(Circulation. 2000;101:2047.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Low Fasting Plasma Glucose Level as a Predictor of Cardiovascular Disease and All-Cause Mortality
From the Cooper Institute (M.W., J.B.K., S.N.B.) and the Cooper Clinic (L.W.G., T.L.M.), Dallas, and the Department of Medicine (M.P.S.), University of Texas Health Science Center, San Antonio, Tex.
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Abstract |
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Background—Although medical textbooks usually classify fasting plasma glucose <70 or 80 mg/dL (<3.89 or 4.44 mmol/L) as abnormal, the prognosis for patients with low fasting plasma glucose is unclear.
Methods and Results—We conducted prospective cohort studies among 40 069 men and women to investigate the association between fasting plasma glucose levels and cardiovascular disease and all-cause mortality. We documented a U-shaped relation between fasting plasma glucose and mortality. In addition to diabetes and impaired fasting glucose levels, low fasting plasma glucose levels were also associated with high mortality. After multivariate adjustment for age, sex, study population, ethnicity, current smoking status, high blood pressure, total cholesterol, body mass index, triglycerides, history of cardiovascular disease and cancer, and a family history of cardiovascular disease, patients with fasting plasma glucose <70 mg/dL (<3.89 mmol/L) had a 3.3-fold increased risk of cardiovascular disease mortality, and patients with fasting plasma glucose 70 to 79 mg/dL (3.89 to 4.43 mmol/L) had a 2.4-fold increased risk compared with the risk in patients with fasting plasma glucose 80 to 109 mg/dL (4.44 to 6.05 mmol/L) (tests for trend P<0.0001). Participants with low fasting plasma glucose levels also had increased risk of all-cause mortality (test for trend P<0.0001).
Conclusions—Participants with low fasting plasma glucose levels had a high risk of cardiovascular disease and all-cause mortality.
Key Words: glucose • cardiovascular diseases • mortality
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Introduction |
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Under normal physiological conditions, plasma glucose concentration is maintained within narrow limits by a tightly regulated balance between glucose efflux from and influx into the circulation.1 A normal plasma glucose level is important for human energy and nutrition. It is known that high fasting plasma glucose (FPG) levels and diabetes are associated with a high incidence of cardiovascular disease (CVD) and all-cause mortality.2 3 4 5 On the other hand, low plasma glucose levels may cause brain and heart problems.1 6 Early studies of low FPG focused on brain damage during hypoglycemia.6 7 8 Although medical textbooks usually classify FPG <70 or 80 mg/dL (<3.89 or 4.44 mmol/L) as abnormal,9 10 symptoms usually appear only when FPG is <50 mg/dL (<2.78 mmol/L).11 There is a paucity of information about the association between low plasma glucose levels and cause-specific and all-cause mortality. In the present study, we address this issue in 2 prospective studies with a total follow-up of 350 552 person-years.
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Methods |
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Subjects
Subjects for this study were 40 069 men and women 20 to 82 years of age at baseline (mean, 43 years) from either the Aerobics Center Longitudinal Study (ACLS) or the San Antonio Heart Study (SAHS). The participants from the ACLS completed
1 preventive medical
evaluation at the Cooper Clinic in Dallas, Tex, between 1970 and 1989.
Details of the study design and population characteristics of this
study are available in previous reports.12 13 Briefly,
this is a population-based prospective study. More than 97% of the
35 140 patients are white, 78% are men, and most had white-collar or
professional occupations. The baseline evaluation was performed after
participants gave their informed written consent for the initial
medical examination and subsequent registration in the follow-up study.
Examinations followed an overnight fast of 12 hours and included
personal and family health histories and a questionnaire on demographic
characteristics and health habits. All procedures were administered by
technicians who followed a standard manual of
operations.12 The study was reviewed and approved annually
by the Institutional Review Board at the Cooper Institute for
Aerobics Research.
The participants in the SAHS were randomly recruited between 1979 and
1988 from 3 types of neighborhoods: low-income barrios, middle-income
transitional neighborhoods, and high-income suburbs. All men and
nonpregnant women between 25 and 64 years of age residing in the
selected households were considered eligible for the study. Of 4929
subjects, 62% were Mexican Americans, and 57% were women. The
baseline evaluation was performed after participants gave their
informed written consent for the medical examination. Examinations
followed an overnight fast of 12 hours and included a questionnaire
on demographic characteristics and health habits. Technicians who
followed a standard manual of operations administered all procedures.
