Angiographic coronary artery disease is associated with progressively higher levels of fasting plasma glucose

This study evaluated the association between progressively higher levels of fasting glycemia (G) and insulin resistance parameters with coronary artery disease (CAD) in patients referred for coronary angiography. All 145 patients (age 58.4+/-0.9 years, 51.7% men) underwent clinical and laboratory evaluation before coronary angiography and subjects were divided into four groups: normal (N, <88 mg/dl), high-normal (H-N, 89-99 mg/dl), impaired fasting glucose (IFG, 100-125 mg/dl) and diabetes (DM, >126 mg/dl or known diabetics). Arteriographic evidence of CAD was determined by two criteria: (1) a 30% or greater diameter stenosis in at least one major coronary artery; (2) a 70% or greater diameter stenosis in at least one major coronary artery. HOMA-IR increased progressively according to each group: N=1.74+/-0.2, H-N=3.14+/-0.3, IFG=4.67+/-0.6 and DM=8.00+/-2.9; p=0.001. The proportion of patients with CAD according to both criteria increased with each G level: CAD criteria 1: N=39.4%, H-N=50%, IFG=60% and DM=69.6%, p=0.006; CAD criteria 2: N=27.3%, H-N=30%, IFG=36% and DM=50%, p=0.03. We demonstrated a significant association between subtle disturbances of the glucose metabolism, assessed by subnormal levels of fasting glucose and insulin resistance parameters, and angiographically documented coronary artery disease.     

High fasting glucose levels as a predictor of worse clinical outcome in patients with coronary artery disease: results from the Bezafibrate Infarction Prevention (BIP) study

Background

A high fasting glucose level may be a marker not only for microvascular complications, but also for macrovascular complications. We evaluated the clinical significance of a high fasting glucose level (≥110 mg/dL), detected either at baseline or during follow-up, in the Bezafibrate Infarction Prevention (BIP) study.

Methods

The BIP study was a secondary prevention prospective double-blind study comparing bezafibrate to placebo. A total of 3122 patients with documented coronary artery heart disease who were aged 45 to 74 years and had a total cholesterol level between 180 and 250 mg/dL, low-density lipoprotein cholesterol level ≤180 mg/dL, a high-density lipoprotein cholesterol level ≤45 mg/dL, a triglyceride level ≤300 mg/dL, and a fasting glucose ≤160 mg/dL were randomized to receive 400 mg of bezafibrate daily or placebo.

Results

The primary end point of the BIP study was fatal myocardial infarction, non-fatal myocardial infarction, or sudden death. Secondary end points included hospitalization for unstable angina, percutaneous transluminal coronary angioplasty, and coronary artery bypass grafting. At baseline, 330 patients (11%) had diabetes mellitus, and 293 patients (9%) had an impaired fasting blood glucose level (IFG). During 6.2 years of follow-up, diabetes mellitus developed in 186 patients (6%), IFG developed in 366 patients (12%), and 62% of patients remained with normal fasting glucose levels (NFG). Patients with diabetes mellitus and IFG both at baseline or developing during follow-up had a significantly higher rate of secondary end points than paients with NFG (P <.0001). Bezafibrate treatment reduced secondary end points only in patients with NFG (P = .04).

Conclusion

Diabetes mellitus and IFG were common in the BIP study and were predictive of a worse clinical outcome that was not attenuated with bezafibrate treatment.     

Impact of fasting glycemia on short-term prognosis after acute myocardial infarction

