valves: This MRI was not protocoled to assess for significant valvular regurgitation or stenoses. However, mild mitral regurgitation noted.
■ Gadolinium Enhanced Images: Late gadolinium enhanced images demonstrate abnormal late gadolinium enhancement of the mid-septal walls, which is commonly seen in dilated cardiomyopathy. No evidence of myocardial infarction or inflltrative process.
Differential Diagnosis
Mechanical back pain
Degenerative disc disease
Spinal Stenosis
Osteoporotic compression fracture
Spondylolysis
Kidney disease Neoplasm
Osteomyelitis
Inflammatory arthritis
Cervical disc herniation
Cervical strain/sprain
Thoracic strain/sprain
Lumbar strain/sprain
Lumbar disc herniation
Lumbar radiculopathy
Impingement syndrome
Supraspinatus sprain
Supraspinatus tear
Cervical subluxation
Thoracic subluxation
Lumbar subluxation
Sacral subluxation
Pelvic subluxation
When the patient initiated care following the MVC she did not have a cardiac condition. However, later it presented itself with the following Differential Diagnosis:
● Pneumonia
● Pulmonary Embolism
● Cardiomyopathy
● Acute systolic heart failure
Degenerative disc disease
Spinal Stenosis
Osteoporotic compression fracture
Spondylolysis
Kidney disease Neoplasm
Osteomyelitis
Inflammatory arthritis
Cervical disc herniation
Cervical strain/sprain
Thoracic strain/sprain
Lumbar strain/sprain
Lumbar disc herniation
Lumbar radiculopathy
Impingement syndrome
Supraspinatus sprain
Supraspinatus tear
Cervical subluxation
Thoracic subluxation
Lumbar subluxation
Sacral subluxation
Pelvic subluxation
When the patient initiated care following the MVC she did not have a cardiac condition. However, later it presented itself with the following Differential Diagnosis:
● Pneumonia
● Pulmonary Embolism
● Cardiomyopathy
● Acute systolic heart failure
Case Diagnosis
Post MVC Cervical Disc Herniation, Lumbar Discopathy and Comorbidity of Severe Dilated Cardiomyopathy with LVEF of 25% and RVEF of 31%
Diagnosis By
Clinical examination, MRI Spine, BNP, EKG, echo, cardiac catheterization, and cardiac MRI.
Treatment & Follow Up
The patient received Cox Table flexion-distraction care. The patient was unable to lie on her back for care due to the cardiac problem but was able to lie prone. This worked out well for the patient as Cox procedures have the patient in the prone position.
Relative to the Cardiac Problem:
● LifeVest for increased risk of sudden cardiac death, followed by ICD implantation
● Medication adjustments: Furosemide, Lisinopril, Metoprolol, Spironolactone, Farxiga, Aspirin, Atorvastatin
● Evaluation for transplant/LVAD
● LifeVest for increased risk of sudden cardiac death, followed by ICD implantation
● Medication adjustments: Furosemide, Lisinopril, Metoprolol, Spironolactone, Farxiga, Aspirin, Atorvastatin
● Evaluation for transplant/LVAD
Discussion
Etiology and Pathophysiology
DCM is characterized by ventricular chamber enlargement and systolic dysfunction, which can occur in the absence of coronary artery disease or abnormal loading conditions like hypertension or valve diseases. The etiology of DCM is multifactorial, encompassing both genetic and acquired factors. Genetic predispositions contribute to primary DCM, while acquired factors include myocardial damage due to infections, exposure to toxins, autoimmune responses, and adverse effects of certain cancer therapies. Recent studies estimate that 5-15% of patients with acquired DCM have a pathogenic gene variant, underscoring the importance of genetic screening in DCM diagnosis and management [1]. Diagnostic Approaches
Diagnosis of DCM primarily involves imaging techniques such as echocardiography, which reveals left ventricular dilation and impaired contractility. Cardiac MRI provides detailed information about ventricular structure, function, and the presence of fibrosis, which is a key marker of adverse prognosis in DCM. Genetic testing is becoming increasingly relevant, especially for familial cases of DCM, to identify specific mutations that may guide treatment and family screening [2]. Treatment Strategies
The management of DCM has evolved significantly, with a shift towards comprehensive care that includes both pharmacologic and non-pharmacologic approaches. Pharmacotherapy commonly involves the use of ACE inhibitors, beta-blockers, and diuretics, which reduce myocardial stress and improve symptoms. Advanced heart failure in DCM may require the use of device therapy, such as implantable cardioverter-defibrillators (ICDs) for arrhythmia management and ventricular assist devices as a bridge to transplantation or as destination therapy. Emerging therapies are also focusing on targeting specific pathways involved in DCM pathogenesis, including inflammatory and metabolic pathways [3] Prognosis and Follow-Up:
