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Increased numbers of small, dense low-density lipoprotein particles may be present in patients with low high-density lipoprotein cholesterol and normal plasma triglycerides and cholesterol. Measurment of apolipoprotein B is the key to diagnosis and such patients should be considered for statin therapy. [ABSTRACT FROM AUTHOR]

The characteristics and predictors of long-term recurrent ischemic cardiovascular events (RICEs) after myocardial infarction with ST-segment elevation (STEMI) have not yet been clarified. We aimed to characterize the 10-year incidence, types, and predictors of RICE. We obtained 10-year follow-up of STEMI survivors at 17 Quebec hospitals in Canada (the AMI-QUEBEC Study) in 2003. There were 858 patients; mean age was 60 years and 73% were male. The majority of patients receive reperfusion therapy; 53.3% and 39.2% of patients received primary percutaneous coronary intervention (PCI) and fibrinolytic therapy, respectively. Seventy-five percent of patients underwent in-hospital PCI (elective, rescue, and primary). At 10 years, 42% of patients suffered a RICE, with most RICEs (88%) caused by recurrent cardiac ischemia. The risk of RICE was the highest during the first year (23.5 per patient-year). At 10 years, the all-cause mortality was 19.3%, with 1/3 of deaths being RICE-related. Previous cardiovascular event, heart failure during the index STEMI hospitalization, discharge prescription of calcium blocker increased the risk of RICE by almost twofold. Each point increase in TIMI (Thrombolysis In Myocardial Infarction) score augmented the risk of RICE by 6%, whereas discharge prescription of dual antiplatelets reduced the risk of RICE by 23%. Our findings suggested that survivors of STEMI remain at high long-term risk of RICE despite high rate of reperfusion therapy and in-hospital PCI. Patients with previous cardiovascular event, in-hospital heart failure, and high TIMI score were particularly susceptible to RICE. Future studies are needed to confirm the impacts of calcium blocker and dual antiplatelets on long-term risk of RICE., (Copyright © 2018 Elsevier Inc. All rights reserved.)

We examined whether plasma apolipoprotein-B (apo-B) levels add further information on the risk of coronary heart disease (CHD) after taking into account low-density lipoprotein (LDL) cholesterol concentrations and other traditional risk factors. Among 2,072 CHD-free men from the Québec Cardiovascular Study at entry and followed for 13 years, 230 had a first CHD event (CHD death or nonfatal myocardial infarction). Increased apo-B (tertile 1 vs 3) levels were associated with a significant increased risk of CHD after adjustment for nonlipid and lipid risk factors other than LDL cholesterol levels (relative risk 1.89, 95% confidence interval 1.31 to 2.73). High plasma LDL cholesterol concentrations (tertile 1 vs 3) were also associated with an increased risk of CHD independently of nonlipid and lipid risk factors (relative risk 2.02, 95% confidence interval 1.44 to 2.84). However, apo-B levels modulated to a significant extent the risk of CHD associated with increased concentrations of LDL cholesterol (>/=4.3 mmol/L). For instance, among men with high LDL cholesterol levels, those with an apo-B level <128 mg/dl were not at increased risk for CHD (relative risk 1.53, 95% confidence interval 0.89 to 2.62). In contrast, high levels of apo-B and LDL cholesterol were associated with a significant twofold increased risk of CHD (p <0.001). Receiver-operating curve analysis also indicated that plasma apo-B levels improved the ability to discriminate incident CHD cases among patients with high LDL cholesterol levels compared with a model based on LDL cholesterol levels (p = 0.04). In conclusion, plasma apo-B levels modulated the risk of CHD associated with LDL cholesterol over a 13-year follow-up.

The objective of the present study was to examine concordance/discordance among 4 atherogenic indexes of cardiovascular risk: plasma total cholesterol, low-density lipoprotein (LDL) cholesterol, non-high-density lipoprotein (non-HDL) cholesterol, and apolipoprotein B-100 (apoB). Analyses were conducted in a cohort of 2,103 men without coronary artery disease (CAD) at the onset of the Quebec Cardiovascular Study. Although there were strong and highly significant correlations among the 4 risk indexes (0.78 < r < 0.97), only 50% of all subjects had concordant apoB and LDL cholesterol levels (i.e., values that fell into the same quintile of the population distribution). Moreover, concordance/discordance was not the same throughout the range of both variables; it was greater at the extremes of their respective distributions (65%), but significantly less in the midpoints (<40%). ApoB appeared to be more concordant with non-HDL cholesterol than with LDL cholesterol, although >1/3 of all subjects had discordant levels. Kappa analysis confirmed that there was only fair agreement between apoB and total or LDL cholesterol (0.38 and 0.36, respectively) and only moderate agreement between non-HDL cholesterol and apoB (0.47). Finally, a significant proportion of subjects (528 of 2,103) who had disproportionately higher apoB levels than would have been predicted based on their LDL cholesterol concentrations was more obese and manifested several features of the metabolic syndrome. They also had a significantly increased cardiovascular risk. In summary, plasma apoB and the various cholesterol indexes are complementary rather than competitive indexes of atherosclerotic risk and provide further evidence as to why measurement of apoB should be part of a standard lipoprotein assessment of CAD risk.

