Please select the outcome measures that correspond to the clinical trial below.
Title: Randomized, Double Blind, Active-controlled, Parallel Study to Analyse Effects of the Combination of Aliskiren and Valsartan on the Vascular Structure and Function of Retinal Vessels
Brief Summary: Hypertension affects approximately one fourth of the world population and therefore contributes substantially to the worldwide burden of cardiovascular (CV) disease and end-organ damage.

Changes in small artery structure characterized by an increased wall-to-lumen ratio (WLR) are characteristic feature of target organ damage in hypertension. Of clinical importance, structural arteries of small subcutaneous arteries have been shown to be of prognostic significance, with adverse prognosis in subjects with higher WLR. However, the assessment of arteriolar structure from biopsies of subcutaneous tissue is invasive and impractical in clinical practice. A new approach focuses on retinal arteriolar structural parameters by using scanning laser Doppler flowmetry (SLDF) with automatic full-field perfusion imaging analyses (9). This approach allows the non-invasive assessment of both the outer diameter (OD) and inner diameter (ID) of retinal arterioles in vivo and, thus, analyses vascular remodeling of retinal arterioles by calculating WLR = (OD - ID) / ID).

A crucial role in the efforts of prevention of end-organ damage plays the renin angiotensin system (RAS). The increased mechanical strain on the vasculature at a higher BP can cause injury to the endothelial wall. Activation of the RAS increases BP and stimulates a local inflammatory response to repair the injury. Long-term or repeated response to injury leads to endothelial dysfunction and microvascular damage, and hence end-organ damage.

Combining RAS inhibitors may provide greater end-organ protection than use of either class alone. However, ONTARGET has failed to show superiority of the dual RAS blockade (ACE-I and ARB) in patients at high cardiovascular risk. The combination of ARBs and direct renin inhibitors (DRIs) emerged as the only available, valid and innovative option for blocking the RAS at two different sites (sequential blockade). Indeed, AVOID study and ALLAY study demonstrated that the DRI aliskiren has additional and to some extent blood pressure independent effects on albuminuria and left ventricular hypertrophy, both signs of subclinical organ damage in hypertension, respectively.

However, no data are available with respect to the effects of ARBs and DRIs on vascular properties in the short and long term To close this gab we focus in this study on vascular structural and functional changes since vascular adaptation to high blood pressure occurs in the early phase of hypertensive disease.


Options:
A: Change from baseline in diastolic blood pressure after 52 weeks
B: Change from baseline in mean sitting diastolic blood pressure after 8 weeks
C: Percentage of Participants With Occurrence of Primary Composite Endpoint (Core : Active Treatment Phase) (Time from randomization to the first event (Maximum 50 months)); Percentage of Participants With Cardiovascular (CV) Death (Core: Active Treatment Phase) (Time from randomization to the first event (Maximum 50 months)); Percentage of Participants With Resuscitated Sudden Death (Core: Active Treatment Phase) (Time from randomization to the first event (Maximum 50 Months)); Percentage of Participants With Fatal/Non-fatal Myocardial Infarction (MI) (Core: Active Treatment Phase) (Time from randomization to the first event (Maximum 50 Months)); Percentage of Participants With Fatal/Non-fatal Stroke (Core: Active Treatment Phase) (Time from randomization to the first event (Maximum 50 Months)); Percentage of Participants With Onset of End-stage Renal Disease (ESRD) (Core: Active Treatment Phase) (Time from randomization to the first event (Maximum 50 Months)); Percentage of Participants With Doubling of Baseline Serum Creatinine Concentration, Sustained for at Least One Month (Core: Active Treatment Phase) (Time from randomization to the first event (Maximum 50 Months)); Percentage of Participants With Unplanned Hospitalization for Heart Failure (Core: Active Treatment Phase) (Time from randomization to the first event (Maximum 50 Months)); Percentage of Participants With All Cause Mortality (Core: Active Treatment Phase) (Time from randomization to the first event (Maximum 50 months)); Percentage of Participants With Occurrence of Primary Composite Endpoint (Extension Phase) (From cut-off date (20Dec2011/End of Treatment (EOT) ) to the first event after cut-off date (9 months in average)); Percentage of Participants With Cardiovascular (CV) Death (Extension Phase) (from cut-off date (20Dec2011/End of Treatment (EOT) ) to the first event after cut-off date (9 months in average)); Percentage of Participants With Resuscitated Sudden Death (Extension Phase) (From cut-off date (20Dec2011/End of Treatment (EOT) ) to the first event after cut-off date (9 months in average)); Percentage of Participants Fatal/Non-fatal Myocardial Infarction (MI) (Extension Phase) (From cut-off date (20Dec2011/End of Treatment (EOT) ) to the first event after cut-off date (9 month in average)); Percentage of Participants With Fatal/Non-fatal Stroke (Extension Phase) (From cut-off date (20Dec2011/End of Treatment (EOT) ) to the first event after cut-off date (9 months in average)); Percentage of Participants With Onset of End-stage Renal Disease (ESRD) (Extension Phase) (From cut-off date (20Dec2011/End of Treatment (EOT) ) to the first event after cut-off date (9 months in average)); Percentage of Participants Doubling of Baseline Serum Creatinine Concentration, Sustained for at Least One Month (Extension Phase) (From cut-off date (20Dec2011/End of Treatment (EOT) ) to the first event after cut-off date (9 months in average)); Percentage of Participants With Unplanned Hospitalization for Heart Failure (Extension Phase) (From cut-off date (20Dec2011/End of Treatment (EOT) ) to the first event after cut-off date (9 months in average)); Percentage of Participants With All Cause Mortality (Extension Phase) (from cut-off date (20Dec2011/End of Treatment (EOT) ) to the first event after cut-off date (9 months in average))
D: To investigate the combined effect of aliskiren and valsartan on vascular structure, assessed by wall to lumen ratio of retinal arterioles, in hypertensive patients. (After 8 weeks of treatment with aliskiren versus placebo)

Answer: D