Endovascular retrieval of an elongated Supera stent.

Stenting is used to achieve artery patency, and the Supera stent, a self-expanding interwoven nitinol stent, has produced good clinical outcomes. A 70-year-old woman with peripheral artery disease had experienced intermittent claudication (Fontaine stage IIb). Endovascular treatment was performed for a chronic total occlusion TransAtlantic InterSociety Consensus class II type B lesion. A Supera stent (Abbott Vascular, Santa Clara, CA) was used. However, it had become severely elongated to the proximal end in the superficial femoral artery and was removed using a balloon inserted from the side and trapped to the guide sheath with the distal end of the stent outside the sheath. After this bailout, an alternate stent could be placed through an antegrade approach to the contralateral common femoral artery.

Comparative study of fractional flow reserve and diastolic pressure ratio using a guidewire with a sensor for measuring intravascular pressure.

PURPOSE: This study aimed to evaluate the correlation and diagnostic agreement between diastolic pressure ratio (dPR) and fractional flow reserve (FFR) in a Japanese real-world setting. DESIGN: Prospective multicenter observational study. METHODS: This study included 100 patients with intermediate coronary artery stenosis at 4 Japanese hospitals. For these lesions, FFR and dPR were measured using a guidewire with a sensor and a monitor to measure intravascular pressure. The correlation and diagnostic agreement between FFR and dPR were assessed. When both FFR and dPR were negative or positive, the results were considered to be concordant. When one was positive and the other was negative, the result was regarded as discordant (positive discordance, FFR > 0.80 and dPR ≤ 0.89; negative discordance, FFR ≤ 0.80 and dPR > 0.89). RESULTS: Overall, the FFR and dPR were well-correlated (R = 0.841). FFR and dPR were concordant in 89% of cases (concordant normal, 43%; concordant abnormal, 46%) and discordant in 11% (positive discordance, 7%; negative discordance, 4%). No significant difference was observed in the rate of concordant results between patients with and without diabetes mellitus. The diagnostic concordance rate was significantly different among the 3 coronary arteries (right coronary artery, 93.3%; left anterior descending artery, 93.2%; and left circumflex artery, 58.3%; P = .001). Additionally, the rate of concordant results tended to be higher when using intravenous administration of adenosine than when using intracoronary bolus injection of nicorandil (adenosine, 95.1%; nicorandil, 84.7%; P = .103). CONCLUSION: We found that dPR was highly correlated with FFR, and diagnostic discordance was observed in 11% of the lesions. Several factors, including lesion location and medication for hyperemia, may cause the diagnostic discordance between dPR and FFR.

Impact of Coronary Stent Fracture on Restenotic Neointimal Tissue Characterization After Drug-Eluting Stent Implantation.

Although drug-eluting stents (DESs) reduce the rates of in-stent restenosis (ISR) and subsequent target lesion revascularization, stent fracture (SF) after DES implantation has become an important concern because of its potential association with restenosis and stent thrombosis. We aimed to assess the pathogenic impact of SF on in-stent restenotic neointimal tissue components after DES implantation. We analyzed 43 consecutive patients (14 with SF and 29 without SF) with ISR requiring revascularization after DES implantation between January 2008 and March 2014. For evaluation of in-stent tissue components, integrated backscatter intravascular ultrasound (IB-IVUS) was performed. SF was defined as complete or partial separation of stent segments observed using plain fluoroscopy or intravascular ultrasound. On volumetric IB-IVUS analyses, patients with SF had a significantly higher percentage of lipid tissue volume within the neointima and a significantly lower percentage of fibrous tissue volume than those without (37.3 ± 18.9% versus 24.9 ± 12.4%, P = 0.02, and 61.2 ± 18.3 versus 72.6 ± 12.1%, P = 0.04, respectively). Moreover, SF was positively correlated with the percentage of lipid volume on multiple linear regression analysis after adjustment for confounding factors (ß = 0.36, P = 0.03). The interval from stent implantation was similar in both groups (47.0 ± 28.7 versus 37.7 ± 33.3 months; P = 0.39). In conclusion, SF is associated with larger lipid tissue volume within the neointima after DES placement, suggesting a contribution to the development of neoatherosclerosis and vulnerable neointima. Thus SF might lead to future adverse coronary events.

