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Increased Pulse Pressure Causes Vascular Injury in Pulmonary and Systemic Arteries. Decreasing the Pulsatility with Banding and Vasodilators Can Stabilize Pulmonary Hypertension

Warren G. Guntheroth

In congenital heart disease with large shunts at the ventricular or arterial level the mean pulmonary artery pressure is increased to systemic levels. In addition, these shunts also increase the pulse pressure (PP) in the pulmonary arteries; the increased pulsatility, acts apart from mean pressure. Increased PP injures the arterial wall from exaggerated distension with each heart beat, producing medial hypertrophy that narrows the lumen, increasing pulmonary vascular resistance--a positive feedback. Thus, pulmonary arterial hypertension (PAH) is progressive and surgical intervention was considered dangerous. However we have observed adults with PAH who are stable and asymptomatic; they had central PAH but the pressure was reduced in the distal pulmonary arteries by valvular or bilateral distal stenosis. We present brie fl y two adults: one illustrates the stabilizing effect of damping pulsatility in the pulmonary arteries, and the second illustrates the catastrophic effects of excessive pulsatility from a shunt.

Recently, surgical advances have demonstrated that stabilization of patients with a large ventricular septal defect by short term surgical banding can be achieved with modest mortality, adding pre- and post-operative pharmacologic vasodilators, such as calcium channel blockers, nitric oxide, acetylcholine, endothelin receptor antagonists, and prostacyclin.

Excess PP has also been recognized to cause vascular injury in the systemic circulation predicting adverse cardiovascular outcomes, unaffected by current antihypertensive therapy. Perhaps increased PP in the systemic circulation might respond to pharmacologic measures that have been successful with PAH.