The prognosis of DCM varies widely and depends on the etiology, severity of cardiac dysfunction, and response to treatment. Patients with DCM are at increased risk for arrhythmias, heart failure progression, and thromboembolic events. Regular follow-up and monitoring of cardiac function, rhythm disturbances, and response to therapy are essential components of DCM management. Lifestyle modifications, including diet, exercise, and avoidance of alcohol and tobacco, play a crucial role in the overall management and prognosis of DCM patients. [1] In summary, DCM is a complex cardiovascular disorder with diverse etiologies and a wide spectrum of clinical manifestations. Its management requires a multidimensional approach that encompasses genetic evaluation, advanced imaging, targeted pharmacotherapy, device therapy, and lifestyle modifications. Ongoing research and clinical trials continue to enhance our understanding and treatment of this challenging condition. As one radiologist (Dr. Buehler personal communication), has said the patient always reserves the right to have more than one condition. In the course of treatment this patient then experienced another condition that required the treating Doctors of Chiropractic to be cognizant and modify treatment care. Although initially she could tolerate electrical muscle stimulation to areas of muscle spasm the onset of cardiac myopathy and placement of the Life Vest required a cessation of that type of care. It is important for the Doctor of Chiropractic to understand and have a working knowledge of visceral conditions as such can directly impact care. With regard to the Cox Table flexion-distraction therapy: The treatment plan for this patient includes Flexion-Distraction therapy, electrical stimulation along the thoracic and lumbar spine, chiropractic manipulation, ultrasound therapy to the cervical region and exercises to stabilize the paraspinal muscles and improve biomechanics. Flexion-Distraction therapy applies gentle traction to the spinal column in order to widen the intervertebral space, spinal canal, and foraminal openings [4,5,6,7]. Flexion distraction manipulation is monitored with careful tolerance testing of patient reaction to the performance. The foramen magnum pump is first tested for tolerance testing to determine if it causes dural stretch pain in the low back; this can help to identify the level of mechanical or inflammatory presence. The value in this treatment is that as she found herself uncomfortable to lie supine due to her cardiac problem and could lie prone for this gentle mobilization. The presence of disc herniation on MRI although definitive in and of itself, must be correlated with functional findings. In worker’s compensation and under No-Fault Law it is important to establish the causal relationship. The importance of the ROM-sEMG (DynaROM) [8] evaluation is to demonstrate the physiological relationship between the patient’s symptoms, MRI findings and what is in this case aberrant findings on evaluation. In this case she has right sided upper extremity pain that extends to the right hand felt to be related to MRI findings of disc herniation at C5/C6. Cervical compression testing did produce cervical pain that extended down the right upper extremity to the hand. Activation of right sided muscles will likely aggravate her symptoms. As such, she uses a guarded and learned mechanism during cervical ranges of motion where she protects the right side and activates left sided muscles. This then demonstrates a supporting relationship between the injury from the MVC and the functional effect. 1. Heymans S, Lakdawala NK, Tschöpe C, Klingel K. Dilated cardiomyopathy: causes, mechanisms, and current and future treatment approaches. Lancet. 2023;402(10406):998-1011. doi:10.1016/S0140-6736(23)01241-2. 2. Merlo M, Masè M, Cannatà A, et al. Management of nonischemic-dilated cardiomyopathies in clinical practice: a position paper of the working group on myocardial and pericardial diseases of the Italian Society of Cardiology. J Cardiovasc Med (Hagerstown). 2020;21(12):927-943. doi:10.2459/JCM.0000000000001050. 3. Castelli G, Fornaro A, Ciaccheri M, et al. Improving survival rates of patients with idiopathic dilated cardiomyopathy in Tuscany over 3 decades: impact of evidence-based management. Circ Heart Fail. 2013;6(5):913-921. doi:10.1161/CIRCHEARTFAILURE.112.000120. 4. Cox JM. Neck Shoulder, Arm Pain: Mechanism, Diagnosis and Treatment (4th ed/). Cox® Technic Resource Center, Inc. Fort Wayne, IN ; 2014 5. Oh, H., Lee, S., Lee, K., & Jeong, M. (2018). The effects of flexion-distraction and drop techniques on disorders and Ferguson's angle in female patients with lumbar intervertebral disc herniation. Journal of physical therapy science, 30(4), 536–539.
https://doi.org/10.1589/jpts.30.536 6. Choi, J., Lee, S., & Jeon, C. (2015). Effects of flexion-distraction manipulation therapy on pain and disability in patients with lumbar spinal stenosis. Journal of physical therapy science, 27(6), 1937–1939.
