What happens to aortic and left ventricular (LV) pressures after a premature ventricular contraction (PVC) in hypertrophic obstructive cardiomyopathy (HOCM) compared to fixed obstruction like aortic stenosis?

Hemodynamic Response to PVCs in HOCM versus Aortic Stenosis

In hypertrophic obstructive cardiomyopathy (HOCM), a premature ventricular contraction (PVC) typically causes a dramatic increase in left ventricular outflow tract (LVOT) gradient and a corresponding drop in aortic pressure in the post-PVC beat, while in fixed aortic stenosis, the post-PVC beat shows minimal change in gradient with a potential increase in aortic pressure due to post-extrasystolic potentiation. 1, 2

Pathophysiological Differences

HOCM Response to PVC

• Mechanism: The post-PVC beat experiences:
  • Increased contractility due to post-extrasystolic potentiation
  • Reduced ventricular volume (from incomplete filling after PVC)
  • These conditions worsen dynamic LVOT obstruction 1, 2
• Hemodynamic consequences:
  • Dramatic increase in LV pressure
  • Significant drop in aortic pressure
  • Marked increase in LVOT gradient
  • Worsened mitral regurgitation due to enhanced SAM (systolic anterior motion)
  • Potential for post-PVC hypotension 1, 2

Aortic Stenosis Response to PVC

• Mechanism: The post-PVC beat experiences:
  • Increased contractility due to post-extrasystolic potentiation
  • Fixed anatomical obstruction that doesn't change with hemodynamics
  • No dynamic component to obstruction 3
• Hemodynamic consequences:
  • Increased LV pressure
  • Increased aortic pressure (due to increased stroke volume)
  • Relatively unchanged gradient across the aortic valve
  • No significant worsening of symptoms 3, 4

Clinical Implications

Diagnostic Value

• The dramatic post-PVC increase in gradient in HOCM (sometimes called the Brockenbrough-Braunwald-Morrow sign) can help differentiate between:
  • Dynamic obstruction (HOCM) - where gradient increases after PVC
  • Fixed obstruction (aortic stenosis) - where gradient remains relatively constant 1, 2

Management Considerations

• In HOCM:
  • PVCs may trigger symptomatic episodes due to post-PVC gradient increase
  • Antiarrhythmic therapy may be beneficial in symptomatic patients with frequent PVCs
  • Beta-blockers help reduce post-PVC gradient augmentation by blunting contractility 1, 2
• In aortic stenosis:
  • PVCs generally have less hemodynamic impact
  • Management focuses on the fixed obstruction rather than dynamic changes 3

Physiological Explanation

The fundamental difference lies in the nature of obstruction:

1. HOCM: Obstruction is dynamic and highly sensitive to:

   • Ventricular preload (reduced after PVC)
   • Contractility (enhanced after PVC)
   • These changes dramatically worsen SAM and LVOT obstruction 1, 2

2. Aortic Stenosis: Obstruction is fixed and anatomical:

   • The valve opening remains constant regardless of hemodynamic changes
   • Post-extrasystolic potentiation increases contractility but doesn't significantly alter the valve gradient 3, 4

This hemodynamic response to PVCs represents a key distinguishing feature between these two forms of outflow tract obstruction and has important implications for both diagnosis and management of these conditions.