Abstract
Objective: HTA is considered to be a silent killer. TOD is an indicator of cardiovascular risk in people with hypertension. The main objective of our study is to describe the sub-clinical TOD in hypertensive patients. Design and method: This is a descriptive study, conducted between October 2016 and October 2019. It included all asymptomatic hypertensive patients over the age of 35 of both sexes. Screening for infraclinical cardiac, vascular and renal damage is carried out with; the evaluation of the left ventricular hypertrophy (LVH) ultrasound and electric. Intima media thickness measurement by 2D carotid ultrasound and screening and evaluation of plaques. The measurement of pulsed pressure. Measuring the ABI for obliterating arterial disease. And finally, the estimate of urinary albumin excretion (UEA) and creatinine clearance according to MDRD. Results: 300 patients included in our series, these are 120 men and 180 women. The average age is 59.75 years. The prevalence of TOD is estimated at 72.3%, the prevalence of electrical LVH is 17.3%, the ultrasound LVH is 29%. Carotid hypertrophy is observed in 34.9% and the presence of stenotic plaques affect 9.1% of patients AOMI is found in 9%. Pathological pulsed pressure is found in 34.3%. UAE is pathological in 23.30% of our patients for A2 and 5.7% for A3. The creatinine clearance is less than 60 ml / min in 11%. The main independent risk factors associated with TOD are the value of SBP and Age. Pulse pressure> 60 mmHg is associated with all TOD and the IMT is correlated with all screening tests for TOD. The SCORE score is predictive only for carotid lesions, it is not predictive for LVH or albuminuria. The SCORE score is not very predictive for AOMI and renal failure. Conclusions: Subclinical TOD is frequent in our series. The major modifiable independent risk factor is the value of SBP. Special attention to pulse pressure as a cardiovascular risk factor and marker of arterial stiffness A strategy for screening for target organ damage coupled with effective therapy targeting SBP is the only way to prevent cardiovascular, neurovascular and renal complications.
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