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Arterial hypertension is an established risk factor for acute coronary syndromes, and physical exertion may trigger the onset of such an event. The mechanisms involved include the rupture of a small, inflamed, coronary plaque and the activation of thrombogenic factors. Blood pressure (BP)-lowering treatment has been associated with beneficial effects on subclinical inflammation and thrombosis at rest and during exercise. This prospective study sought to compare the effect of different antihypertensive drugs on the inflammatory and thrombotic response during exercise. A total of 60 never-treated hypertensive patients were randomized to an angiotensin receptor blocker (ARB)- or non-dihydropyridine calcium channel blocker (CCB)-based regimen. Patients with inflammatory or coronary artery disease were excluded. Six months after pharmaceutical BP normalization, the patients underwent a maximal treadmill exercise testing. High-sensitivity C-reactive protein (hsCRP), serum amyloid A (SAA), white blood cells (WBC), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), total fibrinogen (TF) and von Willebrand factor (vWF) levels, as well as plasminogen activator inhibitor-1 (PAI-1) activity were measured in blood samples taken while the patients were at rest and during peak exercise. All of these biomarkers increased with exercise, except PAI-1, which decreased (P<0.05 for the difference between resting and peak exercise for all biomarkers). The ARB group had less marked (P<0.05) exercise-induced changes than the CCB group in hsCRP (5.8% vs. 7.7%), SAA (4.2% vs. 7.2%), WBC (46.8% vs. 52.6%), TNF-α (16.3% vs. 24.3%), TF (9.5% vs. 16.9%) and PAI-1 (-9.5% vs. -12.3%) but a similar (P=NS) change in IL-6 (39.4% vs. 38.6%) and vWF (29.2% vs. 28.6%). In conclusion, ARBs are most likely more effective than CCBs at suppressing the exercise-induced acute phase response. Potential protection against exercise-related coronary events remains to be elucidated.

The effect of long-term angiotensin II type 1 receptor blocker (ARB) therapy on inflammation indices has not been fully investigated in a hypertensive population. The authors evaluated 323 consecutive nondiabetic patients (mean age, 57 years; 176 men; 92 smokers) with high renin activity and uncomplicated essential hypertension whose blood pressure levels normalized (from 163.9/100.7 mm Hg to 131.6/82.8 mm Hg) after 4 weeks of ARB or ARB/diuretic treatment. All patients underwent full laboratory evaluation (routine examination of blood and urine, liver, kidney, thyroid function, and lipid and glucose profiles), including measurement of high-sensitivity C-reactive protein and serum amyloid A levels, at drug-free baseline, which was repeated after 6 months of ARB or ARB/diuretic treatment. A significant (P<.001) overall decrease was noted in both high-sensitivity C-reactive protein (-0.41+/-1.56 mg/dL) and serum amyloid A (-0.62+/-2.03 mg/dL), but a smaller decrease in high-sensitivity C-reactive protein and serum amyloid A change was seen in the smoker subgroup compared with nonsmokers (P<.05), indicating that the ARB or ARB/diuretic anti-inflammatory effect may be adversely affected by smoking status.

The article focuses on a study that examined the association between dairy consumption and levels of various inflammatory markers among adults with no evidence of cardiovascular or other chronic disease. The study found that C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) levels of individuals consuming between 11 and 14 weekly servings of dairy products had 29%, 9% and 20% lower levels of CRP, IL-6 and TNF-α, respectively.

Summary: During the last decade, several studies have documented the unfavourable effects of inflammation on cardiovascular function and its role in the pathophysiology of atherosclerotic disease. The interplay between inflammation and arterial system is multifaceted. On the one hand, the endothelium contributes to the initiation and the perpetuation of vascular wall inflammation. On the other hand, the inflammatory cascade affects adversely the endothelium-dependent processes and the mechanical properties of the arteries. These effects give rise to impaired vasomotion, arterial stiffening and increased wave reflections and thus result in an unfavourable haemodynamic loading of the heart. Chronic inflammatory diseases (such as rheumatoid arthritis, and others) as well as acute inflammatory stimuli (such as acute infections) may adversely influence the arterial performance. Moreover, systemic subclinical low-grade inflammation, as expressed by high circulating levels of inflammatory markers/mediators, is a common denominator of most cardiovascular risk factors (hypertension, diabetes, etc.) and importantly, it is closely related to impaired arterial elastic properties. In addition, vasculogenic erectile dysfunction, which comprises an alternative phenotype of arterial dysfunction and an emerging cardiovascular risk predictor, is accompanied by low-grade inflammatory activation. Among the several inflammatory markers/mediators, level of C-reactive protein has been consistently associated with indices of arterial function in several populations. However, data regarding a possible direct etiological role of C-reactive protein in arterial dysfunction and atherosclerosis, if any, are yet inconclusive. Current evidence suggests that anti-inflammatory strategies benefit arterial function in several clinical settings. Further research is needed to elucidate whether inflammation may comprise a worthwhile treatment target with regard to the cardiovascular system. [ABSTRACT FROM AUTHOR]