The study was approved by the University of Texas Health Science Center
Institutional Review Board, and all participants gave informed consent.
Details of the study design and sampling, recruitment, and field
procedures of the SAHS have been reported
previously.4 14
We defined diabetes in this study according to the 1997 plasma glucose
criteria of the American Diabetes Association15 : (1) For
impaired fasting glucose, FPG 110 mg/dL (6.11 mmol/L) but
<126 mg/dL (<7.0 mmol/L); and (2) for diabetes, FPG 126 mg/dL
(7.0 mmol/L). Subjects who did not meet this criterion but who
gave a history of diabetes and reported current therapy with either
oral antidiabetic agents or insulin also were considered to have
diabetes. In the SAHS, participants with a 2-hour postload glucose
level 200 mg/dL (11.1 mmol/L) also were considered to have
diabetes. The ACLS material did not include 2-hour postload glucose
data.
Primary outcome measures were CVD and all-cause mortality. The National
Death Index was used to identify possible decedents in the ACLS. The
National Death Index is an effective, accurate means of ascertaining
deaths in the general population with a sensitivity of 
96% and a
specificity of 100%.16 Deaths were identified and
confirmed by follow-up interviews with next-of-kin in the SAHS, and
vital status was ascertained for 98% of the cohort.4
Death certificates were obtained in both studies and coded by
nosologists according to the International Classification of Diseases,
9th Edition, Revised. CVD mortality was defined as codes 390 to 459 and
cancer mortality as codes 140 to 208. Only the underlying cause of
death was used.
The 2 populations were pooled for analysis to increase statistical power. Data were analyzed with the SAS statistical package.17 Interaction terms between population, ethnicity, sex, and other independent variables were entered into the initial models to evaluate possible interactions; however, no significant interactions were found, and the primary analyses were on the pooled data. The adjusted mortality rates were calculated by the direct method. We used survival curves to estimate survival function against time and Log [-log (survival time)] to check proportional hazards model assumption. We used Cox proportional hazards models to estimate the association between mortality and predictor variables after adjustment for potential confounders.17 18 All probability values provided are for 2-sided tests, and values of P<0.05 were considered statistically significant.
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Results |
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Baseline characteristics adjusted for age, sex, ethnicity, and study population are presented in Table 1
. Body mass index, total
cholesterol, triglyceride, systolic
blood pressure, diastolic blood pressure, exercise
tolerance, fasting insulin, and 2-hour postload insulin values were
lower in individuals with low FPG than in individuals with normal FPG.
The prevalence of parental CVD and current smoking were higher in
participants with low FPG; however, the differences for these
variables were small, except for insulin level.
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During an average follow-up of 8 years, there were 954 deaths,
including 413 from CVD and 277 from cancer. We first stratified data by
every 10 mg/dL (0.555 mmol/L) for mortality analysis. We
found increased mortality in participants with diabetes and with FPG
<80 mg/dL (<4.44 mmol/L). There were 1581 participants with diabetes,
4550 with impaired fasting glucose, and 1795 with FPG <80 mg/dL
(<4.44 mmol/L). Among participants with low FPG, 11 had FPG <50
mg/dL (<2.78 mmol/L), 221 had FPG 50 to 69 mg/dL (2.78 to
3.88 mmol/L), and 1563 had FPG 70 to 79 mg/dL (3.89 to 4.43
mmol/L). Figure 1 shows the mortality
rates per 1000 person-years according to FPG levels. Subjects in the
SAHS, which included many Mexican Americans, had a high prevalence of
diabetes (8%) compared with subjects in the ACLS (3%). The prevalence
of low FPG was also higher in Mexican Americans. There was a clear
relation between low FPG and mortality after adjustment for age, sex,
and study population. After exclusion or adjustment for history of
chronic disease, the magnitude of association between low FPG and
mortality did not change.
