ISSN 2398-2969      

Endocardiosis: tricuspid valve

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Contributor(s):

Serena Brownlie

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Introduction

  • Usually concurrent left-sided endocardiosis, rarely tricuspid endocardiosis with right-sided heart failure predominate over left-sided lesion.
  • Cause: insufficient right atrioventricular valve.
  • Signs: right-sided heart failure.
  • Diagnosis: signs, echocardiography.
  • Treatment: symptomatic.

Pathogenesis

Etiology

  • Degenerative process of collagen and glycosaminoglycans in valve leaflets. Mitral valve is usually more severely affected.

Predisposing factors

General

Specific

  • Development of pulmonary hypertension Cor pulmonale - may be due to concurrent chronic airway disease or secondary to chronic left-sided backwards congestive failure.
  • Exertion.
  • Sudden increase in dietary salt intake.
  • Lack of compliance with medication (owner or animal).
  • Raised right ventricular pressure due to concurrent congenital heart disease, eg pulmonic stenosis Pulmonic stenosis.
  • Concurrent congenital tricuspid dysplasia.

Pathophysiology

  • Myxomatous degeneration of tricuspid valve is almost always less severe than mitral valve.
  • Valvular incompetence resulting in tricuspid regurgitation → volume overloading of right atrium and right ventricle, consequently right atrial and right ventricular enlargement.
  • Development of right-sided heart failure is associated with raised end-diastolic right ventricular pressure and right atrial pressure → raised right atrial pressure causes backwards failure with increased venous pressures.
  • Hepatic venous drainage is compromised leading to hepatomegaly and hepatocellular damage → leaky hepatic sinusoids and raised, central venous pressure causes ascites.
  • See also congestive heart failure Heart: congestive heart failure.
  • Tricuspid endocardiosis → tricuspid regurgitation → right-sided volume overload → slow development of right atrial and right ventricular enlargement → right ventricular eccentric hypertrophy → further tricuspid incompetence.
  • Increased right ventricular end-diastolic pressure and right atrial pressure → systemic venous congestion → increased central venous pressure → chronic hepatic venous congestion and hepatocellular cell damage (increased alanine transferase) → hepatic sinusoids are leaky → fluid extravasation into abdomen (ascites).
  • Ascites and gastrointestinal oedema may result in compromised absorption of nutrients (and drugs).
  • Pleural effusion may result from compromised pleural drainage into the systemic circulation.
  • Hypoproteinemia may result due to poor absorption, hepatic sinusoidal loss of protein, compromised liver function and inappetence.
  • With severe long-standing right-sided congestive heart failure associated with ascites and hypoproteinemia, subcutaenous edema may occasionally be recognized due to altered capillary homeostasis (Starlings law).

Timecourse

  • Development of right-sided heart failure is a poor prognostic sign and death (often euthanasia) usually follows within weeks or months.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Boswood A (1999) Rationale for the use of drugs in treatment of cardiovascular disease 3. positive ionotropes. In Practice 21 (5), 253-259 InPractice.
  • Packer M (1998) Neurohormonal interactions and adaptations in congestive heart failure. Circulation 77 (4), 721-730 PubMed.
  • The COVE Study Group (1995) Controlled clinical evaluation of enalapril in dogs with heart failure - results of the Cooperative Veterinary Enalapril Study Group. JVIM 9 (4), 243-252 PubMed
  • The IMPROVE Study Group (1995) Acute and short-term hemodynamic, echocardiographic and clinical effects of enalapril maleate in dogs with naturally acquired heart failure - results of the Invasive, Multicenter, PROspective Veterinary evaluation of Enalapril study. JVIM 9 (4), 234-242 PubMed.
  • Pedersen H D, Koch J, Poulson K, Jemsen A L & Flagstad A (1995) Activation of the renin-angiotensin system in dogs with mildly asymptomatic mitral valvular insufficiency. JVIM 9 (5), 328-331 PubMed.
  • Francis G S & Chu C (1994) Compensatory and maladaptive responses to cardiac dysfunction. Current Opinion in Cardiology 9 (3), 280-288 PubMed.
  • Roudebush P, Allen T A, Kuehn N F, Magerkurth J H & Bowers T L (1994) The effect of combined therapy with captopril, furosemide and a sodium-restricted diet on serum electrolyte concentrations and renal function in normal dogs and dogs with congestive heart failure. J Vet Intern Med 8 (5), 337-342 PubMed.
  • Schlesinger D P & Rubin S I (1994) Potential adverse effects of angiotensin converting enzyme inhibitors in the treatment of congestive heart failure. Comp Cont Educ Pract Vet 16 (3), 275-283 VetMedResource.
  • Dahlstrom U & Karlsson, E (1993) Captopril and spironolactone therapy for refractory congestive heart failure. Am Journ Cardiol 71 (3), 29A-33A PubMed
  • Riegger G A J (1993) ACE inhibitors in early stages of heart failure. Circulation 87 (suppl IV), 117-119 PubMed.
  • Zannad F (1993) Angiotensin-converting anzyme inhibitor and spironolactone combination therapy. New objectives in congestive heart failure management. Am Journ Cardiol 71 (3), 34A-39A PubMed.

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