Maria Concepción Guisasola1. 1. Unidad de Medicina y Cirugía Experimental, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Madrid, España. Electronic address: mguisasola@hggm.es.
Abstract
BACKGROUND AND OBJECTIVES: To study whether the cardioprotective effect of regular alcohol consumption can be explained by the heat shock proteins (HSP), given their pathogenic role in atherosclerosis. MATERIAL AND METHODS: Cross-sectional epidemiological study on 452 men and women aged 40-60. Clinical history, epidemiological survey (frequency of average alcohol consumption) and biochemical analysis was performed; Task Force Chart was applied for classification according to the risk of vascular disease. Intracellular HSPA1A, circulating HSPA1A and HSPD1, and anti-Hsp70/anti-Hsp60 antibodies were quantified by ELISA. RESULTS: Two hundred and thirty-eight (52.7%) were abstemious or drank<20 g/d of alcohol; 123 (27.2%) drank 20-40 g/d, 66 (14.6%) 40-60 g/d and 25>60 g/d (5.5%). Two hundred and thirty-nine had no vascular risk (VR) factor or a risk<5%, 161 had moderate VR (10-20%) and 52 had established atherosclerotic disease. Drinkers of 40-60 g/d showed the highest concentrations of intracellular HSPA1A, which were not significant in subjects with moderate VR. Extracellular HSPA1A didn't differ and HSPD1 was undetectable. Drinkers of 40-60 g/d and moderate VR or atherosclerotic disease presented the lowest concentrations of anti-Hsp70. The highest levels of serum anti-Hsp60 were shown in heavy male drinkers of>60 g/d especially in subjects with moderate VR, and female drinkers of 40-60 g/d. CONCLUSIONS: The cardioprotective effect of 40-60 g/d of alcohol consumption could be due in part, to increased intracellular HSPA1A, a potent anti-inflammatory protein. Excessive intake of alcohol increases antibodies anti-Hsp60, stimulating proinflammatory cytokines. This fact may explain the mortality from cardiovascular disease in heavy drinkers. The clinical application of antibody anti-Hsps quantification has been proposed in patients at risk in order to detect atherosclerotic disease.
BACKGROUND AND OBJECTIVES: To study whether the cardioprotective effect of regular alcohol consumption can be explained by the heat shock proteins (HSP), given their pathogenic role in atherosclerosis. MATERIAL AND METHODS: Cross-sectional epidemiological study on 452 men and women aged 40-60. Clinical history, epidemiological survey (frequency of average alcohol consumption) and biochemical analysis was performed; Task Force Chart was applied for classification according to the risk of vascular disease. Intracellular HSPA1A, circulating HSPA1A and HSPD1, and anti-Hsp70/anti-Hsp60 antibodies were quantified by ELISA. RESULTS: Two hundred and thirty-eight (52.7%) were abstemious or drank<20 g/d of alcohol; 123 (27.2%) drank 20-40 g/d, 66 (14.6%) 40-60 g/d and 25>60 g/d (5.5%). Two hundred and thirty-nine had no vascular risk (VR) factor or a risk<5%, 161 had moderate VR (10-20%) and 52 had established atherosclerotic disease. Drinkers of 40-60 g/d showed the highest concentrations of intracellular HSPA1A, which were not significant in subjects with moderate VR. Extracellular HSPA1A didn't differ and HSPD1 was undetectable. Drinkers of 40-60 g/d and moderate VR or atherosclerotic disease presented the lowest concentrations of anti-Hsp70. The highest levels of serum anti-Hsp60 were shown in heavy male drinkers of>60 g/d especially in subjects with moderate VR, and female drinkers of 40-60 g/d. CONCLUSIONS: The cardioprotective effect of 40-60 g/d of alcohol consumption could be due in part, to increased intracellular HSPA1A, a potent anti-inflammatory protein. Excessive intake of alcohol increases antibodies anti-Hsp60, stimulating proinflammatory cytokines. This fact may explain the mortality from cardiovascular disease in heavy drinkers. The clinical application of antibody anti-Hsps quantification has been proposed in patients at risk in order to detect atherosclerotic disease.