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Vasospastic (Prinzmetal) Angina

Cardiology > Tricuspid Regurgitation

Tricuspid Regurgitation

1. Knuuti J, Wijns W, Saraste A, Capodanno D, Barbato E, Funck-Brentano C, et al. 2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes. Eur Heart J. 2020;41(3):407-477.
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2. Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas AP, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease. J Am Coll Cardiol. 2012;60(24):e44-e164.
PMID: 23182125
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3. Khan MA, Hashim MJ, Mustafa H, Baniyas MY, Al Suwaidi SKBM, AlKatheeri R, et al. Global epidemiology of ischemic heart disease: Results from the Global Burden of Disease Study. Cureus. 2020;12(7):e9349.
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5. Amsterdam EA, Wenger NK, Brindis RG, Casey DE Jr, Ganiats TG, Holmes DR Jr, et al. 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2014;64(24):e139-e228.
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 Background

Tricuspid regurgitation (TR), also known as tricuspid insufficiency, is the backward flow of blood from the right ventricle into the right atrium during systole due to incomplete closure of the tricuspid valve. This leads to right atrial and right ventricular volume overload, progressive chamber dilation, systemic venous congestion, and eventually right-sided heart failure. TR can be functional (secondary to annular dilation or right ventricular pressure overload) or organic (due to structural damage of the valve). 

 

II) Classification or Types

By Etiology: 

    • Primary (Organic) TR: 
      • Rheumatic heart disease 
      • Carcinoid syndrome 
      • Infective endocarditis 
      • Congenital abnormalities (e.g., Ebstein anomaly) 
      • Trauma (e.g., pacemaker or ICD lead) 
    • Secondary (Functional) TR: 
      • Left-sided heart disease (e.g., mitral stenosis or regurgitation) 
      • Pulmonary hypertension 
      • Right ventricular dilation or dysfunction 
      • Atrial fibrillation (atrial TR due to annular dilation) 

By Chronicity: 

    • Chronic TR: Gradual development with compensatory right heart dilation; symptoms develop late. 
    • Acute TR: Sudden volume overload; rare, often seen in endocarditis or trauma. 

 

III) Epidemiology 

    • Sex: More common in women 
    • Age: Typically seen in middle-aged and elderly adults 
    • Geography: Functional TR is prevalent globally; rheumatic TR more common in low-income countries 
    • Comorbidities: Often associated with pulmonary hypertension, atrial fibrillation, and left-sided heart disease 

 Etiology

I) What Causes It

Primary Causes: 

    • Rheumatic fever 
    • Endocarditis (especially with IV drug use or devices) 
    • Congenital anomalies (e.g., Ebstein anomaly) 
    • Carcinoid heart disease 
    • Myxomatous degeneration 

Secondary Causes: 

    • Left-sided heart failure (e.g., mitral valve disease) 
    • Pulmonary hypertension 
    • Right ventricular infarction 
    • Chronic atrial fibrillation 
    • Right ventricular pacing leads 

 

II) Risk Factors

    • Chronic left-sided heart disease 
    • Pulmonary hypertension 
    • Atrial fibrillation 
    • Intracardiac devices (e.g., pacemaker, ICD) 
    • IV drug use 
    • Rheumatic heart disease 
    • Connective tissue disorders 

  Clinical Presentation

I) History (Symptoms)

Chronic TR: 

    • Fatigue 
    • Lower extremity edema 
    • Abdominal fullness and bloating 
    • Right upper quadrant discomfort (hepatic congestion) 
    • Anorexia and weight loss 
    • Ascites 

Acute TR: 

    • Sudden onset of right heart failure 
    • Hypotension (if severe) 
    • Dyspnea (if associated with left-sided lesions or pulmonary edema) 

 

II) Physical Exam (Signs)

Vital Signs: 

    • Normal or low blood pressure 
    • Elevated jugular venous pressure (JVP) 

Cardiac Exam: 

    • Holosystolic murmur best heard at the left lower sternal border, increases with inspiration (Carvallo’s sign) 
    • Right ventricular heave 
    • S3 gallop at left lower sternal border 

Peripheral Signs: 

