scholarly journals Internal Flow Choking in Cardiovascular System: A Radical Theory in the Risk Assessment of Asymptomatic Cardiovascular Diseases

2021 ◽  
Author(s):  
Valsalayam Raghavapanicker Sanal Kumar ◽  
Shiv Kumar Choudhary ◽  
Pradeep Kumar Radhakrishnan ◽  
Rajaghatta Sundararam Bharath ◽  
Nichith Chandrasekaran ◽  
...  

The theoretical discovery of Sanal flow choking in the cardiovascular system (CVS) demands for interdisciplinary studies and universal actions to propose modern medications and to discover new drugs to annul the risk of flow-choking leading to shock-wave generation causing asymptomatic-cardiovascular-diseases. In this chapter we show that when blood-pressure-ratio (BPR) reaches the lower-critical-hemorrhage-index (LCHI) the flow-choking could occur in the CVS with and without stent. The flow-choking is uniquely regulated by the biofluid/blood-heat-capacity-ratio (BHCR). The BHCR is well correlated with BPR, blood-viscosity and ejection-fraction. The closed-form analytical models reveal that the relatively high and the low blood-viscosity are cardiovascular-risk factors. In vitro data shows that nitrogen, oxygen, and carbon dioxide gases are predominant in fresh blood samples of the human being/Guinea-pig at a temperature range of 37–40 °C (98.6–104 °F). In silico results demonstrate the occurrence of Sanal flow choking leading to shock wave generation and pressure-overshoot in CVS without any apparent occlusion. We could conclude authoritatively, without any ex vivo or in vivo studies, that the Sanal flow choking in CVS leads to asymptomatic-cardiovascular-diseases. The cardiovascular-risk could be diminished by concurrently lessening the viscosity of biofluid/blood and flow-turbulence by increasing the thermal-tolerance level in terms of BHCR and/or by decreasing the BPR.

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Sanal Kumar V R ◽  

Introduction: Consequence of lopsided blood-thinning-drug, lowering blood-viscosity (BV), is bleeding and very frequently asymptomatic-hemorrhage (AH) and the acute-heart-failure (AHF) happen. V.R.S.Kumar et al. (2020) reported that such asymptomatic episodes are due to the internal flow choking in the cardiovascular system (CVS) at a critical blood pressure ratio (BPR), which is regulated by biofluid/blood heat capacity ratio (BHCR). Methods: The closed-form-analytical-methodology is used for correlating BV, BPR, BHCR, vessel geometry and ejection fraction (EF). In vitro method is used for the BHCR estimation of healthy subjects. In silico method is used for demonstrating the Sanal flow choking. Results: The analytical models reveal that the relatively high and low BV are risk factors of internal flow choking. In vitro study shows that N 2 , O 2 , CO 2 & Ar gases are predominant in fresh-blood samples of the healthy subjects at a temperature range of 37-40 0 C (98.6-104 0 F), which increases the risk of flow-choking. In silico results demonstrated the Sanal flow choking followed by the shock wave generation and pressure-overshoot in a simulated artery with the divergent/bifurcation region. Conclusions: An overdose of blood-thinning drug reduces BV and increases Reynolds number causing high-turbulence leading to the Sanal flow choking. Asymptomatic stroke could be diminished by concurrently lessening the BV and flow turbulence by rising thermal tolerance level in terms of BHCR or by decreasing the BPR. In conclusion, BPR must always be lower than 1.8257 as dictated by the lowest BHCR of the evolved gas (CO 2 ) for prohibiting asymptomatic stroke.


