Effect of nicorandil administration on cardiac burden and cardio-ankle vascular index after coronary intervention.

Myocardial injury is a problem associated with percutaneous coronary intervention (PCI). This study aimed to clarify the role of nicorandil administration in preventing myocardial injury. This study included patients with stable angina who underwent PCI from November 2013 to June 2016. Of 58 consecutive patients, the first 20 patients received only saline infusion after PCI (control group); the other 38 patients received a continuous intravenous infusion of nicorandil and saline after PCI (nicorandil group). Troponin I and brain natriuretic peptide (BNP) levels were measured. Vascular parameters, such as blood pressure (BP), cardiac output, cardio-ankle vascular index (CAVI), and estimated systemic vascular resistance (eSVR), were measured. Troponin I of both groups increased 12 h after PCI. Changes in BNP levels between immediately after PCI and 12 h after PCI were significantly higher in the control than in the nicorandil group (10.8 ± 44.2 vs. - 2.6 ± 14.6 pg/ml, p = 0.04). In the nicorandil group, BP, eSVR, and CAVI decreased significantly at 12 h after PCI compared with those immediately after PCI (p < 0.0001), whereas no change was observed in the control group. In a single linear analysis, the change in BP (r = 0.36, p < 0.01) and nicorandil administration (r = - 0.47, p < 0.001) was significantly correlated with the change in CAVI, multiple regression analysis revealed that the changes in CO and eSVR were significant contributing factors for the changes in CAVI. PCI could result in myocardial injury and/or cardiac burden in patients with stable angina. Nicorandil administration after PCI may be effective in relieving the burden by decreasing arterial stiffness (CAVI).

Cardio-ankle vascular index relates to left ventricular ejection fraction in patients with heart failure. A retrospective study.

The cardio-ankle vascular index (CAVI) has been proposed as a new noninvasive marker of arterial stiffness independent of blood pressure. Arterial stiffness is closely related to afterload, and elevated afterload aggravates heart failure. We hypothesized that CAVI is a potential marker of afterload in patients with heart failure. Thirty patients who were admitted because of acute heart failure were identified retrospectively from a review of clinical records. Plasma brain natriuretic peptide (BNP) levels, CAVI, cardiothoracic ratio (CTR), and echocardiographic parameters obtained during acute and chronic phases of heart failure were analyzed. Left ventricular ejection fraction (LVEF) increased significantly and CTR, BNP and CAVI decreased significantly after treatment of heart failure. A significant negative correlation was observed between the change in CAVI and change in LVEF in all subjects (r = -0.3272, P < 0.05). To examine the relationship between CAVI and LVEF, we divided the patients into two subgroups (∆CAVI < -0.5; CAVI decrease group, ∆CAVI ≥ -0.5; CAVI non-decrease group). CAVI was significantly improved after heart failure treatment only in the CAVI decrease group. LVEF decreased significantly in both groups, but the P value was smaller in the CAVI decrease group than in the CAVI non-decrease group. The change in LVEF correlated significantly with the change in CAVI in the CAVI decrease group (r = -0.4201, P < 0.05), whereas no significant correlation was found in the CAVI non-decrease group. CAVI correlates inversely with LVEF after heart failure treatment. Our results suggest that CAVI might partially reflect the afterload in patients with heart failure.

Relationship between two AMI risk factors: low serum lipoprotein lipase mass and hypoadiponectinemia.

AIM: Recent clinical studies have reported that low lipoprotein lipase mass in preheparin serum (s-LpL) and hypoadiponectinemia are important risk factors for acute myocardial infarction (AMI). The aim of this study was to elucidate the relationship between low s-LpL and hypoadiponectinemia, both of which are risk factors for AMI. METHODS: One hundred and thirty-seven male patients with AMI and fifty-three males with normal coronary arteries (NCA) were enrolled in the study. Coronary risk factors, including s-LpL and serum total adiponectin concentrations (t-adiponectin), were compared. RESULTS: Both s-LpL and t-adiponectin were significantly lower in patients with AMI than in subjects with NCA (s-LpL, NCA: 48.1±11.0 ng/mL, AMI: 38.9±11.1 ng/mL, p< 0.01; t-adiponectin, NCA: 7.7±2.9 µg/mL, AMI: 6.1±3.3 µg/mL, p< 0.01). In AMI patients, there was a significant positive correlation between s-LpL and t-adiponectin (r=0.46, p< 0.01). Furthermore, multivariate analysis indicated that both s-LpL and t-adiponectin were independent variables for AMI (s-LpL: p< 0.05, t-adiponectin: p< 0.05). CONCLUSION: These results indicate that although low s-LpL and hypoadiponectinemia are associated with each other, they are independent risk factors for AMI.