OBJECTIVE: The prognosis of patients with acute myocardial infarction (MI), according to the new criteria for impaired fasting glucose (IFG) (FG 100-126 mg/dl), has not been evaluated. RESEARCH DESIGN AND METHODS: A total of 2353 patients with acute MI and surviving at d 5 after admission were analyzed for short-term morbidity and mortality. FG was obtained at d 4 and 5. Patients were classified as diabetes mellitus (known diabetes or FG > or = 126 mg/dl), high IFG (110 < or = FG < 126 mg/dl), low IFG (100 < or = FG < 110 mg/dl), and normal fasting glucose (NFG) (FG < 100 mg/dl). RESULTS: Among the 2353 patients, 968 (41%) had diabetes mellitus, 262 (11%) had high IFG, 332 (14%) had low IFG, and 791 (34%) had NFG. Compared with NFG patients, 30-d cardiovascular mortality was increased in high but not low IFG subjects. In-hospital heart failure was increased in high IFG subjects (42 vs. 20% for NFG, P < 0.0001) but not low IFG subjects (21 vs. 20%). High IFG, but not low IFG, was an independent factor associated with 30-d cardiovascular mortality [odds ratio 2.33 (1.55-3.47)] and in-hospital heart failure [odds ratio 1.70 (1.36-2.07)]. The optimal threshold levels of FG on the receiver-operating characteristic curves were 114 and 112 mg/dl to predict mortality and in-hospital heart failure, respectively. CONCLUSION: The present study, based on a nonselected cohort of MI patients, underscores the high prevalence of IFG (25%) and highlights the clinical relevance of 110 mg/dl, but not 100 mg/dl, as a cutoff value to define the risk for worse outcome.     

Impact of impaired fasting glucose on cardiovascular disease: the Framingham Heart Study.

OBJECTIVES: We sought to determine whether impaired fasting glucose (IFG) predicts cardiovascular disease (CVD) events. BACKGROUND: It is unclear which glucose threshold should define prediabetes. We compared the 1997 and 2003 American Diabetes Association (ADA) definitions of IFG to predict CVD. METHODS: Framingham offspring participants free of CVD, categorized by the 1997 ADA IFG definition (fasting plasma glucose 110 to 125 mg/dl; 6.1 to 6.9 mmol/l) or the 2003 definition (100 to 125 mg/dl; 5.6 to 6.9 mmol/l), were followed from 1983 to 2004. Pooled logistic regression was used to calculate multivariable-adjusted odds ratios (ORs) for incident coronary heart disease (CHD; 291 events) or CVD (423 events). RESULTS: Four-year CHD event rates among women were 1.3% (100 to 109 mg/dl), 2.3% (110 to 125 mg/dl), and 2.9% (diabetes); whereas corresponding rates in men were 2.9%, 3.0%, and 8.7%. For the 2003 IFG definition, the OR for CHD among women was 1.7 (95% confidence interval [CI] 1.0 to 3.0, p = 0.048), whereas for the 1997 IFG definition, the OR for CHD in women was 2.2 (95% CI 1.1 to 4.4, p = 0.02), which was almost as high as for women with diabetes (OR 2.5, 95% CI 1.2 to 5.2, p = 0.01). For CVD, only the 1997 IFG definition yielded significantly greater odds of CVD in women (OR 2.1, 95% CI 1.2 to 3.6, p = 0.01). Men were not at increased odds of developing CVD or CHD by either definition. CONCLUSIONS: In women, both IFG definitions were associated with increased CHD risk, whereas neither IFG definition identified men at increased short-term risk for CHD or CVD. The finding that women with FPG 110 to 125 mg/dl had similar CHD risk compared with women with diabetes suggests that CHD risk in women may be elevated at a lower glucose level than for men.     

Comparison of the 1997 and 2003 American Diabetes Association classification of impaired fasting glucose: impact on prevalence of impaired fasting glucose, coronary heart disease risk factors, and coronary heart disease in a community-based medical practice.

OBJECTIVES: The goals of this study were to assess the effect of the 2003 American Diabetes Association definition of impaired fasting glucose (IFG) on prevalence of IFG, coronary heart disease (CHD) risk factors, and CHD compared with the 1997 IFG definition. BACKGROUND: Although IFG is viewed as increasing CHD risk, this association is unclear and has not been well studied after changing the IFG criterion, especially in a clinical practice setting. METHODS: This was a cross-sectional evaluation of 8,295 members (3,763 men and 4,532 women) of a community medical center who were between the ages of 30 and 69 years, without a history of diabetes mellitus, and who had available measurements of fasting plasma glucose and lipid concentrations within the past 2 years. The prevalence of IFG, CHD risk factors, and CHD with the 1997 and 2003 IFG definition was compared. RESULTS: The prevalence of IFG increased from 8% to 35% with the 2003 criterion. Individuals with glucose of 100 to 109 mg/dl had lower prevalence of most CHD risk factors (hypertension, triglyceride > or =150 mg/dl, high-density lipoprotein cholesterol <40 mg/dl, meeting 2 components of the metabolic syndrome criteria, CHD risk > or =10% by Framingham score) compared with individuals with glucose 110 to 125 mg/dl. Individuals identified with the 2003 IFG definition did not have an increase in known CHD when adjusted for covariates (odds ratio 1.4 [95% confidence interval (CI) 0.7 to 2.3] vs. 3.2 [95% CI 1.8 to 5.9]). CONCLUSIONS: One-third of the population has IFG with the 2003 definition, yet many of these individuals do not have increased prevalence of CHD risk factors or CHD.     

