Medical Treatment of Congestive Cardiac Failure from Cerebral Arteriovenous Fistulas at Bicêtre Hospital

Abstract

Arteriovenous fistulas create an increase in venous return and subsequent right heart overload. The result is right heart dilatation, pulmonary arterial hypertension, and increased pulmonary blood flow. Reduction in arterial diastolic pressure (as observed in arteriovenous shunt), an increase in end diastolic pressure (due to increased preload), a reduction in diastolic period (due to tachycardia) are all detrimental to myocardial perfusion and hence oxygen delivery and may precipitate left ventricular failure.

Furthermore, the transition from a foetal circulatory pattern to an adult circulatory pattern is complex and both pulmonary and systemic circulations remain highly unstable during the first week after birth. This can explain a persistent transitional circulation with shunts through the ductus arteriosus, the foramen ovale and a pulmonary hypertension which worsen the systolic and diastolic wall stress.

The clinical presentation depends on the size of the left-to-right shunt and its tolerance. The aims of symptomatic therapy are to improve oxygen delivery to the tissues and decrease tissue oxygen consumption. Measures that improve the patient's effective ventilation, arterial oxygen saturation, and hematocrit need to be the first steps. Diuretics are the first step for reducing preload. Cardiac output can be improved by increasing cardiac contractility with inotropic agents. Digoxin is the main agent used to increase myocardial contractility.

However, its use in a hyperkinetic state due to arteriovenous fistulas remains controversial: pretreatment myocardial function indices may already be above normal, and there is no clear evidence that their further increase produces clinical benefit. Vasodilators are obviously contraindicated if systemic arterial pressure is low. If the failure cannot be controlled, embolisation of the lesion should be considered.

The goal of this paper is to provide a rational approach to the treatment of circulatory failure due to cerebral arteriovenous shunts.