Changes in cardio-ankle vascular index in smoking cessation.

AIM: To investigate the effect of smoking and smoking cessation on cardio-ankle vascular index (CAVI). METHODS: The subjects were 82 smokers (77 men, 64+/-10 years) and 20 non-smokers (18 men, 61+/-7 years). CAVI was measured every 3 months and CAVI severity was classified into 3 levels. Decreased, unchanged, and increased CAVI severity levels were coded as "improvement," "no change," and "exacerbation," respectively. Smoking status was coded as "success" for complete abstinence, "partial success" for a reduced number of cigarettes, and "failure" for an unchanging number of cigarettes. RESULTS: Compared with non-smokers, smokers showed a higher CAVI (p<0.05) prior to smoking cessation. Post-cessation, CAVI improved from 9.4 to 8.6 (p<0.01) in "success" cases (n=22), and the significant pre-cessation difference from non-smokers (n=20, CAVI=8.8) disappeared. With regard to the change in CAVI severity of each smoking status, "improvement" occurred in 17%, 24%, and 68% of "failure" (n=35), "partial success" (n=25), and "success" (n=22) groups, respectively, and the "success" group was significantly higher than the other two groups. CONCLUSION: The study showed that CAVI was increased by smoking, and complete smoking cessation improved CAVI.

Bidirectional precordial ST changes during angioplasty to right coronary artery.

Emergency coronary angiography of a 53-year-old man with acute coronary syndrome revealed stenosis in right coronary artery. During angioplasty, the ECG change showed three kind of ST deviation, namely inferior ST elevation with precordial ST depression, inferior ST elevation with precordial ST elevation, and inferior ST depression with precordial ST elevation. The present case shows that the ST deviation of the inferior ischemia with right ventricular ischemia takes various patterns. This phenomenon is decided by degree of right main coronary and right side branch blood flow.

Clinical significance of serum 7-ketocholesterol concentrations in the progression of coronary atherosclerosis.

AIM: 7-Ketocholesterol concentrations can be measured in a blood sample; however, the relationship between blood 7-ketocholesterol concentrations and atherosclerotic disease is not well-known. The aim of this study was to clarify the clinical significance of serum 7-ketocholesterol concentrations (s-7KCHO) in the progression of coronary atherosclerosis. METHODS: One hundred and thirty-nine subjects with coronary artery disease (CAD, subjects with stable angina pectoris or acute myocardial infarction) and 43 subjects with normal coronary arteries were enrolled in the study. s-7KCHO was measured using gas chromatography mass spectrometry. RESULTS: s-7KCHO was significantly higher in subjects with CAD than in those with normal coronary arteries (normal coronary artery: 19.0+/-11.3 ng/mL, CAD: 32.4+/-23.1 ng/mL, p<0.01). Furthermore, patients with multiple vessel disease had significantly higher s-7KCHO than those with single vessel disease. Multivariate analysis revealed that s-7KCHO was an independent variable for CAD (p<0.01). In CAD subjects, the presence of acute myocardial infarction, number of affected vessels, and high sensitive C-reactive protein concentrations strongly correlated with s-7KCHO (p<0.01, <0.05, <0.05, respectively). CONCLUSION: These results indicate that high s-7KCHO is closely associated with the progression of coronary atherosclerosis and inflammation.

Association between cardio-ankle vascular index and serum cystatin C levels in patients with cardiovascular risk factor.

AIM: The aim of this study was to clarify the relationship between CAVI and serum cystatin C levels to understand the role of arterial stiffness in the presence of renal insufficiency. METHODS: We enrolled 206 consecutive patients with cardiovascular risk factors and/or coronary artery disease (CAD) in the study. Serum cystatin C, estimated glomerular filtration rate (eGFR), and plasma levels of von Willebrand factor (vWF) and plasminogen activator inhibitor (PAI-1) were measured. CAVI was determined as an index of arterial stiffness. RESULTS: For all patients, the mean serum cystatin C level was 0.81+/-0.21 mg/L and mean eGFR was 65.8+/-15.5 mL/min per 1.73 m(2). In univariate analysis, CAVI levels significantly correlated with cystatin C levels (r=0.414, p<0.001), eGFR (r=-0.315, p<0.01), PAI-1 (r=0.269, p<0.01), and vWF (r=0.207, p<0.01). Multiple regression analysis showed that age, cystatin C, PAI-1, and a history of CAD were independent variables of CAVI. Age-adjusted CAVI was highest in the presence of both CAD and renal impairment. CONCLUSION: CAVI was closely associated with cystatin C levels. These results suggest a significant role of arterial stiffness in renal insufficiency.

