The purpose of the study is to prove the effectiveness of pharmacological preconditioning caused by nicorandil in patients with stable coronary heart disease (CHD) during the elective percutaneous coronary intervention (PCI). Materials and methods. We included 88 patients with a stable form of CHD, who were going to pass the elective PCI, in the study. As the method of blind randomization envelope method was used. There were formed two groups or patients: the first group involved 45 patients - were treated with nicorandil (Cordinic, PIQ-FHARMA LLC) (the main group) the other group included 43 patients who were treated by the standard therapy (the comparison group). The basic antianginal therapy was allowed to use in both groups: beta-blockers, calcium antagonists, ATE inhibitors / angiotensin II receptor blockers, statins, acetylsalicylic acid, blockers of P2Y12 receptor platelets. The admission of prolonged form of nitrates before the PCI was allowed in the second group. Patients from the 1st group were to take nicorandil 2 days and 1 day before the PCI at the 30 mg/day dose, then 20 mg orally 2 hours just before PCI, and one more time 6 hours after the PCI - 10 mg nicorandil. Highly sensitive troponin (HS-Tp) as a biomarker of irreversible damage to the myocardium was evaluated before PCI and after PCI in 24 hours. Were used highly sensitive troponin (HF-Tr) and creatine phosphokinase-MB as an irreversible myocardial damage biomarkers. The analysis of which was conducted before PCI and 24 hours after the surgery. Results. The obtained data shows the significant differences of an increase in hs-Tp in 24 hours after PCI in patients with no admission of nicorandil (117 ng/l) as compared with the nicorandil group (73 ng/l), p = 0.04. There were significant differences in the 24 hours increment in hs-Tp in the control group, it was higher (112 ng/l) than in the nicorandil group (67 ng/l), p = 0.03. There was also a significant decrease in CK-MB after 24 hours in the nicorandil group (2.7 ng/L) compared to the control group (2.0 ng/L), p = 0.008. Also the frequency of the troponin increase above the UNL(upper normal level) in the nicorandal group, was significantly (p = 0.03) lower (in 62% of cases compared to 85% of the control group). Conclusion. The prevention of the complications during the percutaneous myocardial revascularization should be considered with the position of the most suitable pharmacological support. The appointment of the oral form of nicorandil (Cordinic, PIQ-FHARMA LLC) for 2 days and 1 day before PCI 30 mg/day, then 20 mg 2 hours before the PCI and 10 mg after 6 hours after the surgery reduces the risk of intraoperative myocardial damage. The obtained data give an opportunity to extend the indications for nicorandil's appointment in the drug support during PCI in patients with stable coronary artery disease.
Vasovagal syncope (VVS) is the most common cause of sudden loss of consciousness. VVS results from cerebral hypoperfusion, due to abnormal autonomic control of blood circulation, leading to arterial hypotension. It is a complex disease, and its development is largely associated with genetic susceptibility. Since abnormal neurohumoral regulation plays an important role in VVS development, we analyzed the association of VVS with polymorphic variants of
ADRA1A
,
ADRB1
,
HTR1A
,
ADORA2A
,
COMT
, and
NOS3
genes, the products of which are involved in neurohumoral signaling, in patients with a confirmed VVS diagnosis (157 subjects) and individuals without a history of syncope (161 subjects). We were able to identify the associations between VVS and alleles/genotypes
ADRA1A
rs1048101,
ADRB1
rs1801253,
ADORA2A
rs5751876, and
COMT
rs4680, as well as
NOS3
rs2070744 in biallelic combination with
COMT
rs4680. Thus, we are the first to observe, within a single study, the role of the genes that encode α- and β-adrenergic receptors, catechol-O-methyltransferase, adenosine receptors and nitric oxide synthase in VVS development. These findings demonstrate that the genes involved in neurohumoral signaling pathways contribute to the formation of a genetic susceptibility to VVS.
This paper presents state of the art of the problem of diagnosis and treatment of orthostatic hypotension (OH). It focuses on the developed algorithms for diagnostics of classical orthostatic hypotension (COH), initial orthostatic hypotension (IOH) and delayed orthostatic hypotension (DOH). It describes the necessary methods for the differential diagnosis of the OH causes. Comparative analysis of the European Society of Cardiology and American College of Cardiology/American Heart Association/Society of Cardiac Rhythm was performed. The treatment options for different groups of patients with orthostatic hypotension are described.
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