Effects of Low Dose versus High Dose Statin Therapy on the Changes of Endothelial Function and Carotid Intima-Media Thickness in Patients with Variant Angina.

BACKGROUND: To compare the effects of low dose and high dose of statin treatment on endothelial function and carotid intima-media thickness (IMT) in patients with variant angina (VAP). METHODS: A total of 70 patients with VAP were divided into two groups; atorvastatin 10 mg treatment group (group I: n = 35, 54.2 ± 12.5 years) versus atorvastatin 40 mg treatment group (group II: n = 35, 52.6 ± 9.8 years). Flow mediated vasodilation (FMD) of the brachial artery and IMT of the carotid artery were compared between the groups after 6 months of statin treatment. RESULTS: The baseline FMD and carotid IMT were not different between the groups. After 6 months of statin therapy, FMD was significantly improved in both groups (7.7 ± 2.5% to 8.9 ± 2.2% in group I, p = 0.001, 7.9 ± 2.7% to 9.5 ± 2.8% in group II, p < 0.001), but the degree of FMD change and FMD at 6 month were not different between the groups. Carotid IMT were not changed in both groups after 6 months of statin therapy. CONCLUSION: The use of statin for 6 months significantly improved endothelial function in patients with VAP, but carotid IMT was not changed. The use of high dose statin did not show significant additional benefit as compared with the use of low dose statin. The present study suggested that statin therapy would be beneficial in the treatment of VAP.

Endothelial dysfunction and increased carotid intima-media thickness in the patients with slow coronary flow.

Flow mediated brachial dilatation (FMD) and carotid intima-media thickness (IMT) have been a surrogate for early atherosclerosis. Slow coronary flow in a normal coronary angiogram is not a rare condition, but its pathogenesis remains unclear. A total of 85 patients with angina were evaluated of their brachial artery FMD, carotid IMT and conventional coronary angiography. Coronary flow was quantified using the corrected thrombosis in myocardial infarction (TIMI) frame count method. Group I was a control with normal coronary angiography (n = 41, 56.1 ± 8.0 yr) and group II was no significant coronary stenosis with slow flow (n = 44, 56.3 ± 10.0 yr). Diabetes was rare but dyslipidemia and family history were frequent in group II. Heart rate was higher in group II than in group I. White blood cells, especially monocytes and homocysteine were higher in group II. The FMD was significantly lower in group II than in group I. Elevated heart rate, dyslipidemia and low FMD were independently related with slow coronary flow in regression analysis. Therefore, endothelial dysfunction may be an earlier vascular phenomenon than increased carotid IMT in the patients with slow coronary flow.

[Effects of a smoking cessation education on smoking cessation, endothelial function, and serum carboxyhemoglobin in male patients with variant angina].

PURPOSE: The aim of this study was to evaluate the effects of a smoking cessation education on endothelial function and carboxyhemoglobin levels in smokers with variant angina. METHODS: A nonequivalent control group pretest-posttest design was used. Participants were 60 male smokers with variant angina admitted to one hospital: the control group (30) between September and December, 2009, and the experimental group (30) between February and May, 2010. Endothelial function, as defined by flow-mediated vasodilation (FMD) of the brachial artery, and serum carboxyhemoglobin (COHb) were determined at baseline and at 3 months after the initiation of education in both groups. RESULTS: Three months after the program, smoking cessation was successful in 22 of the 30 smokers in the experimental group, but only in 4 of 30 smokers in the control group (p<.001). After the education, the experimental group showed a significant increase in FMD, and a significant decreased in serum COHb compared with the control group. CONCLUSION: The findings indicate that this smoking cessation education program is effective for hospitalized smokers with variant angina.

Diagnostic value of nitroglycerin-induced headache as a negative predictor of coronary atherosclerosis.

