August 13, 2019 523 Yogesh N.V. Reddy, MD, MSc Joseph P. Murgo, MD Rick A. Nishimura, MD There has been a gradual transition in the epidemiology of mitral stenosis (MS) in the Western world, with rheumatic disease in rapid decline and an increasing recognition of degenerative mitral annular calcification (MAC)– related MS in the elderly. In both diseases, the patient will present with dyspnea and an elevated transmitral gradient, but the anatomy and pathophysiology differ substantially. With the emerging advent of catheter-based therapies for the mitral valve,1 it is clinically important to understand these differences.

Objectives This study examines the intrapatient variability in peak instantaneous left ventricular outflow tract (LVOT) gradients and aortic pulse pressures during rest, exercise, and after ventricular ectopy. Background Although the variability in LVOT gradients in patients with hypertrophic cardiomyopathy (HCM) is well known, the predictors of such variation are not. We hypothesized that quantitative invasive analysis of gradient variation could identify useful predictors of maximal gradients. Methods Variability in continuously recorded, high-fidelity left ventricular and aortic pressure waveforms were evaluated by computer-assisted analysis in the resting state (N = 659 beats) and during supine exercise (N = 379 beats) in a symptomatic patient with a resting LVOT gradient >30 mmHg and frequent ventricular ectopy. Results At rest, the peak left ventricular and aortic pressures at the time of the peak instantaneous LVOT gradient for all sinus and postectopic beats followed consistent regression slopes characterizing the potential energy loss between the LV cavity and aorta. During exercise, similar regression slopes were identified, and these converged with the resting slopes at the point of the maximal measured LVOT gradient. Component analysis of the LVOT gradient suggests that resting beat-to-beat variability provides information similar to post-ectopic pressures for predicting maximal gradients in obstructive-variant HCM. Conclusions Our study suggests that computer-assisted analysis of hemodynamic variability in HCM may prove useful in characterizing the severity of obstruction. Further study is warranted to confirm the reproducibility and utility of this finding in a population with clinically significant exercise-induced gradients.

Introduction: Although the variability in left ventricular outflow tract (LVOT) gradients in patients with hypertrophic cardiomyopathy (HCM) is well known, the value of pulse pressure (PP) changes with ectopy for predicting changes in LVOT gradient remains unreported. Hypothesis: This study examines the intrapatient variability in peak instantaneous LVOT gradients and aortic pulse pressure (PP) associated with the Brockenbrough-Braunwald-Morrow sign (BBM sign) compared with beat-to-beat variability. Methods: Variability in continuously recorded, high-fidelity left ventricular and aortic pressure waveforms were evaluated by computer-aided analysis in the resting state (N = 659 beats) and during supine exercise (N = 379 beats) in a symptomatic patient with a resting LVOT gradient >30 mmHg. Results: BBM sign was observed in 92.9% (26/28) of post-PVC beats at rest and the post PVC PP decreased 11.8±8.2% (P<0.001) compared with a 148.3±49.5% (P<0.001) increase in the LVOT gradient. During exercise, BBM sign was noted in 84.2% (32/38) of post-PVCs beats and PP decreased 4.0±6.3% (P<0.001) compared with a 74.2±37.5% (P<0.001) increase in LVOT gradient. PP decreases were also noted in 89.5% (17/19) beats during sinus arrhythmia following prolonged RR intervals. Changes in pulse pressure with ectopy poorly predicted quantitative changes in the LVOT gradient (R 2 ≤ 0.198). However, component analysis of the LVOT gradient suggests that beat-to-beat variability provides information similar to ectopic provocation in characterizing gradients in HCM and that rest and exercise changes converge to a common reference value. Conclusions: Although caution is suggested when interpreting pulse pressure changes with the BBM sign as surrogate for measuring LVOT gradients, this study suggests that analysis of hemodynamic variability in HCM may prove useful in characterizing the severity of obstruction.