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We then focused on the comparison between low FPG and normal FPG. We
first performed subgroup analyses in women versus men,
individuals aged 50 years versus those aged <50 years, Mexican
Americans versus non-Hispanic whites, deaths in the first 4 years
versus deaths later than 4 years, and SAHS versus ACLS separately. All
associations between low FPG and mortality were directionally similar
in these subgroup analyses. Compared with participants without
low FPG, those with low FPG had a substantially higher risk of CVD and
all-cause mortality in each subgroup analysis. For example,
age- and sex-adjusted relative risks (with 95% CIs) associated with
low FPG were 2.1 (1.2 to 3.8) for CVD mortality and 2.1 (1.4 to 2.8)
for all-cause mortality in the ACLS data. Age- and sex-adjusted
relative risks (with 95% CIs) were 3.4 (1.6 to 7.1) for CVD mortality
and 1.7 (1.0 to 3.0) for all-cause mortality in the SAHS data. Age- and
sex-adjusted relative risks (with 95% CIs) associated with low FPG
were 2.3 (1.4 to 3.8) for CVD mortality and 2.2 (1.5 to 2.9) for
all-cause mortality in the non-Hispanic whites. Age- and sex-adjusted
relative risks (with 95% CIs) were 3.1 (1.4 to 6.8) for CVD mortality
and 1.6 (0.8 to 3.0) for all-cause mortality in Mexican Americans. The
interactions between study or ethnicity and low FPG on mortality were
not statistically significant. No significant differences for CVD and
all-cause mortality were found between nondiabetics with low FPG and
diabetics.
We used Kaplan-Meier curves to test for differences in mortality rates
between participants with low glucose and those with normal glucose.
There were strong associations between low FPG and CVD and all-cause
mortality (Figure 2). Both
Wilcoxon and log-rank tests were highly significant for CVD and
all-cause mortality (P<0.0001). Log (-log [survival
function]) estimates were approximately parallel across the low FPG
group and normal glucose group (figure not shown).
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Table 2 shows the association between low
FPG and CVD, cancer, deaths other than cancer or CVD, and all-cause
mortality. Participants with low FPG had substantially higher CVD,
all-cause, and other mortality. The relation between low FPG and cancer
mortality was weak and nonsignificant. Additional adjustments by
multivariate analyses and exclusion of persons
with chronic diseases did not alter these associations. For example,
the multivariate-adjusted relative risks (with 95%
CIs) of low FPG for CVD and all-cause mortality were 2.7 (1.7 to 4.3)
and 2.0 (1.5 to 2.6) in all study subjects, 2.7 (1.5 to 4.7) and 2.0
(1.4 to 2.9) in restricting events after 4 years of follow-up, and 2.7
(1.6 to 4.5) and 2.1 (1.5 to 2.9) in individuals without a history of
CVD and cancer. Among 21 participants who died from CVD in the low FPG
group, 52% of the deaths were due to acute myocardial infarction, 19%
were due to cerebrovascular hemorrhage, and 10% were due to
cardiac arrest. Because of the small number of cerebrovascular disease
deaths in the low FPG group, no significant association between low FPG
and cerebrovascular disease was detected.
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To investigate the possible dose-response relation of low FPG
levels to mortality, we classified those with low FPG into <70 mg/dL
(<3.89 mmol/L) and 70 to 79 mg/dL (3.89 to 4.43 mmol/L)
groups (Table 3). We found an
inverse gradient (P<0.0001) for CVD and all-cause mortality
across FPG categories in analyses adjusted for age, sex, and
study population. Other models included adjustment for age, sex, study
population, ethnicity, current smoking status, high blood pressure,
total cholesterol, body mass index,
triglycerides, history of CVD and cancer, and a family
history of CVD. In the fully adjusted model, those with FPG <70 mg/dL
(<3.89 mmol/L) had a 3.3-fold increased risk of CVD mortality,
and those with FPG 70 to 79 mg/dL (3.89 to 4.43 mmol/L) had a
2.0-fold increased risk compared with patients with FPG 80 to 109 mg/dL
(4.44 to 6.05 mmol/L) (test for trend P<0.0001). In
similar analyses, those with FPG <70 mg/dL (<3.89
mmol/L) had a 2.4-fold increased risk of all-cause mortality, and those
with FPG 70 to 79 mg/dL (3.89 to 4.43 mmol/L) had a 1.8-fold
increased risk (test for trend P<0.0001). Low FPG was
associated with low body mass index (<18.5), low
cholesterol level, low diastolic blood
pressure, and current smoking. However, the association between low FPG
and mortality remained the same after adjustment for or excluding these
risk factors. Low FPG was not associated with ex-drinkers or
nondrinkers in the data.
