Open Access e-Journal Cardiometry No.16 May 2020
We should mention that Cardiometry is a fine diagnostics tool to assess heart life expectancy. Our experts, using Cardiocode in “red zones” in intensive care units, have confirmed effectiveness of noninvasive measuring of the hemodynamics data on the cardiovascular system performance in critical patients with different severity degrees. The medical staff involved had a possibility not only to monitor the state in each critical patient, but also to predict and control the progression of a disease. We are going to publish some results of this pilot study in our next issues. We should mention that Cardiometry is a fine diagnostics tool to assess heart life expectancy. Our experts, using Cardiocode in “red zones” in intensive care units, have confirmed effectiveness of noninvasive measuring of the hemodynamics data on the cardiovascular system performance in critical patients with different severity degrees. The medical staff involved had a possibility not only to monitor the state in each critical patient, but also to predict and control the progression of a disease. We are going to publish some results of this pilot study in our next issues.
that provides normal perfusion; its stability guaranteesan adequate blood supply to tissues; all compensatoryhemodynamic responses are aimed at maintaining thenormal AP level. The relatively rare occurrence of thenormal hemodynamic profile is an indication of thecompleted compensatory hemodynamic responses atthe early stages of AH.The obtained data confirm the given concept: thenormal SHD profile is almost absent in the patientswith DAP> 90 mm Hg (0.9%); the profile has not beenobserved in the patients with SAP>152 mm Hg. Allthis clearly indicates that the exhaustion of the compensatorySHD mechanisms appears with grade 1 arterialhypertension.In contrast thereto, in the patients with a decreasedSAP (SAP <120) the normal SHD profile has been recorded2 times more frequently (39%) than in thosewith the normal SAP. In our opinion, the logical explanationof this phenomenon is that a reduction inSAP is one of the earliest compensatory mechanismsof the response to an increase in the CO and TPVRparameters (see Figure 2 herein).Among the examinees aged 18-25 years, a separategroup is formed with healthy individuals according totheir anamneses having the normal AP (n = 144). Inthe above category, only every fifth examinee (19.4%)has shown SHD profile 222 that is consistent with theprevious results and gives us a reason to believe thathemodynamic disorders found prior to developingAH are formed well in advance before the first episodesof the abnormal AP increase [5].The most frequently recorded case among theindividuals with the normal SAP is SHD profile 212(25.3%); less often found is SHD profile 221 (19.3%);every tenth (9.6%) has been reported to have SHDprofile 122. The above distribution indirectly characterizesthe polymorphism of the starting mechanismsin hemodynamic disorders preceding hypertension:in a third of patients (28.9%) the disorders start withincreasing CO (SHD profile 221 and 122), and in everyfifth individual (SHD profile 212) they begin withincreasing TPVR (see Figure 3 herein).A redistribution of the SHD profiles is a mandatoryattribute of AH; at the same time, hemodynamicsmay change either according to the hyperkinetic type,which is characterized by an increase in the performanceof the cardiac pumping activity (SV, HR), or inline with the hypokinetic type (distinguishing featureis the preferential growth of TPVR) or in accordancewith the eukinetic type, when the values of all threeparameters are in the middle of the oscillation range.At the onset of the disease, as a rule, the hyperkinetichemodynamics prevails, while at its later stages the hypokinetictype is dominant [6, 7].The obtained evidence data support the specifiedpattern regularity: in the patients with higher SAP observedis a tendency towards CO decreasing, while theshare of individuals with an increased TPVR is directlyproportional to the level of SAP (see Figure 4 herein).Depending on the ratio between CO and TPVR,the SHD profiles are integrated by us in 3 groups: thehyperkinetic group (122, 221), the eukinetic group(222, 211, 321, 112, 113, 121, 123) and the hypokineticgroup (311, 212). The relationship between the differentSHD forms and SAP is shown in Figures 5, 6 and7 herein.Among the most common hyperkinetic SHD profiles,recorded has been profile 122; among the eukineticprofile types we have detected SHD profile 123;and among the hypokinetic profiles we have identifiedSHD profile 311.ConclusionsThe obtained results show that even in a healthy individualwith the normal AP levels recording of a SHDphysiological profile, which is characterized by thenormal levels of CO and TPVR, is the exception ratherthan the rule. The share of individuals with impairedperformance parameters CO and TPVR aged 18-25years (80.6%) approximately correlates with the prevalenceof AH among the individuals older than 60 years(80.7%). This correlation allows us suggesting that theAH onset should be related not to the age 40-50, as itis generally accepted, but much earlier life spans. It canbe supposed that the hemodynamic disorder of thissort at the age of 25 may predict the onset of arterialhypertension with 60!Latest research shows a close relationship betweenhypertension and the metabolic syndrome. It is believedthat hyperinsulinemia and hyperleptinemiadeveloping against the background of visceral obesity,associated with metabolic syndrome, contribute toan increase in CO and TPVR, thereby triggering thepathophysiological mechanisms of AH [8].Knowing the SHD personal profile, we can selectthe proper AHD, taking into account its targeted effecton each component of the hemodynamics profile (seeTable 3 herein).38 | Cardiometry | Issue 16. May 2020