Decreased Serum Albumin Predicts Bleeding Events in Patients on Antiplatelet Therapy After Percutaneous Coronary Intervention.

BACKGROUND: Antiplatelet therapy (APT) after percutaneous coronary intervention (PCI) prevents ischemic events with increased risk of bleeding. Little is known about the relationship between hypoalbuminemia and bleeding risk in patients receiving APT after PCI. This study investigated the association between serum albumin level and bleeding events in this population.Methods and Results:We enrolled 438 consecutive patients who were prescribed dual APT (DAPT; aspirin and thienopyridine) beyond 1 month after successful PCI without adverse events. The patients were divided into 3 groups according to serum albumin tertile: tertile 1, ≤3.7 g/dL; tertile 2, 3.8-4.1 g/dL; and tertile 3, ≥4.2 g/dL. Adverse bleeding events were defined as Bleeding Academic Research Consortium criteria types 2, 3, and 5. During the median follow-up of 29.5 months, a total of 30 adverse bleeding events were observed. Median duration of DAPT was 14 months. The tertile 1 group had the highest risk of adverse bleeding events (event-free rate, 83.1%, 94.3% and 95.8%, respectively; P<0.001). On Cox proportional hazards modeling, serum albumin independently predicted adverse bleeding events (HR, 0.10, 95% CI: 0.027-0.39, P=0.001, for tertile 3 vs. tertile 1). CONCLUSIONS: Decreased serum albumin predicted bleeding events in patients with APT after PCI.

Impact of Skeletal Muscle Mass on Long-Term Adverse Cardiovascular Outcomes in Patients With Chronic Kidney Disease.

Sarcopenia, defined as skeletal muscle loss and dysfunction, is attracting considerable attention as a novel risk factor for cardiovascular events. Although the loss of skeletal muscle is common in chronic kidney disease (CKD) patients, the relation between sarcopenia and cardiovascular events in CKD patients is not well defined. Therefore, we aimed to investigate the relation between skeletal muscle mass and major adverse cardiovascular events (MACE) in CKD patients. We enrolled 266 asymptomatic CKD patients (median estimated glomerular filtration rate: 36.7 ml/min/1.73 m2). To evaluate skeletal muscle mass, we used the psoas muscle mass index (PMI) calculated from noncontrast computed tomography. The patients were divided into 2 groups according to the cut-off value of PMI for MACE. There were significant differences in age and body mass index between the low and high PMI groups (median age: 73.5 vs 69.0 years, p = 0.002; median body mass index: 22.6 vs 24.2 kg/m2, p <0.001, respectively). During the follow-up period (median: 3.2 years), patients with low PMI had significantly higher risk of MACE than those with high PMI (31.7% and 11.2%, log-rank test, p <0.001). The Cox proportional hazard model showed that low PMI is an independent predictor of MACE in CKD patients (hazard ratio 3.98, 95% confidence interval 1.65 to 9.63, p = 0.0022). In conclusion, low skeletal muscle mass is an independent predictor of MACE in CKD patients. The assessment of skeletal muscle mass may be a valuable screening tool for predicting MACE in clinical practice.

Nutrition Status Predicts Severity of Vascular Calcification in Non-Dialyzed Chronic Kidney Disease.