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Discussion |
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Currently, known risk factors predict
50% to 60% of clinical
CVD,19 20 and it is important to find additional
predictors to improve clinical risk stratification. In the present
study, we found a potential new predictor of CVD with the observation
of an association between low FPG and CVD and all-cause mortality. This
association was strong, independent, graded across strata of low FPG,
and present in 2 separate cohort studies, the ACLS and the SAHS. To
our knowledge, this is the first report on low FPG associated with CVD
and all-cause mortality. Most of the previous studies categorized
plasma glucose into diabetes or nondiabetes. However, a recent cohort
study in men showed that crude CVD and all-cause mortality seems to be
higher in patients with FPG <81 mg/dL (4.5 mmol/L), but the
authors did not test this hypothesis.21 The most important adverse effect of hypoglycemia has been associated with brain damage.22 As an important fuel of the brain, severely low FPG may induce brain damage and dysfunction. However, there were only 11 participants with classic hypoglycemia with FPG <50 mg/dL (<2.78 mmol/L) in the present study, and the exclusion of these participants did not alter the results. ECG changes, including ectopic activity, flattening of the T wave, ST depression, ventricular tachycardia, and atrial fibrillation, have been reported in cases of low plasma glucose.6 7 8 Marques et al23 reported alteration of ventricular repolarization with lengthening of the QT interval during insulin-induced experimental low FPG. Low plasma glucose has been suspected as the cause of high CVD mortality in diabetic patients with an unstable FPG.24 It is known that >60% of adults aged 20 to 30 years have already had atherosclerosis25 and that the prevalence of atherosclerosis increases as age increases.25 26 We hypothesize that long-term exposure to low FPG may serve as a risk factor of CVD mortality, perhaps through abnormal cardiac activity and thrombosis, especially in patients with atherosclerosis.
The relation between moderately low FPG and mortality in the
present study was not confounded by preexisting chronic disease.
After exclusion or adjustment for history of chronic disease, including
CVD and cancer, the magnitude of association between low FPG and
mortality did not change. Some kinds of occult cancer have been
reported to be associated with symptomatic
hypoglycemia1 27 ; however, the association between
low FPG and cancer mortality in our data was weak and nonsignificant.
We reported that low cardiorespiratory fitness is associated with
diabetes and impaired fasting glucose28 and that low
fitness was also somewhat associated with low FPG (Table 1
).
Some investigators have reported that
hyperinsulinemia is a cause of
hypoglycemia1 ; however, compared with persons without low
FPG, study participants with low FPG in the SAHS had lower fasting
insulin and 2-hour postload insulin levels (Table 1). Uric acid
levels also were similar in individuals with low FPG and in those with
normal FPG in our data (Table 1). Heavy alcohol intake and liver
diseases could be associated with liver dysfunction and hypoglycemia,
but alcohol intake and 
-glutamyltranspeptidase were not higher in
individuals with low FPG. When we excluded patients with a history of
jaundice, hepatitis, cirrhosis, or abnormal -glutamyltranspeptidase,
the results were unchanged. Low FPG was associated with low body mass
index, low cholesterol, low diastolic blood
pressure, and current smoking. Low body mass index and current smoking
may partly explain low FPG; however, the association between low FPG
and mortality remained the same after adjustment for these potential
confounders.
Limitations
The subjects in ACLS were well educated, and >95% were
white.12 13 The subjects in the SAHS were randomly
recruited from 3 types of low-, middle-, and high-income neighborhoods,
which included a large proportion of Mexican
Americans.4 14 20 Despite the differences in
characteristics, results from both populations for conventional risk
factors of CVD are consistent with each other and with those
from other populations.4 5 12 13 19 20 But whether our
results also apply to African Americans and Asian Americans remains to
be determined. There may be some measurement errors in the assessment
of fasting plasma glucose and a small amount of patients lost to
follow-up. However, it is unlikely that misclassification accounts for
the observed association. It is possible that low FPG was partially due
to inflammation, metabolic abnormalities, or specific
diets, but we did not have data to evaluate these possibilities.
Additional human studies and animal data are needed to investigate
these issues.
