scholarly journals Role of Arterial Pressure, Wall Stiffness, Pulse Pressure and Waveform in Arterial Wall Stress/Strain and Its Clinical Implications

2021 ◽  
Author(s):  
Thomas K. Day
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Vessel Wall ◽  
Arterial Wall ◽  
Clinical Implications ◽  
Pulse Waveform ◽  
Wall Stiffness ◽  
Wall Compliance ◽  
Formaldehyde Vapour

Biomechanical stress applied to the intima of arteries has long been suspected as a factor in the initiation and localisation of atherosclerotic plaque, and it is implicated in the separation of plaque from the underlying arterial wall giving rise to the acute clinical consequences of thrombosis, dissection and embolism. The factors underlying transmural stress were investigated in-vitro using fresh porcine abdominal aortas on an experimental rig in which pulse pressure, pulse waveform, fluid viscosity, pulse rate, vessel wall compliance and systolic and diastolic blood pressure could be varied at will. Vessel wall compliance was progressively reduced by exposure of the artery to formaldehyde vapour for increased periods of time, a saline-treated artery being used as control. Centripetal transmural stress (CTS) and strain were studied by direct observation of the displacement of a compliant false intima (FI) using real-time B and M mode ultrasound, and by measuring the differential pressure between the space beneath the FI and the adjacent vessel lumen. CTS was found to be directly related to pulse pressure (r = 0.907, p < 0.001) and inversely related to vessel wall compliance. It was independently affected by ranked peak pressure waveform (R = 0.93, p < 0.01) being higher with sharp peak pressure and lower when the waveform was rounded, and it peaked in early diastole in untreated vessels, and both in diastole and peak systole in ones stiffened by formaldehyde vapour. Mean arterial pressure exerted a profound effect via its effect on vessel wall stiffness, which was found to rise 7-fold across the mean arterial pressure range 50-130 mmHg and continued to increase in a logarithmic fashion as the upper physiological range of mean arterial pressure was exceeded. There are two potential clinical implications: in mitigating the postulated biomechanical aspects atherogenesis and atherosclerotic plaque detachment, maintaining large vessel wall compliance is important, and the main factor determining this in a healthy artery is mean arterial pressure; if the arterial wall has already become stiffened as a result of disease, and in the absence of critical stenosis, the findings suggest that the appropriate therapeutic targets are modification of pulse pressure and pulse waveform profile. Simply reducing the diastolic pressure in elderly patients may be unwise if the result is a widened pulse pressure and increased transmural strain. The distribution of atheroma at points of focal mechanical strain in the vessel wall may be explicable if the stress induced by an excessive pulse pressure provokes the inflammatory changes seen in repetitive strain injury. Investigation of inflammatory signalling in the vessel wall provoked by repeated mechanical stress may represent a productive area for future research.

Isolated diastolic hypertension, pulse pressure, and mean arterial pressure as predictors of mortality during a follow-up of up to 32 years

2002 ◽  
Vol 20 (3) ◽  
pp. 399-404 ◽  
Author(s):  
Timo E. Strandberg ◽  
Veikko V. Salomaa ◽  
Hannu T. Vanhanen ◽  
Kaisu Pitkälä ◽  
Tatu A Miettinen
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Predictors Of Mortality ◽  
Diastolic Hypertension

Evaluation of cardiac output variations with the peripheral pulse pressure to mean arterial pressure ratio

2018 ◽  
Vol 33 (4) ◽  
pp. 581-587 ◽  
Author(s):  
Audrey Tantot ◽  
Anais Caillard ◽  
Arthur Le Gall ◽  
Joaquim Mateo ◽  
Sandrine Millasseau ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Pressure Ratio ◽  
Peripheral Pulse

Characterization of acute reversible systemic hypertension in a model of heme protein-induced renal injury

1999 ◽  
Vol 277 (1) ◽  
pp. F58-F65 ◽  
Author(s):  
David H. Warden ◽  
Anthony J. Croatt ◽  
Zvonimir S. Katusic ◽  
Karl A. Nath
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Vessel Wall ◽  
Heme Proteins ◽  
Blood Vessel Wall ◽  
Vasodilatory Response

