Hypertension, arterial haemodynamics and left ventricular disease: historical observations.
The importance of arterial stiffening in the pathogenesis of cardiovascular disease has been gaining acceptance in recent years but is still widely overlooked, with the present preoccupation being atherothrombosis.1,2 Arteriosclerosis is a result of a combination of endothelial dysfunction and structural abnormalities of the media of conduit arteries (in contrast to atherosclerosis which is an intimal disease) including increased collagen content, calcification and hypertrophy of vascular smooth muscle cells.3,4 Chronic kidney disease (CKD) is known to confer an elevated risk of cardiovascular disease with an inverse graded relationship with glomerular filtration rates (GFR) independent of other risk factors.3 It is now widely accepted that the major driver of premature cardiovascular death and disease in CKD is left ventricular hypertrophy (LVH) and fibrosis rather than occlusive arterial disease.4

Arterial stiffening is best understood as a disturbance of one of the major functions of the arterial system, namely buffering of oscillatory changes in blood pressure that result from intermittent ventricular ejection. The highly distensible arterial system ensures that most tissues receive near steady flow with no exposure to peak systolic pressures. This mechanism is so efficient that there is almost no drop in diastolic pressure from ascending aorta to peripheral arteries.5 Loss of arterial distensibility results in a more rigid aorta that is less able to accommodate the volume of blood ejected by the left ventricle, resulting in greater pressure augmentation in systole and higher pulse pressures.6 As arterial stiffness increases, the myocardium, brain and kidneys are exposed to higher systolic pressures and greater pressure fluctuations resulting in microvascular damage.7 The increased impedance results in LVH. Furthermore, the effects on the left ventricle are exacerbated by lower diastolic pressure which reduces diastolic coronary perfusion, promoting subendocardial ischaemia and myocardial fibrosis.8 …