the pathogenesis of pulmonary "arterial" hypertension (who group i) involves the narrowing of blood vessels connected to and within the lungs. this makes it harder for the heart to pump blood through the lungs, much as it is harder to make water flow through a narrow pipe as opposed to a wide one. over time, the affected blood vessels become stiffer and thicker, in a process known as fibrosis. the mechanisms involved in this narrowing process include vasoconstriction, thrombosis, and vascular remodeling (excessive cellular proliferation, fibrosis, and reduced apoptosis/programmed cell death in the vessel walls, caused by inflammation, disordered metabolism and dysregulation of certain growth factors). over time, vascular remodeling causes the affected blood vessels to become progressively stiffer and thicker. this further increases the blood pressure within the lungs and impairs their blood flow. in common with other types of pulmonary hypertension, these changes result in an increased workload for the right side of the heart. the right ventricle is normally part of a low pressure system, with systolic ventricular pressures that are lower than those that the left ventricle normally encounters. as such, the right ventricle cannot cope as well with higher pressures, and although right ventricular adaptations (hypertrophy and increased contractility of the heart muscle) initially help to preserve stroke volume, ultimately these compensatory mechanisms are insufficient; the right ventricular muscle cannot get enough oxygen to meet its needs and right heart failure follows. as the blood flowing through the lungs decreases, the left side of the heart receives less blood. this blood may also carry less oxygen than normal. therefore, it becomes harder and harder for the left side of the heart to pump to supply sufficient oxygen to the rest of the body, especially during physical activity.