Objective This study describes results of iCPET from the past, which used submaximal stress and multisensor high‐fidelity catheters to exclude heart disease in a unique population of young adults. Background There has been resurgence in comprehensive hemodynamic evaluation of complex cardiovascular patients. Although dynamic assessments during cardiac catheterization have become commonplace, there remains limited information regarding left and right heart hemodynamic changes during supine exercise in young adults. Methods The study population was derived from a retrospective review of catheterization records at Brooke Army Medical Center for active duty patients (ages: 19–40 years) in whom hemodynamic waveforms were obtained with multisensor high‐fidelity catheters and supine exercise testing (53.1 ± 12.6 watts) and angiography performed to exclude heart disease. We report findings from 41 males and 1 female (ages: 19–40 years) found free of heart disease. Results Submaximal exercise was associated with ≈ fourfold ( P < 0.001) increase in minute ventilation (VE), O 2 consumption (VO 2 ) and carbon dioxide production (VCO 2 ). VE/VCO 2 ratio decreased (−16.8 ± 13.9%, P < 0.001) and VE/VCO 2 slope was 22.6 ± 0.6 (±SE). Cardiac index (CI) increased with VO 2 (ΔCI/ΔVO 2 slope = 7.6 ± 2.2). Heart rate increased nearly 10 bpm per 100 mL O 2 /min/M 2 , whereas, changes in stroke volume were more variable. Pulmonary artery (PA) saturations fell from 77 to 55% ( P < 0.001). No change was noted in mean right atrial pressures; PA pressures increased ≈10 mm Hg ( P < 0.001). Pulmonary capillary wedge and left ventricular end‐diastolic pressures increased ≈2 mm Hg ( P < 0.001) but variability noted between individuals. Conclusion This study provides insight into past practices of invasive cardiopulmonary testing and furthers the understanding of metabolic and hemodynamic changes in a young population during supine submaximal exercise. © 2017 Wiley Periodicals, Inc.

: Clinical concerns raising suspicion for cardiovascular disease in active duty military require definitive evaluations to diagnose disease at an early stage given high risk occupation. There remains limited information for assessing left and right heart hemodynamic response during supine exercise in young adults in high risk occupations.

Thecirculatory effects associated withlifelong plasma atrial natriuretic factor (ANF)elevation wereexam- inedbygenerating transgenic mice, whichconstitutively ex- press afusion geneconsisting ofthetransthyretin promoter andtheANF structural gene.Thesemicehavechronically elevated ANF levels ascompared withtheir nontransgenic siblings. Transgenic animals exhibited immunoreactive ANF levels that werenearly fivefold higher thanthose measured in nontransgenic littermates. Systemic andregional hemodynam- icsandblood volumes wereexplored byusing modifications of thereference microsphere anddilution techniques. Mean arterial pressure wasreduced by24mm Hg,associated witha 27%reduction intotal heart weight. Thischronic reduction in blood pressure wasduetoa21%reduction intotal peripheral A trial natriuretic factor (ANF) isperhaps thebest- A knownpeptide inafamily ofcompounds inti- ..Lk mately involved inpressure andvolume homeo- stasis.'-3 Although bolus injection oracuteinfusion of ANF isgenerally linked withhypotensive and/or natri- uretic responses,4,5 thechronic effects ofANF arenot clearly understood. Harrison-Bernard eta16andParkes eta17haveshownthatchronic infusion ofANF to normotensive animals inthepathophysiological range is associated withareduction inmeanarterial pressure (MAP),mediated initially byafall incardiac output (CO). Thisresponse isfollowed byadiminished total peripheral resistance (TPR), while CO returns tonor- mal.However, this isnotauniversal finding.8 Further- more,these "chronic" studies normally involve only a fewdaysofANF infusion because oftechnical and economic limitations. Hemodynamic variables maynot reach steady-state values during these infusion periods; someeffects ofANF mayrequire muchlonger to develop. To overcome theseobstacles, a transgenic mouse modelwithchronically elevated ANF levels wasgener- ated.9 Inthismodel, constitutive expression ofthe murine ANFgenewastargeted tohepatocytes withthe transthyretin (TTR)promoter. Thetransgenic mice haveelevated ANF levels andreductions inMAP compared withthenontransgenic siblings. These changes occurwithout modifications inbasalurine output orsodium excretion, suggesting aleftward shift

