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P W Wilson

Publications and source records attributed to P W Wilson.

At least 19 recordsLinked to original sources
PubMed1992

Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease.

The prevalence of abnormalities of lipoprotein cholesterol and apolipoproteins A-I and B and lipoprotein (a) [Lp(a)] was determined in 321 men (mean age 50 +/- 7 years) with angiographically documented coronary artery disease and compared with that in 901 control subjects from the Framingham Offspring Study (mean age 49 +/- 6 years) who were clinically free of coronary artery disease. After correction for sampling in hospital, beta-adrenergic medication use and effects of diet, patients had significantly higher cholesterol levels (224 +/- 53 vs. 214 +/- 36 mg/dl), triglycerides (189 +/- 95 vs. 141 +/- 104 mg/dl), low density lipoprotein (LDL) cholesterol (156 +/- 51 vs. 138 +/- 33 mg/dl), apolipoprotein B (131 +/- 37 vs. 108 +/- 33 mg/dl) and Lp(a) levels (19.9 +/- 19 vs. 14.9 +/- 17.5 mg/dl). They also had significantly lower high density lipoprotein (HDL) cholesterol (36 +/- 11 vs. 45 +/- 12 mg/dl) and apolipoprotein A-I levels (114 +/- 26 vs. 136 +/- 32 mg/dl) (all p less than 0.005). On the basis of Lipid Research Clinic 90th percentile values for triglycerides and LDL cholesterol and 10th percentile values for HDL cholesterol, the most frequent dyslipidemias were low HDL cholesterol alone (19.3% vs. 4.4%), elevated LDL cholesterol (12.1% vs. 9%), hypertriglyceridemia with low HDL cholesterol (9.7% vs. 4.2%), hypertriglyceridemia and elevated LDL cholesterol with low HDL cholesterol (3.4% vs. 0.2%) and Lp(a) excess (15.8% vs. 10%) in patients versus control subjects, respectively (p less than 0.05). Stepwise discriminant analysis indicates that smoking, hypertension, decreased apolipoprotein A-I, increased apolipoprotein B, increased Lp(a) and diabetes are all significant (p less than 0.05) factors in descending order of importance in distinguishing patients with coronary artery disease from normal control subjects. Not applying a correction for beta-adrenergic blocking agents, sampling bias and diet effects leads to a serious underestimation of the prevalence of LDL abnormalities and an overestimation of HDL abnormalities in patients with coronary artery disease. However, 35% of patients had a total cholesterol level less than 200 mg/dl after correction; of those patients, 73% had an HDL cholesterol level less than 35 mg/dl.

Apolipoproteins↗
PubMed1992

White blood cell count and cardiovascular disease. Insights from the Framingham Study.

OBJECTIVE: To examine the relation of white blood cell (WBC) count to the development of cardiovascular disease (CVD), including coronary heart disease, stroke, peripheral arterial disease, and cardiac failure. Traditional CVD risk factors, hematocrit, and vital capacity were considered. DESIGN: Prospective cohort analysis with one baseline examination of relevant risk factors and 12 years of follow-up for CVD. PARTICIPANTS AND METHODS: A community-based sample (Farmingham Offspring Study) of 1393 men and 1401 women who were free of CVD at the onset of the study and who were between the ages of 30 and 59 years at baseline. Time-dependent multiple variable logistic regression methods were used. RESULTS: There were 180 CVD events in men and 80 in women. The WBC count was correlated most strongly with the number of cigarettes smoked per day, hematocrit, and vital capacity. Among nonsmoking men with WBC counts within the normal range, the age-adjusted WBC count was significantly associated with CVD and coronary heart disease incidence. For each 1.0 x 10(9)/L-cell difference in WBC count, the CVD risk increased 32%. In women, each 1.0 x 10(9)/L-cell increment in WBC count was associated with a 17% increase in CVD risk, but only in smokers, and the relationship was not statistically significant after adjustment for relevant risk factors. CONCLUSIONS: The degree of elevation of WBC count within the normal range is a marker for increased risk of CVD that is partially explained by cigarette smoking. Future studies should include differential WBC determinations to assess their association with CVD.