Effect of the metabolic syndrome and hyperuricemia on outcome in patients with coronary artery disease (from the Bezafibrate Infarction Prevention Study)

Hyperuricemia appears to be related to metabolic syndrome (MS), but its impact on cardiovascular risk in patients with MS is unclear. We evaluated the impact of hyperuricemia on cardiovascular risk in patients with MS. Of 2,963 patients with coronary artery disease enrolled in the Bezafibrate Infarction Prevention study, 1,410 had MS, as established by the presence of ≥3 of the following 5 criteria: serum fasting glucose >110 mg/dl, triglycerides >150 mg/dl, high-density lipoprotein cholesterol <40 mg/dl in men and <50 mg/dl in women, systolic and diastolic blood pressures >130 and 80 mm Hg, respectively, and body mass index >28 kg/m2. The remaining 1,553 patients had no MS. Primary end points were defined as occurrence of acute myocardial infarction or sudden cardiac death. Hyperuricemia was defined as serum uric acid levels >7.0 mg/dl in men and >6.0 mg/dl in women, respectively. Higher rate of primary end point was noted in hyperuricemic patients (n = 284) versus normouricemic patients (n = 1,126) with MS (20.1% and 15.3%, respectively, p = 0.05). After adjustment for age, gender, smoking, diabetes, previous myocardial infarction, hypertension, New York Heart Association classes II to IV, estimated glomerular filtration rate, body mass index, total cholesterol, triglycerides, diuretics, antiplatelets, angiotensin-converting enzyme inhibitors, β blockers, and bezafibrate treatment, hyperuricemic patients with MS demonstrated significantly higher risk for the primary end point compared to normouricemic patients with MS (hazard ratio 1.45, 95% confidence interval 1.00 to 2.17, p = 0.05). In conclusion, hyperuricemia is associated with increased risk of myocardial infarction and sudden cardiac death in patients with MS.     

Prognostic value of uric acid in patients with ST-elevated myocardial infarction undergoing primary coronary intervention

Elevated uric acid (UA) levels have been associated with cardiovascular disease in epidemiologic studies. The relation between UA levels and long-term outcomes in patients with ST-segment elevation myocardial infarction who undergo primary percutaneous coronary intervention is not known. Data from 2,249 consecutive patients with ST-segment elevation myocardial infarction who underwent primary percutaneous coronary intervention were evaluated. Patients were divided into 2 groups with high or low UA using upper limits of normal of 6 mg/dl for women and 7 mg/dl for men. There were 1,643 patients in the low-UA group (mean age 55.9 ± 11.6 years, 85% men) and 606 patients in the high-UA group (mean age 60.5 ± 12.6 years, 76% men). Serum UA levels were 8.0 ± 1.5 mg/dl in the high-UA group and 5.2 ± 1.0 mg/dl in the low-UA group (p <0.001). The in-hospital mortality rate was significantly higher in patients with high UA levels (9% vs 2%, p <0.001), as was the rate of adverse outcomes in patients with high UA. The mean follow-up time was 24.3 months. Cardiovascular mortality, reinfarction, target vessel revascularization, heart failure, and major adverse cardiac events were all significantly higher in the high-UA group. In a multivariate analyses, high plasma UA levels were an independent predictor of major adverse cardiac events in the hospital (odds ratio 2.03, 95% confidence interval 1.25 to 3.75, p = 0.006) and during long-term follow-up (odds ratio 1.64, 95% confidence interval 1.05 to 2.56, p = 0.03). In conclusion, high UA levels on admission are independently associated with in-hospital and long-term adverse outcomes in patients with ST-segment elevation myocardial infarction who undergo primary percutaneous coronary intervention.     