https://doi.org/10.1589/jpts.27.1937 7. Cox JM. Low back pain: Mechanism, diagnosis, treatment (7th ed.). Philadelphia, PA: Wolters Kluwer/Lippincott Williams; Wilkins Health; 2011. 8. Myovision.com
DCM is characterized by ventricular chamber enlargement and systolic dysfunction, which can occur in the absence of coronary artery disease or abnormal loading conditions like hypertension or valve diseases. The etiology of DCM is multifactorial, encompassing both genetic and acquired factors. Genetic predispositions contribute to primary DCM, while acquired factors include myocardial damage due to infections, exposure to toxins, autoimmune responses, and adverse effects of certain cancer therapies. Recent studies estimate that 5-15% of patients with acquired DCM have a pathogenic gene variant, underscoring the importance of genetic screening in DCM diagnosis and management [1]. Diagnostic Approaches
Diagnosis of DCM primarily involves imaging techniques such as echocardiography, which reveals left ventricular dilation and impaired contractility. Cardiac MRI provides detailed information about ventricular structure, function, and the presence of fibrosis, which is a key marker of adverse prognosis in DCM. Genetic testing is becoming increasingly relevant, especially for familial cases of DCM, to identify specific mutations that may guide treatment and family screening [2]. Treatment Strategies
The management of DCM has evolved significantly, with a shift towards comprehensive care that includes both pharmacologic and non-pharmacologic approaches. Pharmacotherapy commonly involves the use of ACE inhibitors, beta-blockers, and diuretics, which reduce myocardial stress and improve symptoms. Advanced heart failure in DCM may require the use of device therapy, such as implantable cardioverter-defibrillators (ICDs) for arrhythmia management and ventricular assist devices as a bridge to transplantation or as destination therapy. Emerging therapies are also focusing on targeting specific pathways involved in DCM pathogenesis, including inflammatory and metabolic pathways [3] Prognosis and Follow-Up:
The prognosis of DCM varies widely and depends on the etiology, severity of cardiac dysfunction, and response to treatment. Patients with DCM are at increased risk for arrhythmias, heart failure progression, and thromboembolic events. Regular follow-up and monitoring of cardiac function, rhythm disturbances, and response to therapy are essential components of DCM management. Lifestyle modifications, including diet, exercise, and avoidance of alcohol and tobacco, play a crucial role in the overall management and prognosis of DCM patients. [1] In summary, DCM is a complex cardiovascular disorder with diverse etiologies and a wide spectrum of clinical manifestations. Its management requires a multidimensional approach that encompasses genetic evaluation, advanced imaging, targeted pharmacotherapy, device therapy, and lifestyle modifications. Ongoing research and clinical trials continue to enhance our understanding and treatment of this challenging condition. As one radiologist (Dr. Buehler personal communication), has said the patient always reserves the right to have more than one condition. In the course of treatment this patient then experienced another condition that required the treating Doctors of Chiropractic to be cognizant and modify treatment care. Although initially she could tolerate electrical muscle stimulation to areas of muscle spasm the onset of cardiac myopathy and placement of the Life Vest required a cessation of that type of care. It is important for the Doctor of Chiropractic to understand and have a working knowledge of visceral conditions as such can directly impact care. With regard to the Cox Table flexion-distraction therapy: The treatment plan for this patient includes Flexion-Distraction therapy, electrical stimulation along the thoracic and lumbar spine, chiropractic manipulation, ultrasound therapy to the cervical region and exercises to stabilize the paraspinal muscles and improve biomechanics. Flexion-Distraction therapy applies gentle traction to the spinal column in order to widen the intervertebral space, spinal canal, and foraminal openings [4,5,6,7]. Flexion distraction manipulation is monitored with careful tolerance testing of patient reaction to the performance. The foramen magnum pump is first tested for tolerance testing to determine if it causes dural stretch pain in the low back; this can help to identify the level of mechanical or inflammatory presence. The value in this treatment is that as she found herself uncomfortable to lie supine due to her cardiac problem and could lie prone for this gentle mobilization. The presence of disc herniation on MRI although definitive in and of itself, must be correlated with functional findings. In worker’s compensation and under No-Fault Law it is important to establish the causal relationship. The importance of the ROM-sEMG (DynaROM) [8] evaluation is to demonstrate the physiological relationship between the patient’s symptoms, MRI findings and what is in this case aberrant findings on evaluation. In this case she has right sided upper extremity pain that extends to the right hand felt to be related to MRI findings of disc herniation at C5/C6. Cervical compression testing did produce cervical pain that extended down the right upper extremity to the hand. Activation of right sided muscles will likely aggravate her symptoms. As such, she uses a guarded and learned mechanism during cervical ranges of motion where she protects the right side and activates left sided muscles. This then demonstrates a supporting relationship between the injury from the MVC and the functional effect. 