What causes right ventricular dilation?

Causes of Right Ventricular Dilation

Right ventricular dilation occurs due to various pathological conditions that increase right ventricular pressure or volume, with the most common cause being secondary (functional) tricuspid regurgitation resulting from right ventricular remodeling due to left-sided heart diseases, pulmonary hypertension, congenital heart defects, and cardiomyopathies. 1

Primary Causes of RV Dilation

• Volume Overload Conditions:

  • Tricuspid regurgitation (primary or secondary) 1
  • Pulmonary regurgitation (often following repair of congenital heart defects) 1
  • Atrial septal defect or other congenital shunts 1, 2
  • Anomalous pulmonary venous return 2

• Pressure Overload Conditions:

  • Pulmonary hypertension (primary or secondary) 1
  • Pulmonary valve stenosis or right ventricular outflow tract obstruction 1
  • Pulmonary embolism (acute or chronic thromboembolic disease) 1
  • Double-chambered right ventricle 1

• Right Ventricular Myocardial Disease:

  • Right ventricular ischemia/infarction 1, 3
  • Arrhythmogenic right ventricular cardiomyopathy 2
  • Myocarditis affecting the right ventricle 1
  • Infiltrative cardiomyopathies (e.g., sarcoidosis, amyloidosis) 2
  • Dilated cardiomyopathy (affecting both ventricles) 1

• Other Causes:

  • Tachycardia-induced cardiomyopathy 4
  • Post-cardiac surgery 1
  • Pacemaker lead-induced tricuspid regurgitation 1

Pathophysiological Mechanisms

Volume Overload Pathway

Volume overload conditions lead to RV dilation through the following mechanisms:

• Increased preload causes initial RV dilation 5
• Progressive RV remodeling with chamber enlargement 1
• Tricuspid annular dilation with worsening tricuspid regurgitation 1, 6
• Further RV dilation creating a vicious cycle 1

Pressure Overload Pathway

Pressure overload initially causes RV hypertrophy, but eventually leads to dilation:

• Initial RV hypertrophy as a compensatory mechanism 1
• Development of isovolumic phases of contraction and relaxation 1
• Progressive RV dilation when compensation fails 1
• Declining pulmonary artery pressure despite elevated pulmonary vascular resistance (an ominous sign) 1

Ventricular Interdependence

RV dilation affects left ventricular function through ventricular interdependence:

• RV dilation shifts the interventricular septum toward the left ventricle 1
• This mechanical flattening increases LV end-diastolic pressure 1
• Reduces LV transmural filling pressure and impedes LV diastolic filling 1
• Results in biventricular diastolic dysfunction 1
• Can lead to systemic hypoperfusion 1

Clinical Significance

RV dilation has important clinical implications:

• Associated with increased mortality in heart failure patients 1
• Creates substrate for arrhythmias, including ventricular tachycardia 7
• QRS prolongation >180 ms is a significant risk factor for sudden cardiac death 7
• Severe tricuspid regurgitation accompanying RV dilation is associated with poor prognosis 1
• RV dilation can compress the LV cavity, impeding LV filling 1

Diagnostic Considerations

When evaluating RV dilation, consider:

• Echocardiographic assessment of RV size, function, and associated valve abnormalities 1, 2
• Cardiac MRI for accurate assessment of RV volumes and tissue characterization 7, 5
• ECG evaluation for right bundle branch block, QRS prolongation, and rhythm abnormalities 1, 7
• Assessment of tricuspid valve morphology and function 1

Common Pitfalls and Caveats

• RV dilation may be misinterpreted as normal variant in athletes 2
• Isolated tricuspid regurgitation without pulmonary hypertension can still be associated with RV remodeling and dysfunction 6
• Once tricuspid annular dilation occurs, it may not spontaneously return to normal size 4
• Declining pulmonary artery pressure in the setting of high pulmonary vascular resistance is an ominous clinical finding 1
• RV dilation may be difficult to detect on plain radiographs due to the anterior position of the RV 5