In the recent review of hypertrophic cardiomyopathy (HCM) by Maron et al. ([1][1]), historical controversies relating to the relationship between left ventricular outflow tract (LVOT) pressure gradients and left ventricular (LV) ejection dynamics are revisited. The crux of these controversies is an

HomeHypertensionVol. 53, No. 1Response to Aortic Pulse Wave Velocity, Reflection Site Distance, and Augmentation Index Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBResponse to Aortic Pulse Wave Velocity, Reflection Site Distance, and Augmentation Index Nico Westerhof Jeroen P. van den Wijngaard Joseph P. Murgo Berend E. Westerhof Nico WesterhofNico Westerhof Laboratory for Physiology, Department of Pulmonary Diseases, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands Search for more papers by this author Jeroen P. van den WijngaardJeroen P. van den Wijngaard Department of Medical Physics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands Search for more papers by this author Joseph P. MurgoJoseph P. Murgo Cardiology Division, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Tex Search for more papers by this author Berend E. WesterhofBerend E. Westerhof BMEYE B.V., Amsterdam, The Netherlands Search for more papers by this author Originally published24 Nov 2008https://doi.org/10.1161/HYPERTENSIONAHA.108.125005Hypertension. 2009;53:e10Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: November 24, 2008: Previous Version 1 We thank Nichols and O'Rourke1 for their remarks about our recent article showing that the effective reflection site is elusive.2 The main point of our article is that wave speed calculations from ascending aortic pressure and flow are inaccurate, because it is implicitly assumed the arterial tree can be modeled with a single uniform tube with real reflection (a resistor) at its distal end.McDonald and Taylor3 indeed studied reflections, but they never discussed the implications regarding aortic wave speed calculations from the ascending aorta pressure and flow. Taylor4 discussed reflections by describing the arterial system in the frequency domain, whereas we purposely avoided going into this type of analysis. Taylor showed that the use of a single, uniform tube with reflection at its end is a very poor model of the systemic arterial tree. We agree, but perhaps did not emphasize this sufficiently. One of Taylor’s arguments is that, for high frequencies, the input impedance and apparent wave velocity reach a constant, frequency-independent, value, characteristic impedance, and phase velocity, respectively, suggesting a reflectionless system. In other words, this implies that reflection depends on frequency.We agree with Nichols and O'Rourke1 that reflections occur at junctions, most of them located in the arterioles, and these reflections may possibly lead to an effective reflection site. However, at this site each harmonic of pressure (and flow) encounters a reflection coefficient with a different magnitude and phase shift. We do not agree with Nichols and O'Rourke1 that the phase shift of reflections at branch points can be considered insignificant, because Womersley5 showed otherwise (phase shift considerable and dependent on Womersley’s α). Another way to see that an arterial tree cannot be modeled with a uniform tube loaded with a resistor is that the load on the distal abdominal aorta, ie, the impedance of the iliac arteries, is not a simple resistance.It is not clear to us what Nichols and O'Rourke1 mean with disputing the theory applied. We see no basic difference between Taylor’s frequency domain and our time domain theory.We did on purpose not discuss errors in the Δt by estimating the foot of the forward and backward waves in the determination of pulse wave velocity. We also do not want to discuss errors in estimating Δt from the shoulder of the pressure wave,6 because we consider them technical rather than basic aspects. Nichols and O'Rourke1 remark that changes in Δt and pulse wave velocity cause effective length to increase, in agreement with our data and those of others. We did not suggest a relation between an increase in effective length with a decrease in augmentation index.There is no second tennis player in our model, and we do not take into account frictional (balloon air) losses. We just stated that when you do not know how the ball is reflected you cannot calculate the distance of the reflection site.We are happy to read that Nichols and O'Rourke1 agree that the location of the reflection site is elusive, but we do not see that our reasoning could be incorrect, because it is not different from that of Taylor.We want to emphasize that the calculation of forward and backward pressure is correct, and that the magnitude and time difference, Δt, are valuable parameters. Augmentation index is less accurate but also valuable.7 These quantities do not depend on a model choice. Our point is that investigators calculate pulse wave velocity from Δt by assuming the uniform tube loaded with a resistor, and this model is incorrect.Sources of FundingJ.P.v.d.W. was supported in part by The Netherlands Heart Foundation (grant 2006B226) and by a scholarship from the Niels Stensen Foundation.DisclosuresB.E.W. owns shares of the BMEYE Company. There is no conflict of interest. The remaining authors report no conflicts.1 Nichols WW, O'Rourke MF. Aortic pulse wave velocity, reflection site distance, and augmentation index. Hypertension. 