In the glycerol model of renal injury we describe an acute rise in systemic arterial pressure which is attended by a reduced vasodilatory response to acetylcholine in vivo; vasodilatory responses to verapamil, however, were not impaired. Neither arginine nor sodium nitroprusside diminished this rise in blood pressure; N ω-nitro-l-arginine methyl ester (l-NAME) elevated basal mean arterial pressure and markedly blunted the rise in mean arterial pressure following the administration of glycerol. Aortic rings from the glycerol-treated rat demonstrate an impaired vasodilatory response to acetylcholine, an effect not repaired by arginine; the vasodilatory responses to nitric oxide donors, sodium nitroprusside and SIN-1, were also impaired; 8-bromo-cGMP, at higher doses, evinced a vasodilatory response comparable to that observed in the control rings. This pattern of responses was not a nonspecific effect of aortic injury, since aortic rings treated with mercuric chloride, a potent oxidant, displayed an impaired vasodilatory response to acetylcholine but not to sodium nitroprusside. We conclude that in the glycerol model of heme protein-induced tissue injury, there is an acute elevation in mean arterial pressure attended by impaired endothelium-dependent vasodilatation in vitro and in vivo. We suggest that the acute scavenging of nitric oxide by heme proteins depletes the blood vessel wall of its endogenous vasodilator and permeation of heme proteins into the blood vessel wall may contribute to such sustained effects as observed in vitro.

scholarly journals Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure

2011 ◽  
Vol 43 (10) ◽  
pp. 1005-1011 ◽  
Author(s):  
Louise V Wain ◽  
◽  
Germaine C Verwoert ◽  
Paul F O'Reilly ◽  
Gang Shi ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Association Study ◽  
Pulse Pressure ◽  
Genome Wide Association Study ◽  
Genome Wide Association ◽  
Genome Wide

The influence of different surgical procedures on hypertension after repair of coarctation

2005 ◽  
Vol 15 (5) ◽  
pp. 477-480 ◽  
Author(s):  
Ugo Giordano ◽  
Salvatore Giannico ◽  
Attilio Turchetta ◽  
Fatma Hammad ◽  
Flaminia Calzolari ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Systolic Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Pulse Pressure ◽  
Ambulatory Monitoring ◽  
Peak Exercise ◽  
End To End

We measured resting and exercise haemodynamics, as well as 24-hour ambulatory blood pressure, so as to study the influence on development of hypertension in children after repair of coarctation by either construction of a subclavian flap or end-to-end anastamosis. The patients in both groups were studied a mean time of 13 years after surgery. Thus, we divided 43 children who had undergone surgical repair of coarctation, and who were not on antihypertensive therapy, into a group of 22 patients who had undergone subclavian flap repair, with a mean age of 14 plus or minus 2.6 years, and another group of 21 patients undergoing end-to-end anastomosis, with a mean age of 13.5 plus or minus 3.9 years. We examined blood pressure at rest and during exercise, along with the measurement of cardiac output using impedance cardiography, and during 24-hour ambulatory monitoring. We recorded systolic and diastolic blood pressures, pulse pressure, cardiac output and total peripheral vascular resistance at rest and at peak exercise. During ambulatory monitoring, we measured mean pressures over 24 hours, in daytime and nighttime, 24-hour pulse pressure, and 24-hour mean arterial pressure. Student's t test was used to judge significance, accepting this when p was less than 0.05. The group repaired using the subclavian flap showed significantly disadvantageous differences for diastolic blood pressure at rest, systolic blood pressure at peak exercise and for 24-hour systolic and diastolic blood pressure, 24-hour mean arterial pressure, and daytime and nighttime systolic blood pressure during ambulatory monitoring. Our findings suggest that, after repair using the subclavian flap in comparison to end-to-end anastomosis, patients show a higher incidence of late hypertension, both during exercise and ambulatory monitoring. The data indicate different residual aortic stiffnesses, these being lower after end-to-end anastomosis, which may be due to the greater resection of the abnormal aortic tissue when coarctation is repaired using the latter technique.

Comparative effects of levosimendan, OR-1896, OR-1855, dobutamine, and milrinone on vascular resistance, indexes of cardiac function, and O2 consumption in dogs

2008 ◽  
Vol 294 (1) ◽  
pp. H238-H248 ◽  
Author(s):  
Patricia N. Banfor ◽  
Lee C. Preusser ◽  
Thomas J. Campbell ◽  
Kennan C. Marsh ◽  
James S. Polakowski ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Myocardial Oxygen Consumption ◽  
Plasma Concentrations ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Dose Dependent