Conclusions
The association between low FPG and CVD and all-cause mortality is
clinically relevant. Actually, the higher relative risks of CVD and
all-cause mortality in patients with low FPG were similar to those in
patients with diabetes.2 4 5 Clinicians should be aware of
this situation and search for special causes in cases of low FPG.
Although association does not necessarily indicate cause and effect,
our data suggest that low FPG itself may be a cause of high mortality
risk. If our results are confirmed, low FPG could be a modifiable risk
factor in nondiabetics. The optimal goals associated with FPG in
diabetics taking insulin or oral antidiabetic agents might be to
achieve an FPG level not <80 mg/dL. Further study is needed to
explore the cause of low FPG and the association between low plasma
glucose and CVD and all-cause mortality.
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Acknowledgments |
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This study was supported in part by a grant from the National Institutes of Health, National Institute on Aging (AG-06945), by grants from the National Heart, Lung, and Blood Institute (R01 HL-24799, R37 HL-36820, and R01 HL-62508), and by several private contributions. We thank patients, physicians, and technicians at the Cooper Clinic for their participation, Dr Kenneth H. Cooper for establishing the Aerobics Center Longitudinal Study, Carolyn E. Barlow for data management, and Melba Morrow for editorial assistance.
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Footnotes |
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Reprint requests to Dr Ming Wei, the Cooper Institute, 12330 Preston Rd, Dallas, TX 75230.
Received September 7, 1999; revision received December 1, 1999; accepted December 10, 1999.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
-
Clutter WE, Cryer PE. Hypoglycemia. In: Stein JH,
ed. Internal Medicine. Boston, Mass: Little Brown & Co;
1990:2267–2272.
-
Geiss LS, Herman WH, Smith PJ. Mortality in
non-insulin-dependent diabetes. In: National Diabetes Data Group, ed.
Diabetes in America. Bethesda, Md: National Institutes of
Health, National Institute of Diabetes and Digestive and Kidney
Diseases; 1995:233–257. Publication No. (NIH) 95–1468.
-
Lowe LP, Liu K, Greenland P, Metzger BE, Dyer AR,
Stamler J. Diabetes, asymptomatic hyperglycemia, and
22-year mortality in black and white men: The Chicago Heart Association
Detection Project in Industry Study. Diabetes Care. 1997;20:163–169.[Abstract]
-
Wei M, Gaskill SP, Haffner SM, Stern MP. Effects of
diabetes and level of glycemia on all-cause and
cardiovascular mortality: The San Antonio Heart Study.
Diabetes Care. 1998;21:1167–1172.[Abstract]
-
Wei M, Gibbons LW, Mitchell TL, Kampert JB, Blair SN.
Undiagnosed diabetes and impaired fasting glucose as predictors of
cardiovascular disease and all-cause mortality.
CVD Prev. 1998;1:123–128.
-
Galizia AC, Fava S, Foale R.
Nesidioblastosis-associated hypoglycaemia presenting with prominent
cardiac manifestations. Postgrad Med J. 1996;72:231–232.[Abstract]
-
Duh E, Feinglos M. Hypoglycemia-induced angina
pectoris in a patient with diabetes mellitus. Ann Intern
Med. 1994;121:945–946.
[Free Full Text]
-
Collier A, Matthews DM, Young RJ, Clarke BF. Transient
atrial fibrillation precipitated by hypoglycaemia: two case reports.
Postgrad Med J. 1987;63:895–897.[Abstract]
-
Bennett JC, Plum F, eds. Cecil Textbook of
Medicine. Philadelphia, Pa: WB Saunders Co; 1996.
-
Stein JH, ed. Internal Medicine. Boston,
Mass: Little Brown & Co; 1990:2453–2460.
-
Boyle CA, Decouflé P. National sources of vital
status information: extent of coverage and possible selectivity in
reporting. Am J Epidemiol. 1990;131:160–168.
