The purpose of this statement is to provide specific recommendations in regard to evaluation and intervention in each of the core components of cardiac rehabilitation (CR) to assist CR staff in the design and development of their programmes; the statement should also assist health care providers, insurers, policy makers and consumers in the recognition of the comprehensive nature of such programmes. Those charged with responsibility for secondary prevention of cardiovascular disease, whether at European, at national or at individual centre level, need to consider where and how structured programmes of CR can be delivered to the large constituency of patients now considered eligible for CR.

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SummaryIn the present study we evaluated whether two polymorphisms of β2-adrenergic receptors (β2-AR) gene (R16G and Q27E) could modify the risk of myocardial infarction (MI).Using a case-control design, we analyzed the data from 125 male patients who had experienced a first episode of MI before the age of 45 years and 108 male controls matched for age. The allele frequencies for R16G and Q27E were: G16=0.56 and E27=0.36 in patients with MI and G16=0.61 and E27=0.42 in the control group. There was a trend (not statistically significant) of decreasing MI risk according to E27 or G16 alleles. Combined effect between E27 allele and history of dyslipidemia has been observed. Whereas dyslipidemia conferred a relative risk of MI of 4.8 (P<0.001) compared with normolipidemia in the entire study population, the relative risk increased to 9.0 (P<0.001) in Q27 homozygotes with dyslipidemia, and decreased to 1.8 (P=0.36) in E27 homozygotes.Our results show that the E27 allele of the β2-adrenergic receptor has a significant protective effect on MI in dyslipidemic young male.

Summary Objective: The exposure of tissue factor (TF) to blood flow is the initial step in the coagulation process and plays an important role in thrombogenesis. We investigated the role of genetic polymorphisms and haplotypes of the TF gene in the risk of ischemic vascular disease. Methods: Four hundred and twenty-two Italian patients with juvenile myocardial infarction (MI) and 434 controls, 808 US cases with MI and 1005 controls, 267 Italian cases with juvenile ischemic stroke and 209 controls and 148 German cases with juvenile ischemic stroke and 191 controls were studied. rs1361600, rs3917629 (rs3354 in the US population), rs1324214 and rs3917639 Tag single nucleotide polymorphisms were genotyped. Additionally, a meta-analysis of all previous studies on TF loci and the risk of ischemic coronary disease (ICD) was performed. Results: After multivariable analysis none of the SNPs, major SNP haplotypes or haplotype-pairs showed any consistent association with MI. Pooled meta-analysis of six studies also suggested that TF polymorphisms are not associated with CHD. A significant, independent association between SNP rs1324214 (C/T) and juvenile stroke was found in Italian and German populations (OR for TT homozygotes = 0.47, 95% CI 0.24-0.92, in combined analysis). Pooled analysis also showed a significant association for haplotype H3 (OR = 0.76, 95% CI 0.57-1.00) and haplotype-pair H3-H3 (OR = 0.43, 95% CI 0.20-0.92). Conclusions: TF genetic variations were associated with the risk of ischemic stroke at young age, but did not affect ischemic coronary disease.

Recently, Giannuzzi et al 1 eloquently described the beneficial effect of long-term exercise training on left ventricular remodeling in postinfarction patients. An earlier report from Coats et al 2 demonstrated that training can improve autonomic function (mainly in terms of RR variability and norepinephrine spillover) in patients with chronic heart failure but failed to show significant changes in resting catecholamine levels after a short-term exercise program.In an attempt to explain their findings, Giannuzzi et al used a series of reports describing the reduction of catecholamine levels by exercise training in subjects with normal left ventricular function 3,4 and speculated that this effect exists in patients with left ventricular dysfunction as well. However, this phenomenon is no longer conjectural because it has been demonstrated clearly in postinfarction patients with severe left ventricular dysfunction after long-term exercise rehabilitation. 5 Moreover, that study 5 also showed a beneficial effect of the rehabilitation program on atrial natriuretic peptide. We hope that clarification of these points will provide additional support for the findings of Giannuzzi and his team. ResponseWe greatly appreciate the letter of Drs Tenenbaum and Shemesh, who give us the opportunity to provide additional comments concerning the role of exercise training in the remodeling process among postinfarction patients with left ventricular dysfunction and the long-term effect of physical training on the autonomic balance and neurohormonal activation.After the initial conflicting results, an increasing body of evidence has now demonstrated clearly that patients with poor left ventricular function after an uncomplicated myocardial infarction may benefit from regular exercise training without any additional deterioration of ventricular volumes and function.1,2 More importantly, we 2 recently documented in a large group of postinfarction patients with left ventricular dysfunction that long-term exercise training may attenuate the unfavorable remodeling process and even improve both regional and global function over time. We 3 also reported similar results in preliminary form in patients with chronic heart failure, in whom training actually lessened left ventricular dilatation and dysfunction.Exercise training has been shown to increase functional work capacity and at the same time to reduce catecholamine levels and vascular peripheral resistances and enhance heart rate variability and baroreflex gain, both in subjects with normal ventricular function as well as in patients with left ventricular dysfunction and heart failure. Shemesh et al 4 briefly reported significantly lower levels of resting norepinephrine and atrial natriuretic peptide in postinfarction patients with reduced ejection fraction who were undergoing longterm cardiac rehabilitation. This result and previous observations strongly indicate a lower sympathetic activity after training. The real point of speculation in our article was not the existence of this e...