Nitric oxide synthase gene G298 allele. Is it a marker for microvascular angina in hypertensive patients?
BACKGROUND
Nitric oxide (NO) has an important effect on blood pressure, arterial wall, and the basal release of endothelial NO in hypertension (HPN) may be reduced. Until now, there is no solid data revealing the potential role of the polymorphism of the nitric oxide synthase gene (NOS) in patients with HPN and microvascular angina.


OBJECTIVE
The aim of the present study is to investigate the gene of endothelial nitric oxide synthase (eNOS), as the polymorphism of this gene may be a putative candidate for HPN and initiate the process of atherosclerosis.


METHODS
Sixty participants were recruited for this study; 50 were hypertensive patients complaining of chest pain [30 of them have electrocardiogram (EKG) changes of ischemia], 20 had isolated HPN, and 10 healthy volunteers served as control. All patients underwent stress myocardial perfusion imaging (MPI) and coronary angiography. Genotyping of eNOS for all patients and controls was performed. The linkages between HPN, microvascular angina and eNOS gene polymorphism were investigated.


RESULTS
MPI and coronary angiography revealed that 15 patients had chest pain with true ischemia and reversible myocardial perfusion defects (multiple and mild) but normal epicardial coronary arteries (microvascular angina), while 15 patients had significant coronary artery disease (CAD), and 20 hypertensive patients showed normal perfusion scan and coronary angiography. The prevalence of the NOS G(298) allele was higher in the hypertensive group with microvascular angina (documented by MPI) than it was among the control participants (P<.005). The eNOS allele was significantly higher in the hypertensive group than in the control participants, but there was no significant difference in homozygote mutants among hypertensive participants, x-syndrome and patients with CAD.


CONCLUSIONS
eNOS gene polymorphism is proved to be an important etiology in microvascular angina (x-syndrome) among hypertensive patients. In addition, the eNOS mutant gene showed a significant increase in isolated HPN and in patients with CAD.
Nagib El-Kilany
Galal E
GE
Cardiology Department, Tanta University Hospital, Egypt. galal_elkilany@yahoo.com
Nayel
Ehab
E
Hazzaa
Sahar
S
D000483:Alleles; D016022:Case-Control Studies; D017023:Coronary Angiography; D004252:DNA Mutational Analysis; D004562:Electrocardiography; D005080:Exercise Test; D005819:Genetic Markers; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000201:enzymology / Q000235:genetics*; D017566:Microvascular Angina / Q000000981:diagnostic imaging / Q000201:enzymology / Q000235:genetics*; D019001:Nitric Oxide Synthase / Q000235:genetics*; D012307:Risk Factors; D015899:Tomography, Emission-Computed, Single-Photon
D005819:Genetic Markers; D019001:Nitric Oxide Synthase