Time course of rapid C-reactive protein reduction by pravastatin in patients with stable angina.

The evidence has indicated that rapid reduction of inflammatory marker, such as C-reactive protein (CRP) could be achieved by administration of a statin. However, limited information is available in evaluating the short-term time course of CRP reduction in patients with coronary artery disease by use of a statin. Forty-two patients with stable angina were randomly assigned to 20 mg/d or 40 mg/d group of pravastatin.

Activation of nuclear factor-kappaB and correlation with elevated plasma c-reactive protein in patients with unstable angina.

Background: Unstable coronary syndromes are currently believed to be caused by rupture of an atherosclerotic plaque due to local events, which may be of general inflammatory etiology. There is increasing evidence that nuclear factor-kappaB (NF-kappaB) is a key transcription factor in controlling gene expression concerning inflammatory response, and that plasma concentrations of C-reactive protein (CRP) is a sensitive marker of inflammation in unstable coronary syndromes. However, whether NF-kappaB activation is associated with coronary heart disease (CHD) activity as well as plasma CRP level has been less well investigated.

Effects of xuezhikang, an extract of cholestin, on lipid profile and C-reactive protein: a short-term time course study in patients with stable angina.

Background: Reduction of cholesterol and inflammation can be achieved by administration of a statin. Xuezhikang, an extract of cholestin, available from Chinese red yeast rice, could effectively modify the lipid profile. However, limited information is available regarding rapid effects of Xuezhikang on plasma C-reactive protein (CRP) and the lipid profile in patients with stable angina.

Is hypertension an inflammatory disease?

Hypertension has been recognized as a multi-factorial trait resulting from the effect of a combination of environmental and genetic factors, including excess dietary salt or alcohol intake, stress, age, genetics and family history, obesity, physical inactivity, as well as high saturated fat diet. During the past few years, however, a large amount of information has been collected on the vascular inflammation, indicating that inflammation may involve in the initiation as well as development of hypertension and allowing us to reconsidering the pathogenic mechanisms of hypertension. Evidence from animal models as well as patients, have indicated that hypertension, an established major risk factor for coronary artery disease, has been suggested to exert pro-inflammatory actions through the increased expression of several mediators, including leukocyte adhesion molecules, chemokines, specific growth factors, heat shock proteins, endothelin-1, and angiotensin.

Statin, like aspirin, should be given as early as possible in patients with acute coronary syndrome.

It is estimated that about 1 million patients are hospitalized for acute coronary events each years in the United States. An acceptable theory is that the acute coronary syndrome is caused by rupture of the atherosclerotic plaque with superimposed thrombus, which is a complex process and involving a number of different stages. Previous studies indicated that inflammation is one of the most important features of vulnerable plaque, and occurs in most vulnerable plaque, comprised of monocytes, macrophages, and lymphocytes in both the cap and in the adventitia.

Time course of inflammatory response after renal artery stenting in patients with atherosclerotic renal stenosis.

Background: Inflammatory response has been demonstrated in patients with coronary artery disease after percutaneous coronary intervention (PCI). Such response following renal artery stenting has not yet been established, however, in patients with atherosclerotic renal artery stenosis.

Methods: A total of 44 patients were enrolled in this study.

Increased C-reactive protein level after renal stent implantation in patients with atherosclerotic renal stenosis.

Elevated C-reactive protein (CRP) level has been demonstrated in patients with coronary artery disease after coronary stent implantation, but no data are available in patients with atherosclerotic renal artery stenosis concerning whether such changes of CRP also exist after renal artery stent implantation. The authors hypothesize that elevated CRP level may also be present in patients with atherosclerotic renal artery stenosis after stent implantation owing to mechanical disruption of atherosclerotic plaque. In total, 24 patients were enrolled in this study.

Atheroscleritis is a more rational term for the pathological entity currently known as atherosclerosis.

The term "atheroma", a Latin word was first used in 1755 by Albrecht von Halles to designate the plaque deposited on the innermost layer of systemic artery walls. In 1940, however, Félix Marchand suggested the word "atherosclerosis" should be better instead of "atheroma", which is derived from two Greek roots: athéré means gruel or porridge and sclerosis signifies hardening. It is obviously an improvement over the older designation arteriosclerosis.

C-reactive protein is not only an inflammatory marker but also a direct cause of cardiovascular diseases.

Inflammatory processes play a pivotal role in the pathogenesis of atherosclerosis and mediate many of the stages of atheroma development from initial leukocyte recruitment to eventual rupture of the unstable atherosclerotic plaque. C-reactive protein (CRP), an acute phase reactant that reflects different degree of inflammation, has been indicated an independent risk factor in a variety of cardiovascular disease (CVD), especially in unstable coronary syndrome. Our data have showed that increased level of CRP in patients with unstable angina was associated with short-term clinical outcomes, response for conventional therapy, and activation of nuclear factor-kappa B (NF-kappaB), but it is not correlated to coronary artery stenosis as well as lipid profile.

Rapid effects of simvastatin on lipid profile and C-reactive protein in patients with hypercholesterolemia.

Background: Rapid lowering of low-density lipoprotein (LDL) cholesterol levels as well as C-reactive protein (CRP) by administration of drugs may produce early benefit to the coronary endothelium in patients with coronary heart disease and reduce angina and coronary events after revascularization. Limited information has been available in evaluating a potentially effective first 2-week therapeutic approach for the treatment of patients with hypercholesterolemia using a statin.

Hypothesis: The study was undertaken to investigate whether a rapid LDL cholesterol and CRP reduction can be achieved by 2-week simvastatin therapy using a common lipid-lowering protocol in patients with hypercholesterolemia.

Ischemic preconditioning detected by treadmill exercise tests in patients with stable angina.

The aim of this study was to explore the ischemic preconditioning (IP) phenomenon in patients with chronic stable angina (SA) by using treadmill exercise tests (TETs). Twenty-nine patients with SA were divided into 2 groups: group A (n = 15) and group B (n = 14). There was no difference between the 2 groups in both clinical characteristics and extent of coronary stenosis.

Circadian variation in ischemic threshold in patients with stable angina: relation to plasma endothelin-1.

To investigate circadian variation in ischemic threshold in chronic coronary heart disease (CHD) and its relation to plasma endothelin-1 (ET-1), 21 patients with stable angina underwent treadmill exercise tests twice within a day, performed at 8-9 AM for the first test and at 3-4 PM for the second one. Ischemic threshold was defined as the heart rate at the onset of 1 mm ST segment depression during exercise tests. Blood samples were taken at 5 minutes before each exercise test, and plasma ET-1 was measured for determining the possible relation to ischemic threshold in patients with CHD.

Elevated level of plasma C-reactive protein in patients with unstable angina: its relations with coronary stenosis and lipid profile.

C-reactive protein (CRP) is a sensitive marker of inflammation, and elevated levels have been associated with future risk of cardiovascular events. To explore the role and relationship of CRP and coronary stenosis in the development of unstable angina (UA), plasma levels of CRP were determined on admission in 45 patients with UA, and in 42 patients with stable angina (SA) using high-sensitivity ELISA. Coronary angiography was performed in all patients with coronary heart disease (CHD), and severity of coronary stenosis was evaluated by a quantitative analysis.