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Smoking accelerates albumin excretion in hypertensive patients with metabolic syndrome

Session Lifestyle choices and blood pressure

Speaker Panagiota Pietri

Congress : ESC Congress 2018

  • Topic : hypertension
  • Sub-topic : Hypertension: Lifestyle Modification
  • Session type : Advances in Science
  • FP Number : 1411

Authors : P Pietri (Athens,GR), A Kordalis (Athens,GR), D Tsiachris (Athens,GR), C Vlachopoulos (Athens,GR), G Vyssoulis (Athens,GR), C Stefanadis (Athens,GR)

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Authors:
P. Pietri1 , A. Kordalis1 , D. Tsiachris1 , C. Vlachopoulos2 , G. Vyssoulis2 , C. Stefanadis2 , 1Athens Medical Center, Athens Heart Center - Athens - Greece , 21st Cardiology Department, Athens Medical School, Hippokration Hospital - Athens - Greece ,

Citation:
European Heart Journal ( 2018 ) 39 ( Supplement ), 266

Introduction: Microalbuminuria is a marker of kidney organ damage and has independent prognostic value for future cardiovascular events. Metabolic syndrome (MS) is prognostic of cardiovascular disease, either as a distinct entity or through its clustering cardiometabolic abnormalities. Whether smoking may accelerate microalbuminuria in patients with MS, is not well clarified.

Purpose: The aim of the present study was to investigate the effect of smoking on albumin excretion in hypertensive patients with MS.

Methods: We studied 524 patients with never-treated arterial hypertension and metabolic syndrome defined by the ATP III criteria. Smoking status was assessed by recording the current habit of smoking. Albumin excretion was evaluated in all patients after 24h urine collection, using immunonephelometry and albumin to creatinine ratio (ACR) was calculated. High-sensitivity C-reactive protein (hsCRP) was measured as an inflammatory biomarker. All participants were free from overt cardiovascular disease.

Results: Smokers (n=274) were younger compared to non-smokers (mean age: 51 vs 56 years old, p<0.001), had increased levels of hsCRP (1.9±1.2 vs 1.7±1.1 mg/L, p<0.01) and, marginally, lower mean arterial pressure (MAP) levels, compared to non-smokers (111.3±11.8 vs 113.2±12.8 mmHg, p=0.06). Albumin excretion was significantly higher in smokers compared to non-smokers (mean ACR: 40.4 vs 32.9 mg/g, p=0.04). In linear regression analysis, ACR was independently associated with smoking (b=0.10, p=0.01) after adjustment for age, gender, BMI, plasma glucose, MAP and hsCRP.

Conclusions: Smoking accelerates microalbuminuria in hypertensive patients with MS, independently of other classic or novel risk factors. Given the prognostic significance of microalbuminuria, it might be assumed that smoking may enhance the cardiovascular risk associated with MS through its adverse effect on albumin excretion. Whether quitting smoking may be associated with regression of microalbumiuria, thus with a more favorable cardiovascular risk profile, is a question that warrants further investigation.

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