Open Access e-Journal Cardiometry No.16 May 2020

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an inefficacy of the conceptual approaches offered bythem thereto. It is not the way to base the treatmentstrategies on taking into account comorbidities, whenselecting the medication lines, since there are no accompanyingdiseases at the first stage of treatment; thetarget organs are not yet affected by the AH disease atthe first stage; the presence of some associated clinicalconditions points to a highly neglected disease case. Inthe meantime, in the scientific debates "hypertensionremains the major preventable cause of cardiovasculardisease (CVD) and all-cause death globally"; so thatsearching for fresh solutions to this problem is perhapsthe most topical challenge for modern medicine [1].AimsThe aims of our studies are systematization and applicationsof hemodynamic patterns in the diagnosticsand treatment of AH.Every medical student knows the following formula:AP = CO . TPVR,where AP is an arterial pressure; CO is cardiac output;TPVR is total peripheral vascular resistance [2].Taking into account the fact that the CO is the productof the stroke volume (SV) by the heart rate (HR),i.e. CO = HR . SV, the AP value is directly dependenton three key factors: HR, SV and TPVR. By influencingthese parameters, the level of AP can be controlled, bothupwards and downwards. The only thing is to identifythe relevant treating factors. This truth is so simple thatit is really surprising why it has not been so far usedas the primary conceptual approach to the treatment ofAH, as well as arterial hypotension. But, unfortunately,there is even no attempt to discuss this conceptual assumptionat all. This is much stranger, since the effectof antihypertensive drugs (AHD) on the systemic hemodynamics(SHD) is a well studied subject; the evidencedata are directly available, including annotationsto drugs (see Table 1 herein).The only justification is that, until recently, the"gold standard” in SHD studies has been the Swan-Ganz pulmonary artery catheterization, which impliesan insertion of a special catheter into one of the mainbranches in the pulmonary trunk. Such procedure isnot safe; 2-3% of cases are complicated by serious disturbancesin the heart rhythm and conduction thathinders the widespread use of the method, even underthe in-hospital conditions [3].At present, the above mentioned drawback hasbeen removed; moreover, appeared are accessible and,Table 1. Effects produced by AHD* on SHDGroup SAP DAP HR TPVR SVBB ↓↓ ↓ ↓ ↑↓ ↓CCB ↓ ↓ ↓↑ ↓ –TD ↓ ↓ – ↓ ↓–ACEi ↓ ↓ – ↓ ↑–ARB ↓↓ ↓ – ↓ ↑–*Legend: BB - beta-blockers; CCB - calcium antagonists;TD - thiazide diuretics, ACEi - ACE inhibitors, ARB - angiotensinreceptor blockers; ↑ - increase, ↓ - decrease, – - no effectavailable.most importantly, non-invasive techniques for investigatingSHD, which reveal vast prospects for their use ingeneral medical practice [4].Materials and methodsThe materials of our studies cover 1447 examineesaged from 18 to 89 (mean age 37.5 years), including832 (57.5%) males and 615 (46.5%) females.Our method of examination is the compression oscillometry:for this purpose, we have used device KAPTsG osm “GLOBUS" (Manufactured by Globus Ltd.,Registration Certificate No. RZN2017/6582 dd. December15, 2017), which allows non-invasively measuring22 SHD parameters, including systolic arterialpressure (SAP), diastolic arterial pressure (DAP), HR,SV and TPVR. Since the values of SV and TPVR dependon the patient's height and weight and do nothave clear standard boundaries, in our calculations weused their integral analogues: SI (stroke index), calculatedas SV/T where T is a human body surface area(m2), and SPVR (specific peripheral vascular resistance)equal to TPVR/T. The standard SI value is 30-45ml/m2, and the standard SPVR parameter is 32 ± 6%arbitrary units. It is assumed that the normal values ofHR, SAP and DAP are as follows: HR 60-80 beats permin., SAP 120-130 mm Hg, DAP 70-80 mm Hg.ResultsResults obtained from our studies are given furtherbelow.In the above examinees we have revealed variouscombinations of HR, SI and SPVR parameters; we havepooled them to form 15 SHD profiles. In this case,noteworthy is the detected dependence of each profileon the corresponding AP level (see Table 2 herein).The following SHD profiles have not been detectedin any examinee: 111, 131, 132, 133, 232, 233, 312,313, 323, 331, 332 and 333. Besides, in patients withincreased SAP and DAP we have never recorded theSHD profiles as listed below: 213, 223, and 322. The36 | Cardiometry | Issue 16. May 2020