2009; 53: e9.LinkGoogle Scholar2 Westerhof BE, van den Wijngaard JP, Murgo JP, Westerhof N. Location of a reflection site is elusive: consequences for the calculation of aortic pulse wave velocity. Hypertension. 2008; 52: 478–483.LinkGoogle Scholar3 McDonold DA, Taylor MG. The hydrodynamics of the arterial circulation. Progress in Biophysics and Biophysical Chemistry. 1959; 9: 107–173.Google Scholar4 Taylor MG. Wave transmission through an assembly of randomly branching elastic tubes. Biophys J. 1966; 6: 697–716.CrossrefMedlineGoogle Scholar5 Womersley JR. Technical Report Wade-TR 56–614. The Mathematical Analysis of the Arterial Circulation in a State of Oscillatory Motion. Dayton, OH: Wright Air Development Center; 1957.Google Scholar6 Segers P, Rietzschel ER, De Buyzere ML, De BD, Van Bortel LM, De BG, Gillebert TC, Verdonck PR. Assessment of pressure wave reflection: getting the timing right! Physiol Meas. 2007; 28: 1045–1056.CrossrefMedlineGoogle Scholar7 Westerhof BE, Guelen I, Westerhof N, Karemaker JM, Avolio A. Quantification of wave reflection in the human aorta from pressure alone: a proof of principle. Hypertension. 2006; 48: 595–601.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails January 2009Vol 53, Issue 1 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.108.125005 Originally publishedNovember 24, 2008 PDF download Advertisement SubjectsHypertension

HomeHypertensionVol. 53, No. 1Response to Uncertainties in Estimating the Site of Arterial Wave Reflection Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBResponse to Uncertainties in Estimating the Site of Arterial Wave Reflection Berend E. Westerhof Jeroen P. van den Wijngaard Joseph P. Murgo Nico Westerhof Berend E. WesterhofBerend E. Westerhof BMEYE BV, Amsterdam, The Netherlands Jeroen P. van den WijngaardJeroen P. van den Wijngaard Department of Medical Physics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands Joseph P. MurgoJoseph P. Murgo Cardiology Division–Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Tex Nico WesterhofNico Westerhof Laboratory for Physiology and, Department of Pulmonary Diseases, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands Originally published17 Nov 2008https://doi.org/10.1161/HYPERTENSIONAHA.108.123695Hypertension. 2009;53:e8Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: November 17, 2008: Previous Version 1 We thank Schillaci et al1 for their interest in our work.2 We appreciate the opportunity to answer the questions that they put forward. The first question concerns the change in return time of the reflected pressure wave at the proximal end of a uniform tube when the load at its distal end changes. First, we occluded the tube (loaded it with an infinite impedance), giving a real refection coefficient of 1: no phase shift occurred, and the time of return was determined by twice the travel time. Next, we loaded the tube with the 3-element Windkessel and set its characteristic impedance equal to that of the tube. The Windkessel is a lumped model, wave travel does not exist, and the reflection site remains at the same position. However, in this case, there was a phase shift of reflected waves (complex reflection coefficient), and this gave the delay in the backward wave seen in our Figure 2B.2 In the anatomically correct model, the reflected wave increases with distal aortic occlusion but arrives back in the ascending aorta at approximately the same time, whether the distal aorta is occluded or not. In the anatomically correct model, the aorta is not a single uniform tube, and many reflections sites exist (as in the real systemic tree). The low harmonics of pressure, ie, those that are reflected, happen to exhibit the same phase shift after occlusion, suggesting a reflection site at the bifurcation but not proof of it. Latham et al3 experienced great difficulty in attempting to determine the reflection site and suggested 2 major sites of reflection. From the perspective of the heart, the exact