Prognostic value of fibrinogen in patients admitted with suspected unstable angina and non-q-wave myocardial infarction

INTRODUCTION AND OBJECTIVE: In recent years, the relation between biological markers of inflammation and prognosis in patients suffering from acute coronary syndromes has been investigated. The aim of this study was to evaluate the association between baseline fibrinogen concentrations and the development of clinical events in patients admitted with suspicion of unstable angina and non-Q-wave myocardial infarction. MATERIAL AND METHOD: Levels of fibrinogen at enrollment were analyzed in 325 consecutive patients with acute coronary syndromes. Fibrinogen values were divided into tertiles and the incidence of clinical events was evaluated at each level. The combination of death and/or myocardial infarction was the main endpoint. RESULTS: Fibrinogen levels were significantly higher in patients who subsequently had myocardial infarction, cardiac death, or both during follow up. The probabilities of death and/or myocardial infarction were 6%, 13%, and 29% (p < 0.0001), respectively, in patients grouped by fibrinogen tertiles (304, 305-374 and 375 mg/dl). Multivariate predictors of combined events were age, previous angina, ST-segment depression in the admission ECG, and fibrinogen into tertiles. The adjusted hazard ratio (95% CI) for patients in the upper tertile was 4.8 (1.6-14; p = 0.004). CONCLUSIONS: High fibrinogen levels were related to a less favorable long-term or short-term outcome in patients admitted for suspicion of unstable angina and non-Q-wave myocardial infarction. This association persists after adjustment for other classical risk factors such as age, prior angina, and ST-segment depression in the ECG.     

Cardiovascular risk in patients with fasting blood glucose levels within normal range

Fasting glucose levels elevated beyond the normal range have been associated with increased cardiovascular risk. However, it is unknown whether this association exists for variations of fasting glucose within the normal range. The present study was conducted using the computerized database of the Sharon-Shomron District of Clalit Health Services. Included in the present study were subjects with fasting glucose levels within the normal range (< 100 mg/dl). We excluded patients with a history of cardiovascular disease or diabetes. The primary outcome was the incidence of coronary revascularization with either percutaneous coronary intervention or coronary artery bypass grafting. The 28,263 participants (age 53.7 ± 12.2 years) were divided into quartiles according to the fasting glucose level (75.4 ± 4.5, 83.6 ± 1.7, 88.9 ± 1.4, and 95.1 ± 2.2 mg/dl). During a mean follow-up of 5.9 ± 0.7 years, 424 subjects required coronary revascularization. A progressive increase was seen in the risk of coronary revascularization as the fasting glucose levels increased within the normal range (hazard ratio 1.73, 95% confidence interval 1.3 to 2.3, p > 0.001, between the fourth and first quartiles). However, this association lost its statistical significance after adjustments for the conventional coronary risk factors (hazard ratio 1.17, 95% confidence interval 0.85 to 1.62, p = 0.328). In conclusion, elevated fasting glucose levels within the normal range were associated with an increased cardiovascular risk. This association was caused by the greater prevalence of the other conventional risk factors and not by the glucose level itself.     

Lipoprotein (a) is increased in acute coronary syndromes (unstable angina pectoris and myocardial infarction), but it is not predictive of the severity of coronary lesions

Lipoprotein (a) [Lp(a)] concentrations were determined in 365 patients undergoing coronary angiography for stable angina (n = 159), unstable angina (n = 99), recent myocardial infarction (n = 45), and nonischemic heart disease (cardiomyopathy or valvular disease, n = 62, non-IHD). Mean ± SD and median Lp(a) concentrations in stable angina (29.9 ± 29.2; 22 mg/dl) did not differ from those in non-IHD (26.9 ± 26.3; 17), but were significantly lower than in patients with unstable angina (52.7 ± 36.6; 58) and myocardial infarction (44.8 ± 36.4; 34) (p < 0.01). Coronary angiography revealed that 261 patients, including 4 patients in the non-IHD group, had significant (≥ 50%) coronary lesions. Lp(a) was higher in patients with (41 ± 35; 32) than in those without (28 ± 27; 19) angiographic evidence of significant coronary stenosis (p < 0.05) and showed a weak univariate correlation with the angiographic index (Total Score) of the severity of the disease (r = 0.106; p < 0.05). However, in the subgroup of 303 patients with stable/unstable angina or myocardial infarction, Lp(a) was predictive neither of angiographic presence nor of severity of coronary disease. Patients were then ranked according to the Total Score values. Among patients with comparable angiographic severity of coronary artery disease, Lp(a) appeared to be remarkably higher in patients with acute ischemic syndromes (unstable angina, myocardial infarction) than in patients with stable angina. In conclusion, Lp(a) was roughly twice as high in acute (unstable angina, myocardial infarction) than in chronic (stable angina) ischemic syndromes, but there was no difference between chronic stable angina and non-IHD. Serum level determination of Lp(a) made a poor contribution in predicting the extent of coronary artery disease.     