Adult↗
PubMed1992

Efficacy of lipid profiles in prediction of coronary disease.

National guidelines in the United States and Europe have stimulated interest in controlling blood lipid levels to prevent CHD. In this review, the efficiency of lipid profiles in predicting CHD has been examined, and total cholesterol, HDL and LDL cholesterol, and triglyceride values have been compared on the basis of 12 to 14 years of surveillance in the Framingham Study. The average value of total cholesterol and LDL cholesterol in patients who had coronary disease was at or below values that are considered dangerous, which indicates the need for more specific and sensitive lipid profiles. Measurement of LDL cholesterol levels predicted CHD only marginally better than measurement of serum total cholesterol. Measurement of triglyceride levels was the weakest predictor. The total cholesterol to HDL cholesterol ratio was the most efficient predictor both in those with apparently safe and those with abnormal cholesterol values. Measurement of HDL cholesterol was the best single lipid predictor and use of this measurement avoids needlessly alarming or falsely reassuring persons at risk for CHD who have high total cholesterol values. Since the risk associated with any serum cholesterol value varies over a 10-fold range depending on coexistent cardiovascular risk factors, these lipid factors must be taken into account in judging the hazards and efficacy of treatment needed. Evidence is available that controlling elevated cholesterol by diet and administration of pharmaceutical agents can reduce the rate of coronary events, slow progression of angiographically visualized lesions, and regress xanthomata.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

The MspI restriction fragment length polymorphism 3' to the apolipoprotein A-II gene: relationships with lipids, apolipoproteins, and premature coronary artery disease.

In previous studies, a restriction fragment length polymorphism (RFLP) has been identified using MspI restriction endonuclease in the 3' region of the apo A-II gene. The rare variant site for this MspI (M2) has been reported to be associated with higher levels of HDL cholesterol and apo A-II. We have studied the frequency and lipid associations of this RFLP in a population of 168 coronary artery disease (CAD) male and female patients, who had more than 50% narrowing of one or more arteries prior to age 60 years, as well as 255 aged-matched males and females from the Framingham Offspring Study. We also studied 31 kindreds in which the proband had premature CAD. The frequency of the M2 allele was higher in CAD cases (0.20) than in the controls (0.13) (P less than 0.05). In general, those subjects carrying the M2 allele had lower HDL cholesterol and apo A-I plasma levels; however, this difference was only significant (P less than 0.02 and 0.002, respectively) in females with CAD. No cosegregation of the M2 allele with hypoalphalipoproteinemia was found in 31 kindreds studied. However, in both generations there was a trend for those subjects carrying the M2 allele to have lower HDL cholesterol levels than those carrying the M1 allele. Sequence analysis of the apo A-II gene of subjects homozygous for either the M1 (n = 1) or the M2 allele (n = 2) revealed that this RFLP is due to a T----C single base mutation 528 bp 3' to the apo A-II gene. In the subjects homozygous for the M2 allele no other mutations were found within the coding region of the apo A-II gene that could result in changes in the primary sequence of the protein. These data indicate that the MspI RFLP 3' to the apo A-II gene is somewhat more frequent in the CAD group. However, there was no significant association between this RFLP and any of the parameters examined. In conclusion, this DNA marker lacks the specificity to be clinically useful for CAD risk assessment in the population studied.

Adult↗
PubMed1992

Change in LDL particle size is associated with change in plasma triglyceride concentration.

Low density lipoprotein (LDL) particle size is inversely associated with plasma triglyceride concentration in cross-sectional analyses. In the present study, changes in the LDL particle size of 227 participants of the Framingham Offspring Study were analyzed longitudinally by nondenaturing gradient gel electrophoresis at two examinations that were separated by 3-4 years. All subjects had triglyceride concentrations < 400 mg/dl at both exams. Using laser scanning densitometry to assess mean LDL particle size, 56% of samples displayed a change in size: 41% had a one-band size change, 13% had a two-band change, and 2% had a three-band change. These changes in size corresponded to a 15% change in pattern type, based on pattern A and B terminology. There was a significant inverse association between change in LDL size and change in triglyceride (p < 0.0001) and glucose (p < 0.004) concentrations, body weight (p < 0.02), and age (p < 0.03). There was also a significant positive association with change in high density lipoprotein (HDL) cholesterol concentration (p < 0.0001). Change in LDL cholesterol concentration, as calculated by use of the Friedewald formula, however, showed no significant association with change in LDL size (p < 0.9). There was also no significant association with change in smoking or blood pressure, but there was a nonsignificant inverse trend associated with alcohol intake (p < 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

LDL particle size distribution. Results from the Framingham Offspring Study.