BACKGROUND: Vascular calcification is a major complication in chronic kidney disease (CKD) that increases the risk of adverse clinical outcomes. Geriatric nutritional risk index (GNRI) is a simple nutritional assessment tool that predicts poor prognosis in elderly subjects. The purpose of the present study was to evaluate the correlation between GNRI and severity of vascular calcification in non-dialyzed CKD patients.Methods and Results:We enrolled 323 asymptomatic CKD patients. To evaluate abdominal aortic calcification (AAC), we used aortic calcification index (ACI) determined on non-contrast computed tomography. The patients were divided into three groups according to GNRI tertile. Median ACI significantly decreased with increasing GNRI tertile (15.5%, 13.6%, and 7.9%, respectively; P=0.001). On multivariate regression analysis GNRI was significantly correlated with ACI (ß=-0.15, P=0.009). We also investigated the combination of GNRI and C-reactive-protein (CRP) for predicting the severity of AAC. Low GNRI and high CRP were significantly associated with severe AAC, compared with high GNRI and low CRP (OR, 4.07; P=0.004). CONCLUSIONS: GNRI was significantly associated with AAC in non-dialyzed CKD patients.

Impact of nutritional assessment and body mass index on cardiovascular outcomes in patients with stable coronary artery disease.

BACKGROUND: An inverse association between obesity, as defined by body mass index (BMI) and prognosis has been reported in patients with cardiovascular disease ("obesity paradox"). The aim of this study was to investigate whether adding nutritional information to BMI provides better risk assessment in patients undergoing elective percutaneous coronary intervention (PCI). METHOD: This study comprised 1004 patients undergoing elective PCI. We calculated each patient's controlling nutritional status (CONUT) score for nutritional screening at baseline. Patients were divided into 4 groups based on CONUT score (low, 0-1 [<75th percentile]; or high, ≥2 [≥75th percentile]) and BMI (normal, 18.5-24.9kg/m2; or high, ≥25kg/m2). The endpoint was major adverse cardiac events (MACE) defined as cardiac death and/or myocardial infarction. RESULTS: Low CONUT score+normal BMI, low CONUT score+high BMI, high CONUT score+normal BMI, and high CONUT score+high BMI were determined in 374, 242, 275, and 113 patients, respectively. During a median follow-up of 1779 days, 73 events occurred. High CONUT score+normal BMI showed a 2.72-fold increase in the incidence of MACE (95% CI 1.46-5.08, p=0.002) compared with low CONUT score+normal BMI after adjusting for confounding factors. On the other hand, no significant difference in the incidence of MACE was observed in the other three groups. CONCLUSION: The combination of CONUT score and BMI was a useful predictor of MACE in this population. Using BMI to assess the cardiovascular risk may be misleading unless the nutritional information is considered.

Correlations between geriatric nutritional risk index and peripheral artery disease in elderly coronary artery disease patients.

AIM: Malnutrition is associated with the development of atherosclerosis and an increased risk of cardiovascular mortality in elderly patients. The present study aimed to investigate the association between the Geriatric Nutritional Risk Index (GNRI), a simple nutritional assessment tool, and the prevalence of peripheral artery disease (PAD) in elderly coronary artery disease patients. METHODS: We evaluated 228 elderly coronary artery disease patients (mean age 74.0 ± 5.7 years). Ankle-brachial index (ABI) measurements were routinely carried out to investigate the prevalence of lower extremity PAD. Patients showing ABI <0.9 were defined as having PAD. RESULTS: Based on our findings, 20.6% of the study patients had PAD. The median GNRI values were significantly lower in patients with PAD than those in patients without PAD (93.8 vs 100.0, P < 0.001). Even after multivariate adjustment, GNRI values were independently associated with PAD (odds ratio 0.94; 95% confidence interval 0.89-0.99; P = 0.024). Furthermore, patients with low GNRI and high C-reactive protein levels had a 5.5-fold higher risk of having PAD than those with high GNRI and low C-reactive protein levels. CONCLUSIONS: GNRI values showed a strong relationship with PAD in elderly coronary artery disease patients. These data reinforce the utility of GNRI as a screening tool in clinical practice. Geriatr Gerontol Int 2017; 17: 1057-1062.

Impact of Geriatric Nutritional Risk Index on cardiovascular outcomes in patients with stable coronary artery disease.