1. Heymans S, Lakdawala NK, Tschöpe C, Klingel K. Dilated cardiomyopathy: causes, mechanisms, and current and future treatment approaches. Lancet. 2023;402(10406):998-1011. doi:10.1016/S0140-6736(23)01241-2. 2. Merlo M, Masè M, Cannatà A, et al. Management of nonischemic-dilated cardiomyopathies in clinical practice: a position paper of the working group on myocardial and pericardial diseases of the Italian Society of Cardiology. J Cardiovasc Med (Hagerstown). 2020;21(12):927-943. doi:10.2459/JCM.0000000000001050. 3. Castelli G, Fornaro A, Ciaccheri M, et al. Improving survival rates of patients with idiopathic dilated cardiomyopathy in Tuscany over 3 decades: impact of evidence-based management. Circ Heart Fail. 2013;6(5):913-921. doi:10.1161/CIRCHEARTFAILURE.112.000120. 4. Cox JM. Neck Shoulder, Arm Pain: Mechanism, Diagnosis and Treatment (4th ed/). Cox® Technic Resource Center, Inc. Fort Wayne, IN ; 2014 5. Oh, H., Lee, S., Lee, K., & Jeong, M. (2018). The effects of flexion-distraction and drop techniques on disorders and Ferguson's angle in female patients with lumbar intervertebral disc herniation. Journal of physical therapy science, 30(4), 536–539.
https://doi.org/10.1589/jpts.30.536 6. Choi, J., Lee, S., & Jeon, C. (2015). Effects of flexion-distraction manipulation therapy on pain and disability in patients with lumbar spinal stenosis. Journal of physical therapy science, 27(6), 1937–1939.
https://doi.org/10.1589/jpts.27.1937 7. Cox JM. Low back pain: Mechanism, diagnosis, treatment (7th ed.). Philadelphia, PA: Wolters Kluwer/Lippincott Williams; Wilkins Health; 2011. 8. Myovision.com
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Congestive Heart Failure with an Emphasis on Imaging
Disease Discussion
Definitions:
Congestive Heart Failure (CHF) is a complex clinical syndrome characterized by the heart's inability to pump sufficient blood to meet the body's needs (1). It is broadly classified into two types based on ejection fraction, which is a measurement of the percentage of blood leaving the heart each time it contracts. Heart Failure with Reduced Ejection Fraction (HFrEF), often referred to as systolic heart failure, is defined by a significantly impaired ejection fraction, typically considered to be below 40%. This condition is characterized by a weakened heart muscle that cannot contract effectively (2). On the other hand, Heart Failure with Preserved Ejection Fraction (HFpEF), also known as diastolic heart failure, occurs when the heart muscle becomes stiff and is unable to relax properly, leading to inadequate filling of the heart with blood. In HFpEF, the ejection fraction is usually normal (above 50%), but the heart's ability to relax and fill is compromised (3). Key terms associated with heart failure include "cardiac output," which is the amount of blood the heart pumps in a minute, and "cardiac index," a measure of cardiac output relative to body size (4). "Stroke volume" refers to the amount of blood pumped by the left ventricle of the heart in one contraction, and "preload" and "afterload" are terms that describe the volume of blood in the ventricle at the end of diastole (preload) and the resistance the heart must overcome to eject blood (afterload) (4). Understanding these different types of heart failure and related terms is crucial for diagnosis, treatment planning, and management of the condition. History:
The historical understanding of CHF has undergone significant evolution. In ancient times, theories of heart failure were primarily based on the imbalance of the four humors. The concept of cardiac failure as a clinical entity emerged in the 17th century with the work of English physician William Harvey, who described the circulatory system. However, it was not until the 20th century that major strides in understanding and treating CHF were made. The development of diagnostic tools like the electrocardiogram and later, echocardiography, revolutionized the ability to assess heart function (5). Significant milestones in CHF research and treatment include the introduction of diuretics in the 1950s, beta-blockers in the 1960s, and ACE inhibitors in the 1970s (5). The late 20th and early 21st centuries saw an expansion in the understanding of the molecular and neurohormonal mechanisms underlying heart failure, leading to more targeted therapies (5). The recognition of the distinct entity of HFpEF, alongside HFrEF, marked a crucial development in tailoring treatment strategies (5). These advancements have transformed CHF from a once invariably fatal condition to one that can often be managed effectively with a combination of lifestyle changes, medication, and in some cases, surgical intervention. Anatomical and Etiological Considerations:
CHF is characterized by significant structural changes in the heart, primarily affecting its ability to pump blood efficiently (1). In CHF, the heart muscle may become weakened (in HFrEF) or stiffened (in HFpEF), leading to either reduced contraction or impaired relaxation capabilities, respectively. These alterations can result in dilated or hypertrophied ventricles, impacting the heart's pumping efficacy (6). The etiology of CHF is multifactorial, involving a combination of lifestyle factors, genetic predispositions, and underlying diseases. Key contributors include coronary artery disease, leading to reduced blood supply to the heart muscle; hypertension, imposing excessive workload on the heart; valvular heart diseases, affecting the flow of blood through the heart; and cardiomyopathies, which directly impair the heart muscle's structure and function. Lifestyle factors such as obesity, sedentary habits, and smoking can exacerbate these conditions or independently contribute to heart failure (7). Genetic factors also play a role, with certain genetic mutations being linked to an increased risk of developing specific types of heart failure (7). Incidence:
CHF represents a significant global health concern, with its incidence and prevalence demonstrating notable demographic variations. Globally, CHF affects millions, with higher prevalence rates observed in developed countries, partly due to better diagnostic capabilities and aging populations (8). The incidence of CHF is notably higher in older adults, making it a leading cause of hospitalization for those over 65 (8). Additionally, improvements in medical treatments for acute cardiac events, such as myocardial infarctions, have led to increased survival rates, subsequently contributing to a rise in the number of individuals living with CHF (8). This trend underscores the growing need for effective CHF management strategies tailored to diverse populations and age groups. Symptoms:
Symptoms of CHF vary widely among patients and are closely tied to the severity and progression of the disease. Common symptoms include shortness of breath (dyspnea), particularly during exertion or while lying flat (orthopnea); fatigue and weakness, which may limit daily activities; and swelling (edema) in the legs, ankles, and feet (9). Fluid retention can also lead to rapid weight gain and bloating. As CHF progresses, these symptoms typically become more severe and may occur even at rest. Advanced stages of CHF can lead to severe pulmonary congestion, causing breathlessness and coughing, especially at night (termed paroxysmal nocturnal dyspnea) (9). The severity and combination of these symptoms are critical in assessing the stage of heart failure and guiding treatment strategies. Clinical Findings:
In patients with CHF, clinical findings during physical examination are pivotal for assessment and diagnosis. Common findings include jugular venous distension, indicating increased right atrial pressure (10). Pulmonary examination might reveal crackles or wheezes, suggestive of pulmonary congestion. Patients often exhibit peripheral edema, especially in the lower extremities, indicative of fluid retention. Cardiac auscultation can reveal third or fourth heart sounds (S3 or S4 gallop), which are significant markers of CHF (11). Additionally, arrythmias might be noted (11). These clinical findings, when combined with patient history and symptoms, play a crucial role in diagnosing CHF, assessing its severity, and guiding the course of treatment. Diagnosis:
The diagnosis of CHF involves a combination of clinical evaluation and various diagnostic tools. The primary criteria for diagnosis include patient history, physical examination, and symptoms such as dyspnea, fatigue, and edema. Diagnostic methodologies extend beyond these basic assessments, incorporating advanced imaging technologies which play a crucial role (12). Echocardiography is the gold-standard imaging tool in CHF diagnosis, providing detailed information about the heart's structure, function, and the presence of any abnormalities. It helps in assessing ejection fraction, a key indicator in differentiating between HFrEF and HFpEF (13). Cardiac Magnetic Resonance Imaging (MRI) offers a more detailed view of the heart's anatomy and function, particularly useful in complex cases, evaluating for sarcoidosis or when echocardiography results are inconclusive. It excels in assessing myocardial scarring and viability, which can guide treatment decisions (14). Chest X-rays, though less specific than echocardiography and MRI, are often used to identify pulmonary congestion and other structural changes in the chest that may be associated with heart failure (15). Additionally, laboratory tests, including natriuretic peptide levels, provide supportive diagnostic information and can help in assessing the severity of CHF. The integration of these diagnostic methodologies allows for a comprehensive evaluation of CHF, facilitating accurate diagnosis and effective management of the condition (15). Differential Diagnosis:
The differential diagnosis of CHF includes a range of conditions that present with similar symptoms, such as dyspnea, fatigue, and edema. Primary among these are respiratory disorders like chronic obstructive pulmonary disease (COPD) and asthma, which can cause shortness of breath and wheezing. Pulmonary embolism is another condition that mimics CHF, characterized by acute onset dyspnea and chest pain (1). Renal diseases leading to fluid overload and liver cirrhosis with ascites can also present with symptoms similar to CHF (1). Imaging plays a crucial role in differentiating CHF from these conditions. For example, echocardiography can help distinguish cardiac causes of dyspnea from pulmonary causes, and chest X-rays can provide insights into pulmonary status, helping to exclude primary respiratory disorders (1). Conservative Management:
Conservative management of CHF primarily focuses on lifestyle modifications and non-pharmacological approaches. These include dietary changes, notably salt restriction to help manage fluid retention, and limiting fluid intake as advised by a healthcare provider (16). Regular, moderate exercise is encouraged, adapted to the patient's capabilities, to improve cardiovascular health and overall well-being. Weight management is crucial, as obesity can exacerbate CHF symptoms (16). Smoking cessation and limiting alcohol intake are also recommended, as these habits can worsen heart function. Stress management techniques can be beneficial, considering the impact of stress on cardiovascular health. Monitoring and self-management of symptoms, such as keeping track of weight and recognizing early signs of fluid overload, are important for timely intervention (16). These lifestyle interventions, when effectively implemented and adhered to, can significantly improve the quality of life, reduce hospitalizations, and potentially slow the progression of CHF (16). Regular follow-up with healthcare professionals is vital to monitor the effectiveness of these strategies and make adjustments as necessary. Allopathic and Operative Management:
The allopathic and operative management of CHF encompasses a range of pharmacological treatments and surgical interventions. Pharmacologically, the management typically includes ACE inhibitors or ARBs to improve heart function and reduce blood pressure, beta-blockers to slow the heart rate and decrease its workload, and diuretics to reduce fluid overload (17). Additionally, medications like aldosterone antagonists and digitalis may be used to improve heart function and control symptoms. For advanced cases, surgical interventions can include the implantation of devices like pacemakers to manage arrhythmias or ventricular assist devices (VADs) to aid heart function. In severe cases, heart transplantation may be considered (18). These treatments and interventions are tailored to individual patient needs based on the severity and progression of their CHF. In guideline-directed medical therapy for CHF, several medications have shown mortality benefits in clinical trials. ACE inhibitors, evidenced by the CONSENSUS and SOLVD trials, reduce mortality and morbidity by decreasing afterload and ventricular remodeling. Beta-blockers, such as in the MERIT-HF, CIBIS-II, and COPERNICUS trials, have been shown to reduce mortality and hospitalization in CHF patients (19-23). Mineralocorticoid receptor antagonists, demonstrated in the RALES and EPHESUS trials, reduce mortality and hospitalization in severe CHF (24,25). More recently, ARNIs, as seen in the PARADIGM-HF trial, have shown a mortality benefit over ACE inhibitors in reducing cardiovascular death and hospitalization in HFrEF patients (26). Each of these medications targets different pathways in the pathophysiology of heart failure, contributing to improved outcomes. Prognosis:
The prognosis of CHF is influenced by several factors including the underlying etiology, the severity of cardiac dysfunction, patient comorbidities, and response to treatment. Early and accurate diagnosis, followed by comprehensive management, significantly impacts patient outcomes (27). Adherence to guideline-directed medical therapy and lifestyle modifications play critical roles in improving the trajectory of the disease. The advancement in treatments and management strategies over the years has led to improved survival rates and quality of life for CHF patients (27). However, the condition remains a major cause of morbidity and mortality, underscoring the importance of ongoing patient monitoring and management adjustments.