Using 2-16% gradient gel electrophoresis, we examined low density lipoprotein (LDL) particle size in relation to plasma lipoproteins in 1,168 women and 1,172 men from the Framingham Offspring Study. In addition, we studied the effect of dietary intake on LDL size in a subset of the population. Seven LDL size peaks were identified, with the largest, LDL 1, being found in the density range 1.019-1.033 g/ml; LDL 2 and LDL 3 in d = 1.033-1.038 g/ml; LDL 4 and LDL5 in d = 1.038-1.050 g/ml; and the smallest, LDL 6 and 7, in d = 1.050-1.063 g/ml. Seventy-seven percent of the population had one major and at least one minor LDL peak. Secondary LDL peaks accounted for 23% of the total LDL relative area, based on laser scanning densitometry. LDL size distribution was skewed toward larger LDL particles in women (prevalence of LDL 1, 30% and of LDL 2, 31%), whereas men exhibited a more symmetric distribution (prevalence of LDL 3, 42%). The prevalence of small (< 255 A), dense (d > 1.038 g/ml) LDL particles 4-7 was 33% in men, 5% in premenopausal women, and 14% in postmenopausal women. In agreement with previous reports, small, dense LDL particles were significantly (p < 0.0001) associated with increased triglyceride and apolipoprotein (apo) B levels and decreased HDL cholesterol and apo A-I levels. In addition, we found a significant (p < 0.0001) association between LDL cholesterol and LDL size. The highest LDL cholesterol levels were found among women with LDL 4 (148 mg/dl) and men with LDL 3-5 (138 mg/dl). In addition, the presence of LDL 3 or 4 as secondary peaks was significantly associated with higher LDL cholesterol levels, while smaller secondary LDL peaks were associated with higher triglyceride levels. We also found that compared with subjects with optimal LDL cholesterol levels (< 130 mg/dl), individuals with high-risk LDL cholesterol levels (> or = 160 mg/dl) had 1) a higher prevalence of LDL 3 and 4 (women only) and a lower prevalence of LDL 1 and 2 (women only) and 2) 11% higher LDL cholesterol to apo B ratios, even when matched for LDL particle size. Furthermore, low saturated fat and cholesterol intakes were significantly associated (p < 0.01) with smaller LDL particles. Therefore, the identification of small, dense LDL particles per se may not be a good indicator of coronary artery disease risk in population studies.(ABSTRACT TRUNCATED AT 400 WORDS)

Apolipoproteins↗
PubMed1992

Low density lipoprotein particle size and coronary artery disease.

Decreased plasma low density lipoprotein (LDL) particle size has been associated with premature coronary artery disease (CAD). We examined LDL particle size by 2-16% gradient gel electrophoresis in 275 men with CAD (greater than 75% cross-sectional-area stenosis) and 822 controls. Seven major LDL size bands (with LDL-1 [d = 1.025-1.033 g/ml] being the largest and LDL-7 [d = 1.050-1.063 g/ml, the smallest]) were identified. Because most subjects had two or more adjacent LDL bands, an LDL score was calculated for each subject, with the relative area in each band taken into consideration. Four major LDL particle size groups were classified in the present studies: large LDL, intermediate LDL, small LDL, and very small LDL. The use of beta-blockers was significantly associated with smaller LDL particles. After adjusting for use of this medication, small LDL particles were still more prevalent in CAD patients (39%) compared with controls (27%). The prevalence of large LDL particles was lower in CAD patients (3%) than in controls (24%). Intermediate LDL particles were the most prevalent in both groups, 49% in CAD patients and 46% in controls. The difference in LDL particle size between CAD patients and controls was not independent but was highly associated (p less than 0.0001) with elevated triglyceride levels and decreased high density lipoprotein (HDL) cholesterol levels. Significantly higher LDL cholesterol levels were found in subjects with intermediate and small LDL particles than in those with large or very small LDL particles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Familial lipoprotein disorders in patients with premature coronary artery disease.

