RAAS and adrenergic genes in heart failure: Function, predisposition and survival implications

Table 4 Effect of renin-angiotensin-aldosterone system gene polymorphisms on survival of patients with heart failure

Ref.	Sample, design1	Endpoints	Follow-up (mo)	Mortality rate (%)	SNP	Main findings
Angiotensinogen
[75]	822	AD, HZ	12	24	M235T	No association with endpoints
[78]	2273	AD, HT	48	18	M235T	No association with endpoints
[83]	4513	AD	48	49.7	M235T, T174M	Increased mortality in 174M patients
Angiotensin-converting enzyme
[75]	822	AD, HZ	12	24	I/D	No association with endpoints
[73]	1943	AD, HT	60	42	I/D	Increased risk of death in DD patients
[78]	2273	AD, HT	48	18	I/D	No association with endpoints
[84]	3283	AD, HT	3-38	23	I/D	Decreased survival in D allele patients untreated with beta-blockers. No differences in treated patients
[85]	4793	AD, HT	3-62	28.6	I/D	Decreased survival in D allele patients untreated with β-blockers. No differences in treated patients and decreased impact with high dose ACE inhibitors
[86]	3233	AD, HZ	10 (median)	9.6	I/D	Associated with severity of disease (NYHA class)
Angiotensin-II receptor type 1
[73]	1943	AD, HT	60	42	A1166C	Not associated with end-points. Increased risk of mortality as haplotype (ACE DD)
[75]	822	AD, HZ	12	24	A1166C	No correlation with mortality rate
[78]	2273	AD, HT	48	18	A1166C	No association with endpoints
Aldosterone
[87]	3542	AD, HZ	12	3.4	-344 T/C	Decreased survival in C allele patients. Isosorbide dinitrate and hydralazine improved composite score in TT genotype but had no impact on C allele

¹Study design;

²Placebo controlled randomized trial;

³Non-randomized, single group assignment. SNP: Single nucleotide polymorphism; AD: All cause mortality; CD: Cardiac mortality; HT: Heart transplantation; HZ: Hospitalizations; ACE: Angiotensin-converting enzyme.