site of pressure reflection is not important; it is the timing and magnitude of the reflected wave arriving in the ascending aorta that determine the widening of the pulse pressure. Indeed, a doubling of aortic pulse wave velocity does not result in a decrease of the return time by a factor of 2, showing that the distance of the reflection site is not constant. In effect, each harmonic of pressure is reflected with a different phase.Segers et al4 determined several measures of time of return of the reflected wave, such as inflection point and shoulder of the carotid pressure. Although the decrease of inflection-based return time wave was inversely related to an increase of pulse wave velocity, these authors also report that this return time did not correspond with the timing obtained from wave separation analysis, which they consider the reference method. In a group with a wider age range studied by McEniery et al,5 the change in pulse wave velocity was much larger than the change in inflection time. From these data we calculated an increase in effective length with age, as did Mitchell et al,6 whereas Segers et al4 observed a decrease in effective length. Thus, in any case, all of these studies show that effective length is not constant.Sources of FundingJ.P.v.d.W. was supported in part by The Netherlands Heart Foundation (grant 2006B226) and by a scholarship from the Niels Stensen Foundation.DisclosuresB.E.W. owns shares of the BMEYE Company. There is no conflict of interest. The remaining authors report no conflicts.1 Schillaci G, Pucci G, Cziráki A. Uncertainties in estimating the site of arterial wave reflection. Hypertension. 2009; 53: e7.LinkGoogle Scholar2 Westerhof BE, van den Wijngaard JP, Murgo JP, Westerhof N. Location of a reflection site is elusive: consequences for the calculation of aortic pulse wave velocity. Hypertension. 2008; 52: 478–483.LinkGoogle Scholar3 Latham RD, Westerhof N, Sipkema P, Rubal BJ, Reuderink P, Murgo JP. Regional wave travel and reflections along the human aorta: a study with six simultaneous micromanometric pressures. Circulation. 1985; 72: 1257–1269.CrossrefMedlineGoogle Scholar4 Segers P, Rietzschel ER, De Buyzere ML, De BD, Van Bortel LM, De BG, Gillebert TC, Verdonck PR. Assessment of pressure wave reflection: getting the timing right! Physiol Meas. 2007; 28: 1045–1056.CrossrefMedlineGoogle Scholar5 McEniery CM, Yasmin, Hall IR, Qasem A, Wilkinson IB, Cockcroft JR. Normal vascular aging: differential effects on wave reflection and aortic pulse wave velocity: the Anglo-Cardiff Collaborative Trial (ACCT). J Am Coll Cardiol. 2005; 46: 1753–1760.CrossrefMedlineGoogle Scholar6 Mitchell GF, Parise H, Benjamin EJ, Larson MG, Keyes MJ, Vita JA, Vasan RS, Levy D. Changes in arterial stiffness and wave reflection with advancing age in healthy men and women: the Framingham Heart Study. Hypertension. 2004; 43: 1239–1245.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails January 2009Vol 53, Issue 1 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.108.123695 Originally publishedNovember 17, 2008 PDF download Advertisement SubjectsHypertension

Aortic pulse wave velocity (PWV), a measure of aortic stiffness, is an important indicator of cardiovascular risk. Derivation of PWV from uncalibrated proximal aortic or carotid pressure alone has practical advantages. However, when the time of return of the reflected wave, Delta t, is used to calculate PWV, inaccurate data are obtained. With aging PWV increases but Delta t hardly decreases, suggesting that the reflection site moves toward the periphery. We hypothesized that the forward and reflected waves in the distal aorta are not in phase, leading to an undefined reflection site. We derived forward and backward waves, at the entrance and distal end of a uniform tube, with length " L." With the tube closed at the end, forward and reflected waves are there in phase, and PWV = 2L/Delta t. When the tube is ended with the input impedance of the lower body, forward and backward waves at its end are not in phase, and Delta t is increased, suggesting that the reflection site is further away (tube seems longer), and PWV calculated from 2L/Delta t is underestimated. Using an anatomically accurate model of the human arterial system, we show that the forward and backward waves in the distal aorta are not in phase. When aortic PWV increases, Delta t changes only little, and the reflection site appears to move to the periphery, similar to what is observed in humans. We conclude that to define the location of a reflection site is elusive and that PWV cannot be calculated from time of return of the reflected wave.