[Abstract/Free Full Text]
-
Blair SN, Kohl HW III, Paffenbarger RSJ, Clark DG,
Cooper KH, Gibbons LW. Physical fitness and all-cause mortality: a
prospective study of healthy men and women. JAMA. 1989;262:2395–2401.[Abstract]
-
Blair SN, Kampert JB, Kohl HW, Barlow CE, Macera CA,
Paffenbarger RSJ, Gibbons LW. Influences of cardiorespiratory fitness
and other precursors on cardiovascular disease and
all-cause mortality in men and women. JAMA. 1996;276:205–210.[Abstract]
-
Stern MP, Rosenthal M, Haffner SM, Hazuda HP, Franco
LJ. Sex difference in the effects of sociocultural status on diabetes
and cardiovascular risk factors in Mexican Americans:
The San Antonio Heart Study. Am J Epidemiol. 1984;120:834–851.
[Abstract/Free Full Text]
-
The Expert Committee on the Diagnosis and
Classification of Diabetes Mellitus. Report of the Expert Committee on
the Diagnosis and Classification of Diabetes Mellitus. Diabetes
Care. 1997;20:1183–1197.[Medline]
[Order article via Infotrieve]
-
Stampfer MJ, Willett WC, Speizer FE, Dysert DC, Lipnick
R, Rosner B, Hennekens CH. Test of the National Death Index.
Am J Epidemiol. 1984;119:837–839.
[Free Full Text]
-
SAS Institute Inc. SAS/STAT User’s Guide,
Version 6. Cary, NC: SAS Institute Inc; 1989.
-
Greenland S. Modeling and variable selection in
epidemiologic analysis. Am J Public Health. 1989;79:340–349.
[Abstract/Free Full Text]
-
Heller RF, Chinn S, Pedoe HDT, Rose G. How well can we
predict coronary heart disease? Findings in the United Kingdom
Heart Disease Prevention Project. BMJ. 1984;288:1409–1411.
-
Wei M, Mitchell BD, Haffner SM, Stern MP. Effects of
cigarette smoking, diabetes, high cholesterol, and
hypertension on all-cause mortality and cardiovascular
disease mortality in Mexican Americans: The San Antonio Heart Study.
Am J Epidemiol. 1996;144:1058–1065.
[Abstract/Free Full Text]
-
Bjornholt JV, Erikssen G, Aaser E, Sandvik L,
Nitter-Hauge S, Jervell J, Erikssen J, Thaulow E. Fasting blood
glucose: an underestimated risk factor for
cardiovascular death. Diabetes Care. 1999;22:45–49.
[Abstract/Free Full Text]
-
Malouf R, Brust JC. Hypoglycemia: causes, neurological
manifestations, and outcome. Ann Neurol. 1985;17:421–430.[Medline]
[Order article via Infotrieve]
-
Marques JLB, George E, Peacey SR, Harris ND, Macdonald
IA, Cochrane T, Heller SR. Altered ventricular
repolarization during hypoglycaemia in patients with diabetes.
Diabet Med. 1997;14:648–654.[Medline]
[Order article via Infotrieve]
-
Muggeo M, Verlato G, Bonora E, Zoppini G, Corbellini M,
de Marco R. Long-term instability of fasting plasma glucose, a novel
predictor of cardiovascular mortality in elderly
patients with non-insulin-dependent diabetes mellitus: The Verona
Diabetes Study. Circulation. 1997;96:1750–1754.
[Abstract/Free Full Text]
-
Berenson GS, Srinivasan SR, Bao W, Newman WP III, Tracy
RE, Wattigney WA. Association between multiple
cardiovascular risk factors and
atherosclerosis in children and young adults: The
Bogalusa Heart Study. N Engl J Med. 1998;338:1650–1656.
[Abstract/Free Full Text]
-
Tejada C, Strong JP, Montenegro MR, Restrepo C, Solberg
LA. Distribution of coronary and aortic
atherosclerosis by geographic location, race, and sex.
Lab Invest. 1968;18:509–526.[Medline]
[Order article via Infotrieve]
-
Trivedi N, Mithal A, Sharma AK, Mishra SK, Pandey R,
Trivedi B, Daughaday WH. Non-islet cell tumour induced hypoglycaemia
with acromegaloid facial and acral swelling. Clin Endocrinol
(Oxf). 1995;42:433–435.[Medline]
[Order article via Infotrieve]
-
Wei M, Gibbons LW, Mitchell TL, Kampert JB, Lee CD,
Blair SN. The association between cardiorespiratory fitness and
impaired fasting glucose and type 2 diabetes mellitus in men. Ann
Intern Med. 1999;130:89–96.
[Abstract/Free Full Text]
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