Table 2. Dependence of SHD profile on AP levelSHD* profile (HR/SPVR/SI)All AP<120 АP120-130 АP>140 АP>160 АP>170 DAP>90112 10.9 3.9 4.8 17.6 3.6 0 23.2113 3.1 9.1 0 5.2 0 0 4.7121 0.3 0 0 0.7 4.5 2 0.2122 9.4 11.7 9.6 15.3 0 0 2.7123 0.7 0 1.2 1.1 0 0 0211 8.5 0 3.6 11.8 12.5 10.4 18.4212 19.5 14.3 25.3 4.5 32.1 37.6 24.3213 1.3 10.4 0 0 0 0 0.9221 16.4 6.5 19.3 18.1 14.3 8.3 4.8222 14.3 39 22.9 7 0 0 0.9223 0.1 1.2 0 0 0 0 0231 0.4 0 0 0.2 0 0 0311 4.7 0 7.3 7.1 18.7 22.9 13.9321 10.2 1.3 6 11.2 14.3 18.8 6322 0.3 2.6 0 0 0 0 0*Notes: SHD profile is ratio HR / SPVR/ SI, where 1 - increased value of the parameter; 2 - normal value of the parameter; 3 -decreased value of the parameter.Figure 1 Figure 2123 and 211SHD have not been found in the hypotensionpatients. The combination of the normal valuesof HR, SI and SPVR (SHD profile 222) occurred in16.4% of the patients (see Figure 1 herein).It would be logical to expect the prevalence of SHDprofile 222 among the examinees with the normallevels of SAP and DAP. Indeed, in this category of examineesSHD, profile 222 occurs more often (22.9%),though not as often as one would expect. The abovephenomenon may indicate only the following: AH isnot only (and not as much as) an increase in AP. Earlypathological manifestations of the AH disease in theform of impaired cardiac reflex activity and vasculartone imbalance for a long time are compensated bythe redistribution of the hemodynamic constants. APis the main hemodynamic parameter in the organismFigure 3Issue 16. May 2020 | Cardiometry | 37
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Page 3 and 4: Dear Reader!Our life dictates what
Page 5 and 6: Prof. Mohammad AleemCairo Universit
Page 7 and 8: 74808597The study of hemodynamics i
Page 9 and 10: We commemorate great Russian scient
Page 11 and 12: and, in particular, activated is th
Page 13 and 14: decline in the rate of those who fo
Page 15 and 16: Table 1.Mass parameters of some org
Page 17 and 18: REVIEW Submitted: 20.02.2020; Accep
Page 19 and 20: teides. As a rule, under the hypoxi
Page 21 and 22: Table 1Changes in ratios between th
Page 23 and 24: Consequences of anaerobic formation
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Page 31 and 32: 12], we may assume that PC-assisted
Page 33 and 34: Figure 2. Demonstration of the para
Page 35 and 36: of doubts has been expressed by tho
Page 37: ORIGINAL RESEARCH Submitted: 2.04.2
Page 41 and 42: Figure 4Figure 5Figure 6 Figure 7Ta
Page 43 and 44: The mapping between the SHD profile
Page 47 and 48: measurement thereof cannot detect a
Page 49 and 50: AimsThe aim of this study is to ass
Page 51 and 52: vascular system condition, using an
Page 53 and 54: 4. Papers devoted to the AH treatme
Page 55 and 56: 2019;2(12):18-23. https://doi.org/1
Page 57 and 58: ORIGINAL RESEARCH Submitted: 17.01.
Page 59 and 60: The statistical analysis of the obt
Page 61 and 62: Table 7Eigenvalues and percentage o
Page 63 and 64: but also as a means for active mode
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Page 79 and 80: Conflict of interestNone declared.A
Page 83 and 84: the action of high level energy. Ac
Page 85 and 86: Figure 5. Diagram of “a multipuls
Page 87 and 88: REPORT Submitted: 25.02.2020; Accep
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REVIEW Submitted: 5.03.2020; Accept
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ORIGINAL RESEARCH Submitted: 12.01.
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ORIGINAL RESEARCH Submitted: 4.12.2
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Open Access e-Journal Cardiometry No.16 May 2020

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