Prognostic value of uric acid in patients with acute coronary syndromes

The association between uric acid and cardiovascular disease is incompletely understood. In particular, the prognostic value of uric acid in patients with acute coronary syndromes who undergo percutaneous coronary intervention has not been studied. This study included 5,124 patients with acute coronary syndromes who underwent percutaneous coronary intervention: 1,629 with acute ST-segment elevation myocardial infarction, 1,332 with acute non-ST-segment elevation myocardial infarction, and 2,163 with unstable angina. The primary end point was 1-year mortality. Patients were divided into quartiles according to uric acid level as follows: quartile 1, 1.3 to <5.3 mg/dl; quartile 2, 5.3 to <6.3 mg/dl; quartile 3, 6.3 to <7.5 mg/dl; and quartile 4, 7.5 to 18.4 mg/dl. There were 450 deaths during follow-up: 80 deaths in quartile 1, 77deaths in quartile 2, 72 deaths in quartile 3, and 221 deaths in quartile 4 of uric acid (Kaplan-Meier estimates of 1-year mortality 6.4%, 6.2%, 5.6%, and 17.4%, respectively; unadjusted hazard ratio 3.05, 95% confidence interval 2.54 to 3.67, p <0.001 for fourth vs first quartile of uric acid). After adjustment for traditional cardiovascular risk factors, renal function, and inflammatory status, the association between uric acid and mortality remained significant, with a 12% increase in the adjusted risk for 1-year mortality for every 1 mg/dl increase in the uric acid level. Uric acid improved the discriminatory power of the predictive model regarding 1-year mortality (absolute integrated discrimination improvement 0.008, p = 0.005). In conclusion, elevated levels of uric acid are an independent predictor of 1-year mortality across the whole spectrum of patients with acute coronary syndromes treated with percutaneous coronary intervention.     

Effect of sustained virological response to treatment on the incidence of abnormal glucose values in chronic hepatitis C

BACKGROUND/AIMS: To investigate the effect of sustained virological response (SVR) on impaired fasting glucose (IFG) and/or type 2 diabetes (T2DM); to assess the influence of glucose abnormalities on the SVR rate. METHODS: 1059 patients with chronic HCV; normal glucose (< 100 mg/dl) in 734, IFG (between 100 and 125 mg/dl) in 218, and T2DM (126 mg/dl) in 107 cases, were treated with interferon plus ribavirin over 24 or 48 weeks, depending on viral genotype. RESULTS: The SVR rate was lower in patients with IFG and/or T2DM than in patients with normal glucose concentrations [143/325 (44%) vs. 432/734 (58.8%); P=0.002]. In the follow-up, abnormal glucose concentrations were observed in 74 of 304 (24.3%) non-responders and in 49 of 430 (11.4%) sustained responders (log-rank: 13.8; P=0.00002). Reverse stepwise logistic regression analysis identified the independent variables predictive of IFG or T2DM development as: sustained response (OR: 0.44; 95%CI=0.20-0.97; P=0.004) and fibrosis stage (OR: 1.46; 95%CI=1.06-2.01;P=0.02). Family history of DM, steatosis, gender, HCV viral load, genotype, triglycerides, cholesterol and BMI did not enter the multivariate analysis equation. CONCLUSIONS: SVR reduces the risk of IFG and/or T2DM development in patients with chronic hepatitis C while altered glucose metabolism impairs sustained response to viral treatment.     

Does eptifibatide confer a greater benefit to patients with unstable angina than with non-ST segment elevation myocardial infarction? Insights from the PURSUIT Trial.

