Lipoprotein (a) and Apoprotein B in an Apparently Healthy Population of Fighter Pilots and Ground Personnel: Their Significance as Potential Markers of Atherosclerosis
Restricted accessResearch articleFirst published online April, 1999
Lipoprotein (a) and Apoprotein B in an Apparently Healthy Population of Fighter Pilots and Ground Personnel: Their Significance as Potential Markers of Atherosclerosis
Individuals who carry cardiovascular risk factors (CVRF) have a higher incidence of cardiovascular pathology. Among the most commonly screened CVRF are apoprotein A and B and lipoprotein (a), which represent ‘independent’ risk factors for atherosclerosis. In the air force community, cardiovascular pathology has been reported as the primary reason for grounding pilots.
Design
The aim of this study was to evaluate the frequency of CVRF in an apparently healthy population of military fighter pilots (group B, n = 50), and military ground personnel (group A, n = 50) who were matched for age, sex and body mass index but not involved in flight activity, and to evaluate whether any particular pattern of CVRF might be related to flight
Methods
Each subject fasted overnight, and underwent the following measurements: blood pressure and resting ECG recording; and determination of serum levels of total and high-density lipoprotein cholesterol, triglycerides, uric acid and plasma levels of glucose. In addition, serum levels of apolipoprotein A, B and lipoprotein (a) were detected.
Results
An overall risk index for coronary artery disease was calculated using the Framingham equation. This risk index was slightly but not significantly increased in group A compared with group B. By contrast, a significant increase in both apoprotein B (P<0.005) and lipoprotein (a) (P<0.0005) was found in group B compared with group A. No significant differences between groups were detected for the other parameters evaluated.
Conclusions
We suggest the presence in group B of an underlying trend towards the development of atherosclerosis, which may not be identified by a routine approach. Moreover, on a purely theoretical basis with no experimental evidence, the issue of the possible pathophysiological mechanism of these findings and their relationship to flight environment is also addressed.
AndersonKMWilsonPWOdellPMKannelWB. An update coronary risk profile. Circulation1991; 83: 357–363.
2.
BuhlerFR. Cardiovascular risk factors: a unifying sympathetic concept. Schweiz Med Wochenschr1991; 121: 1793–1802.
3.
CastelliWP. A population at risk: prevalence of high cholesterol in hypertensive patients in the Framingham study. JAMA1986; 80 (suppl 2A): 23–32.
4.
KannelWB. Hypertension: relationship with other risk factors. Drugs1986; 31 (suppl): 1–11.
5.
LichtensteinMJShipleyMJRoseG. Systolic and diastolic blood pressure as predictors of coronary artery mortality in the Whitehall study. Br J Med1985; 291: 243–247.
6.
NIH Consensus Development Conference Statement. Lowering blood cholesterol to prevent heart disease. Arteriosclerosis1985; 5: 404–412.
7.
Multiple risk intervention trial, risk factor changes and mortality results. The multiple risk factors intervention trial research group. JAMA1982; 248: 1465–1477.
8.
BrunzellJDSnidermanADAlbersJJKwiterowighPOJrApoprotein B and A-1 and coronary artery disease in man. Arteriosclerosis1984; 4: 79–83.
9.
MaciejkoJJHolmesDRKottkeBAZinsmeisterARDinhDMMaoSJ. Apolipoprotein A-1 as a marker of angiographically assessed coronary artery disease. N Engl J Med1983; 309: 385–389.
10.
BergKDahlenGFrickMH. Lp(a) lipoprotein and pre-beta-1-lipoprotein in patients with coronary heart disease. Clin Genet1974; 6: 230–235.
HoeflerGHarnorncourtFPaschkeEMirtlWPfiefferKHKostnerGM. Lipoprotein Lp(a) as a risk factor for myocardial infarction. Arteriosclerosis1988; 8: 329–401.
13.
SandkampMFunkeHSchulteHKohelerEAssmannG. Lipoprotein Lp(a) is an independent risk factor for myocardial infarction at young ageClin Chem1990; 36: 20–23.
14.
SchriewerHAssmannGSandkampMSchulteH. The relationship of lipoprotein (a) to risk factors of coronary heart disease. Initial results of the prospective epidemiological study on company employees in Westfalia. J Clin Chem Clin Biochem1984; 22: 591–596.
15.
BennetP. Stress management approach to the prevention of coronary artery disease. Br J Clin Psychol1990; 29: 1–12.
16.
GlassJCMcKinneyMEHofshirePJFedorkoS. Cardiovascular reactivity to stress: an examination of familial trends. Int J Psychophysiol1990; 9: 1–11.
17.
LashSHEislerRMSchulmanRS. Cardiovascular reactivity to stress in man. Effects of masculine gender role stress appraisal and masculine performance challenge. Behav Modif1990; 14: 3–20.
18.
NetterstromBKristensenTSDamsgaardMTOlsenOSjolA. Job strain and cardiovascular risk factors: a cross-sectional study of employed Danish men and women. Br J Ind Med1991; 48: 684–689.
19.
RosengrenATibblinGWilhelmsenL. Self-perceived psychological stress and incidence of coronary artery disease in middle aged men. Am J Cardiol1991; 68: 1171–1175.
20.
