Acute myocardial infarction in young adults: prognostic role of angiotensin-converting enzyme, angiotensin II type I receptor, apolipoprotein E, endothelial constitutive nitric oxide synthase, and glycoprotein IIIa genetic polymorphisms at medium-term follow-up.
BACKGROUND
A number of reports have investigated the association between various gene polymorphisms and the phenotypic expression of myocardial infarction. No investigations have evaluated the prognostic role of genetic factors in young people with premature coronary disease. The aim of this study was to investigate the influence of genetic factors compared with that of conventional risk factors on follow-up events in a population of Italian young adults with myocardial infarction.


RESULTS
The study population consisted of 106 young patients (mean age 40 +/- 4 years, range 23 to 45 years) with diagnosis of acute myocardial infarction. Clinical and genetic data from the group of patients with events during follow-up were compared with those from patients without events. The following genetic polymorphisms were tested: angiotensin I converting enzyme, angiotensin II type I receptor, apolipoprotein E (ApoE), endothelial constitutive nitric oxide synthase, and platelet glycoprotein IIIa. Coronary angiography was performed in 94 patients. Coronary angiography showed coronary artery disease in 93% of patients. During follow-up (46 +/- 12 months, range 25 to 72) the overall combined end points (cardiac death, myocardial infarction, and revascularization procedures) accounted for 21 events. Family history of coronary artery disease, smoking, stenosis of the left anterior descending artery at coronary angiography, and ApoE polymorphism (presence of epsilon4 allele) were significantly more prevalent (univariate analysis) in the group of patients with events. Logistic multivariate analysis showed that ApoE polymorphism (P =. 004, odds ratio [OR] 6.8, 95% confidence interval [CI] 2 to 22), family history (P =.005, OR 8.3, 95% CI 2 to 35), smoking after acute myocardial infarction (P =.008, OR 10.9, 95% CI 2 to 62), and left anterior descending coronary artery disease (P =.02. OR 6.6, 95% CI 1.3 to 33) were independent predictors of adverse events.


CONCLUSIONS
Myocardial infarction at a young age is commonly characterized by evidence of multiple cardiovascular risk factors and by a favorable prognosis in short- and medium-term follow-up. Evidence of significant disease at coronary angiography suggests the presence of a premature atherosclerotic process. ApoE polymorphism (presence of epsilon4 allele) appears to be a strong independent predictor of adverse events, suggesting a remarkable influence in the accelerated coronary disease.
Brscic
E
E
Dipartimento di Medicina Interna, Università di Torino, Italia.
Bergerone
S
S
Gagnor
A
A
Colajanni
E
E
Matullo
G
G
Scaglione
L
L
Cassader
M
M
Gaschino
G
G
Di Leo
M
M
Brusca
A
A
Pagano
G F
GF
Piazza
A
A
Trevi
G P
GP
D000328:Adult; D015703:Antigens, CD / Q000235:genetics*; D001057:Apolipoproteins E / Q000235:genetics*; D017023:Coronary Angiography; D004247:DNA / Q000032:analysis; D005260:Female; D005500:Follow-Up Studies; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D006801:Humans; D039661:Integrin beta3; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000235:genetics*; D019001:Nitric Oxide Synthase / Q000235:genetics*; D052250:Nitric Oxide Synthase Type III; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010641:Phenotype; D010980:Platelet Membrane Glycoproteins / Q000235:genetics*; D011110:Polymorphism, Genetic; D011379:Prognosis; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000235:genetics*; D012189:Retrospective Studies
D015703:Antigens, CD; D001057:Apolipoproteins E; D005819:Genetic Markers; D039661:Integrin beta3; D010980:Platelet Membrane Glycoproteins; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D004247:DNA; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D007703:Peptidyl-Dipeptidase A