Why the study?
Does higher pulse pressure correlate with increased subclinical cardiovascular damage in middle-aged patients with untreated primary hypertension?
Does higher pulse pressure correlate with increased subclinical cardiovascular damage in middle-aged patients with untreated primary hypertension?
Pulse pressure is an independent marker of preclinical cardiovascular damage in relatively young patients with primary hypertension, identifying those at higher risk of cardiovascular events.
May aid risk stratification in untreated hypertension; leaves open causal and therapeutic implications.
BACKGROUND: High pulse pressure (PP) values have recently been implicated in the development and progression of large vessel atherosclerosis, small vessel disease, and in the occurrence of cardiovascular events. The aim of the present study is to investigate the relationship between PP and subclinical cardiovascular damage in a cohort of unselected middle-aged patients (204 male, 129 female) with untreated primary hypertension. METHODS: PP was calculated as the difference between systolic (SBP) and diastolic blood pressure (DBP). Left ventricular mass index (LVMI) was assessed by M-B mode echocardiography (LVH=LVMI>51 g/m(2.7)), and carotid intima-media thickness (IMT) by high-resolution US scan. Albuminuria was measured as the albumin to creatinine ratio (ACR) in three non-consecutive first morning urine samples. RESULTS: PP was positively correlated to gender (P<0.05), duration of disease (P<0.001), age (P<0.0001), LDL cholesterol (P=0.007), and to early signs of target organ damage (TOD), namely LVMI (P<0.0001), IMT (P<0.0001), and ACR (P=0.036). Patients in the upper quartile of PP showed higher LVMI (P<0.001), thicker carotid walls (P<0.001), as well as higher ACR (P<0.04). Multiple linear regression analysis showed that PP and ACR independently influence LVMI (F=26.476, r(2)=0.29, P<0.0001) and IMT (F=17.813, r(2)=0.26, P<0.0001). Patients with LVH, increased carotid IMT and microalbuminuria showed higher PP values as compared with those with lesser degrees of target organ involvement (F=4.97, P<0.003 inter-group comparison). Moreover, the risk of having the simultaneous occurrence of various signs of TOD increases significantly with each SD increase in PP or SBP, but is not influenced by DBP. CONCLUSIONS: PP is an independent marker of preclinical cardiovascular damage in relatively young patients with primary hypertension and, therefore, can be useful for identifying those at higher risk of cardiovascular events.
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Francesca Viazzi (2002) studied this question.
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