    • Prominent v-wave in JVP 
    • Hepatomegaly (pulsatile) 
    • Ascites 
    • Peripheral edema 
    • Cyanosis (in severe chronic TR with right-to-left shunt) 

Pulmonary: 

    • Usually clear unless left-sided failure or pulmonary edema coexists 

 Differential Diagnosis (DDx)

    • Pulmonary hypertension 
    • Constrictive pericarditis 
    • Pericardial tamponade 
    • Right ventricular failure (non-valvular) 
    • Atrial septal defect 
    • Mitral stenosis or regurgitation 
    • Hepatic cirrhosis (due to similar signs) 

  Diagnostic Tests

Initial Tests: 

Transthoracic Echocardiogram (TTE): 

    • Determines TR severity (jet area, vena contracta, hepatic vein flow reversal) 
    • Assesses right atrial and ventricular size and function 
    • Evaluates valve morphology 

Transesophageal Echocardiogram (TEE): 

    • Better visualization of valve leaflets 
    • Used in endocarditis, device-related TR 

Electrocardiogram (ECG): 

    • Right atrial enlargement 
    • Right ventricular hypertrophy 
    • Atrial fibrillation 

Chest X-ray: 

    • Cardiomegaly (right heart enlargement) 
    • Pleural effusion (occasionally) 
    • Clear lungs unless left-sided involvement 

BNP/NT-proBNP: 

    • May be mildly elevated in isolated TR 
    • More elevated if biventricular failure 

Cardiac MRI: 

    • Accurate quantification of right ventricular size/function and regurgitant volume 

Right Heart Catheterization: 

    • Confirms pulmonary hypertension 
    • Measures right-sided pressures and cardiac output 

 Treatment

I) Medical Management

Functional TR: 

    • Treat underlying cause (e.g., left-sided heart failure, pulmonary hypertension) 
    • Diuretics: mainstay for symptom relief (edema, ascites) 
    • Aldosterone antagonists for volume overload 
    • Avoid excessive preload or afterload reduction (may worsen symptoms) 

Primary TR (mild to moderate): 

    • Monitor with serial imaging 
    • Manage risk factors (e.g., endocarditis prophylaxis if indicated) 

Acute TR: 

    • Diuresis, vasopressors, treat underlying cause 
    • Consider urgent surgical evaluation in endocarditis or trauma 

 

II) Interventional/Surgical

Indications for Tricuspid Valve Repair or Replacement: 

    • Severe symptomatic TR not responsive to medical therapy 
    • Severe TR with other left-sided surgery planned 
    • Progressive right ventricular dysfunction 
    • Annular dilation >40 mm even without severe TR 

Surgical Options: 

    • Annuloplasty (preferred in functional TR) 
    • Valve replacement (bioprosthetic preferred due to lower thrombosis risk) 

Transcatheter Options: 

    • Emerging therapies for high-risk surgical candidates (e.g., edge-to-edge repair, valve-in-valve procedures) 

  Patient Education, Screening, Vaccines

    • Educate on early signs of right heart failure (leg swelling, fatigue, ascites) 

    • Emphasize adherence to diuretics and follow-up 

    • Encourage sodium restriction in severe cases 

    • Promote good dental hygiene to prevent endocarditis 

    • Vaccinations: 

    • Influenza 

    • Pneumococcal 

    • COVID-19 

  Consults/Referrals

    • Cardiology: Diagnostic evaluation, TR severity grading, and optimization 
    • Cardiothoracic Surgery: If surgical correction is needed 
    • Infectious Disease: For infective endocarditis management 
    • Gastroenterology/Hepatology: If hepatic congestion or ascites dominates 
    • Primary Care: Management of comorbidities and routine follow-up 

  Follow-Up

Echocardiography: 

    • Mild TR: every 3–5 years 
    • Moderate TR: every 1–2 years 
    • Severe TR (asymptomatic): every 6–12 months 

Monitoring Goals: 

    • Right ventricular function and size 
    • Progression of TR severity 
    • Symptoms and response to diuretic therapy 
    • Evaluate candidacy for surgical/interventional therapy 

 

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