Effect of the angiotensin II receptor antagonist telmisartan on lipoprotein lipase mass in preheparin serum.

AIM: Lipoprotein lipase protein exists in preheparin serum (preheparin LpL mass), even though lipoprotein lipase activity is rarely detected. Recent clinical studies have clarified that low preheparin LpL mass concentration is an important coronary risk factor. The aim of this study was to clarify the effect of telmisartan, which is an angiotensin II receptor antagonist with partial peroxisome proliferator-activated receptor-gamma agonist activity, on preheparin LpL mass concentration in the serum of patients with hypertension. METHODS: Fifty untreated hypertensive patients were treated with telmisartan 40 mg/day for 12 weeks and the subjects were divided into two groups by their mean value of preheparin LpL mass concentration at baseline (cut-off level: Male 55 ng/mL, Female 65 ng/mL). RESULTS: Before telmisartan therapy, low preheparin LpL mass concentration was closely associated with the pathogenesis of insulin resistance and the presence of coronary atherosclerosis. Preheparin LpL mass concentration significantly increased after telmisartan therapy in subjects with a low preheparin LpL mass concentration (baseline/12 weeks after, 46 +/- 12 ng/mL/54 +/- 14 ng/mL, p=0.001). CONCLUSION: This finding indicated that telmisartan could prevent the occurrence of coronary events in subjects with hypertension by increasing the preheparin LpL mass concentration.

Relationship between metabolic syndrome and early stage coronary atherosclerosis.

AIM: Recent clinical studies using intra-vascular ultrasound have clarified that coronary artery plaque already exists in subjects with normal coronary artery which is diagnosed by coronary angiography; furthermore, culprit lesion on acute coronary syndrome often occurs in mild to moderate angiographical stenotic lesion. The aim of this study is to clarify relationship between metabolic syndrome and early stage coronary atherosclerosis using a 3-dimensional intra-vascular ultrasound. METHODS: 70 subjects with normal coronary artery diagnosed by coronary angiography were enrolled. Proxymal range of left anterior descending coronary artery was observed by intra-vascular ultrasound using autopullback methods. RESULTS: Subjects with metabolic syndrome had significantly high percent plaque volume (31 +/- 8% vs 21 +/- 8%, p < 0.0001) and frequently detected abnormal plaque quality such as eccentricity, calcification and lipid pool into plaque than those without metabolic syndrome. Multivariate analysis showed that serum adiponectin concentration was the most strongest variable for percent plaque volume (t value= - 3.0, p < 0.01). On the other hand, subjects with hypoadiponectinemia were detected high incidence of mild calcification into plaque. CONCLUSION: Metabolic syndrome needs to be detected and treated as early as possible. Furthermore, measurement of serum adiponectin concentration and appropriate treatment would prevent acute coronary syndrome.

Relationship between preheparin lipoprotein lipase mass concentration in serum and bare metal stent restenosis.

OBJECTIVES: Insulin resistance or inflammation is known to be related with lipoprotein lipase activity and these factors are also closely associated with the pathogenesis of bare-metal stent restenosis. This study examined the relationship between preheparin lipoprotein lipase protein (preheparin LpL mass) concentration in serum and bare-metal stent restenosis. METHODS: A total of 121 lesions in 112 patients who underwent bare-metal stent implantation using NIR stent or S660/670 stent were examined. Subjects were divided into two groups (N group; patients with normal preheparin LpL mass concentration, n = 50 or L group; patients with low preheparin LpL mass concentration, n = 71) according to the mean levels of preheparin LpL mass concentration (male 39.3 ng/ml, female 50.6 ng/ml). RESULTS: There were no differences in percutaneous coronary intervention or angiographical characteristics. The L group had a significantly higher incidence of restenosis rate and target lesion revascularization than the N group (N group vs L group: 8.0% vs 42.3%, p < 0.0001; 8.0% vs 33.8%, p = 0.0008, respectively). Homeostatic model assessment of insulin resistance as a marker of insulin resistance and high sensitive C-reactive protein concentration were significantly higher in the L group than the N group. Multiple regression analysis showed that only low preheparin LpL mass concentration was an independent factor for restenosis (t value = 3.6, p = 0.0005). CONCLUSIONS: Preheparin LpL mass concentration is closely associated with bare-metal stent restenosis and preheparin LpL mass concentration may be an important marker for the selection of bare-metal stent or drug-eluting stent.

