Briefly, Isolated Systolic Hypertension is due to increased arterial stiffness of large and medium conductance arteries that loose their "cushioning" properties. In these patients peripheral arterial resistances are usually normal and diastolic pressure is not increased.

You may find useful the article attached.

Very appreciated

As M. Sardina well said, the stiffness of the arteries reflect reduced complience (the ability to stretch under pressure). As the arterial walls resist expanding during systole, the pressure builds up.

Because diastolic arterial pressure depends upon mainly peripheral arterial resistance, thet are not necessarily increased when large and medium arteries wall is more rigid

Arterial stiffness is associated with isolated systolic hypertension due to reduced elastic property of the large arteries of which it has lower effect on diastolic hypertension. The momentary resting period before the next phase of systolic may be responsible for this phenomenon.

Diastolic pressure does not increase due to lower recovery of venous blood due to venous insufficiency, but also due to the weakening of the heart's strength due to aging changes.

central aortic waveform is made up of percussion wave ( due to direct ejection of blood from LV to aorta), then tidal wave ( felt to be forward wave in late systole merging with reflected wave primarily from upper extremity), and dicrotic wave( early diastolic wave due to reflected wave from lower extremity)

arteries expand during systole and store some of ejected blood and then recoil releasing blood during diastole. Normaly pressure wave travels faster than blood itself.

In young due to elastic nature of vessels waveform travels slowly to periphery and when it gets reflected back to aorta it boosts pressure in diastole( reflected wave falls on diastolic pressure)

Hi, Muhammad, very good question. As already been told diastolic pressure is mainly depends upon peripheral resistance offered mainly at arteriolar level. In elderly patients with aging there is increased stiffening of arteries mainly of aorta and large arteries which cause decreased ratio of lumen to arterial wall thickness ratio and there is no effect on arteriolar level and responsible for isolated systolic hypertension. It is an important cause of mortality and morbidity in elderly specially in terms of cerebrovascular accident. Caution should be given to reduce the systolic blood pressure because there is always is a chance of reducing the diastolic pressure to much which may be harmful and beta blocker preferably to be avoided.. Thanks

From invasive blood pressure measurements one can get a great deal of factual information. Invasive blood pressure monitoring using fluid-filled transducers which have been upgraded rapidly so that the eighties would not trap air, be effected by ambient temperature changes, and finally by providing fluid in collapsible containers do not trap air. These devices have become extremely reliable so that we have been performing operations requiring strict control of the perfusion pressure. Professionals caring for these patients have been given the tools to provide proper treatment in a very short time; unfortunately most epidemiologists do not have these means. I have had the chance to work in medical centers that had facilities and people who always care for the how and why. I started observing PWs in an attempt to find why the SP in radial PWs became completely unreliable during cardiac surgery, just before aortic cannulation for cardiopulmonary by pass. We found that the radial SP was up to 35 mmHg higher than that in the aorta, but equal in 9 of 51 middle-aged and older hypertensives, who turned out to have their SPs represented by the second peak (P2), which is hypertension due to aortic degeneration. We also found that the diastolic pressure in these patients (who also had ISH) could be measured accurately only invasively and they were equivalent in radial and aortic PWs. However, the DP can be read accurately in older normotensives.

It would be nice if scientist could find a way to measure intravascular pressures accurately, by physical means. Modulation will never achieve this. If you follow the work going at Calgary University and some at the Imperial College, you will see that our thought are going in the same direction.

I think we have some learning to do, and then more

Alfredo L Pauca MD

As Alfreo correctly highlights invasive blood pressure measurements could provide additional and important information that in my humble opinion are very important for research purposes but hardly to be applied on large scale practice.

As a matter of facts pulse pressure (i.e. the difference between systolic blood pressure and diastolic blood pressure) a very easy and non invasive method is the best risk predictor for patients with isolated systolic hyperternsion (ISH) that as correctly Biswajit quote is a major risk factor for mortality and morbidity in the elderly. Furthermore this easy evalutation can be performed routinely by GPs. Unfortunatley so far there are no targeted therapies for ISH.

M Sardinia

Some of us do not publish very much, but instead observe and document reproducible results. Try to get reproducible results with a great deal of self criticism. In other words, try as hard as possible to get real cause effect relationships before going into metanalysis.

I am afraid modern research relies too much on large scale observations. Take for example an older study now, Murgo’s et al Circulation 1980; 62:105-11 in 18 patients, very well done at any time. Right on the dot except for his assumption that the front flow was bLunt therefore producing reflected waves which produced P2. This study had only 18 patientS.

The only way we can take care of patients is by understanding what is wrong with them.

Without invasive blood pressure monitoring we could not have done the surgery we have. We do not have to monitor BP invasively, but we could do well by knowing what this shows us and try to adjust our thinking. Michael O’Rourke, my coauthor, believes that the blood pressure measured by a blood pressure cuff should be the standard to compare any other method. It has been useful for more than 100 years. “Central aortic pressure calibration ; I a bridge too far’ J of Hypertension 2017, 35:893-901.

Alfredo L Pauca MD

@Alfreo L pauca

Thank you sir .

The same as an explanation from my student times after the WWII , when pathophysiology was in her early baby-days, that "neurohumoral" adaptations are responsible in "adjusting " the relationship of the strenght of every cardiac contraction and the width of the supposed lumen of the whole arterial part of circulation in a situation of rigid arterial wall, in order to secure an adequate tissue perfusion.

@Aleksandar Nedok

Thank you sir !

Diastolic pressure decreases greatly in patients with so-called isolated SHypertension because of loss of elasticity. Some hypertensive treatments can make the rest of their life miserable.

unfortunately theit DP can be measured accurately lnvasively.

Alfredo L Pauca MD