BACKGROUND: The association between malnutrition and cardiovascular prognosis in patients with stable coronary artery disease remains unclear. The aim of this study was to evaluate the association between Geriatric Nutritional Risk Index (GNRI), a simple tool to assess nutritional risk, and long-term outcomes after elective percutaneous coronary intervention (PCI). METHODS: This study consisted of 802 patients (age, 70±10 years, male, 69%) who underwent elective PCI. GNRI was calculated at baseline as follows: GNRI=[14.89×serum albumin (g/dl)+[41.7×(body weight/body weight at body mass index of 22)]]. Patients were then divided into three groups as previously reported: GNRI <92, 92 to ≤98, and >98. The endpoint of this study was the composite of cardiac death or non-fatal myocardial infarction. RESULTS: During a median follow-up period of 1568 days, 56 cardiac events occurred. Using Kaplan-Meier analysis, the 4-year event-free rates were found to be 79% for GNRI <92, 90% for GNRI 92 to ≤98, and 97% for GNRI >98 (log-rank test p<0.001). GNRI <92 and GNRI 92 to ≤98 showed 6.76-fold [95% confidence interval (CI) 3.13-14.56, p<0.001] and 3.03-fold (HR 3.03, 95%CI 1.36-6.78, p=0.007) increase in the incidences of cardiac death or non-fatal myocardial infarction compared with GNRI >98 after adjusting for confounding factors. CONCLUSION: GNRI significantly associated with cardiac events after elective PCI. Further studies should be performed to establish appropriate therapeutic strategies for this vulnerable patient group.

Impact of Paradoxical Decrease in High-density Lipoprotein Cholesterol Levels After Statin Therapy on Major Adverse Cardiovascular Events in Patients with Stable Angina Pectoris.

PURPOSE: Statin therapy usually increases HDL-C levels. However, a paradoxical decrease in HDL-C levels after statin therapy is often seen in clinical settings. The relationship between a paradoxical decrease in HDL-C levels after statin therapy and adverse cardiovascular events in patients with stable angina pectoris (SAP) is not well understood. The purpose of this study was to analyze the relationship between paradoxical HDL-C decreases after statin therapy and major adverse cardiovascular events (MACEs) in patients undergoing percutaneous coronary intervention (PCI) for SAP. METHODS: Between January 2006 and March 2015, 867 patients underwent PCI for SAP. Of them, we enrolled 209 patients who were newly started on statin therapy before PCI. We excluded patients who had started statin therapy earlier than 6 months before PCI, patients who had not started statin therapy after PCI, and patients who were diagnosed with acute coronary syndrome. They were divided into 2 groups according to the change in their HDL-C levels between baseline and 6 to 9 months after the index PCI: decreased HDL group after statin treatment (80 patients) and increased HDL group (129 patients). The primary end points were MACEs defined as a composite of all-cause death, nonfatal acute myocardial infarction, and target vessel revascularization (TVR). FINDINGS: Using Kaplan-Meier analysis, the 7-year event rate for composite MACEs in the decreased HDL group was found to be higher than that for the increased HDL group (38% versus 24%, log-rank P = 0.02). TVR occurred more frequently in the decreased HDL group than in the increased HDL group (32% versus 12%, log-rank P = 0.01). With the use of multivariate analysis, changes in HDL-C levels after statin therapy indicated a significant inverse association with the increased risk of MACEs, (hazard ratio [HR] = 0.94; 95% CI, 0.92-0.97; P < 0.01). The incidence of MACEs was more strongly associated with ΔHDL than with ΔLDL. Moreover, BMS usage also independently predicted MACEs (HR = 2.18; 95% CI, 1.14-4.17; P < 0.01). IMPLICATIONS: A paradoxical decrease in HDL-C levels after statin therapy might be a risk factor for MACEs, especially TVR, in patients with SAP.

Predictors of abdominal aortic calcification progression in patients with chronic kidney disease without hemodialysis.