Congestive Heart Failure (CHF) is a complex clinical syndrome characterized by the heart's inability to pump sufficient blood to meet the body's needs (1). It is broadly classified into two types based on ejection fraction, which is a measurement of the percentage of blood leaving the heart each time it contracts. Heart Failure with Reduced Ejection Fraction (HFrEF), often referred to as systolic heart failure, is defined by a significantly impaired ejection fraction, typically considered to be below 40%. This condition is characterized by a weakened heart muscle that cannot contract effectively (2). On the other hand, Heart Failure with Preserved Ejection Fraction (HFpEF), also known as diastolic heart failure, occurs when the heart muscle becomes stiff and is unable to relax properly, leading to inadequate filling of the heart with blood. In HFpEF, the ejection fraction is usually normal (above 50%), but the heart's ability to relax and fill is compromised (3). Key terms associated with heart failure include "cardiac output," which is the amount of blood the heart pumps in a minute, and "cardiac index," a measure of cardiac output relative to body size (4). "Stroke volume" refers to the amount of blood pumped by the left ventricle of the heart in one contraction, and "preload" and "afterload" are terms that describe the volume of blood in the ventricle at the end of diastole (preload) and the resistance the heart must overcome to eject blood (afterload) (4). Understanding these different types of heart failure and related terms is crucial for diagnosis, treatment planning, and management of the condition. History:
The historical understanding of CHF has undergone significant evolution. In ancient times, theories of heart failure were primarily based on the imbalance of the four humors. The concept of cardiac failure as a clinical entity emerged in the 17th century with the work of English physician William Harvey, who described the circulatory system. However, it was not until the 20th century that major strides in understanding and treating CHF were made. The development of diagnostic tools like the electrocardiogram and later, echocardiography, revolutionized the ability to assess heart function (5). Significant milestones in CHF research and treatment include the introduction of diuretics in the 1950s, beta-blockers in the 1960s, and ACE inhibitors in the 1970s (5). The late 20th and early 21st centuries saw an expansion in the understanding of the molecular and neurohormonal mechanisms underlying heart failure, leading to more targeted therapies (5). The recognition of the distinct entity of HFpEF, alongside HFrEF, marked a crucial development in tailoring treatment strategies (5). These advancements have transformed CHF from a once invariably fatal condition to one that can often be managed effectively with a combination of lifestyle changes, medication, and in some cases, surgical intervention. Anatomical and Etiological Considerations:
CHF is characterized by significant structural changes in the heart, primarily affecting its ability to pump blood efficiently (1). In CHF, the heart muscle may become weakened (in HFrEF) or stiffened (in HFpEF), leading to either reduced contraction or impaired relaxation capabilities, respectively. These alterations can result in dilated or hypertrophied ventricles, impacting the heart's pumping efficacy (6). The etiology of CHF is multifactorial, involving a combination of lifestyle factors, genetic predispositions, and underlying diseases. Key contributors include coronary artery disease, leading to reduced blood supply to the heart muscle; hypertension, imposing excessive workload on the heart; valvular heart diseases, affecting the flow of blood through the heart; and cardiomyopathies, which directly impair the heart muscle's structure and function. Lifestyle factors such as obesity, sedentary habits, and smoking can exacerbate these conditions or independently contribute to heart failure (7). Genetic factors also play a role, with certain genetic mutations being linked to an increased risk of developing specific types of heart failure (7). Incidence:
CHF represents a significant global health concern, with its incidence and prevalence demonstrating notable demographic variations. Globally, CHF affects millions, with higher prevalence rates observed in developed countries, partly due to better diagnostic capabilities and aging populations (8). The incidence of CHF is notably higher in older adults, making it a leading cause of hospitalization for those over 65 (8). Additionally, improvements in medical treatments for acute cardiac events, such as myocardial infarctions, have led to increased survival rates, subsequently contributing to a rise in the number of individuals living with CHF (8). This trend underscores the growing need for effective CHF management strategies tailored to diverse populations and age groups. Symptoms:
Symptoms of CHF vary widely among patients and are closely tied to the severity and progression of the disease. Common symptoms include shortness of breath (dyspnea), particularly during exertion or while lying flat (orthopnea); fatigue and weakness, which may limit daily activities; and swelling (edema) in the legs, ankles, and feet (9). Fluid retention can also lead to rapid weight gain and bloating. As CHF progresses, these symptoms typically become more severe and may occur even at rest. Advanced stages of CHF can lead to severe pulmonary congestion, causing breathlessness and coughing, especially at night (termed paroxysmal nocturnal dyspnea) (9). The severity and combination of these symptoms are critical in assessing the stage of heart failure and guiding treatment strategies. Clinical Findings:
In patients with CHF, clinical findings during physical examination are pivotal for assessment and diagnosis. Common findings include jugular venous distension, indicating increased right atrial pressure (10). Pulmonary examination might reveal crackles or wheezes, suggestive of pulmonary congestion. Patients often exhibit peripheral edema, especially in the lower extremities, indicative of fluid retention. Cardiac auscultation can reveal third or fourth heart sounds (S3 or S4 gallop), which are significant markers of CHF (11). Additionally, arrythmias might be noted (11). These clinical findings, when combined with patient history and symptoms, play a crucial role in diagnosing CHF, assessing its severity, and guiding the course of treatment. Diagnosis:
The diagnosis of CHF involves a combination of clinical evaluation and various diagnostic tools. The primary criteria for diagnosis include patient history, physical examination, and symptoms such as dyspnea, fatigue, and edema. Diagnostic methodologies extend beyond these basic assessments, incorporating advanced imaging technologies which play a crucial role (12). Echocardiography is the gold-standard imaging tool in CHF diagnosis, providing detailed information about the heart's structure, function, and the presence of any abnormalities. It helps in assessing ejection fraction, a key indicator in differentiating between HFrEF and HFpEF (13). Cardiac Magnetic Resonance Imaging (MRI) offers a more detailed view of the heart's anatomy and function, particularly useful in complex cases, evaluating for sarcoidosis or when echocardiography results are inconclusive. It excels in assessing myocardial scarring and viability, which can guide treatment decisions (14). Chest X-rays, though less specific than echocardiography and MRI, are often used to identify pulmonary congestion and other structural changes in the chest that may be associated with heart failure (15). Additionally, laboratory tests, including natriuretic peptide levels, provide supportive diagnostic information and can help in assessing the severity of CHF. The integration of these diagnostic methodologies allows for a comprehensive evaluation of CHF, facilitating accurate diagnosis and effective management of the condition (15). Differential Diagnosis:
The differential diagnosis of CHF includes a range of conditions that present with similar symptoms, such as dyspnea, fatigue, and edema. Primary among these are respiratory disorders like chronic obstructive pulmonary disease (COPD) and asthma, which can cause shortness of breath and wheezing. Pulmonary embolism is another condition that mimics CHF, characterized by acute onset dyspnea and chest pain (1). Renal diseases leading to fluid overload and liver cirrhosis with ascites can also present with symptoms similar to CHF (1). Imaging plays a crucial role in differentiating CHF from these conditions. For example, echocardiography can help distinguish cardiac causes of dyspnea from pulmonary causes, and chest X-rays can provide insights into pulmonary status, helping to exclude primary respiratory disorders (1). Conservative Management:
Conservative management of CHF primarily focuses on lifestyle modifications and non-pharmacological approaches. These include dietary changes, notably salt restriction to help manage fluid retention, and limiting fluid intake as advised by a healthcare provider (16). Regular, moderate exercise is encouraged, adapted to the patient's capabilities, to improve cardiovascular health and overall well-being. Weight management is crucial, as obesity can exacerbate CHF symptoms (16). Smoking cessation and limiting alcohol intake are also recommended, as these habits can worsen heart function. Stress management techniques can be beneficial, considering the impact of stress on cardiovascular health. Monitoring and self-management of symptoms, such as keeping track of weight and recognizing early signs of fluid overload, are important for timely intervention (16). These lifestyle interventions, when effectively implemented and adhered to, can significantly improve the quality of life, reduce hospitalizations, and potentially slow the progression of CHF (16). Regular follow-up with healthcare professionals is vital to monitor the effectiveness of these strategies and make adjustments as necessary. Allopathic and Operative Management:
The allopathic and operative management of CHF encompasses a range of pharmacological treatments and surgical interventions. Pharmacologically, the management typically includes ACE inhibitors or ARBs to improve heart function and reduce blood pressure, beta-blockers to slow the heart rate and decrease its workload, and diuretics to reduce fluid overload (17). Additionally, medications like aldosterone antagonists and digitalis may be used to improve heart function and control symptoms. For advanced cases, surgical interventions can include the implantation of devices like pacemakers to manage arrhythmias or ventricular assist devices (VADs) to aid heart function. In severe cases, heart transplantation may be considered (18). These treatments and interventions are tailored to individual patient needs based on the severity and progression of their CHF. In guideline-directed medical therapy for CHF, several medications have shown mortality benefits in clinical trials. ACE inhibitors, evidenced by the CONSENSUS and SOLVD trials, reduce mortality and morbidity by decreasing afterload and ventricular remodeling. Beta-blockers, such as in the MERIT-HF, CIBIS-II, and COPERNICUS trials, have been shown to reduce mortality and hospitalization in CHF patients (19-23). Mineralocorticoid receptor antagonists, demonstrated in the RALES and EPHESUS trials, reduce mortality and hospitalization in severe CHF (24,25). More recently, ARNIs, as seen in the PARADIGM-HF trial, have shown a mortality benefit over ACE inhibitors in reducing cardiovascular death and hospitalization in HFrEF patients (26). Each of these medications targets different pathways in the pathophysiology of heart failure, contributing to improved outcomes. Prognosis:
The prognosis of CHF is influenced by several factors including the underlying etiology, the severity of cardiac dysfunction, patient comorbidities, and response to treatment. Early and accurate diagnosis, followed by comprehensive management, significantly impacts patient outcomes (27). Adherence to guideline-directed medical therapy and lifestyle modifications play critical roles in improving the trajectory of the disease. The advancement in treatments and management strategies over the years has led to improved survival rates and quality of life for CHF patients (27). However, the condition remains a major cause of morbidity and mortality, underscoring the importance of ongoing patient monitoring and management adjustments.
ACR Code
5.6
Location
Spine
Category
Cardiac & Renal
Keywords
Heart Failure
Trauma
Artificial Heart
Trauma
Artificial Heart
Reference
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