The purpose of the present study was to clarify the possible relationship between nitroglycerin (NTG)-induced headache and both vascular functional and organic atherosclerosis. The study included 96 patients with NTG-induced headache (group I: 54.7±9.5 years, 52 males) and 204 patients without headache (group II: 58.1±9.1 years, 127 males) who suffered from new-onset chest pain. Flow-mediated dilation and nitroglycerin-mediated dilation were significantly greater in group I than in group II (8.8±4.1% vs. 7.1±3.5%, p=0.001, and 23.1±7.3% vs. 17.1±11.8%, p<0.001, respectively). The carotid intima-media thickness was significantly smaller in group I than in group II (0.55±0.15 mm vs. 0.67±0.22 mm, p=0.001). Heart-carotid pulse wave velocity was significantly lower in group I than in group II (784.5±160.1 m/s vs. 979.1±215.6 m/s, p=0.003). In the multiple regression analysis, the absence of NTG-induced headache was a predictor of coronary artery disease (CAD) (odds ratio: 17.89, 95% confidence interval: 7.89-40.02, p<0.001). NTG-induced headache developed more frequently in patients with normal coronary arteries or minimal CAD than in patients with obstructive CAD. The presence of NTG-induced headache might be helpful and provide additional information in evaluating patients with chest pain syndrome.

Comparison of effects of rosuvastatin and atorvastatin on plaque regression in Korean patients with untreated intermediate coronary stenosis.

BACKGROUND: Serial intravascular ultrasound (IVUS) was used to compare the effects of moderate doses of rosuvastatin and atorvastatin on plaque regression in patients with intermediate coronary stenosis. METHODS AND RESULTS: This was a prospective, randomized, and comparative study for lipid-lowering therapy with rosuvastatin 20mg (n=65) and atorvastatin 40mg (n=63) using serial IVUS (baseline and 11-month follow-up). Efficacy parameters included changes in total atheroma volume (TAV) and percent atheroma volume (PAV) from baseline to follow-up. Changes of TAV (-4.4±7.3 vs. -3.6±6.8mm(3), P=0.5) and PAV (-0.73±2.05 vs. -0.19±2.00%, P=0.14) from baseline to follow-up were not significantly different between the 2 groups. Plaque was increased in 15% in the rosuvastatin group and in 30% in the atorvastatin group at follow-up (P=0.064). The plaque increase group had higher baseline high-sensitivity C-reactive protein (hs-CRP; 1.28±2.70mg/dl vs. 0.54±1.16mg/dl, P=0.034) and higher follow-up low-density lipoprotein cholesterol (LDL-C) (78±24mg/dl vs. 63±21mg/dl, P=0.002) compared with the plaque non-increase group. Follow-up LDL-C (odds ratio [OR]=1.038, 95% confidence interval [CI]=1.003-1.060, P=0.036) and baseline hs-CRP (OR=1.025, 95%CI=1.001-1.059, P=0.046), not the type of statin, were the independent predictors of plaque increase at follow-up. CONCLUSIONS: Moderate doses of rosuvastatin and atorvastatin could contribute to effective plaque regression. Follow-up LDL-C and baseline hs-CRP are associated with plaque progression in patients with intermediate coronary stenosis.

Gender differences in coronary plaque components in patients with acute coronary syndrome: virtual histology-intravascular ultrasound analysis.

BACKGROUND: The aim of this study was to evaluate the gender differences in plaque components in acute coronary syndrome (ACS) patients. METHODS: We used virtual histology-intravascular ultrasound to evaluate the plaque components in culprit lesions in 362 ACS patients (254 men, 108 women). RESULTS: Women were more likely to be diabetic (34% vs 23%, p=0.030), had greater percentage necrotic core (%NC) volume (19.0±12.7% vs 16.8±11.9%, p=0.040), and had trends toward higher high-sensitivity C-reactive protein (hs-CRP) (0.85±1.28 mg/dl vs 0.53±0.48 mg/dl, p=0.063), and higher incidence of thin-cap fibroatheroma (TCFA) (62% vs 52%, p=0.078) compared with men. %NC volume was significantly greater in diabetic patients compared with nondiabetic patients (20.4±10.2% vs 16.0±8.9%, p<0.001) and was significantly greater in patients with elevated hs-CRP (≥0.2 mg/dl) compared with those with normal hs-CRP (<0.2 mg/dl) (18.8±8.9% vs 16.6±9.7%, p=0.021). However, there were no differences in plaque components between diabetic women and men, and between women and men with elevated hs-CRP levels. Diabetes [odds ratio (OR): 2.44, 95% confidence interval (CI): 1.35-3.82, p=0.003] and hs-CRP (OR: 1.54, 95% CI: 1.08-2.65, p=0.032), but not female gender, were the independent predictors of TCFA. CONCLUSIONS: Although it seems likely that female ACS patients have more vulnerable plaque components compared with male ACS patients, these findings may result not from true gender differences in plaque components but higher prevalence of diabetes and hs-CRP elevation in women.

