Key result
Smoking significantly reduced the odds of achieving target lipid levels (OR 0.1; 95% CI 0.13-4.87; p=0.03) in patients with arterial hypertension and cardiovascular disease.
Why the study?
Does smoking status affect lipid profiles and the achievement of target lipid levels in patients with arterial hypertension and cardiovascular disease?
Cohort (n=274)
Does smoking status affect lipid profiles and the achievement of target lipid levels in patients with arterial hypertension and cardiovascular disease?
Odds Ratio: 0.1 (95% CI 0.13–4.87)
p-value: p=0.03
In patients with arterial hypertension, current smoking is associated with a more atherogenic lipid profile and a reduced likelihood of achieving target lipid levels.
Smoking was associated with lower odds of lipid target achievement in hypertensive CVD; this Level 3 finding leaves open causality and requires prospective confirmation before practice change.
Introduction: Smoking is a risk factor for cardiovascular diseases. The direct influence of smoking status on the lipid profile was highlighted in patients with arterial hypertension and associated cardiovascular disease. Objective: We aimed to evaluate lipid profile among patients related to smoking status in a registry-based cohort study. Methods: The data of registry of National Research Сenter of Preventive Medicine were conducted. Patients filled in the special questionnaire in order to identify their smoking status, statins therapy. Results: 274 patients were included; main nosologic disease was arterial hypertension (230 patients), 14.8% were smokers, 62.9% non-smokers, and 22.2% past-smokers. The rank analysis of variations by Kruskal-Wallis (H) test for multiple comparisons between groups revealed significant differences in lipid levels for patients according to smoking status: total cholesterol H (2, n=234) =9.119,p=0.0105; LDL-cholesterol H (2, n=225) =6.2615,p=0.0437; triglycerides H (2, n=216) =9.8485,p=0.0073; these indicators of lipid profile among non-smoking patients were lower than among smokers, these indices among past-smokers were lower than among smokers. The absence of statistically significant differences between groups was confirmed in statin therapy (χ2=3.169, df=4,p=0.529). Logistic regression analysis was conducted to identify factors that influence achievement target lipid levels. Only 2 statistically significant signs were identified in this model: smoking (OR 0.1; 95%CI [0.13;4.87];p=0.03) and statin therapy (OR 8.2;95%CI [-3.6; -,078];p=0.002). Conclusion: Significantly higher lipid levels have been observed in smokers compared to non-smokers in patients with arterial hypertension and associated cardiovascular disease. Smoking is a great factor disincentive to achieve target lipid levels.
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Gaisenok et al. (2018) conducted a cohort in Arterial hypertension and cardiovascular diseases (n=274). Smoking vs. Non-smokers and past-smokers was evaluated on Achievement of target lipid levels (OR 0.1, 95% CI 0.13-4.87, p=0.03). Smoking significantly reduced the odds of achieving target lipid levels (OR 0.1; 95% CI 0.13-4.87; p=0.03) in patients with arterial hypertension and cardiovascular disease.
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