BACKGROUND AND AIMS: Abdominal aortic calcification (AAC) is an important predictor of cardiovascular mortality in patients with chronic kidney disease (CKD). However, little is known regarding AAC progression in these patients. This study aimed to identify risk factors associated with AAC progression in patients with CKD without hemodialysis. METHODS: We recruited 141 asymptomatic patients with CKD without hemodialysis [median estimated glomerular filtration rate (eGFR), 40.3 mL/min/1.73 m2] and evaluated the progression of the abdominal aortic calcification index (ACI) over 3 years. To identify risk factors contributing to the rate of ACI progression, the associations between baseline clinical characteristics and annual change in ACI for each CKD category were analyzed. The annual change of ACI (ΔACI/year) was calculated as follows: (second ACI - first ACI)/duration between the two evaluations. RESULTS: Median ΔACI/year values significantly increased in advanced CKD stages (0.73%, 0.87%, and 2.24%/year for CKD stages G1-2, G3, and G4-5, respectively; p for trend = 0.041). The only independent risk factor for AAC progression in mild to moderate CKD (G1-3, eGFR ≥ 30 mL/min/1.73 m2) was pulse pressure level (ß = 0.258, p = 0.012). In contrast, parathyroid hormone (PTH) level was significantly correlated with ΔACI/year (ß = 0.426, p = 0.007) among patients with advanced CKD (G4-5, eGFR < 30 mL/min/1.73 m2). CONCLUSIONS: This study suggests that the AAC progression rate was significantly accelerated in patients with advanced CKD. In addition, measuring PTH is useful to evaluate both bone turnover and AAC progression in patients with advanced CKD.

Impact of adipose tissue composition on cardiovascular risk assessment in patients with stable coronary artery disease.

BACKGROUND AND AIMS: Visceral adipose tissue (VAT), unlike subcutaneous adipose tissue (SAT), is highly correlated with cardiovascular risk factors. This study aimed to evaluate the predictive value of adipose tissue composition, as measured by computed tomography, for cardiovascular events in patients with stable coronary artery disease. METHODS: 357 consecutive patients who underwent 64-slice computed tomography and elective percutaneous coronary intervention (PCI) were recruited. The ratio of visceral to subcutaneous adipose tissue (VAT/SAT) was calculated. Patients were divided into three groups in accordance with VAT/SAT (low VAT/SAT, <0.55 [<25th percentile]; moderate VAT/SAT, 0.55-1.03 [25th-75th percentile]; high VAT/SAT, ≥1.03 [≥75th percentile]). The investigated risk factors were hypertension, hyperglycaemia, and dyslipidaemia. We analysed the incidence of major adverse cardiovascular events (MACE), defined as the composite of cardiac death, myocardial infarction, and any revascularization. RESULTS: The rate of patients with two or more concomitant risk factors was significantly higher in the high VAT/SAT group (p = 0.006). During 1480 person-years, 109 events were documented. There was a significant association between the incidence of MACE and VAT/SAT, with the worst event-free survival rate in the high VAT/SAT group (log-rank, p = 0.01). In Cox analysis, the hazard ratio of high VAT/SAT for MACE was 2.72 (95% confidence interval 1.04-7.09, p = 0.04) compared with the low VAT/SAT after adjustment for confounding factors. CONCLUSIONS: Increased VAT/SAT is independently associated with the incidence of MACE, indicating that adipose tissue composition is a useful predictor of cardiovascular outcome, after elective PCI.

Association of a polymorphism of BTN2A1 with hypertension in Japanese individuals.

BACKGROUND: We previously showed that the C→T polymorphism (rs6929846) in butyrophilin, subfamily 2, member A1 gene (BTN2A1) was associated with myocardial infarction in Japanese individuals. Given that hypertension is a major risk factor for myocardial infarction, the association of rs6929846 of BTN2A1 with myocardial infarction might be attributable, at least in part, to its effect on susceptibility to hypertension. We have thus examined the relation of rs6929846 of BTN2A1 to hypertension in Japanese individuals. METHODS: A total of 8,567 Japanese individuals from two independent subject panels were examined: Subject panels A and B comprised 2,317 hypertensive individuals and 1,933 controls, and 2,911 hypertensive individuals and 1,406 controls, respectively. The genotype of rs6929846 was determined by a method that combines the PCR and sequence-specific oligonucleotide probes with suspension array technology. RESULTS: Multivariable logistic regression analysis with adjustment for covariates revealed that rs6929846 of BTN2A1 was significantly associated with hypertension in subject panel A (P = 2.6 × 10(-6); odds ratio, 1.69) and in subject panel B (P = 0.0284; odds ratio, 1.24), with the T allele representing a risk factor for hypertension. The rs6929846 was associated with systolic blood pressure (BP) in subject panels A (P = 0.0063) and B (P = 0.0115) and with diastolic BP in subject panel B (P = 0.0323), with the T allele being related to high BP. CONCLUSIONS: BTN2A1 may be a susceptibility gene for hypertension in Japanese individuals. Determination of genotype for this polymorphism may prove informative for assessment of the genetic risk for hypertension.