BACKGROUND: Genetic lipoprotein disorders have been associated with premature coronary artery disease (CAD). METHODS AND RESULTS: The prevalence of such disorders was determined in 102 kindreds (n = 603 subjects) in whom the proband had significant CAD documented by angiography before the age of 60 years. Fasting plasma cholesterol, triglyceride, low density lipoprotein (LDL) cholesterol, apolipoprotein (apo) B, and lipoprotein (a) [Lp(a)] values above the 90th percentile and high density lipoprotein (HDL) cholesterol and apo A-I below the 10th percentile of age- and sex-specific norms were defined as abnormal. An abnormality was noted in 73.5% of probands compared with 38.2% in age-matched controls (p less than 0.001), with a low HDL cholesterol level (hypoalphalipoproteinemia) being the most common abnormality (39.2% of cases). In these kindreds, 54% had a defined phenotypic familial lipoprotein or apolipoprotein disorder. The following frequencies were observed: Lp(a) excess, 18.6% (includes 12.7% with no other dyslipidemias); hypertriglyceridemia with hypoalphalipoproteinemia, 14.7%; combined hyperlipidemia, 13.7% (11.7% with and 2.0% without hypoalphalipoproteinemia); hyperapobetalipoproteinemia (elevated apo B only), 5%; hypoalphalipoproteinemia, 4%; hypercholesterolemia (elevated LDL only), 3%; hypertriglyceridemia, 1%; decreased apo A-I only, 1%. Overall, 54% of the probands had a familial dyslipidemia; unclassifiable lipid disorders (spouse also affected) were found in 3%. No identifiable familial dyslipidemia was noted in 43% of kindreds of those; nearly half (45%) had a sporadic lipid disorder. Parent-offspring and proband-spouse correlations for these biochemical variables revealed that lipoprotein and apolipoprotein levels are in part genetically determined, with Lp(a) showing the highest degree of parent-offspring correlation. CONCLUSIONS: Our data indicate that more than half of patients with premature CAD have a familial lipoprotein disorder, with Lp(a) excess, hypertriglyceridemia with hypoalphalipoproteinemia, and combined hyperlipidemia with hypoalphalipoproteinemia being the most common abnormalities.

Coronary Disease↗
PubMed1992

Association of HbA1c with prevalent cardiovascular disease in the original cohort of the Framingham Heart Study.

We studied the cross-sectional relationship between HbA1c and cardiovascular disease (CVD) in the survivors of the original cohort of the Framingham Heart Study (n = 1045). HbA1c was significantly related to prevalent CVD among women but not men. HbA1c was also related to hypertension and to the ratio of total to high-density lipoprotein cholesterol levels. In regression analyses that controlled for these and other potential risk factors, HbA1c remained significantly related to CVD among women. The relative odds of CVD increased 1.39-fold (95% confidence interval 1.06-1.83) for increases in HbA1c of 1% (e.g., for HbA1c from 5 to 6%). The relationship was not weakened when known diabetic subjects or subjects taking beta-blocker or thiazide medications were excluded from analysis. In contrast, there was no significant relationship between "casual" blood glucose and prevalent CVD. Our results reveal a strong, significant, independent association between hyperglycemia, measured by HbA1c, and CVD among older women.

Aged↗
PubMed1991

Serum cholesterol as a prognostic factor after myocardial infarction: the Framingham Study.

