The aim of treatment for ApHCM is mainly to control symptoms and prevent complications, which are done by means of medications such as beta-blockers or calcium-channel blockers to control the heart rate, and also ACEI to reduce the left
ventricular afterload. Recent discovery also showed that ACEI will reduce the adverse cardiac remodeling and fibrosis in ApHCM.[3] For a patient who is persistently symptomatic or has high risk of sudden cardiac death, an ICD will be inserted.
It should be administered especially to those selected subjects who have increased right
ventricular afterload, low risk of bleeding, and an expectation for a long survival time.
The most common pathologies, which leads to an increase in left
ventricular afterload are systemic hypertension and aortic stenosis with the consequence to develop concentric hypertrophy.
Volume expansion versus norepinephrine in treatment of a low cardiac output complicating an acute increase in right
ventricular afterload in dogs.
With progression of fetal pulmonary and systemic vasoconstriction, an increased right
ventricular afterload and a shift of cardiac output to the left ventricle occur [8], with impact on left diastolic function and possible increased impedance to flow through the foramen ovale (FO) [14].
PH, if left untreated, can cause increased right
ventricular afterload with right heart dilatation and failure, which is compounded by functional TR by annulus dilatation [16].
Due to early recognition of the disease and aggressive supportive care with mechanical ventilation, right
ventricular afterload reduction, and blood transfusion, both patients survived without any significant sequelae.
Positive ventilation might influence the TAPSE by way of increasing right
ventricular afterload.[sup][29] However, in this study, the PEEP and plateau pressures were not different between the two groups.
Choi et al., "Computational analysis of the effect of the type of LVAD flow on coronary perfusion and
ventricular afterload," Journal of Physiological Sciences, vol.
The uteroplacental circulation and systemic vasodilatation contribute to the decline in vascular resistance, which is the steady component of
ventricular afterload. Vascular resistance decreases in the early first trimester, presents its nadir in the middle of the second trimester, and returns close to prepregnancy levels within two weeks after delivery [11].
The i-cor system, which provides Synchronized Cardiac Assist, combines the best elements of cardiac assist and augmented cardiac function associated with IABP and percutaneous ventricular assist devices but does not increase left
ventricular afterload or ventricular work.
Following extubation, inhaled iloprost was started at doses of 2.5 [micro]g, six times per day since iloprost is known to reduce residual postoperative PH, decrease right
ventricular afterload, and may facilitate the early postoperative management after PEA.
