Smoking and lipoprotein abnormalities on platelet aggregation in coronary heart disease

This study aimed to clarify whether smoking had any influence on platelet aggregability in coronary patients with different lipoprotein abnormalities. We studied 297 non-diabetic patients with coronary heart disease, 40 to 85 years of age, 223 (75%) male, 167 smokers and 130 never smokers. After 3 months on Step-One diet, without any regular medication, patients had fasting plasma total cholesterol levels > or = 6.2 mmol/L; low-density lipoprotein > or = 4.14 mmol/L; and different levels of high-density lipoprotein and triglycerides. Platelet aggregation was analyzed by turbidometric method of Born. Patients were classified in groups of smokers and non-smokers. Results showed that platelet hyperaggregability was more prevalent in smokers with lower levels of high-density lipoprotein (47% vs. 20%; P=0.004 for spontaneous platelet aggregation, 56% vs. 33%; P=0.02 for adenosine diphosphate induced platelet aggregation), and in smokers with hypertrygliceridemia (64% vs. 29%; P=0.004 for spontaneous, 81% vs. 43%; P<0.0001 for adenosine diphosphate induced, and 87% vs. 46%; P<0.0001 for adrenaline induced platelet aggregation). Platelet hypoaggregability was greater in non-smokers with normal high-density lipoprotein and triglycerides plasma levels when compared to non-smokers with the same lipid profile (39% vs. 12%; P=0.004). In conclusion, smoking increased platelet reactivity in hypercholesterolemic patients with low high-density lipoprotein levels or high triglycerides levels.