Arterial stiffening and isolated systolic hypertension

Stiffening the arteries — falling compliance at fixed CO×SVR — widens the pulse pressure and shortens τ=RC while mean pressure stays flat, exactly the Framingham aging pattern. The engine reaches an isolated-systolic-hypertension point at C≈0.50 (SBP≈144, DBP≈56, PP≈87). Grade [V]; Franklin 1997 anchor [L].

Isolated systolic hypertension is the highest-confidence disease prediction: it lands directly on the pulse pressure and τ the Windkessel already prints. Reducing arterial compliance widens PP from 32 to 156 mmHg and shortens τ from 1.54 to 0.29 s, with MAP unchanged — SBP rises, DBP falls.

Stiffness, not resistance, widens the pulse

After mid-life the dominant hemodynamic change is central arterial stiffening, not a rise in peripheral resistance. On the Windkessel this is a fall in the compliance C at fixed CO×SVR. Because mean pressure is set by CO×SVR (unchanged), MAP stays flat while the pulse pressure widens and the diastolic decay τ=RC shortens.

An ISH point emerges

Sweeping C from compliant to stiff, the engine holds MAP flat (relative range 1e-06) while PP rises monotonically 32→156 mmHg and τ falls 1.54→0.29 s in lockstep. SBP climbs and DBP falls until, near C≈0.50, the reading crosses an isolated-systolic-hypertension threshold (SBP≥140 with DBP<90: here 144/56). This reproduces the classic Framingham age pattern — little change in mean pressure, a plateau then rise in SBP, a fall in DBP after 50, and a dramatic PP increase — attributed to aortic stiffening with little change in peripheral resistance (Franklin SS et al., Circulation 1997;96:308–315). The hemodynamic shape is forced; the absolute cardiovascular-event rate needs a population hazard model and stays [O].