[Angina pectoris presenting with unusual form of coronary spasm: a case report].

A 46-year-old male with asthma bronchiale and eosinophilia was admitted to our hospital because of continuous severe chest pain. Electrocardiography showed ST segment elevation in leads II, III and aVF during chest pain. Emergency coronary angiography showed a series of coronary arterial narrowings in segments 1 and 2. After injection of nitroglycerin 0.1 mg and nicorandil 2 mg into the right coronary artery, the coronary arterial narrowing was gradually relieved. The artery became completely normal after 10 min. Left coronary arterial angiography showed no abnormalities. The diagnosis was spontaneous coronary arterial spasm based on the coronary angiographic findings. The spasm occurred as multiple short narrow arterial segments. Normalization of the coronary artery took a long time. In a case like this, thrombus is easily formed that may cause acute myocardial infarction and unnecessary coronary angioplasty may be performed.

[Mechanism of exercise-induced ST depression based on hemodynamics during cardiac catheterization].

OBJECTIVES: The cause of exercise-induced ST depression was studied by assessing left ventricular end-diastolic pressure (LVEDP). METHODS: This study included 28 patients with normal coronary artery, 24 patients with vasospastic angina pectoris and 28 patients with fixed organic lesion who underwent both treadmill exercise testing and selective coronary arteriography. Exercise-induced ST deviation was considered as maximal ST deviation during the exercise test and maximum LVEDP was considered as the pressure measured 1 min after left ventriculography. RESULTS: The degree of exercise-induced ST depression in aVF showed no significant differences between the three groups. Exercise-induced ST elevation occurred in the intracardiac leads and exercise-induced ST depression occurred in the epicardial leads. These electrocardiographic changes were not contradictory to subendocardial ischemia. In addition, there was a good correlation (r = - 0.465, p < 0.01) between exercise-induced ST depression and maximum LVEDP elevation. CONCLUSIONS: Exercise-induced ST depression was caused by subendocardial ischemia due to increased LVEDP.

[Relationships between intravascular ultrasonographic findings and coronary risk factors in patients with normal coronary angiography].

OBJECTIVES: Indicators of ischemic heart disease were studied for the practice of preventive medicine. METHODS: Intravascular ultrasonography was performed in 97 patients with no abnormalities by left anterior descending artery angiography. Coronary risk factors were evaluated based on the relationship between plaque formation and lipoprotein levels. RESULTS: Plaque was observed in 81% of patients. The relationship between mean plaque area(%) and the low-density lipoprotein/high-density lipoprotein(LDL/HDL)ratio was examined. Mean plaque area(%) was significantly higher at LDL/HDL < or = 2.5 than at LDL/HDL > 2.5. The border of significant change level of mean plaque area(%)was LDL/HDL = 2.5. There was a good correlation between mean plaque area (%) and LDL/HDL (r = 0.65, p < 0.01). Mean plaque area (%) at LDL/HDL 2.5 was calculated at 15%. Patients with coronary risk factors had LDL/HDL lower than 2.5 at mean plaque area of 15%. CONCLUSIONS: Maintaining LDL/HDL at 2.5 is very important for preventive medicine. However, LDL/HDL should be managed at under 2.5 in patients with coronary risk factors.

[A relationship between insulin resistance and reduction in oxidative stress in vivo by atorvastatin].