This purpose of this study was to investigate how plasma C-reactive protein (CRP), a nonspecific acute-phase reactant, modulates the risk of coronary heart disease (CHD) associated with the small, dense, low-density lipoprotein (LDL) phenotype. LDL particle size and plasma CRP were measured in the Quebec Cardiovascular Study cohort of 2,025 men free of CHD at baseline, among whom 103 had a first CHD event during a 5-year follow-up period. Plasma CRP levels were measured using the Behring Latex-Enhanced (highly sensitive) CRP assay. LDL particle size phenotype was characterized using 2% to 16% polyacrylamide gradient gel electrophoresis. There were weak but significant associations between plasma CRP levels and features of LDL size, such as the proportion of LDL with a diameter <255 A (r = 0.09, p <0.001) and LDL peak particle size (r = -0.09, p <0.001). Variations in plasma CRP levels modulated the risk of CHD associated with small LDL peak particle size (relative risk 4.3 vs 2.5 in men with high vs low plasma CRP levels, respectively) and with an elevated proportion of LDL <255 A (relative risk 6.6 vs 3.0). Thus, increased plasma CRP levels further elevate the risk of CHD associated with having small, dense LDL particles.

Fibrinogen has been prospectively found to correlate with coronary heart disease (CHD) but a similar association has not been well established for lipoprotein (a) (Lp(a)). Plasma lipids, Lp(a), and fibrinogen levels were measured in 2,125 men (aged 47 to 76 years) who were free of clinical CHD. During a 5-year follow-up period, 116 first CHD events were documented. Men with CHD were older, smoked more, had a higher prevalence of diabetes, and higher levels of systolic blood pressure, cholesterol, low-density lipoprotein cholesterol, Lp(a), and fibrinogen, and lower plasma high-density lipoprotein cholesterol levels. Only fibrinogen levels in the upper tertile of the distribution compared with the lower tertiles were associated with a significant risk of CHD (adjusted risk ratio 2.5; 95% confidence interval [CI] 1.4 to 4.2; p = 0.0010). Such an association was not observed with Lp(a). To assess a possible relation between fibrinogen and Lp(a) to the risk of CHD events, men were assigned to 1 of 4 groups according to fibrinogen median levels and a Lp(a) cut-off level of 300 mg/L: group 1: fibrinogen < 4.05 g/L and Lp(a) < 300 mg/L; group 2: fibrinogen < 4.05 g/L and Lp(a) > or =300 mg/L; group 3: fibrinogen > or =4.05 g/L and Lp(a) < 300 mg/L; and group 4: fibrinogen > or =4.05 g/L and Lp(a) > or =300 mg/L. Using group 1 as a reference, a significant risk ratio was only documented in group 4 (2.5; 95% CI 1.2 to 5.1; p = 0.0132). In this population, high fibrinogen levels associated with high Lp(a) levels significantly increased the risk of CHD.

This study was undertaken to evaluate the distribution and the relation of lipoprotein(a) (Lp[a]) concentration with intermittent claudication in a cohort of men aged 35 to 64 years, randomly selected in 1974 and followed until 1990. In 1985, blood samples for a complete fasting lipid profile and Lp(a) were obtained in 2,424 men representing 62% of the living cohort. The diagnosis of intermittent claudication was made by trained nurses using a standardized questionnaire and confirmed by a cardiologist. Lp(a) distribution did not change with age and was similar to that of other Caucasian populations. Because Lp(a) concentration did not vary with age, its relation to the incidence of intermittent claudication was assessed for the years 1974 to 1990. The incidence of intermittent claudication was 42 of 10,000 person-years. The 113 men with intermittent claudication, in contrast to men without this symptomatology, were older at entry (49 +/- 7 vs 45 +/- 7 years), and had higher systolic pressure (144 +/- 20 vs 136 +/- 16 mmHg) and Lp(a) levels (46 +/- 45 vs 33 +/- 35 mg/dl) (all p < 0.05). There was also a significantly greater prevalence of smoking and diabetes among men with intermittent claudication. The risk of intermittent claudication was doubled in men in the second and third tertiles of Lp(a) concentration (p < 0.001). Thus, high Lp(a) levels constitute a significant risk for intermittent claudication in this population.