Endothelial dysfunction, increased carotid artery intima-media thickness and pulse wave velocity, and increased level of inflammatory markers are associated with variant angina.

BACKGROUND: Endothelial dysfunction and vascular inflammation may be associated with variant angina (VA). Flow-mediated vasodilation (FMD), carotid artery intima-media thickness (IMT), and pulse wave velocity (PWV) are widely used as non-invasive modalities for evaluating atherosclerosis. METHODS AND RESULTS: A total of 254 patients with chest pain were divided into three groups according to coronary angiogram (CAG) finding. There were 76 patients (VA group: 53.5+/-10.2 years, 41 males) with normal CAG with positive ergonovine-provocation test (EPT), 58 patients (control group: 55.3+/-8.7 years, 30 males) with normal CAG with negative EPT, and 120 patients with angiographically diagnosed coronary artery disease (CAD group: 56.3+/-9.7 years, 79 males). The level of FMD was lower in the VA group than in the control group (7.7+/-3.5% vs. 9.4+/-3.8%, p=0.014). Carotid IMT was higher in the VA group than in the control group (0.58+/-0.1 mm vs. 0.54+/-0.1 mm, p=0.029). The brachial-ankle PWV (baPWV) was higher in the VA group than in the control group (1445.3+/-211.8 cm/s vs. 1396.7+/-394.5 cm/s, p=0.020). The levels of monocyte cell counts was higher in patients of the VA group than in the other two groups (7545.7+/-2611.1/mm(3) vs. 6548.2+/-2156.4/mm(3) vs. 6740.9+/-1730.4/mm(3), p=0.015, respectively; monocyte cell counts: 657.2+/-242.6/mm(3) vs. 442.5+/-219.3/mm(3) vs. 490.0+/-172.0/mm(3), p=0.025). CONCLUSION: VA is associated with endothelial dysfunction and increased carotid IMT, baPWV, and inflammatory markers.

Clinical effects of calcium channel blocker and Angiotensin converting enzyme inhibitor on endothelial function and arterial stiffness in patients with angina pectoris.

To evaluate the effects of calcium channel blocker (CCB) and angiotensin converting enzyme inhibitor (ACEI) on endothelial function and arterial stiffness in stable angina pectoris (SAP), 87 patients with SAP (57.6+/-10.0 yr, 52 males) were divided into two groups; CCB group (group I: n=44, 57.9+/-9.7 yr, 23 males) vs. CCB plus ACEI group (group II: n=43, 57.2+/-10.5 yr, 29 males). Flow mediated vasodilation (FMD) of the brachial artery, pulse wave velocity (PWV), urinary albumin excretion (UAE), and high sensitivity C-reactive protein (hsCRP) were compared. FMD, PWV, UAE, and hsCRP were not different between the groups at baseline. After 6 months of treatment, FMD were significantly improved in group II (7.5+/-3.7 to 8.8+/-2.7%, p<0.001), but not in group I (7.9+/-2.7 to 8.2+/-2.8%, p=0.535). Brachial-ankle PWV were significantly improved in both groups (1,621.3+/-279.4 to 1,512.1+/-225.0 cm/sec in group I, p<0.001, 1,586.8+/-278.5 to 1,434.5+/-200.5 cm/sec in group II, p<0.001). However, heart-femoral PWV were significantly improved (1,025.7+/-145.1 to 946.2+/-112.2 cm/sec, p<0.001) and UAE were significantly decreased (20.19+/-29.92 to 13.03+/-16.42 mg/g Cr, p=0.019) in group II only. In conclusion, combination therapy with CCB and ACEI improves endothelial function, arterial stiffness, and UAE than CCB mono-therapy more effectively in patients with SAP.