Scherbakova E.S., Zagidullin N.S., Safina Y.F., Zulkarneev R.H., Zagidullin Sh.Z.
Bashkir State Medical University, 3 Lenin Str., 450000, Ufa, Russia
Arterial stiffness and heart rate variability in patients with angina pectoris
Keywords. Stable angina, vascular stiffness, heart rate variability
In most industrialized countries, the incidence of cardiovascular disease is the number one leading cause of death . In particular, increased pulse wave velocity, higher vascular stiffness, and disturbed heart rate variability refer to such factors. A lot of research has been recently devoted to the study of the new markers of cardiovascular risk prediction, such as arterial stiffness . There are several generally accepted and proven arterial stiffness markers. The basic ones are the aortic pulse pressure (PP) and augmentation index (Aix), calculated according to the form of the radial pulse and pulse wave velocity (PWV) that is determined by the shift of the pulse wave in two major arteries. HRV parameters that are determined in a long-term electrocardiography (ECG) are also the markers of adverse cardiovascular events, particularly myocardial infarction, heart failure, etc. . Despite a fairly large number of studies conducted in this area, there is a need for a comprehensive study of new biomarkers in patients with coronary heart disease (CHD) as compared to the control group.
The aim was to examine arterial stiffness, heart rate variability, and pulse wave velocity in patients with stable angina pectoris in prospective open comparative non-randomized study.
Materials and methods. In a randomized controlled study 30 patients with stable angina, and 15 patients in the control group were investigated. Patients with CHD and healthy persons in the control group were examined in the same way. All the patients signed their consent to the following examination: a 10 minute ECG record in supine position for HRV analysis, blood pressure (BP) according to Korotkov, pulse oximetry
(SpO2), pulse wave velocity (PWV) and arteria lstiffness of the vessel wall by applanation tonometry (Sphygmacor,
Patient inclusion and exclusion cri- teria in the group of CHD.
1. CHD, stable angina pectoris (NYHA class II-III);
2. Signed informed consent. Exclusion criteria:
1. Significant arrhythmias (atrial fi- brillation, atrial flutter, frequent pre- mature atrial and ventricular beats, AV block);
2. Implanted electriccardiostimulator;
4. Occlusive atherosclerosis of the lower limbs, radial, carotid and femo- ral arteries;
5. Myocardial infarctionin the past medical history;
6. Severe chronic heart failure;
7. Body mass index >30 kg/m2.
Group results are presented as mean values (M) and standard deviation (m). Reliability was determined by the Student’s t-test for paired variables. The statistically significant result was at p<0.05.
Results. A total of 30 patients with CHD and 15 patients in the control group were investigated (Table. 1). Table 2 shows basic cardiovascular characteristics of the groups. There were no significant changes between the groups in baseline characteristics except for their growth (166.7±1.7 cm vs. 174.7±1.8, p=0.034). In CHD group arterial hypertension was more frequent, namely in 23 patients (76.7%) vs. 4 patients (26.6%) in the control group. In the experimental group 26 patients (86.7%) were diagnosed with stable angina of NYHA II and 4 patients (13.3%) of NYHA III. (Table 1, Table 2).
The analysis of vital parameters has shown that both systolic pressure in the CHD group (137.0±3.3 mm Hg vs. 117.6±3.69 in the control group, p=0.00067) and diastolic pressure (84.66±1.8 mm Hg vs. 75.29±1.7, p=0.00078) were higher, the heart rate being about the same (65.0±2.1 beats/min vs. 66.15±2.6, p=0.67). Moreover, oxygen saturation was also higher in the control group (97.18±0.32% vs. 98.1±0.16, p=0.037). Systolic and diastolic central pressures were significantly higher in the experimental group and corresponded to the peripheral pressure: Sp (p=0.00023), DP (p=0.00044) and Mp (p=0.0041)
respectively. In addition, the following parameters were significantly higher: Pp (50.65±2.8 mm Hgvs. 33.0±2.7, p=0.00032), early systolic peak point P1 (28.6±1.5 mm Hgvs. 23.14±1.3, p=0.018) and end systolic blood pressure (118.3±2.6 mm Hgvs. 101.14±3.75, p=0.00092). However, no significant difference in the pulse wave velocity (PWV) was determined (p=0.18). (Table 3).
The following results were obtained in the HRV analysis. Triangular index (5.78±0.36 vs. 7.35±0.63, p=0.041) and SDANN (9.19±1.4 vs. 15.89±1.98, p=0.0089) were significantly lower in the experimental group than in the control one. A high frequency domain (HF) was greater in the CHD group (73.58±3.6 vs.57.42±7.2, p=0.00071), while a low frequency (LF) – in the control group (73.58±3.6 to 42.58±7.2, p=0.00092). (Table 4).
Discussion. Myocardial ischemia in CHD is manifested not only in the narrowing of the coronary arteries, but it entire endothelium dysfunction, in particular, wide spread arteriosclerosis, increased stiffening of the aorta, decreased elasticity of the vascular wall . Arterial stiffness is an independent cardiovascular risk factor, for example, aortic pulse wave velocity, greater than 10 m/s, is considered to indicate the target organ damage, i.e. the aorta . There are several methods for determining of arterial stiffness, and applanation tonometry is the “gold standard” for this case . As is known, central systolic blood pressure is one of the measures of arterial stiffness, and the parameters such as augmentation index and pulse wave velocity are independent predictors of cardiovascular events (stroke, myocardial infarction, sudden death) [11,12]. On the other hand, cardiovascular risk factors are two or three times higher in patients with an increased arterial stiffness, than in healthy people of the corresponding age . In CHD there is an imbalance of the sympathetic and parasympathetic nervous systems, which results abnormal HRV, namely activation of the sympathetic nervous system  and inhibition of the activity of the parasympathetic one.
In our study, we adopted a comprehensive approach to the study of modern risk factors and examined arterial stiffness, PWV and HRV in CHD patients in comparison with the control group. Since it is known that myocardial infarction significantly impairs HRV andmostly increases vascular stiffness , we excluded the patients who had myocardial infarction in the past. Patients with CHD showed a significant excess of systolic and diastolic blood pressure. It was also consistent with a large proportion of CHD patients with arterial hypertension (76.6% vs. 26.6%, respectively). In addition, the study also showed that arterial stiffness increased central systolic, diastolic and pulse pressure in patients with CHD. Other indicators of stiffness were also higher, both early systolic peak point and systolic blood pressure. At the same time, the patients’ pulse wave velocity in both groups did not differ. This may be explained by the fact that increased conduction velocity presents a greater risk of stroke than of CHD . Overall, such increased vascular wall stiffness points to atherosclerotic lesions of the vascular wall, which can also be proved by the above parameters.
At the same time, by HRV analysis, low-frequency domain (LF) was more pronounced, while a high frequency – significantly reduced, which is slightly different from the literature data . In this case, it can be interpreted as a disbalance of autonomic nervous system heart rateregulation in CHD, the description of which can be also found in some literary sources [3,5]. In the control group the ratio between sympathetic and parasympathetic domains of the autonomic nervous system was more balanced.
Thus, in the study was shown that patients with stable angina in CHD had the increased peripheral and central blood pressure; some other parameters of the arterial stiffness were also higher. In addition, the peripheral oxygen saturation was reduced and there was abnormal balance between sympathetic and parasympathetic nervous systems heart rate control was determined.
The study was supported by the Russian President Grant for Young PhDMD-7395.2016.7 (Naufal Zagidullin) and Russian Humanitarian Scientific Foundation (15-36-01255).
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