2021 ◽  
Author(s):  
SANALKUMAR V R

Lopsided Blood-thinning Drug Increases the Risk of Internal Flow Choking and Shock Wave Generation Causing Asymptomatic Stroke Author Block: V R SANAL KUMAR, ISRO; S.K.Choudhary, AIIMS; P.K.Radhakrishnan, GU; Suresh Menon, GT; Vrishank Raghav, AU; K.K.N Namboodiri, Sapna E.Sreedharan, SCTIMST; Bharath R.S, Nichith C, C.Oommen, IISc; V.Sankar, IITK; A.Sukumaran, KCT; Arun K, DHMMC; A.Pal, Tharikaa R.K, AU, Abhirami R, AIMS. IntroductionConsequence of lopsided blood-thinning-drug, lowering blood-viscosity (BV), is bleeding and very frequently asymptomatic-hemorrhage (AH) and the acute-heart-failure (AHF) happen. V.R.S.Kumar et al. (2020) reported that such asymptomatic episodes are due to the internal flow choking in the cardiovascular system (CVS) at a critical blood-pressure-ratio (BPR), which is regulated by biofluid/blood heat capacity ratio (BHCR). MethodsThe closed-form-analytical-methodology is used for correlating BV, BPR, BHCR, vessel geometry and ejection fraction (EF). In vitro method is used for the BHCR estimation of healthy subjects. In silico method is used for demonstrating the Sanal flow choking. ResultsThe analytical models reveal that the relatively high and low BV are risk factors of internal flow choking. In vitro study shows that N2, O2, CO2 & Ar gases are predominant in fresh-blood samples of the healthy subjects at a temperature range of 37-400 C (98.6-1040 F), which increases the risk of flow-choking. In silico results demonstrated the Sanal flow choking followed by the shock wave generation and pressure-overshoot in a simulated artery with the divergent/bifurcation region. ConclusionsAn overdose of blood-thinning drug reduces BV and increases Reynolds number causing high-turbulence leading to the Sanal flow choking. Asymptomatic stroke could be diminished by concurrently lessening the BV and flow turbulence by rising thermal tolerance level in terms of BHCR or by decreasing the BPR. In conclusion, BPR must always be lower than 1.8257 as dictated by the lowest BHCR of the evolved gas for prohibiting asymptomatic stroke.


2021 ◽  
Author(s):  
SANAL KUMAR V R ◽  
Shiv Kumar Choudhary ◽  
Pradeep Kumar Radhakrishnan ◽  
Bharath R.S. ◽  
Nichith Chandrasekaran ◽  
...  

Abstract BackgroundThe truly popular consequence of management with the blood-thinning-drug, causation of lower blood-viscosity (BV), is bleeding and very frequently asymptomatic-hemorrhage (AH) and the acute-heart-failure (AHF) happen without any preceding symptoms.ObjectivesOur aim was to develop an infallible closed-form analytical model for demonstrating the proof of the concept of the Sanal flow choking in cardiovascular system (CVS) causing AH and AHF by correlating the blood pressure ratio (BPR), biofluid/blood-heat-capacity-ratio(BHCR), blood viscosity(BV), stenosis (in terms of vessel cross-sectional area (VCA)) and ejection fraction(EF). For establishing the proof of the concept we were planned in vitro and in silico studies. MethodsThe closed-form-analytical-methodology is used herein to establish the proof of the concept of Sanal-flow-choking. In vitro method is invoked for the speciation analyses of blood samples of healthy subjects (human being/Guinea pig) for the BHCR estimation. In silico method is used for demonstrating the asymptomatic pressure-overshoot in an artery due to the Sanal flow choking and shock wave generation. ResultsThe closed-form analytical, in vitro and in silico results are presented herein to establish the proof of the concept of internal flow choking in CVS causing cardiovascular risk without prejudice to the percutaneous coronary intervention (PCI). The analytical models reveal that the relatively high and low BV are risk factors of AH and AHF. In vitro study shows that nitrogen(N2), oxygen(O2), carbon dioxide(CO2) and argon(Ar) gases are predominant in fresh-blood samples of the healthy human-being and Guinea-pig at a temperature range of 37-400 C (98.6-1040 F), which increases the risk of flow-choking leading to AH and AHF. The thermal-tolerance level in terms of BHCR of Guinea-pig is found higher than the human being. In silico results demonstrated the Sanal flow choking and shock wave generation in an artery with the divergent/bifurcation region. ConclusionsAn overdose of blood-thinning drug for reducing the blood-viscosity(BV) augments Reynolds number leading to high-turbulence and enhanced boundary-layer-blockage(BLB), which increases the chances of cavitation and the Sanal-flow-choking leading to the shock wave and pressure-overshoot causing memory effect (stroke history) in viscoelastic vessels. Designing the precise blood-thinning regimen is vital for attaining the desired therapeutic efficacy and negating undesirable flow-choking leading to AH and AHF. Herein we established that the disproportionate blood-thinning treatment increases the risk of the Sanal-flow-choking due to the enhanced BLB factor. The cardiovascular risk could be diminished by concurrently lessening the BV and flow turbulence by rising thermal-tolerance-level in terms of BHCR or by decreasing the BPR. Condensed AbstractHerein, we provide a proof of the concept to establish that such asymptomatic diseases are due to the boundary-layer-blockage (BLB) induced flow choking (Sanal-flow-choking) at a critical blood-pressure-ratio (BPR). When the pressure of the nanoscale-fluid increases, average-mean-free-path decreases and thus, the Knudsen number reduces leading to a no-slip boundary condition with compressible-viscous (CV) flow effect. Sanal-flow-choking is a CV flow effect creating a physical situation of the sonic-fluid-throat, at a critical BPR. We concluded that AH and AHF are transient-events due to flow-choking, and not an illness. The cardiovascular risk could be diminished by concurrently lessening the BV and flow turbulence by rising thermal-tolerance-level in terms of BHCR or by decreasing the BPR.