In 1985, plasma cholesterol, triglyceride, high-density lipoprotein cholesterol, and plasma apoprotein (apo) B levels were measured in 2,103 men (aged 45 to 76 years) without ischemic heart disease from the Québec city suburbs. Occurrence of a first ischemic event (i.e., angina pectoris, acute myocardial infarction, or coronary-related death) was recorded in 114 men between 1985 and 1990. Men with and without ischemic heart disease were classified as normal or in various dyslipidemic groups according to an established algorithm. Of the 1,989 men who remained free of ischemic events, 50% had a normal lipid profile compared with 32% in men with ischemic heart disease. Although the prevalence of type IIb and IV dyslipidemias was similar in men with and without ischemic heart disease, type IIa (16% vs 10%), hyperapo B-hypertriglyceridemia (12% vs 6%), hyperapo B-normotriglyceridemia (11% vs 7%), and hypoalphalipoproteinemia (18% vs 13%) were more prevalent in men with than without ischemic heart disease. Adjusted odds ratios (ORs) were not increased in type IIb and IV phenotypes, whereas men with type IIa (OR 2.8), with the 2 hyperapo B phenotypes (hyperapo B-normotriglyceridemia, OR 2.7; hyperapo B-hypertriglyceridemia, OR 3.1) or with isolated hypoalphalipoproteinemia (OR 2.2), were at higher risk. The results of this prospective study confirm the importance of both elevated plasma cholesterol and decreased high-density lipoprotein cholesterol levels as risk factors for ischemic heart disease. They also emphasize the high prevalence of an elevated apo B dyslipidemic state in ischemic heart disease.

In patients with a strongly positive exercise electro-cardiogram, the workload achieved during the test allows the identification of subsets with good or poor survival rates. To determine whether the same criteria also predict acute ischemic heart events such as unstable angina and myocardial infarction, fatal and nonfatal acute manifestations were documented in 241 patients medically treated during an 8-year follow-up. All patients had a Bruce protocol treadmill exercise test with ST-segment depression greater than or equal to 2 mm and coronary angiographic studies. There were 52 deaths; of these 44 were due to coronary artery disease. There were 41 episodes of unstable angina and 21 myocardial infarcts documented as first morbid events. As expected, survival improved with increased workload achieved; patients terminating their exercise at stage I (5.1 METs) had an 8-year survival rate of 45 +/- 9% while those reaching stage IV or more (10 METs) had a survival rate of 93 +/- 6%. In a multivariate analysis, the duration of exercise and the number of narrowed coronary arteries and of left ventricular segment abnormalities correlated significantly with survival. In contrast, nonfatal acute events occurred in about 20 to 35% of patients whatever the stage of the exercise test. Furthermore, neither variables during the exercise test nor angiographic findings predicted nonfatal events. Thus, although the workload achieved did identify patients with different mortality rates, it failed to predict subsets of patients with different morbid event rates.

To determine the prognosis of patients with painless strongly positive exercise electrocardiogram, the 6-year cumulative survival rate was computed for 298 medically treated patients who terminated their exercise test with or without angina. All had horizontal or downsloping ST depression greater than or equal to 2 mm during a treadmill exercise test according to the standardized multistage Bruce protocol. Of the 298 patients, 119 terminated the exercise test because of dyspnea or fatigue and 179 stopped because of angina. Among the 119 patients without angina, there were 18 deaths, 16 from coronary artery disease (CAD), of which 8 occurred suddenly. Among the 179 patients with exercise-induced angina, 36 died, 33 from CAD, of which 13 were sudden deaths. The overall 6-year survival rate was 85 +/- 3% for patients without angina and 80 +/- 3% in those with angina (p less than 0.05). However, patients without angina achieved a significantly longer duration of exercise and had higher maximal heart rate and systolic blood pressure during exercise. In both groups, survival decreased with decreasing duration of exercise. In patients without angina, the 6-year survival rate was 97 +/- 3% in those achieving stage IV (greater than or equal to 541 s), 87 +/- 4% in stage III (361 to 540 s), 64 +/- 13% in stage II (181 to 360 s) and 60 +/- 15% in stage I (less than or equal to 180 s).(ABSTRACT TRUNCATED AT 250 WORDS)