Figure 4Figure 5Figure 6 Figure 7Table 3. Effects produced by AHD on SHDAHP Registration No. (SRMP) HR TPVR 1 TPVR 2 SVAtenolol ЛП002294-051113 decrease increase decrease decreaseBisoprolol ЛП-004617-251117 decrease increase decrease decreaseBetaxolol ЛП-002502-160614 decrease decrease decrease decreaseNevibilol П N011417/01-100809 decrease decrease decrease decreaseMetoprolol ЛП-001760-020712 decrease increase decrease decreaseAmlodipine ЛС-001987 no change decrease decrease no changeDiltiazem ЛС-001987-261211 decrease decrease decrease no changeNifedipine ЛС-001381-190911 increase decrease decrease increaseNitrendipine ЛП-003289-051115 increase decrease decrease no changeMoxonidine ЛП-003255-151015 no change decrease decrease no changeKaptopril ЛП-002918-170315 no change decrease decrease no changeChinapril П N014329/01-010411 no change decrease decrease no changeLizinopril ЛП-003753-260716 no change decrease decrease no changePerindopril ЛП-003712-290616 no change decrease decrease increaseRamipril ЛП-003235-081015 no change decrease decrease no changeFosinopril ЛП-003603-040516 no change decrease decrease no changeEnalapril ЛП-002572-080814 no change decrease decrease increaseCandesartan ЛП-002525-080714 no change decrease decrease no changeEprosartan П N012018/01-110310 no change decrease decrease no changeIrbesartan ЛП-003987-011216 no change decrease decrease no changeLosartan ЛСР-010617/08-261208 decrease decrease decrease increaseTelmisartan ЛП-004442-010917 no change decrease decrease no changeValsartan ЛП-004219-300317 no change decrease decrease no changeIndapamide ЛП-003095-170715 no change decrease decrease no changeLegend: HR - heart rate; TPVR1 - total peripheral vascular resistance in the first month of starting treatment; TPVR2 - totalperipheral vascular resistance after a month of starting treatment; SI - stroke index.Issue 16. May 2020 | Cardiometry | 39
- Page 1 and 2: 124 | Cardiometry | Issue 16. May 2
- 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
- Page 25 and 26: receptor SUCNR1 [72], which is call
- Page 27 and 28: acid and oxalacetic acid. J. Biol.
- Page 29 and 30: Issue 16. May 2020 | Cardiometry |
- 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 and 38: ORIGINAL RESEARCH Submitted: 2.04.2
- Page 39: Table 2. Dependence of SHD profile
- Page 43 and 44: The mapping between the SHD profile
- Page 45 and 46: Issue 16. May 2020 | Cardiometry |
- 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
- Page 65 and 66: values [6]. Both groups are homogen
- Page 67 and 68: Table 2No. of ind.BMIAge, yearsHb,
- Page 69 and 70: ORIGINAL RESEARCH Submitted: 18.03.
- Page 71 and 72: а) b)Figure 1. Fragments of the bl
- Page 73 and 74: а)b)cd)Figure 3. Fragments of seru
- Page 75 and 76: zation of the facias and add to the
- Page 77 and 78: PV5 - blood volume (part of SV), pu
- Page 79 and 80: Conflict of interestNone declared.A
- Page 81 and 82: Issue 16. May 2020 | Cardiometry |
- 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
- Page 89 and 90: used to suppress this sort of noise
Figure 4
Figure 5
Figure 6 Figure 7
Table 3. Effects produced by AHD on SHD
AHP Registration No. (SRMP) HR TPVR 1 TPVR 2 SV
Atenolol ЛП002294-051113 decrease increase decrease decrease
Bisoprolol ЛП-004617-251117 decrease increase decrease decrease
Betaxolol ЛП-002502-160614 decrease decrease decrease decrease
Nevibilol П N011417/01-100809 decrease decrease decrease decrease
Metoprolol ЛП-001760-020712 decrease increase decrease decrease
Amlodipine ЛС-001987 no change decrease decrease no change
Diltiazem ЛС-001987-261211 decrease decrease decrease no change
Nifedipine ЛС-001381-190911 increase decrease decrease increase
Nitrendipine ЛП-003289-051115 increase decrease decrease no change
Moxonidine ЛП-003255-151015 no change decrease decrease no change
Kaptopril ЛП-002918-170315 no change decrease decrease no change
Chinapril П N014329/01-010411 no change decrease decrease no change
Lizinopril ЛП-003753-260716 no change decrease decrease no change
Perindopril ЛП-003712-290616 no change decrease decrease increase
Ramipril ЛП-003235-081015 no change decrease decrease no change
Fosinopril ЛП-003603-040516 no change decrease decrease no change
Enalapril ЛП-002572-080814 no change decrease decrease increase
Candesartan ЛП-002525-080714 no change decrease decrease no change
Eprosartan П N012018/01-110310 no change decrease decrease no change
Irbesartan ЛП-003987-011216 no change decrease decrease no change
Losartan ЛСР-010617/08-261208 decrease decrease decrease increase
Telmisartan ЛП-004442-010917 no change decrease decrease no change
Valsartan ЛП-004219-300317 no change decrease decrease no change
Indapamide ЛП-003095-170715 no change decrease decrease no change
Legend: HR - heart rate; TPVR1 - total peripheral vascular resistance in the first month of starting treatment; TPVR2 - total
peripheral vascular resistance after a month of starting treatment; SI - stroke index.
Issue 16. May 2020 | Cardiometry | 39
Change language