OBJECTIVES: To examine the relationship between insulin resistance (IR) and the reduction of oxidative stress in vivo by the statin atorvastatin. METHODS: This study included 40 patients with hypercholesterolemia without a history of diabetes mellitus (21 males, 19 females, mean age 62 +/- 11 years). Homeostasis assessment insulin resistance (HOMA-IR) was used as a marker for insulin resistance. The patients were divided into two groups [IR group (n = 24) and non-IR group (n = 16), using the cut off level of 1.73]. Urinary 8-iso-prostaglandin F2alpha (U-8-iso) excretion was used as an oxidative stress marker. The subjects were treated with atorvastatin (10 mg/day) for 12 weeks. RESULTS: The IR group had significantly higher U-8-iso levels than the non-IR group before atorvastatin administration (211 +/- 112 vs 137 +/- 33 pg/mg Cr, p = 0.01). Low-density lipoprotein cholesterol, triglyceride, and 8-iso levels were significantly reduced in both groups after 12 weeks, U-8-iso levels were significantly higher in the IR group than the non-IR group (178 +/- 61 vs 110 +/- 38 pg/mg Cr, p = 0.003), and HOMA-IR showed no significant change. Multiple regression analysis after 12 weeks showed that HOMA-IR and triglyceride levels were independent variables for U-8-iso levels (standard regression coefficient = 0.60, 0.59, p < 0.0001, p = 0.0002). CONCLUSIONS: Insulin resistance is important in the occurrence of oxidative stress in patients with hypercholesterolemia. Since atorvastatin does not reduce insulin resistance, further therapy to reduce insulin resistance is necessary for early prevention of cardiovascular events during atorvastatin treatment.

[Relationship between insulin resistance and oxidative stress in vivo].

OBJECTIVES: The relationship between oxidative stress in vivo and insulin resistance was examined. METHODS: This study included 87 patients, 46 males and 41 females (mean age 63 +/- 10 years), without coronary artery disease. The homeostasis assessment insulin resistance (HOMA-IR) (fasting blood sugar x fasting immunoreactive insulin/405), a marker for insulin resistance, was measured. The patients were divided into three groups: the noninsulin resistance group (N-IR group) without diabetes mellitus (DM) and with fasting blood glucose level of 126 mg/dl and HOMA-IR < or = 1.73 (n = 44), the insulin resistance group (IR group) without diabetes mellitus and with fasting blood glucose level of 126 mg/dl and HOMA-IR > 1.73 (n = 29), and the DM group (type 2 diabetes mellitus) (n = 14). Urinary 8-iso-prostaglandin F2 alpha (U-8-iso-PGF2 alpha) excretion was measured as a marker of in vivo oxidative stress. RESULTS: There were significantly more obese patients in the IR group than in the N-IR group (62% vs 25%, p = 0.001), and the remnant-like particle cholesterol level was significantly higher in the IR group than in the N-IR group (7.6 +/- 5.2 vs 4.6 +/- 1.5 mg/dl, p < 0.01). Patients in the IR group had a significantly larger number of coronary risk factors. U-8-iso-PGF2 alpha excretion was significantly higher in the IR group and DM groups (201 +/- 86, 191 +/- 136 vs 129 +/- 50 pg/mg. Cr, p < 0.0001, p = 0.01), and there was a significantly positive correlation between the number of coronary risk factors, fasting blood sugar and U-8-iso-PGF2 alpha concentration (correlation coefficient = 0.32, 0.37, p = 0.002, p = 0.0003). Multiple regression analysis showed that remnant-like particle cholesterol, fasting blood sugar and insulin resistance were independent factors for U-8-iso-PGF2 alpha concentration (p < 0.0001, p = 0.0007, p = 0.02). CONCLUSIONS: Insulin resistance, remnant lipoprotein and hyperglyceridemia are deeply involved in oxidative stress in vivo.

Preventive effect of an antiallergic drug, pemirolast potassium, on restenosis after stent placement: quantitative coronary angiography and intravascular ultrasound studies.

