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Aortic aneurysms are associated with coronary artery ectasia (CAE). However, the relation between the extent of CAE and coronary blood flow in patients with aortic aneurysms is not fully understood. This study was undertaken to assess the angiographic characteristics and effects of the topographical extent of CAE on coronary blood flow in patients with aortic aneurysms. This study consisted of 93 consecutive patients with aortic aneurysms (AA group) and 79 patients without aortic aneurysms who had angiographically normal coronary arteries as the control group (Control group). Coronary flow velocity was determined using the thrombolysis in myocardial infarction frame count (TFC) and the topographical extent of CAE was assessed. In the AA group, 43 patients (46.2 %) had significant coronary artery stenosis and 37 patients (40.2 %) had diffuse CAE. TFC was significantly higher in the AA group than in the control group in all 3 coronary arteries. Furthermore, mean corrected TFC (CTFC) was significantly higher in the AA group than in the control group (40.1 ± 10.7 vs. 25.8 ± 6.5, p < 0.001). In the AA group, mean CTFC in patients with diffuse CAE was significantly higher than that in patients with segmental CAE (50.2 ± 8.7 vs. 33.6 ± 5.2, p < 0.001). The mean CTFC correlated positively with the topographical extent of CAE. Many patients with aortic aneurysms were accompanied with angiographic coronary artery stenosis and CAE. Furthermore, patients with aortic aneurysms had higher CTFC than those without aortic aneurysms and it was primarily driven by more frequent prevalence of diffuse CAE.

Recent studies have shown good correlations between echocardiography and Tl-201 gated single-photon emission computed tomography (SPECT) for the assessment of left ventricular volumes and ejection fraction. We assessed how left ventricular geometry affected correlations between these values measured by the 2 methods in patients with known or suspected coronary artery disease. There were 109 patients with normal left ventricular geometry, 20 patients with concentric remodeling, 32 patients with eccentric hypertrophy and 28 patients with concentric hypertrophy. In all 4 groups, there were good correlations between end-diastolic volume (EDV) and end-systolic volume (ESV) values measured by echocardiography and quantitative gated SPECT (QGS). EDV and ESV values measured by QGS were significantly underestimated than those measured by echocardiography except for ESV in eccentric hypertrophy. In all 4 groups, ejection fraction (EF) value measured by echocardiography significantly correlated with that measured by QGS, but Bland–Altman plot showed a proportional error. EF value measured by QGS was likely to be overestimated when EF value increased from the median value, and to be underestimated when EF value decreased from the median value especially in concentric remodeling. Tl-201 gated SPECT is a useful tool for the assessment of left ventricular volumes and function, but it requires methodological considerations according to left ventricular geometry.

Residual risk of cardiovascular events after treatment with stain might be explained in part because patients have low levels of n−3 polyunsaturated fatty acids (PUFA). We examined how lipid-lowering therapy with strong statin affected serum PUFA levels in patients with coronary artery disease. The study population consisted of 46 patients with coronary artery disease whose low-density lipoprotein (LDL) cholesterol was more than 100 mg/dl. Lipid-lowering therapy was performed with a strong statin including atorvastatin (n = 22), rosuvastatin (n = 9) or pitavastatin (n = 15). Serum PUFA levels were determined by gas chromatography. The treatment with strong statin decreased the sum of dihomo-γ-linolenic acid (DGLA) and arachidonic acid (AA) levels (195 ± 41 to 184 ± 44 μg/ml, P < 0.05) as well as the sum of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) levels (233 ± 71 to 200 ± 72 μg/ml, P < 0.001). These effects of strong statin resulted in a significant decrease in ratio of the sum of EPA and DHA levels to the sum of DGLA and AA levels (1.20 ± 0.27 to 1.10 ± 0.35, P < 0.05). The percent decrease in the LDL cholesterol level correlated significantly with that in the sum of EPA and DHA levels (r = 0.38, P < 0.01). In conclusion, our results showed that lipid-lowering therapy with strong statin mainly reduced n−3 PUFAs in proportion to the decrease in the LDL cholesterol level in patients with coronary artery disease.

Aliskiren is a novel blood pressure-lowering agent acting as an oral direct renin inhibitor. We evaluated the effects of aliskiren on the fibrinolytic system in patients with coronary artery disease who were receiving angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II type 1 receptor blockers (ARBs). We studied 17 patients with coronary artery disease whose systolic blood pressure was more than 130 mmHg despite treatment with ACEIs or ARBs. Aliskiren (150 mg) was added to ACEIs or ARBs, and was continued for 6 weeks. Aliskiren significantly decreased systolic blood pressure (140 ± 6-128 ± 8 mmHg, P < 0.001) and plasma renin activity (1.8 ± 2.3-0.6 ± 0.9 ng/ml/h, P < 0.01) after 6 weeks. However, it did not affect plasminogen activator inhibitor-1 (28.8 ± 14.5-30.6 ± 13.6 ng/ml, P = 0.84), fibrinogen (305 ± 72 vs 301 ± 71 mg/dl, P = 0.33), or D-dimer (0.49 ± 0.24-0.51 ± 0.28 μg/ml, P = 0.70) levels. Our data suggested that patients receiving ACEIs or ARBs would not be expected to have any changes in biomarkers of the fibrinolytic system with additional pharmacologic inhibition of the renin-angiotensin-aldosterone system.