Fixed congenital ventricular outflow obstructions (pulmonary or aortic valvular stenosis, subaortic membrane, PA or aortic hypoplasia) cause concentric left or right ventricular hypertrophy (RVH or LVH). Two constraints play a critical role in how these cases are managed [1].
 

A severe obstruction of the aortic arch (hypoplasia, coarctation) can cause systemic hypoperfusion with metabolic acidosis and mesenteric ischaemia. In cases of valvular or subvalvular aortic stenosis, systemic hypotension may cause myocardial ischaemia due to a fall in coronary perfusion pressure [2].

In cases of muscular aortic and pulmonary stenosis (infundibular), the dynamic aspect is dominant – the stenosis effect increases with contractility and is reduced by β-blockade. The obstruction is reduced by a negative inotropic effect, increased circulating volume (hypervolaemia), and increased afterload (α vasocontrictors). Any β catecholaminergic stimulation must be avoided.

Valvular regurgitation causes eccentric ventricular hypertrophy with volume overload and increased filling pressure. It is highly sensitive to variations in afterload – mitral insufficiency (MI) or aortic insufficiency (AI) increase if SVR rises. In severe cases of tricuspid insufficiency (Ebstein anomaly) or pulmonary insufficiency (PI), regurgitation is exacerbated by rising PVR.
 

 

Obstructive lesions and valvular heart diseases

Outflow obstructions cause concentric ventricular hypertrophy characterised by:     - Diastolic dysfunction     - Threat of systolic dysfunction     - Threat of myocardial ischaemia Valvular insufficiencies are exacerbated by rising ventricular afterload

 

© BETTEX D, BOEGLI Y, CHASSOT PG, June 2008, last update May 2018
 

 

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