HomeHypertensionVol. 50, No. 2Noninvasive Input Impedance of the Human Systemic Circulation Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBNoninvasive Input Impedance of the Human Systemic Circulation Michael F. O'Rourke Wilmer W. Nichols Joseph P. Murgo Michael F. O'RourkeMichael F. O'Rourke St. Vincent's Clinic/University of New South Wales, Sydney, Australia Wilmer W. NicholsWilmer W. Nichols Department of Cardiovascular Medicine, University of Florida, Gainesville, Fla Joseph P. MurgoJoseph P. Murgo Central Cardiovascular Institute of San Antonio, University of Texas Health Science Center, San Antonio, Tex Originally published4 Jun 2007https://doi.org/10.1161/HYPERTENSIONAHA.107.093096Hypertension. 2007;50:e16Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: June 4, 2007: Previous Version 1 To the Editor:The study of noninvasive aortic input impedance by Segers et al1 is a very important step in understanding age-related changes in humans and an advance on previous limited invasive studies conducted decades ago.2,3 One reason that these lapsed was the difficulty in accurately measuring aortic pulsatile flow, attributable to turbulence in the left ventricular outflow tract (LVOT) and proximal aorta. Subsequent emphasis was placed on pressure waveforms2,3 after introduction of high fidelity manometers2 and tonometers3 for noninvasive studies.Segers et al present baseline data for a longitudinal study; long-term information is eagerly awaited. We offer the following explanations for major findings.Fluctuations in modulus and phase of aortic impedance at all ages and both sexes are remarkably consistent and similar to previous invasive studies, and can only be explained on the basis of strong wave reflection.The most obvious and consistent aging changes in this cohort were the simplest to measure (PWV and AIx) and are determined from pressure waveforms alone, using noninvasive tonometry.Segers et al1 measured flow velocity and diameter in the LVOT, where the physical and geometric characteristics are much different from the elastic aorta beyond. Measures of compliance or characteristic impedance (Zc) in the LVOT are not necessarily applicable to the wider elastic aorta. Authors found no change (in females) and a fall (in males) of Zc with age, despite increases in aortic PWV with age in both sexes. Such discrepancy has previously been noted in the aorta and pulmonary artery3,4 and readily explained on the basis of aortic dilation with age (or pulmonary artery dilation with increasing pressure). In all situations there is a constant relationship between PWV and Zc when this is expressed in terms of linear flow velocity. Authors did not measure aortic diameter so could not calculate aortic Zc.Authors discuss relative importance of changes in incident and reflected waves with aging. The incident wave is of necessity greater than the reflected wave. However, as age advances, the reflected wave contributes more to total amplitude of the wave, at least up to 60 years of age. There is no other way to explain the dramatic and consistent increase in AIx in this large cohort.Data presented by Segers et al1 support the view that arterial stiffness, arterial diameter, and wave reflection increase with advancing age.5DisclosuresM.F.O. is a founding director of AtCor Medical, manufacturer of pulse wave analysis systems. W.N. is a consultant to AtCor Medical Pty Ltd. J.M. served as an expert witness for the plaintiff in Hendley et al vs the McIntosh Clinic, P.C. Superior Court of Thomas City, Ga.1 Segers P, Rietzschel ER, De Buyzere ML, Vermeersch SJ, De Bacquer D, Van Borte LM, De Backer G, Gillebert TC, Verdonck PR. Noninvasive (input) impedance, pulse wave velocity, and wave reflection in healthy middle-aged men and women. Hypertension. 