Levosimendan enhances cardiac contractility via Ca2+ sensitization and induces vasodilation through the activation of ATP-dependent K+ and large-conductance Ca2+-dependent K+ channels. However, the hemodynamic effects of levosimendan, as well as its metabolites, OR-1896 and OR-1855, relative to plasma concentrations achieved, are not well defined. Thus levosimendan, OR-1896, OR-1855, or vehicle was infused at 0.01, 0.03, 0.1, and 0.3 μmol·kg−1·30 min−1, targeting therapeutic to supratherapeutic concentrations of total levosimendan (62.6 ng/ml). Results were compared with those of the β1-agonist dobutamine and the phosphodiesterase 3 inhibitor milrinone. Peak concentrations of levosimendan, OR-1896, and OR-1855 were 455 ± 21, 126 ± 6, and 136 ± 6 ng/ml, respectively. Levosimendan and OR-1896 produced dose-dependent reductions in mean arterial pressure (−31 ± 2 and −42 ± 3 mmHg, respectively) and systemic resistance without affecting pulse pressure, effects paralleled by increases in heart rate; OR-1855 produced no effect at any dose tested. Dobutamine, but not milrinone, increased mean arterial pressure and pulse pressure (17 ± 2 and 23 ± 2 mmHg, respectively). Regarding potency to elicit reductions in time to peak pressure and time to systolic pressure recovery: OR-1896 > levosimendan > milrinone > dobutamine. Levosimendan and OR-1896 elicited dose-dependent increases in change in pressure over time (118 ± 10 and 133 ± 13%, respectively), concomitant with reductions in left ventricular end-diastolic pressure and ejection time. However, neither levosimendan nor OR-1896 produced increases in myocardial oxygen consumption at inotropic and vasodilatory concentrations, whereas dobutamine increased myocardial oxygen consumption (79% above baseline). Effects of the levosimendan and OR-1896 were limited to the systemic circulation; neither compound produced changes in pulmonary pressure, whereas dobutamine produced profound increases (74 ± 13%). Thus levosimendan and OR-1896 are hemodynamically active in the anesthetized dog at concentrations observed clinically and elicit cardiovascular effects consistent with activation of both K+ channels and Ca2+ sensitization, whereas OR-1855 is inactive on endpoints measured in this study.

scholarly journals Association of High Levels of Spot Urine Protein with High Blood Pressure, Mean Arterial Pressure and Pulse Pressure with the Development of Diabetic Chronic Kidney Dysfunction or Failure among Diabetic Patients. Statistical Regression Modeling to Predict Diabetic Proteinuria

2019 ◽  
Vol 15 (6) ◽  
pp. 486-496 ◽  
Author(s):  
Kamran M. Ahmed Aziz
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Disease ◽  
Pulse Pressure ◽  
Odds Ratio ◽  
Chronic Renal Disease ◽  
Diabetic Patients ◽  
Urine Protein ◽  
Spot Urine

Introduction:In research elevated Blood Pressure (BP) has been demonstrated to be a risk for the development of nephropathy and chronic renal disease (CKD) Or Diabetic Kidney Disease (DKD) among diabetics. However, no study has find correlation for the spot urine protein (UPr) excretion with elevated BP, Pulse Pressure (PP) and mean arterial pressure MAP). This technique was invented in the current study.Methods:10,270 were recruited for more than 12 years. Demographically, 43%, 38%, and 16% showed hypertension, nephropathy and chronic renal disease, respectively. UPr demonstrated significant correlations with systolic BP (SBP) and diastolic BP (DPB), MAP and PP (p < 0.0001 for all). SBP, DBP, PP and MAP, UPr were observed to be higher among the groups with nephroaphty and CKD/DKD with highly significant p-values (all p < 0.05). With logistic regression, odds ratio of hypertension (HTN) with nephropathy was observed to be 2.99 (95% CI 2.44 to 3.7; p < 0.0001); and odds ratio of HTN with CKD/DK was 7.1 (95% CI 4.3 to 11.84; p<0.0001), indicating that HTN significantly contributes to the development of nephropathy and CKD/DKD in diabetics.Results:Invented regression models for the excretion of UPr from the kidney with elevated SBP, DBP, MAP and PP were highly significant (p < 0.0001 for all); UPr = -138.6 + [1.347 × SBP] ; UPr = -93.4 + [1.62 × DBP] ; UPr = -149.5 + [1.922 × MAP] ; UPr = -41.23 +[1.541 × PP].Conclusion:Current study is the first one to introduce this technique. These invented new equations can be used by physicians to estimate protein excretion in urine at bedside and outpatients departments for monitoring proteinuria and CKD/DKD.

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