This is important…
(not to mention increases in blood pressure AND insulin resistance)
All of this is compatible with slower cellular aging (b/c the nutrients are not IN the cells where they can promote growth/cause damage), but it does mean one needs better diagnostic tools (eg continuous measures of inflammation or 8-oxo-G or ROS)
The effect of rapamycin and rapalogs on the cardiovascular system initially was not clear, especially in humans. In clinical studies with transplant patients, rapalogs induced a negative plasma cardiovascular risk profile, e.g., an increase in LDL cholesterol and triglyceride concentrations in plasma . Rapamycin also has been reported to have deleterious effects on endothelial function (ability of a blood vessel to constrict and dilate) in laboratory animals and in human coronary arteries from sirolimus-eluting stents [48, 49]. Rapamycin also has been reported to accelerate senescence of endothelial progenitor cells ; however, as described below, most of the recent studies indicate that rapamycin reduces cellular senescence. Overall, these early studies are in conflict with the large number of studies in mice listed in Table 4 that have studied the effect of rapamycin on atherosclerosis in mice.
Mueller et al.  reported that the blood levels of LDL and VLDL cholesterol were slightly higher in the everolimus-treated mice but observed no change in triglycerides. It is interesting to note that Ross et al.  observed no effect of rapamycin (1.0 mg/kg/day) treatment on blood triglyceride levels in the non-human primate, marmoset.
I mean, ex-Malaysian PM Mahathir Mohamad is enough proof that heart disease risk is not the same thing as aging rate.