2007; 49: 1248–1255.LinkGoogle Scholar2 Murgo JP, Westerhof N, Giolma JP, Altobelli SA. Aortic input impedance in normal man: relationship to pressure wave forms. Circulation. 1980; 62: 105–116.CrossrefMedlineGoogle Scholar3 Nichols WW. O'Rourke MF. McDonald's Blood Flow in Arteries. 5th ed. London: Arnold; 2005: 264–267, 355–360.Google Scholar4 O'Rourke MF. Vascular impedance in studies of arterial and cardiac function. Physiol Rev. 1982; 62: 570–623.CrossrefMedlineGoogle Scholar5 O'Rourke MF. Aortic diameter, aortic stiffness and wave reflection increase with age and isolated systolic hypertension. Hypertension. 2005; 245: 652–658.Google Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Akhtar S and Ebert T (2018) Cardiovascular System Geriatric Anesthesiology, 10.1007/978-3-319-66878-9_11, (161-178), . O'Rourke M (2008) Time domain analysis of the arterial pulse in clinical medicine, Medical & Biological Engineering & Computing, 10.1007/s11517-008-0370-7, 47:2, Online publication date: 1-Feb-2009. Segers P, Rietzschel E and De Buyzere M (2007) Response to Noninvasive Input Impedance of the Human Systemic Circulation, Hypertension, 50:2, (e17-e17), Online publication date: 1-Aug-2007. August 2007Vol 50, Issue 2 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.107.093096PMID: 17548713 Originally publishedJune 4, 2007 PDF download Advertisement SubjectsHypertension

The basics of pulsatile ejection dynamics are reviewed in order to clarify the relationships among left ventricular and aortic pressures, intra-left ventricular and aortic flow velocities, and cardiovascular sound. The principles of turbulent flow are examined using the Reynolds number concept, and the evidence for cause-and-effect relationships between turbulent flow and murmur generation is presented. Examples of hemodynamics and phonocardiography are given for normal subjects and are compared to patients with aortic stenosis and hypertrophic cardiomyopathy. The concepts presented are used to analyze the results of a new study suggesting increased intraventricular velocities as a new cause for systolic murmurs in adults.

To determine the feasibility and accuracy of digital echocardiography for routine interpretation of two-dimensional and Doppler echocardiography, we studied 93 consecutive patients chosen at random from our daily workload. The parameters studied included cavity sizes, biventricular regional and global systolic and diastolic function, valvular structure and function, and presence or absence of pericardial disease. The results were first interpreted using quad screen, digital format cine loops. These results were then compared with the results obtained from reviewing the video-tape images. Seventy-nine patients (87%) showed complete concordance between the digital system and video tape. Among the 1156 echocardiographic parameters/measurements examined in all patients, a 99% concordance rate (normal vs abnormal) was found. Disagreements between the digital system and video tape in the patients undergoing two-dimensional/Doppler exams included mitral valve prolapse in 3, mild valvular insufficiency in 5, a small pleural effusion in 2, and a wall-motion abnormality in 3 patients. In conclusion, the use of digital technology for evaluation of routine echocardiograms appears to compare favorably with the interpretation of images using the conventional video tape. (ECHOCARDIOGRAPHY, Volume 13, September 1996)