Hypertension: An immune related disorder?

Hypertension is a multifactorial disorder with serious complications and unknown etiology. Among potential contributors, immune dysregulation has been also proposed. The study population included 61 consecutive hypertensive patients and 55 healthy individuals of similar age and sex distribution. All study participants underwent a thorough evaluation for subclinical atherosclerosis. A full immunological profile including quantification of immunoglobulins (IgG, IgM, IgA) and lymphocyte subpopulations was also obtained. Immunoglobulin levels IgG, IgA and IgM and complement factor C3 were found to be significantly increased in the hypertensive compared to the HC group while a statistically significant decrease in peripheral blood CD3+, CD4+ and CD8+ in hypertensive patients versus controls was detected. These findings might support a putative involvement of altered cellular and humoral immune responses in the pathogenesis of hypertension, implying a promising role for immunomodulatory strategies, already implemented in the treatment of autoimmune diseases, in the future management of hypertension.

Factors influencing white-coat effect.

BACKGROUND: The transient blood pressure (BP) rise during clinical visits is usually referred to as white-coat effect (WCE). The aim of the present study was to investigate factors that may influence the WCE. METHODS: A total of 2004 subjects underwent office BP measurements and 24-h ambulatory BP monitoring (ABPM) on the same day. The WCE was estimated as the difference between office and average daytime ambulatory BP (ABP). According to the office and daytime BP values, the study population was divided into normotensives (NTs), white-coat hypertensives (WCHs), masked hypertensives (MHTs), and sustained hypertensives (SHTs). Statistical analyses were performed using one-way analysis of variance and multiple linear regression models. RESULTS: The mean systolic and diastolic WCE was 9 +/- 16 and 7 +/- 12 mm Hg, respectively. In the entire group of patients, multiple linear regression models revealed independent determinants of systolic WCE in the following rank order: office systolic BP (SBP) (beta = 0.727; P < 0.001), female gender (beta = 0.166; P < 0.001), daytime SBP variability (beta = 0.128; P < 0.001), age (beta = 0.039, P = 0.020), and smoking (beta = 0.031, P = 0.048). A 1.0 mm Hg increase in daytime SBP variability correlated with an increment of 0.589 mm Hg (95% confidence intervals, 0.437-0.741) in the systolic WCE. The regression analyses for diastolic WCE revealed the same factors as independent determinants. A 1.0 mm Hg increase in daytime diastolic BP (DBP) variability was independently associated with an increment of 0.418 mm Hg (95% confidence intervals, 0.121-0.715) in the diastolic WCE. CONCLUSIONS: Factors such as gender, age, smoking, office BPV and daytime BPV may exert an important influence on the magnitude of the WCE.

Acute smoke-induced endothelial dysfunction is more prolonged in smokers than in non-smokers.

BACKGROUND: The aim of the study was to compare acute endothelial dysfunction caused by smoking one cigarette between smokers and non-smokers. METHODS: Thirty volunteers, 15 smokers and 15 non-smokers, were asked to smoke the same type of cigarette and endothelial function was assessed by FMD (flow mediated dilatation) at fast, 30, 60 and 90 min post-smoking. RESULTS: Overall response of FMD after smoking was significantly different between smokers and non-smokers (p=0.011). Endothelial dysfunction after smoking remained significant for 1-h in smokers (p=0.002), but only for 30 min in non-smokers (p=<0.001). FMD 1-h after smoking was significantly higher in non-smokers than in smokers (p=0.002). CONCLUSIONS: Smokers seem to have sustained and more intensive unfavourable effects in endothelial function than non-smokers after smoking one cigarette. It is possible that long-term smoking diminishes the capacity of endothelium to counterbalance external factors that cause endothelial dysfunction.

Twenty-four-hour heart rate and blood pressure are additive markers of left ventricular mass in hypertensive subjects.

BACKGROUND: We investigated whether mean heart rate (HR(24)) and blood pressure (BP) parameters during 24-h ambulatory BP monitoring (ABP) are independent or additive markers of left ventricular (LV) mass in subjects with newly diagnosed, untreated hypertension. METHODS: A total of 250 patients (40% women, 60% men; mean age 59.6 +/- 11 years) with essential hypertension who were attending the outpatient Hypertension Unit were studied. All patients underwent 24-h ABP and HR monitoring as well as echocardiography for assessment of left ventricular (LV) dimensions and function. RESULTS: A decreasing HR24 or increasing ABP parameters (ie, systolic, diastolic, mean BP, and pulse pressure) were associated with increasing LV mass (P < .001) and wall thickness (P < .01). In multivariate analysis, after adjusting for age, gender, body surface area, body mass index, hematocrit, glucose, cholesterol, smoking, and each of the measured ABP parameters separately, decreasing HR24 was independently related to increasing LV mass in addition to ABP and body size parameters (P < .001). The addition of HR24 in different multivariate models for prediction of LV mass significantly increased the adjusted model r2 (range of r2 change: 0.039 to 0.064, P for change <.05). Decreasing HR24 or HR during daytime (6 am to 10 pm) was associated with a higher likelihood of LV hypertrophy in addition to ABP parameters (adjusted odds ratio 0.92 (CI 0.87 to 0.98), per 1 beat/min greater HR24 P = .002 and 0.93 (CI: 0.87 to 0.98), per 1 beat/min greater HR in the daytime P = .017). CONCLUSION: The 24-h HR and BP during ABP are independent and additive markers of increased LV mass in untreated hypertensive individuals.