2021 ◽  
pp. 2000076
Author(s):  
Valsalayam Raghavapanicker Sanal Kumar ◽  
Shiv Kumar Choudhary ◽  
Pradeep Kumar Radhakrishnan ◽  
Rajaghatta Sundararam Bharath ◽  
Nichith Chandrasekaran ◽  
...  

2020 ◽  
Vol 28 ◽  
Author(s):  
Justyna Hajtuch ◽  
Karolina Niska ◽  
Iwona Inkielewicz-Stepniak

Background: Cancer along with cardiovascular diseases are globally defined as leading causes of death. Importantly, some risk factors are common to these diseases. The process of angiogenesis and platelets aggregation are observed in cancer development and progression. In recent years, studies have been conducted on nanodrugs in these diseases that have provided important information on the biological and physicochemical properties of nanoparticles. Their attractive features are that they are made of biocompatible, well-characterized and easily functionalized materials. Unlike conventional drug delivery, sustained and controlled drug release can be obtained by using nanomaterials. Methods: In this article, we review the latest research to provide comprehensive information on nanoparticle-based drugs for the treatment of cancer, cardiovascular disease associated with abnormal haemostasis, and the inhibition of tumorassociated angiogenesis. Results: The results of the analysis of data based on nanoparticles with drugs confirm their improved pharmaceutical and biological properties, which gives promising antiplatelet, anticoagulant and antiangiogenic effects. Moreover, the review included in vitro, in vivo research and presented nanodrugs with chemotherapeutics approved by Food and Drug Administration. Conclusion: By the optimization of nanoparticles size and surface properties, nanotechnology are able to deliver drugs with enhanced bioavailability in treatment of cardiovascular disease, cancer and inhibition of cancer-related angiogenesis. Thus, nanotechnology can improve the therapeutic efficacy of the drug, but there is a need for a better understanding of the nanodrugs interaction in the human body, because this is a key factor in the success of potential nanotherapeutics.


2020 ◽  
Vol 20 (8) ◽  
pp. 1253-1261
Author(s):  
Mourad Akdad ◽  
Mohamed Eddouks

Aims: The present study was performed in order to analyze the antihypertensive activity of Micromeria graeca (L.) Benth. ex Rchb. Background: Micromeria graeca (L.) Benth. ex Rchb is an aromatic and medicinal plant belonging to the Lamiaceae family. This herb is used to treat various pathologies such as cardiovascular disorders. Meanwhile, its pharmacological effects on the cardiovascular system have not been studied. Objective: The present study aimed to evaluate the effect of aqueous extract of aerial parts of Micromeria graeca (AEMG) on the cardiovascular system in normotensive and hypertensive rats. Methods: In this study, the cardiovascular effect of AEMG was evaluated using in vivo and in vitro investigations. In order to assess the acute effect of AEMG on the cardiovascular system, anesthetized L-NAME-hypertensive and normotensive rats received AEMG (100 mg/kg) orally and arterial blood pressure parameters were monitored during six hours. In the sub-chronic study, rats were orally treated for one week, followed by blood pressure assessment during one week of treatment. Blood pressure was measured using a tail-cuff and a computer-assisted monitoring device. In the second experiment, isolated rat aortic ring pre-contracted with Epinephrine (EP) or KCl was used to assess the vasorelaxant effect of AEMG. Results: Oral administration of AEMG (100 mg/kg) provoked a decrease of arterial blood pressure parameters in hypertensive rats. In addition, AEMG induced a vasorelaxant effect in thoracic aortic rings pre-contracted with EP (10 μM) or KCl (80 mM). This effect was attenuated in the presence of propranolol and methylene blue. While in the presence of glibenclamide, L-NAME, nifedipine or Indomethacin, the vasorelaxant effect was not affected. Conclusion: This study showed that Micromeria graeca possesses a potent antihypertensive effect and relaxes the vascular smooth muscle through β-adrenergic and cGMP pathways.


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