Association of polymorphisms of BTN2A1 and ILF3 with myocardial infarction in Japanese individuals with different lipid profiles.

Dyslipidemia is an important risk factor for myocardial infarction (MI). We previously showed that gene polymorphisms associated with MI differed among individuals with different lipid profiles. We also showed that rs6929846 of BTN2A1 and rs2569512 of ILF3 were significantly associated with MI in Japanese individuals. In the present study, we examined the relationship between rs6929846 of BTN2A1 or rs2569512 of ILF3 and MI in individuals with low or high serum concentrations of triglycerides, high density lipoprotein (HDL) cholesterol, or low density lipoprotein (LDL) cholesterol, respectively. The study population comprised 5513 unrelated Japanese individuals, including 1537 subjects with MI and 3976 controls. Multivariable logistic regression analyses with adjustment for covariates revealed that rs6929846 of BTN2A1 was significantly associated with MI in individuals with low (P=3.1 x 10-5; odds ratio, OR=1.66) or high (P = 1.1 x 10⁻6; OR = 2.09) triglycerides; in individuals with low (P = 0.0082; OR = 1.75) or high (P = 2.0 x 10⁻9; OR = 1.85) HDL cholesterol; and in individuals with low (P = 3.2 x 10⁻7; OR = 1.75) or high (P = 2.8 x 10⁻5; OR =2.18) LDL cholesterol. Similar analyses revealed that rs2569512 of ILF3 was significantly associated with MI in individuals with low (P = 0.0066; OR = 1.47) or high (P = 0.0013; OR = 1.88) triglycerides; in individuals with low (P = 0.0059; OR = 1.96) or high (P = 0.0020; OR = 1.51) HDL cholesterol; and in individuals with low (P = 0.0004, OR = 1.62) LDL cholesterol, but not in those with high LDL cholesterol. The results suggest that the relationship between rs6929846 of BTN2A1 or rs2569512 of ILF3 and MI is influenced by the serum concentrations of HDL and LDL cholesterol, respectively. Stratification of subjects according to lipid profiles may thus be useful for the personalized prevention of MI based on genetic information.

Association of polymorphisms of BTN2A1 and ILF3 with myocardial infarction in Japanese individuals with or without hypertension, diabetes mellitus or chronic kidney disease.

Recent evidence suggests that genetic variants that confer susceptibility to myocardial infarction (MI) may differ between men and women or between individuals with or without conventional risk factors for MI. We previously showed that rs6929846 of BTN2A1 and rs2569512 of ILF3 were significantly associated with MI in Japanese individuals. In the present study, we examined the associations of rs6929846 of BTN2A1 or rs2569512 of ILF3 to MI among individuals stratified by the absence or presence of hypertension, diabetes mellitus (DM) and chronic kidney disease (CKD). The study population was comprised of 5689 unrelated Japanese individuals, including 1626 subjects with MI and 4063 controls with or without hypertension, DM or CKD. Multivariable logistic regression analyses with adjustment for covariates revealed that rs6929846 of BTN2A1 was significantly associated with MI in individuals with (P=0.0001; odds ratio, 1.49) or without (P=1.6x10-7; odds ratio, 2.32) hypertension; in individuals with (P=0.0002; odds ratio, 1.65) or without (P=8.1x10-7; odds ratio, 1.76) DM; and in individuals without CKD (P=6.0x10-11; odds ratio, 2.03), but not in those with CKD. Similar analyses revealed that rs2569512 of ILF3 was significantly associated with MI in individuals with (P=0.0041; odds ratio, 1.26) or without (P=0.0051; odds ratio, 1.78) hypertension; in individuals with (P=0.0200; odds ratio, 1.46) or without (P=0.0174; odds ratio, 1.43) DM; and in individuals with (P=0.0011, odds ratio, 1.47) or without (P=0.0237; odds ratio, 1.34) CKD. Results suggested that the association of rs6929846 in BTN2A1 with MI was more apparent in low-risk individuals than in high-risk individuals, whereas the association of rs2569512 in ILF3 with MI was not influenced by the absence or presence of hypertension, DM or CKD. Stratification of subjects based on hypertension, DM or CKD may thus be informative in order to achieve personalized prevention of MI with the use of genetic information.

