Carotid intima-media thickness (cIMT) is also known as a predictor of cardiovascular disease. The distensibility of the carotid artery represents a relative change of arterial volume in response to that of pressure, and the compliance represents the absolute change in arterial volume in response to that of pressure. There is an a characteristic increase in impedence, a decrease in total peripheral arterial compliance, and an increase arterial wave reflexion, regardless of the presence of coronary artery lesions. therefore arterial stiffening may be possible reason  that causes the increase of PEP.

more stiffness leads to faster more abrupt changes and thus reduced PEP

Firstly I want  you to know that in my opinion PEP is a very sensitive and hard-to-measure quantity, and caution should be used when evaluating such a quantity.

By the way, i think that one possible explanation invoke the increased maximum elastance of the left ventricle (Chantler 2012 Frontiers in physiology) seen in hypertension. The increased maximum of the elastance function determines and increase steepness of the elastance during the isovolumic contraction phase, that actually corresponds to the PEP. 

In my opinion, the increased force of contraction needed in a condition of HT in order to preserve arterio-ventricular coupling, can decrease the time needed to increase the ventricular pressure above the aortic one, and thus decreases the PEP.

I agree, it is a function of abnormal ventricle-vascular coupling due to a stiff aortic root. also explains link with carotid vascular changes. I think the PEP is an unreliable measure and the clue would come fro looking at dp/dt which will be steeper in these patients.

Thank you all very much! I think the reason also can be  that a decreased arterial compliance in hypertensive patients cause a decreased capacity to store blood in heart during diastole, then aortic diastolic pressure decreases, this thereby lead to a shortened isovolumic contraction time to researching the lower aortic diastolic pressure before ventricular ejection commences.

PEP indeed is not optimally validated. An additional aspect to keep in mind is time-varying wall stress. In our Asklepios population higher peak and early-systolic myocardial wall stress is correlated with better systolic and diastolic function, while the opposite is true for late-systolic wall stress. This late-systolic wall stress is related to wave reflection and leads to maladaptive hypertrophy and cardiovascular events. PMID: 23283359

The PEP, ejection time and Q-S2 are not the same thing and there are differences in their determinants. Two direct determinants of the PEP are the diastolic blood pressure (affecting the onset of ejection) and the heart rate (affecting LV contractility via the force-frequency relationship). Univariate and multivariate regression analyses of PEP including HR, BP and IMT may provide insight into possible mechanisms, as may analyzing the determinants of ejection time and Q-S2. .

Interesting question. The PEP may be inversely related to contractility. Therefore, a possible explanation would be an increased adrenergic drive resulting in both:

1. increasing contractility (with increased dP/dt and higher total contractile force) and thus shortening isovolumetric contraction time.

2. hypertension and related aortic stiffness plus increased IMT.

Thank you very much for your good answers!