AIMS: To evaluate the differential effects of eptifibatide therapy on unstable angina vs non-ST elevation myocardial infarction at enrollment, since the separate impact on these two major diagnostic subsets of acute coronary syndrome patients has not been fully investigated. METHODS AND RESULTS: We examined the 9461 patients in the PURSUIT trial (conducted between 1995 and 1997) to compare the effects of eptifibatide on unstable angina and myocardial infarction. The study showed greater and more consistent effects of eptifibatide therapy on unstable angina than non-ST elevation myocardial infarction in reducing 30-day death/(re)infarction (from the unadjusted rate of 13.0% to 11.2%, P=0.059 for unstable angina; and 18.9% to 17.9%, P=0.387 for myocardial infarction), especially among patients who underwent early percutaneous coronary intervention (odds ratios=0.49 and 0.86, 95% confidence intervals=0.30-0.80 and 0.53-1.42, respectively, for unstable angina and myocardial infarction). The only subgroup for whom the benefit of eptifibatide was not evident was female myocardial infarction patients who did not undergo early percutaneous coronary intervention. CONCLUSIONS: These data suggest that eptifibatide benefited unstable angina patients more than myocardial infarction patients, especially among those who underwent early percutaneous coronary intervention, and support its use as concomitant therapy with early percutaneous coronary intervention especially in female myocardial infarction patients.     

Association between C-reactive protein levels and subsequent cardiac events among patients with stable angina treated with coronary artery stenting

PURPOSE: To investigate the prognostic value of elevated C-reactive protein levels in patients with stable angina who underwent coronary stenting. METHODS: We followed a consecutive series of 1152 patients with stable angina who had undergone coronary stenting. We measured baseline C-reactive protein levels before stenting with a high-sensitivity assay; 651 patients (57%) had elevated C-reactive protein levels (>5 mg/L). The primary endpoint was either death or myocardial infarction within 1 year after the procedure. Angiographic restenosis was defined as a > or =50% diameter stenosis at follow-up angiography. RESULTS: During the 1-year follow-up, 62 (9.5%) of the 651 patients with an elevated C-reactive protein level and 24 (4.8%) of the 501 patients with normal levels died or had a myocardial infarction (P = 0.002). In a multivariate analysis, elevated baseline C-reactive protein levels were associated with almost a twofold increase in the rate of death or myocardial infarction after coronary stenting (hazard ratio = 1.8; 95% confidence interval: 1.1 to 2.9). Most of the difference in the event rates developed within the first 30 days. Baseline C-reactive protein levels did not correlate with restenosis. CONCLUSION: Elevated preprocedural C-reactive protein levels are associated with a less favorable prognosis in patients with stable angina who undergo coronary stenting. The measurement of C-reactive protein levels in these patients may help to identify those who may benefit from a treatment strategy aimed at the attenuation of inflammation.     

Long-term follow-up results after plain balloon coronary angioplasty.

Between September 1987 and June 1992, 571 patients of coronary artery disease underwent percutaneous transluminal coronary angioplasty in our institute. Their ages ranged from 31-82 years (mean 51 +/- 9) and majority (88.3%) were males. At baseline, 318 (55.7%) patients had chronic stable angina, 184 (32.2%) unstable angina, and 57 (10%) underwent PTCA for recurrence of angina in the post-infarction period. Single vessel angioplasty was performed in 406 (71.1%), two-vessel angioplasty in 121 (21.2%) and three or more vessels were dilated in 44 (7.7%). The procedure was successful in 524 (91.8%) patients. Follow-up was available in 438 (83.6%) patients, and ranged from 78 to 135 months (mean 89 +/- 29) with all the patients completing at least 60 months of follow-up. Using Kaplan-Meier statistical analysis, event-free survival (freedom from repeat percutaneous transluminal coronary angioplasty, myocardial infarction, coronary artery bypass surgery, or death) was 72.5 percent at three, 68.0 percent at five, 61.8 percent at seven and 55.6 percent at 10 years of follow-up. Freedom from major adverse cardiac events (myocardial infarction, coronary artery bypass surgery or death) was 88.3, 85.8, 82.0 and 75.4 percent at 3, 5, 7 and 10 years, respectively. Overall survival was 97.4 and 95.2 percent, respectively at 5 and 10 years. Subgroup analysis for all major events was done between males and females, diabetics and non-diabetics, previous history or absence of myocardial infarction, stable versus unstable angina and single versus multivessel disease. Event-free survival rates were compared between the groups using log rank test. On follow-up, the need for surgical revascularisation was more in males compared to females although statistically insignificant, and in patients with unstable angina compared to stable angina (p < 0.02). Similarly, freedom from major adverse cardiac events was significantly better in females compared to males (p < 0.05) and in stable versus unstable angina (p < 0.01). Event-free survival (repeat percutaneous transluminal coronary angioplasty, myocardial infarction, coronary artery bypass surgery, death) was also significantly better in patients with stable angina (p < 0.02). The other outcomes were comparable in all the subgroups. In conclusion, plain balloon angioplasty provides excellent long-term results in patients with coronary artery disease in terms of reduction in major adverse cardiovascular events and need for subsequent revascularisation.     

