Our objective was to examine the association between myocardial infarction (MI) and two DNA-polymorphisms at the proinflammatory chemokine receptors CCR2 (I64V) and CCR5 (32 bp deletion, Δccr5), defining if these polymorphisms influence the age for the onset of MI. A total of 214 patients with an age at the first MI episode< 55 years, 96 patients that suffered the first MI episode when older than 60 years, and 360 population controls were polymerase chain reaction genotyped for the CCR2-V64I and CCR5-Δ32/wt polymorphisms. Patients and controls were male from the same Caucasian population (Asturias, northern Spain). The frequency of the Δccr5 allele was significantly higher in controls compared to patients< 55 years (P= 0.004), or in patients> 60 years compared to patients< 55 years (P= 0.002). Taking the patients> 60 years as the reference group, non-carriers of the Δccr5-allele would have a three-fold higher risk of suffering an episode of MI at< 55 years of age (OR= 3.06; 95% CI= 1.46–6.42). Gene and genotype frequencies for the CCR2 polymorphism did not differ between patients< 55 years and controls or patients> 60 years. Our data suggest that the variation at the CCR5 gene could modulate the age at the onset of MI. Patients carrying the Δccr5-allele would be protected against an early episode of MI. CCR5 and the CCR5-ligands are expressed by cells in the arteriosclerotic plaque. Thus, the protective role of Δccr5 could be a consequence of an attenuated inflammatory response, that would determine a slower progression of the arteriosclerotic lesion among Δccr5-carriers. Our work suggests that the pharmacological blockade of CCR5 could be a valuable therapy in the treatment of MI.