OBJECTIVE: To determine the relation between serum cholesterol levels and the long-term risk for reinfarction, death from coronary heart disease, and all-cause mortality in persons who recover from myocardial infarction. DESIGN: Prospective, longitudinal study. SETTING: A geographically defined population-based cohort of adults participating in the Framingham Heart Study. PATIENTS: Men (n = 260) and women (n = 114), 33 to 88 years of age (mean age, 62 years), who had a history of myocardial infarction. MEASUREMENTS: A complete physical examination, including electrocardiographic evaluation, blood pressure measurement, height and weight measurements, determination of smoking habits, and casual determinations of blood glucose and serum cholesterol, was done approximately 1 year after recovery from initial myocardial infarction. Patients were followed after infarction for the occurrence of reinfarction or death (mean follow-up, 10.5 years; range, 0.8 to 31.6 years). MAIN RESULTS: The mean cholesterol level after infarction was 5.21 mmol/L (242.8 mg/dL); 20% of patients had levels below 5.17 mmol/L (200 mg/dL), and 22% had levels of 7.11 mmol/L (275 mg/dL) or more. Compared with patients who had cholesterol levels below 5.17 mmol/L, patients with levels of 7.11 mmol/L or more were at increased risk for reinfarction (relative risk, 3.8; 95% Cl, 1.6 to 8.7), death from coronary heart disease (relative risk, 2.6; Cl, 1.4 to 4.8), and all-cause mortality (relative risk, 1.9; Cl, 1.2 to 2.9) based on multivariate Cox regression analyses adjusted for other coronary risk factors. Intermediate cholesterol levels (5.17 mmol/L to 7.11 mmol/L) were generally not associated with increased risk. The association between elevated serum cholesterol and increased risk was strongest in men; however, elevated cholesterol levels were found to be most strongly related to death from coronary disease and to all-cause mortality in persons who were 65 years of age or more. CONCLUSIONS: Patients who have recovered from a myocardial infarction and who have high cholesterol levels are at an increased long-term risk for reinfarction, death from coronary heart disease, and all-cause mortality. Our results confirm the prognostic value of cholesterol levels measured after myocardial infarction and support the role of lipid management in this population.

Adult↗
PubMed1991

Echocardiographic evidence for the existence of a distinct diabetic cardiomyopathy (the Framingham Heart Study).

Although several reports have described early changes of cardiac structure and function in diabetic patients, controversy persists regarding the existence of a clinically distinct diabetic cardiomyopathy. To this end, sex-specific linear regression analyses were used to examine the contribution of diabetes mellitus and glucose intolerance to age-adjusted echocardiographic parameters in 1,986 men (mean age 48 years) and 2,529 women (mean age 50 years) from the original Framingham Study cohort and the Framingham Offspring Study. Subjects with evidence of cardiovascular disease at the time of echocardiogram were excluded. Diabetics had higher heart rates than nondiabetics (67.9 vs 64.0 beats/min (p = 0.002) in men, and 73.1 vs 68.3 beats/min (p = 0.004) in women). Diabetic women had increased left ventricular (LV) wall thickness (18.7 vs 17.1 mm, p less than 0.001), relative wall thickness (0.403 vs 0.377, p = 0.008), LV end-diastolic dimension (46.9 vs 45.7 mm, p = 0.03) and LV mass corrected for height (100.4 vs 82.2 g/m, p less than 0.001). Women with glucose intolerance showed similar, less significant trends (p = 0.007 for wall thickness, p less than 0.01 for LV mass). In diabetic men, fractional shortening was slightly reduced (0.355 vs 0.360, p less than 0.05). In a multivariate model that included potentially confounding factors, diabetes remained an independent contributor to LV mass (p = 0.004) and wall thickness (p = 0.008) in women. In a separate linear regression model, which assessed the association of age with LV mass, the age-coefficient for diabetic women was much higher than that for nondiabetics (13.6 vs 6.6 g/m per 10-year increment in age).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Prevalence of lipoprotein (a) [Lp(a)] excess in coronary artery disease.