Influence of impaired fasting glucose on the incidence and prognosis of atherosclerosis in various vascular regions

Patients with cardiovascular disease have a poorer diagnosis if they are diabetic. The risk for cardiovascular events is already increased in individuals with impaired fasting glucose (IFG). The aim of this study was to evaluate the impact of diabetes mellitus (DM) and IFG on the incidence of atherosclerotic manifestations and on the long-term prognosis of patients with atherosclerosis in various vascular regions. METHODS: In a prospective study we included 906 patients (72.5% men, mean age 62 +/- 9 years) preceding heart catheterization. All patients were evaluated for the presence of peripheral stenosis by carotid duplex sonography (pathologic: stenosis >50%) and evaluation of the ankle-brachial index (pathologic <0.9). Blood samples were drawn from each subject after an overnight fasting period and serum glucose was evaluated. RESULTS: Patients were compared with regard to the presence of DM (known DMor fasting glucose > or =126 mg/dL, N = 283, 31.2%) or IFG (fasting glucose >110 and <126 mg/dL, N = 89, 9.8%). Patients with IFG and DM had a higher prevalence of atherosclerotic manifestations in the coronary, carotid and peripheral vessels. Diabetics had the highest prevalence of atherosclerotic manifestations in multiple vascular regions (=advanced atherosclerosis). Cardiovascular events (death, myocardial infarction and stroke) after a median follow-up of 4.1 years were evaluated in 901 patients (99.4%). Presence of IFG and DM significantly increased the incidence of cardiovascular events (event rate: no DM 10.9%, IFG 13.6%, DM 23.4%, P < 0.0001). Moreover, patients with advanced atherosclerosis suffered significantly more often from cardiovascular events (event rate: no stenosis 4.1%, coronary artery disease without peripheral stenosis 9.7%, advanced atherosclerosis 23.9%). Prognosis was worst in patients with DM and advanced atherosclerosis with an event rate of 35%.Patients with cardiovascular disease have a poorer prognosis if they are diabetic. The risk for cardiovascular events is already increased in individuals with impaired fasting glucose (IFG). The aim of this study was to evaluate the impact of diabetes mellitus (DM) and IFG on the incidence of atherosclerotic manifestations and on the long-term prognosis of patients with atherosclerosis in various vascular regions.     

Impaired fasting glucose and impaired glucose tolerance - lack of agreement between the two categories in a North Indian population

This study was carried out to determine the relationship between impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in a North Indian population. The data in 5083 subjects studied earlier was reanalyzed by applying new WHO diagnostic criteria. Reanalysis revealed that 305 (6.0%) subjects had diabetes mellitus (198 on the basis of fasting plasma glucose of > or =7.0 mmol/l (> or =126 mg/dl) and an additional 107 based on a 2-h glucose tolerance test), 381 (7.5%) had IFG and 361 (7.1%) had IGT. Of these 361 subjects with IGT, only 99 (27.4%) had impaired fasting glucose whereas 262 (72.6%) had normal fasting glucose of <6.1 mmol/l (<110 mg/dl). Of 381 subjects with IFG, 99 (26%) had IGT where as 282 (74%) had normal 2-hr glucose. We conclude that there is a poor correlation between IGT and IFG.     