Association of a polymorphism of BTN2A1 with chronic kidney disease in individuals with or without hypertension or diabetes mellitus.

Hypertension and diabetes mellitus are important risk factors for chronic kidney disease (CKD). We previously showed that the C→T polymorphism (rs6929846) of BTN2A1 was significantly associated with myocardial infarction. The purpose of the present study was to examine an association of rs6929846 of BTN2A1 with CKD in individuals with or without hypertension or diabetes mellitus, thereby contributing to the personalized prevention of CKD in such individuals separately. The study population comprised 7,542 unrelated individuals, including 2,289 subjects with CKD [estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m(2)] and 5,253 controls (eGFR ≥60 ml/min/1.73 m(2)) with or without hypertension or diabetes mellitus. The Chi-square test, a multivariable logistic regression analysis with adjustment for covariates, as well as a stepwise forward selection procedure revealed that the C→T polymorphism (rs6929846) of BTN2A1 was significantly associated with CKD in normotensive individuals, in diabetic individuals and in individuals with hypertension and diabetes mellitus, or without either condition, with the T allele representing a risk factor for CKD. Stratification of subjects based on hypertension or diabetes mellitus may thus be important in order to achieve personalized prevention of CKD with the use of genetic information.

Association of genetic variants with myocardial infarction in Japanese individuals with or without metabolic syndrome.

The etiology of metabolic syndrome (MetS) is highly complex, with both genetic and environmental factors being thought to play an important role. Although MetS has been recognized as a risk factor for myocardial infarction (MI), the genetic risk for MI in individuals with or without MetS has remained uncharacterized. We examined a possible association of genetic variants with MI in individuals with or without MetS separately. The study population comprised 4,424 individuals, including 1,918 individuals with MetS (903 subjects with MI and 1,015 controls) and 2,506 individuals without MetS (499 subjects with MI and 2,007 controls). The 150 polymorphisms examined in the present study were selected by genome-wide association studies of MI and ischemic stroke with the use of Affymetrix GeneChip Human Mapping 500K Array Set. Initial screening by the Chi-square test revealed that the C→T polymorphism (rs1794429) of LRPAP1, the A→G polymorphism (rs12373237) of LAMA3 and the A→G polymorphism (rs3782257) of NCOR2 were significantly (false discovery rate of <0.05) associated with MI for individuals with MetS, and that the C→G polymorphism (rs13051704) of TFF1 was significantly related to MI for individuals without MetS. Subsequent multivariable logistic analysis with adjustment for covariates revealed that rs1794429 of LRPAP1 (recessive model; P=0.0218; odds ratio=0.71) and rs3782257 of NCOR2 (dominant model; P=0.0057; odds ratio=1.94) were significantly associated with MI among individuals with MetS, and that rs13051704 of TFF1 (additive model; P=0.0100; odds ratio=0.55) was significantly associated with MI among individuals without MetS. The genetic variants that confer susceptibility to MI differ between individuals with or without MetS. Stratification of subjects according to the presence or absence of MetS may thus be important for personalized prevention of MI based on genetic information.