Lipoprotein (a) [Lp(a)] is composed of 1 low-density lipoprotein (LDL) particle, to which 1 molecule of apolipoprotein (a) is covalently linked. Elevated levels of Lp(a) have been associated with coronary artery disease (CAD) and Lp(a) has been shown to be highly heritable. Our purpose was to determine the prevalence of familial Lp(a) excess in patients with CAD. We determined plasma levels of Lp(a) in 180 patients (150 men and 30 women) with angiographically documented CAD before age 60 years, and in 459 control subjects (276 men and 183 women) clinically free of cardiovascular disease. In addition, Lp(a) levels were determined in families of 102 of the CAD probands (87 men and 15 women). No gender differences in Lp(a) levels were observed between men and women (patients or control subjects). Patients with CAD had higher Lp(a) levels than did control subjects (19 +/- 21 vs 13 +/- 15 mg/dl, p less than 0.001). The prevalence of Lp(a) excess (defined as greater than 90th percentile of controls) was 17% in patients with CAD (p less than 0.05). Lp(a) levels were not correlated with cholesterol, LDL cholesterol, high-density lipoprotein (HDL) cholesterol or apolipoproteins A-I or B. There was a weak correlation between Lp(a) and triglycerides (r = 0.166, p less than 0.05) in patients and control subjects. Stepwise discriminant analysis revealed that Lp(a) was a risk factor for the presence of CAD in men, independent of smoking, hypertension, diabetes, LDL and HDL cholesterol, or apolipoprotein A-I and B levels. Family studies revealed that Lp(a) levels are strongly genetically determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins↗
PubMed1991

The epidemiology of impaired glucose tolerance and hypertension.

Epidemiologic research indicates that glucose intolerance and hypertension are interrelated phenomena, each powerfully predisposing to atherosclerotic cardiovascular disease. Both diabetic and hypertensive patients have greater amounts of atherogenic risk factors, including dyslipidemia, hyperuricemia, elevated fibrinogen, and left ventricular hypertrophy. Diabetic persons have an increased prevalence of hypertension (50%), and glucose intolerance is more common in hypertension (15% to 18%). Both share a strong relationship to excess weight, but the excess of hypertension in diabetic persons occurs in both lean and obese subjects. Diabetes doubles the risk of hypertension associated with overweight. The risk of coronary disease, stroke, and peripheral arterial disease increases with increasing blood pressure to the same degree in diabetic persons as in nondiabetic persons, but at any level of blood pressure, diabetic persons have a doubled risk of these outcomes. Both diabetic and hypertensive patients are particularly prone to silent or unrecognized myocardial infarctions. Greater efforts at primary prevention of both hypertension and diabetes are clearly needed, including efforts at weight control, exercise, limitation of salt intake, and control of blood lipid levels. In either diabetic or hypertensive candidates for cardiovascular disease, optimization of the chances of avoiding sequelae requires a comprehensive multifactorial approach. Prevention requires more than normalization of either the blood sugar or blood pressure. Rational preventive measures must also include weight reduction, a fat-modified diet, cessation of smoking cigarettes, raising high-density lipoprotein, lowering low-density lipoprotein, and reduction of fibrinogen. Hypertension, obesity, insulin resistance, hyperinsulinemia, hypertriglyceridemia, and low high-density lipoprotein cholesterol tend to coexist.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1991

Is hyperglycemia associated with cardiovascular disease? The Framingham Study.

The association of nonfasting blood glucose levels with CVD incidence was determined prospectively in 1382 men and 2094 women aged 45 to 84 years participating in the Framingham Heart Study. For this study, all patients were classified in 1970 as diabetic or nondiabetic. Every 2 years they were examined, categorized according to causal blood glucose samples obtained at the clinic visit, reclassified for development of CVD and diabetes mellitus, and followed 10 years for CVD. During the follow-up period, 350 men and 369 women developed CVD. Age-adjusted CVD rates were positively associated with glucose levels in nondiabetic women who did not develop diabetes during follow-up. No such associations were seen in men. Multivariate analyses confirmed the independent association of blood glucose levels with later CVD in nondiabetic women. This study shows that hyperglycemia in the original Framingham cohort is an independent risk factor for CVD in nondiabetic women, but not among men.

Aged↗
PubMed1991

Cardiovascular disease risk profiles.