SchnallPLPieperCSchwartzJEKarasekRASchlusseYDevereuxDBThe relationship between job strain, work place, diastolic blood pressure and left ventricular mass index: results of a case control study. JAMA1990; 263: 1971–1972.
21.
Van LeusdenAJPrendergastPRGrayGW. Permanent grounding and flying restriction in Canadian Force pilots: a 10 years review: Aviat Space Environ Med1991; 62: 513–516.
22.
WhittonRC. Medical disqualification in USAF pilots and navigators. Aviat Space Environ Med1984; 55: 332–336.
23.
McCallNJWickRLJrBrawleyWLBergerBT. A survey of blood lipid levels of airline pilot applicants. Aviat Space Environ Med1993; 63: 533–537.
24.
BurkeTJ. Estimate of requirements for detection and treatment of hypercholesterolemia in US Army aviators. Aviat Space Environ Med1991; 62: 1119–1244.
25.
CoppEKGreenNR. Dietary intake and blood lipid profile survey of fighter pilots at Tyndall air force base. Aviat Space Environ Med1991; 62: 837–841.
26.
HardarsonTThordarsonUAnarsonEOFranzsonL. Biochemical screening for airmen. Avait Space Environ Med1998; 59: 965–967.
27.
LewisB. Risk factors for coronary heart disease in pilots. Eur Heart J1984;5 (suppl A): 17–24.
28.
Reichenbach-KlinkeKKolkSBurchardEC. HDL-cholesterol related to weight, smoking and physical fitness in German Air force pilots. Aviat Space Environ Med1985; 56: 709–713.
29.
ClarkDATolanGDJohnsonRHickmanJRJacksonWGMcGranahamGM. The West Point study: 40 years of follow up. Aviat Space Environ Med1994; 65 (suppl 5): A71–A74.
30.
EkstrandKBostromPAArboreliusMNilssonJALindellSE. Cardiovascular risk factors in commercial flight aircrew officers compared with those in general population. Angiology1996; 47: 1089–1094.
31.
RomhiltDWEstesEHJr. A point score system for the ECG diagnosis of left ventricular hypertrophy. Am Heart J1968; 75: 752–758.
32.
ShapiroSSWilkRA. An analysis of variance test for normality (complete samples). Biometrika1965; 52: 591–611.
33.
DixonWJ (editor). Statistical software manual. Berkeley, CA: University of California Press; 1990.
34.
SaarniHNiemiLPenttiJHartialaJKuuselaA. Cardiac status and cardiovascular risk factors among Finnish sea pilots. Int J Occup Environ Health1996; 9: 53–58.
35.
WaldNJLawMWattHCWuTBaileyAJohnsonAM. Apolipoproteins and ischemic heart disease: implications for screening. Lancet1994; 343: 75–79.
36.
MillsFJMarkV. Human endocrine response to acceleration stress. Aviat Space Environ Med1982; 53: 537–540.
37.
KjeldsenSERostrupMMoanAMundalHHGjesdalKEideIK. The sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension. J Cardiovasc Pharmacol1992; 20 (suppl 8): 32–39.
38.
PaulettoPScannapiecoGPessinaAC. Sympathetic drive and vascular damage in hypertension and atherogenesis. Hypertension1991; 17 (suppl 4);11175–11181.
39.
KaplanJRPetterssonKManuckSBOlssonG. Role of sympathoadrenal medullary activation in the initiation and progression of atherosclerosis. Circulation1991; 84 (suppl 6): 23–32.
40.
PetterssonKKaplanJRManuckSBOlssonG. Experimental sympathetic activation causes endothelial injury in the rabbit thoracic aorta via beta-1 receptor. Circ Res1990; 67: 1027–1034.
41.
FriedmanMH. How hemodynamic forces in the human affect the topography and development of atherosclerosis. In: GlagovSNewmanWPIIISchafferSA (editors): Pathobiology of the human atherosclerotic plaque. New York: Springer-Verlag; 1990, pp. 303–315.
DeweyCF. Effect of fluid flow on living vascular cells. J Biochem Eng1985; 106: 31–35.
44.
LevesqueMJNeremRM. The elongation and orientation of cultured endothelial cells in response to shear stress. J Biomech Eng1985; 107: 341–347.
45.
FrangosJAEskinSGMcIntireLVIvesCL. Flow effects on prostacyclin production by cultured human endothelial cells. Science1985; 227: 1477–1479.
46.
FriedmanMHHutchinsGMBergeronCBDetersOJMarkFF. Correlation between intimal thickness and fluid shear in human arteries. Atherosclerosis1981; 39: 425–436.
47.
HamadaMNishioIKusuyamaYUraMYoshikawaHMasuyamaM. The effect of centrifugal forces on glycosaminoglycans synthesis and cell proliferation of vascular smooth muscle cells in culture. In: YoshidaYYamaguchiTCaroCGGlacovSNeremRM (editors): Role of blood flow in atherogenesis. Proceedings of the international symposium, Hyogo, October 1987. Tokyo: Springer-Verlag; 1988, pp. 217–222.
48.
MerrileesMJMerrileesMABirnbaumPSScottPJFlintMH. The effect of centrifugal force on glycosaminoglycan production by aortic smooth muscle cells in culture. Atherosclerosis1977; 27: 259–264.
