Cigarette smoking and serum lipids and lipoproteins

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Notes

C&are& smoking and scram lipids and lipoproteins Data from 54 published studies were analyzed to examine the association between cigarette smoking and serum lipid and lipoprotein concentrations in adults. The data were grouped into non-smokers, all current smokers, and light, moderate and heavy current smokers and were analyzed according to both the overall effects and the dose response effects of cigarette smoke exposure. Overall, smokers had significantly higher serum concentrations OF cholesterol (3.0%). triglycerides (9.1%). very low density lipoprotein cholesterol (VLDL-C) (10.4%). and low density lipoprotein cholesterol (LDL-C) (1.7%) and lower serum concentrations of high density lipoprotein cholesterol (HDL-C) (-5.7%) and apolipoprotein (apo) AI (-4.2%). Among non, light, moderate and heavy smokers, a signiFicant dose response effect was present for cholesterol (0. 1.8, 4.3 and 4.5% respectively), triglycerides (0. 10.7, 1I .5 and 18.0%). VLDL-C (0,7.2,44.4 and 39.0%). LDL-C (Or1.1, 1.4 and ll.O%), HDL-C (0, -4.6, -6.3 and 8.9%). and apo AI (0, -3.7 and -5.7% in non, light and heavy smokers). These dose response effects may provide new evidence for a causal relation between exposure to cigarette smoke and changes in serum lipid and lipoprotein concentrations. Altered lipid and lipoprotein levels have been implicated in increased risk For coronary artery disease (CAD): a 1% increase in serum cholesterol concentration being associated with at least a 2% increase in risk. The 3% increase in serum cholesterol concentrations associated with smoking could account For at least 9% of the average 70% increase in CAD mortality risk reported in cigarette smokers overall. Moreover, the dose response data suggests a gradient of increased risk between light and heavy smokers. WJCratg(l) Foundationfar Blood Research. Scarbomu8h. ME 04074, USA

74 mg/dl. In contrast, the mean LDL-cholesterol level in unaffected Family members wss 122 mg/dl. The mutant form of apo-B, apo-B46, was present in all 3 of the conventional lipoprotein density fractions - VLDL, LDL, and HDL. The importance of this study is that it identified a new mutation in the ape-B gene capable of causing low plasma cholestrol levels, and it emphasized the need to consider the diagnosis of familial hypobetalipoproteinemia in subjects with low plasma cholesterol levels. SG Young(2) CardiovascularResearch Institute. SanFrancisco CA 94140-0608, USA

Myocardial infarction risk and smoking in women Cigarettes that are low in nicotine and carbon monoxide have been promoted as being less hazardous than other brands and, are becoming increasingly popular. In a case-control study carried out in several New England States, the effect of smoking “low yield” cigarettes on the risk of nonfatal myocardial infarction in women under 65 years of age was evaluated. Data were obtained on the smoking habits of 910 women with a first myocardial infarction and 2375 hospital controls. Overall, smokers had an estimated relative risk of 3.7 (95% confidence interval, 3.0-4.7) compared to those who had never smoked, and the risk increased with the number of cigarettes smoked per day. Among smokers, how-. ever, the estimated relative risks of myocardial infarction did not vary according to the nicotine or carbon monoxide yield of the cigarette: For women who smoked brands with the lowest levels of nicotine (c 0.40 mg per cigarette) the estimated relative risk was 4.7. and For smokers of the higher yield brands (> 1.30 mg), it was 4.2 These data suggest that women who smoke low yield cigarettes do not have a lower risk of First nonfatal myocardial infarction than women who smoke higher yield brands. JR Palmer(3) BostonUniversitySchoolof Medicine. BrooklineMA 02146. USA

Apolipoprotein B (B-46) For many years, it has been known that abnormally low levels of apolipoprotein (apo-) B and LDL-cholesterol can be inherited within Families in a simple Mendelian Fashion. This syndrome is called Familial hypobetalipoproteinemia. In the past 2 years, several laboratories have shown that mutations in the ape-B gene which interfere with the translation of a Full-length apo-B molecule caq cause familial hypobetalipoproteinemia. In the present study, we examined a kindred with familial hypobetalipoproteinemia in which the plasma of affected subjects contained a truncated Form of apo-B, apoB46. We showed that apo-B46 was the result of a nonsense mutation in the codon For apo-B amino acid residue 2058. Six Family members were heterozygous for the mutation; their mean LDL-cholesterol level was (I) Er Med J (1989) 298. 784

Dental infections and acute myocardial infarction Although the importance of conventional risk Factors For acute myocardial infarction (AMI) has been shown beyond doubt, they do not explain all clinical and epidemiological Featuresof this disease. Previous experimental, epidemiological and case-control studies have suggested a role for viruses and immunogic reactions in the development of AMI. To investigate the possibility that

chronic bacterial infections plays some role, dental status was assessed in 100 AM1 patients and 102. representative random controls. ‘Dvo indexes were used, one of which was assessed blindly. Dental infections were found to be significantly more common (and more (2) N El181J Med (1989) 320. 1605 (3) N E@

J Med (1989) 320. 1569