This article presents prediction equations for several cardiovascular disease endpoints, which are based on measurements of several known risk factors. Subjects (n = 5573) were original and offspring subjects in the Framingham Heart Study, aged 30 to 74 years, and initially free of cardiovascular disease. Equations to predict risk for the following were developed: myocardial infarction, coronary heart disease (CHD), death from CHD, stroke, cardiovascular disease, and death from cardiovascular disease. The equations demonstrated the potential importance of controlling multiple risk factors (blood pressure, total cholesterol, high-density lipoprotein cholesterol, smoking, glucose intolerance, and left ventricular hypertrophy) as opposed to focusing on one single risk factor. The parametric model used was seen to have several advantages over existing standard regression models. Unlike logistic regression, it can provide predictions for different lengths of time, and probabilities can be expressed in a more straightforward way than the Cox proportional hazards model.

Adult↗
PubMed1991

Twelve-year incidence of coronary heart disease in middle-aged adults during the era of hypertensive therapy: the Framingham offspring study.

PURPOSE: To provide information on the incidence of coronary heart disease (CHD) in the offspring of the original cohort from the Framingham Heart Study. PATIENTS AND METHODS: From 1972 to 1974, offspring of the original participants in the Framingham Heart Study underwent a baseline examination for standard cardiovascular risk factors. At entry into the study, these offspring were 30 to 59 years old and free of CHD. They were followed for 12 years, during which time 156 of 1,663 men and 55 of 1,714 women developed CHD. RESULTS: In a multivariate proportional hazards model, CHD was significantly associated with age, lower high-density lipoprotein cholesterol (HDL-C) levels, and number of cigarettes smoked. Fasting glucose levels and low-density lipoprotein cholesterol (LDL-C) were highly associated with CHD in men, but borderline in women, while triglycerides and very-low-density lipoprotein cholesterol were not significantly associated with CHD after adjustment for HDL-C and glucose. Blood pressure medication was used in half of the hypertensive individuals, and systolic pressure was associated with CHD in women only. CONCLUSIONS: This study confirms the importance of the common CHD risk factors of cigarette smoking and LDL-C, and extends the prognostic role of HDL-C in a middle-aged cohort. The impact of blood pressure, with or without use of hypertensive medications, was reduced in this study, and the data suggest that this attenuation was due to successful treatment.

Adult↗
PubMed1991

The NHLBI Twin Study: heritability of apolipoprotein A-I, B, and low density lipoprotein subclasses and concordance for lipoprotein(a).

Heritability of plasma apolipoprotein (apo) A-I, apo B, and low density lipoprotein (LDL) subclasses and concordance for lipoprotein(a) excess were assessed in 109 monozygotic (MZ) and 113 dizygotic (DZ) twin pairs participating in the third examination of the National Heart, Lung, and Blood Institute Twin Study. The intraclass correlation coefficient for apo A-I was significantly greater in MZ twins (0.56) than in DZ twins (0.37, P less than 0.05); however, apo A-I showed an unequal distribution in the two groups, with significantly greater total variance in DZ twins. Therefore the among-component estimate of genetic variance was applied, and the results indicated no significant heritability for apo A-I (P = 0.59). MZ and DZ twins had equal apo B variance. The intraclass correlation coefficient for apo B in MZ twins (0.71) was significantly higher than in DZ twins (0.25) (P less than 0.0001), indicating significant heritability for apo B. Plasma apo A-I levels were significantly correlated with alcohol intake (P less than 0.0001), body mass index (BMI, P less than 0.0001), and physical activity, while apo B levels were significantly correlated only with BMI (P less than 0.05). After plasma apo A-I and apo B concentrations were adjusted for all of these variables and for cigarette smoking, the analysis of variance and intraclass correlation coefficients remained virtually unchanged. The LDL type intraclass correlation coefficient was higher in MZ twins (0.58) than in DZ twins (0.32, P less than 0.005); however, greater total variance for this parameter in DZ twins was observed and after applying the among component estimate of genetic variance, no significant heritability of LDL type was observed. After adjustment for covariate effects the conclusions were not changed. Only 8.4% of MZ twin pairs, as compared with 26.7% of DZ twin pairs, were discordant for elevated lipoprotein(a) on gradient gels (P less than 0.0001). Our data indicate that there is a strong heritability for plasma apo B and lipoprotein(a), with only weak evidence for heritability of LDL type or plasma apo A-I levels within this population sample.

Aged↗