Effects of asymptomatic ischemia on long-term prognosis in chronic stable coronary disease

BACKGROUND. Ischemia on ambulatory electrocardiographic monitoring has been shown to adversely affect short-term prognoses in patients with unstable angina, after myocardial infarction, and with chronic stable angina. METHODS AND RESULTS. In this long-term study, we followed 138 patients (mean age, 59 +/- 9 years) with chronic stable angina and positive exercise tests for cardiac events (e.g. death, myocardial infarction, percutaneous transluminal coronary angioplasty, or coronary artery bypass graft surgery). In 105 patients, ambulatory electrocardiographic monitoring was performed after all antianginal medication was withheld for 48 hours. In 26 patients, the diagnostic tests were repeated while on their usual medication. In addition to the 105 patients, 33 patients had their monitoring performed only while on their usual medication. During 37 +/- 17 months of follow-up, there were nine deaths, nine myocardial infarctions, and 35 revascularization procedures. In patients monitored off medication, Cox survival analysis showed that the occurrence of ischemia on electrocardiographic monitoring was the most significant predictor of death and myocardial infarction in the subsequent 2 years (p = 0.02) and all adverse events for 5 years (p = 0.009). Patients who were monitored on medication and did not have ischemia (n = 18) appeared to have more adverse events than patients who had no ischemia while being monitored off medication (n = 43). CONCLUSIONS. Asymptomatic ischemia on ambulatory electrocardiographic monitoring in patients with stable angina predicts death and myocardial infarction for 2 years and all adverse events for 5 years. Monitoring performed while on medication may show no ischemia; however, this may not indicate low risk of future coronary events.     

Metabolic risk factors in southern Taiwanese with impaired fasting glucose of 100 to 109 mg/dL

This study investigates the influence of changes in impaired fasting glucose (IFG) criteria by the American Diabetes Association in 2003 in estimating the prevalence and cardiovascular risks in Taiwanese with fasting plasma glucose (FPG) between 100 and 109 mg/dL. Data came from a cross-sectional study on 1411 participants aged 30 years and older without known diabetes in southern Taiwan. Besides collection of anthropometric and biochemistry data, a 75-g oral glucose tolerance test was performed. The new IFG criteria additionally identified 14.2% of all participants as having IFG100, with FPG between 100 and 109 mg/dL, among which the percentage of normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and diabetes mellitus were 7.7%, 5.0%, and 1.5%, respectively. Mean body weight, body mass index, abdominal girth, systolic blood pressure, diastolic blood pressure (DBP), 2-hour glucose, and triglyceride were significantly higher in the IFG100 group than in normal fasting glucose (NFG) group (FPG, <100 mg/dL). Moreover, body weight, body mass index, systolic blood pressure, DBP, and 2-hour glucose were statistically higher in subgroups of IFG100/IGT than in NFG/NGT. In contrast, only DBP and 2-hour glucose were significantly higher in the IFG100/NGT group than in the NFG/NGT group. The 2003 criteria increased the prevalence of IFG and identified more IGT and diabetes. However, the increase of cardiovascular risks among newly identified IFG100 subjects came from those who concomitantly had IGT.     

Prevalence of the impaired glucose metabolism and its association with risk factors for coronary artery disease in women with gestational diabetes

Gestational diabetes (GDM) has increased risk of diabetes (DM2), a coronary artery disease (CAD) equivalent. The aim of this study was to determine the prevalence of impaired glucose metabolism (IGM) in GDM and its association with risk factors for CAD. A cohort of 109 women with GDM underwent a glucose tolerance test which classified them into three groups: diabetic (DM2) (fasting glucose (G) >or=126mg/dl or plasma glucose 2h (2-h G) >or=200mg/dl); impaired glucose tolerance (IGT) (G 100-125mg/dl and/or 2-h G 140-199mg/dl); and normal (N) (G<100mg/dl and/or 2-h<140mg/dl). They were compared for pre-gestational (PBMI) and current (CBMI) body mass index, systolic (SBP) and diastolic blood pressure (DBP), G, lipids, fibrinogen and C-reactive protein (hsCRP). Thirty two months after delivery, 17.4% presented DM2, 39.4% IGT and 43.1% were N. PBMI, CBMI, SBP and DBP were significantly higher in the DM2 than N. G was higher in DM2 and IGT. HDL-cholesterol (HDL-C) was higher in the N (p=0.02) and the triglycerides (TG) were higher in DM2 (p=0.02). The groups showed significantly different levels of hsCRP (p=0.002). We conclude that the high prevalence of IGM, overweight/obesity, dyslipidemia and altered inflammatory markers, make GDM a high-risk situation for CAD.