OBJECTIVES: The preventive effect of pemirolast against restenosis after coronary stent placement was evaluated. METHODS: Eighty-four patients with 89 de novo lesions who underwent successful coronary stenting were assigned to the pemirolast group(40 patients, 45 lesions) and the control group(44 patients, 44 lesions). Administration of pemirolast(20 mg/day) was initiated from the next morning after stenting and continued for 6 months of follow-up. Quantitative coronary angiography was performed immediately after stenting and at follow-up. Angiographic restenosis was defined as diameter stenosis > or = 50% at follow-up. Intravascular ultrasound study conducted at follow-up angiography was used to measure vessel cross-sectional area(CSA), stent CSA, lumen CSA, neointima CSA(stent CSA--lumen CSA), and percentage neointima CSA(neointima CSA/stent CSA x 100%) at the minimal lumen site. RESULTS: There were no significant differences in baseline characteristics between the two groups. Restenosis rate was significantly lower in the pemirolast group than in the control group(15.0% vs 34.1% of patients, 13.3% vs 34.1% of lesions, p < 0.05, respectively). The intravascular ultrasound study at follow-up(36 lesions in the pemirolast group, 33 in the control group) found no significant differences in vessel CSA and stent CSA between the two groups(17.3 +/- 2.2 vs 16.8 +/- 2.4 mm2, 8.6 +/- 1.9 vs 8.4 +/- 1.7 mm2, respectively). However, lumen CSA was significantly larger in the pemirolast group than in the control group(5.5 +/- 1.3 vs 4.4 +/- 1.1 mm2, p < 0.05). Moreover, neointima CSA and percentage neointima CSA were significantly smaller in the pemirolast group(3.1 +/- 1.1 vs 4.0 +/- 1.2 mm2, p < 0.05 and 36.2 +/- 15.9% vs 47.4 +/- 15.6%, p < 0.01). CONCLUSIONS: Pemirolast has a preventive effect against restenosis after stent placement, possibly by inhibiting neointimal hyperplasia.

[Headache due to nitroglycerin administration and its clinical significance].

OBJECTIVES: This study assessed the side effects of nitroglycerin administration and their clinical significance. METHODS: Adverse reactions associated with sublingual nitroglycerin administration were investigated in 103 patients, 71 men and 32 women (mean age 56 +/- 11 years), 32 patients with coronary artery stenosis and 71 without coronary artery stenosis. RESULTS: Fifty-one percent of patients experienced headache and 30% experienced other adverse reactions, whereas 19% experienced no adverse reactions. The relationship was investigated between headache, the most common adverse reaction, and the following eight clinical background factors: coronary angiographic findings, sex, age, hyperlipidemia, hypertension, diabetes mellitus, smoking and drinking. Multiple regression analysis was conducted by treating sublingual nitroglycerin-induced headache as an object variable and the clinical background factors as explanatory variables. Statistically, the onset of headache correlated most closely to coronary angiographic findings, followed by smoking, hypertension, diabetes mellitus and drinking. The first four factors suppressed the onset of headache, whereas drinking facilitated the onset of headache. CONCLUSIONS: There is a close relationship between the onset of headache following sublingual nitroglycerin administration and coronary angiographic findings. Sublingual nitroglycerin-induced headache as a predictor of coronary angiographic findings has a sensitivity and specificity of 81% and 66%, respectively, for patients without coronary artery stenosis based on the absence of headache.

[Clinical significance of preheparin serum lipoprotein lipase mass in normocholesterolemic patients with coronary artery disease].

OBJECTIVES: Some normocholesterolemic patients have coronary artery disease (CAD) in Japan. This study evaluated the clinical significance of preheparin lipoprotein lipase mass as a risk factor for normocholesterolemic patients with CAD. METHODS: This study included 89 normocholesterolemic male patients with CAD (CAD group, 40 with stable organic angina pectoris, 19 with vasospastic angina pectoris, and 30 with acute myocardial infarction), and 13 normocholesterolemic males with normal coronary arteries (control group) with no stenotic lesion and negative reaction to intracoronary administration of acetylcholine. Preheparin lipoprotein lipase mass was measured by enzyme-linked immunosorbent assay. Coronary risk factors including preheparin lipoprotein lipase mass were compared between the two groups. Low-density lipoprotein (LDL) particle size and presence of midband were estimated by polyacrylamide gel disc electrophoresis. RESULTS: Mild hypertriglyceridemia and low high-density lipoprotein (HDL) cholesterolemia were observed in the CAD group, and small particle size LDL and presence of midband were also common in the CAD group. Preheparin lipoprotein lipase mass level was significantly lower in the CAD group than the control group (52 +/- 18 vs 40 +/- 13 ng/ml, p = 0.005) as well as in each type of patient in the CAD group. Multiple regression analysis showed that small particle size LDL, low preheparin lipoprotein lipase mass and smoking were independent risk factors for CAD (p < 0.001, p = 0.007, p = 0.037). Low preheparin lipoprotein lipase mass concentration was observed in the small particle size LDL group and/or the midband positive group. CONCLUSIONS: These results indicate that low preheparin lipoprotein lipase mass reflects insulin resistance and may be deeply involved in the progression of coronary arteriosclerosis.