Decreased plasminogen activator inhibitor-1 levels in coronary artery aneurysmatic patients.

BACKGROUND: Matrix metalloproteinases (MMPs) have been implicated in the pathogenesis of arterial aneurysms through increased proteolysis of extracellular matrix proteins. Increased proteolysis due to elevated matrix degrading enzyme activity in the arterial wall may act as a susceptibility factor for the development of coronary aneurysms. Plasmin strongly stimulates pro-MMP enzyme conversion to the active form. Plasmin hyperactivity due to decreased plasminogen activator inhibitor-1 (PAI-1) may cause MMP over activity and coronary aneurysms. The aim of this study was to investigate the association between PAI-1 and presence of coronary aneurysms. METHODS: Twenty-three patients with aneurysmal coronary artery disease and stable angina were enrolled into study (Group 1). Twenty-two patients without coronary aneurysm were selected as a control group (Group 2). PAI-1 was measured in peripheral venous blood. RESULTS: The plasma PAI-1 level was lower in the coronary artery aneurysmatic patients compared to the control group (8.41 +/- 4.28 vs. 13.32 +/- 10.05 ng/ml, p = 0.037). Serum C-reactive protein (CRP) values were not significantly different between groups (3.83 +/- 1.08 vs. 4.01 +/- 1.35 mg/l, p >0.05). CONCLUSION: Increased matrix degrading enzyme activity can cause arterial wall destruction through increased proteolysis of extracellular matrix proteins. Unregulated plasmin hyperactivity due to decreased inhibition by PAI-1 may play an important role in coronary aneurysm formation.

Atorvastatin treatment decreases inflammatory and proteolytic activity in patients with hypercholesterolemia.

BACKGROUND: Statins have anti-inflammatory and anti-platelet effects, which are known as non-lipid effects. Statin treatment can decrease endogenous inflammatory response. AIM: To study the effects of atorvastatin on matrix metalloproteinase-9 (MMP-9) and high sensitive C-reactive protein (hs-CRP) - markers of the proteinolytic and inflammatory activity. METHODS: In this prospective study 44 patients with hypercholesterolemia were randomly assigned into 2 groups; Group 1 (n=22) treated with atorvastatin and diet for 2 months, and Group 2 (n=22) - diet alone. MMP-9 and hs-CRP were measured at baseline and two months later. RESULTS: Groups were matched for age, sex and baseline characteristics. Lipid levels decreased by 32% (LDL from 153.9+/-26.6 to 94.5+/-20.8 mg/dl, p<0.005) in the atorvastatin group and by 9% in the diet alone group. Atorvastatin lowered plasma CRP from 5.16+/-1.9 to 2.88+/-1.06 mg/L (p<0.001) and MMP-9 activity from 64.3+/-28.1 to 35.4+/-20.0 ng/ml (p<0.0001). Atorvastatin-induced reductions in CRP and MMP-9 were greater than in the diet alone group. MMP-9 levels did not show significant changes in Group 2 after two months of diet. CONCLUSIONS: Atorvastatin treatment decreases inflammatory and proteolytic activity in patients with hypercholesterolemia.

Left ventricular hypertrophy and endothelial functions in patients with essential hypertension.

OBJECTIVE: In this study, we used a non-invasive method in patients with essential hypertension and without any overt clinical evidence of atherosclerosis to investigate the role of left ventricular hypertrophy (LVH) in endothelial functions. METHODS: We assessed endothelial function in 32 hypertensive patients with LVH (group 1), 28 hypertensive patients without LVH (group 2) and 29 normotensive subjects (control group). Flow-mediated (endothelium-dependent) and nitrate induced (endothelium-independent) dilatation of the brachial artery was evaluated in all groups. RESULTS: Flow-mediated dilatation was considerably higher in the control group than in group 1 and 2 (13.98 +/- 2.92%, 4.67 +/- 1.09% and 7.02 +/- 1.79% respectively, p < 0.001). In addition, endothelium-dependent dilatation was significantly lower in group 1 than in group 2 (p < 0.001), whereas nitrate induced changes were similar in all groups. CONCLUSION: Vascular endothelial functions are impaired in hypertensive patients. There may be heterogeneity of endothelial dysfunction among patients with hypertension. Presence of LVH has an additional negative effect on endothelial function in hypertensive patients.

Femoral signal intensity: a new method for prediction of embolic risk.

Mitral stenotic patients with left atrial spontaneous echo contrast (LA SEC) are associated with high risk of thromboembolism. The aim of this study was to predict thromboembolic risk in mitral stenotic patients. Femoral artery signal intensity alteration (%) was compared among the groups. Group 1 had severe mitral stenosis with LA SEC and group 2 slight mitral stenosis without LA SEC. Group 3 patients had normal transthoracic echocardiography. Femoral artery longitudinal view was studied with a linear USG probe (7.5 MHz, HP 2500). The femoral cuff was inflated to 300 mmHg, 7-12 cm below the inguinal ligament. Cuff inflation resulted in femoral arterial blood stasis. Intraluminal signal intensity increased in seconds. The femoral signal intensity alteration (%) at 180 seconds was compared to baseline. After femoral cuff inflation, femoral signal intensity alteration (%) was significantly higher in group 1 than groups 2 and 3 (P < 0.001). Group 1 patients had higher thromboembolic risk on the basis of their echocardiographic, clinical, and laboratory parameters. Increased signal intensity alteration (%) can be detected in the femoral artery in mitral stenotic patients with LA SEC.

Elevated serum CA 125 levels in mitral stenotic patients with heart failure.

BACKGROUND: Elevated tumor marker levels have been reported in heart failure patients with left ventricular (LV) systolic dysfunction and enlargement. The levels of several tumor markers, including CA 125, CA 19-9, CA 15-3 and CEA, in rheumatic mitral stenotic patients were compared to the control group. MATERIALS AND METHODS: Tumor markers were measured in 60 mitral stenotic patients and in 30 normal subjects who served as the control group. Mitral stenotic patients were classified into two categories of cardiac dysfunction based on the classification of the New York Heart Association (NYHA). Group I consisted of 31 patients in NYHA class 3-4 and group II of 29 patients in NYHA class 1-2. Echocardiographic examinations and invasive hemodynamic monitoring were performed in all patients. RESULTS: Group I patients had decreased mitral valve area (p = 0.004) and higher left atrial diameter (p = 0.003) than group II patients. Right atrial, mean pulmonary artery and pulmonary capillary wedge pressures and transmitral gradient were higher in group I than in group II (p = 0.010, 0.0001, 0.0001 and 0.0001, respectively). CA 125 levels were statistically higher in mitral stenotic patient groups than in the control group (p < 0.0001). No statistically significant differences were shown for the other tumor markers. Group I patients had higher CA 125 levels compared to group II (p < 0.0001). CONCLUSION: Elevated CA 125 levels may be due to venous congestion and activation of peritoneal mesothelium or increased signal peptides.