Tracking of brachial and central aortic systolic pressure over the normal human lifespan: insight from the arterial pulse waveforms.

Despite multiple studies, it has not been possible to account for the normal changes of blood pressure that occur from infancy to old age. We sought a comprehensive explanation, by linking brachial pressure with the well documented changes in the arterial pulse waveform, whose peak and nadir determine systolic, diastolic and pulse pressure in brachial arteries. Changes in humans arterial pulse wave contour from birth to old age can be readily explained on (i) growth, with increasing length of the body from birth to adolescence, and adult height maintained thereafter, and (ii) degeneration and dilation of the aorta from elastic fibre fracture throughout life, causing progressive increase in aortic pressure wave amplitude from early return of wave reflection, and summation of incident with reflected waves in systole. These changes throughout life complement arterial pulse waveform analysis and explain brachial cuff pressure values, with optimal pulse wave pattern for cardiac interaction apparent in adolescence.

Central Pulsatile Pressure and Flow Relationship in the Time and Frequency Domain to Characterise Hydraulic Input to the Brain and Cerebral Vascular Impedance.

In the time domain, pulsatile flow and pressure can be characterised as the ratio of the late systolic boost of flow or pressure to the pulse amplitude so as to estimate the hydraulic input to the brain. While vascular impedance has been widely used to represent the load presented to the heart by the systemic circulation, it has not been applied to the cerebral circulation.We set out to study the relationship between the pressure and the flow augmentation index (AIx) in the time domain and to determine cerebral vascular impedance using aortic blood pressure and cerebral blood flow waveforms in the frequency domain. Twenty-four young subjects (aged 21-39 years) were recruited; aortic pressure was derived using SphygmoCor from radial pressure. Flow waveforms were recorded from the middle cerebral artery. In three subjects, we performed the Valsalva manoeuvre to investigate their response to physiological intervention. There was a linear relationship between flow and pressure AIx, and cerebral impedance values were similar to those estimated for low resistance vascular beds. Substantial change in pressure and flow wave contour was observed during the Valsalva manoeuvre; however, the relationship in both the time and the frequency domains were unchanged. This confirms that aortic pressure and cerebral flow waveform can be used to study cerebral impedance.

Intracranial Pressure Waveforms are More Closely Related to Central Aortic than Radial Pressure Waveforms: Implications for Pathophysiology and Therapy.

In patients with subarachnoid haemorrhage, pulsatile intracranial pressure (ICP) is more strongly associated with adverse events than mean ICP. Furthermore, patients with idiopathic normal-pressure hydrocephalus (iNPH), and pulsatile ICP of 5 mmHg or more, gain more benefit from cerebrospinal fluid (CSF) shunting than those whose pulsatile ICP is lower than 5 mmHg.Our study aims to investigate the morphological relationship between ICP pulsations, aortic pressure pulsations and radial artery pulsations. Central aortic pulse pressure has been known to be the best predictor of adverse cardiac events, whereas radial artery pulse pressure is generally measured and displayed in intensive care environments.We studied 10 patients with iNPH, and their ICP and aortic and radial pressures were digitised, ensemble-averaged and compared in the time and frequency domains. The ICP wave contour was quite different to the radial pressure waveform. By contrast, the ICP waveform was similar to the aortic pressure wave contour. The ICP amplitude averaged <10 % of aortic pulse pressure. In the frequency domain, the relative amplitude of the first three harmonics was similar for the ICP and aortic pressure. Hence, monitoring central aortic pressure through derivation from the radial pressure wave is superior to measurement of radial pressure alone.

Change in Pulsatile Cerebral Arterial Pressure and Flow Waves as a Therapeutic Strategy?

While intracranial pressure (ICP), arterial pressure and transcranial middle cerebral artery flow velocity (MCAFV) are often monitored in unconscious patients following stroke or head injury, the value of waveform indices has not been fully established. We retrospectively analysed the data of eight adults (aged 19-36 years) with closed head injury who had spontaneous and repeated episodes of elevated ICP (i.e. "plateau waves"). MCAFV was measured using transcranial Doppler, ICP using a Codman catheter and radial artery pressure using cannulation. Ascending aortic pressure (AAP) was generated from the radial artery using SphygmoCor(TM). Cerebral perfusion pressure (CPP) was calculated as AAP - ICP in the time domain.During the period of increased ICP, ICP and cerebral flow velocity amplitude increased significantly compared with the basal condition, while cerebral mean flow decreased. Amplitude of the secondary peak in ICP, AAP and MCAFV waveform became apparent.An increase in the amplitude of ICP, AAP and MCAFV waves can be attributed to the greater prominence of reflected waves from the lower body, which was apparent in pulse waveform analysis. Arterial vasodilators such as nitrates reduce reflected pressure waves from the lower body and, by decreasing the amplitude of AAP, ICP and MCAFV, may be as beneficial for the cerebral circulation as they are for the left ventricle of the heart.

Noninvasive studies of central aortic pressure.

Our purpose is to review noninvasive methods for measuring central arterial pressure. Indices of central arterial pressure measured from central aortic and peripheral arterial waveforms have shown value in predicting cardiovascular events and death, as well as in guiding therapeutic management. This article reviews noninvasive techniques of measuring central arterial pressure that have been validated against intra-arterial pressure. This paper explains methods to derive central (aortic and carotid) pressure from radial and brachial sites. It focuses on specific issues of brachial calibration applied to carotid pressure waveforms, which were regarded as a surrogate of aortic pressures used in three major studies (Framingham, Asklepios, and Australian National Blood Pressure 2 studies). We explain why radial-based methods are superior to carotid-based methods for estimating central pressure. Physiological principles of pressure measurement need be satisfied to ensure accurate recording.

Association between Brachial-Ankle Pulse Wave Velocity as a Marker of Arterial Stiffness and Body Mass Index in a Chinese Population.

Objectives: Arterial stiffness is widely accepted as an important predictor of cardiovascular disease (CVD) development. While obesity is generally associated with increased CVD risk, there is evidence that overweight patients with existing CVD may have better clinical outcomes than their lean counterparts. Our study sought to observe any potential association between brachial−ankle pulse wave velocity (BAPWV), a marker of arterial stiffness related to CVD risk, and Body Mass Index (BMI), a crude and widely used measure of obesity. Methods: Adult individuals (n = 857) assessed for routine CV risk were included and grouped according to their BMI (<25 kg/m2: normal; 25−30 kg/m2: overweight, ≥30 kg/m2: obese). Their anthropometric parameters, brachial cuff pressures, and BAPWV were measured. Results: Brachial pressure was significantly higher as BMI increased. BAPWV showed a positive linear association with systolic (r = 0.66, p < 0.01), mean (r = 0.60, p < 0.01), diastolic (r = 0.51, p < 0.01), and pulse (r = 0.53, p < 0.01) pressures. However, a linear relationship between BMI and BAPWV was only apparent in males aged <50 years (p = 0.01) and in females aged ≥50 years (p < 0.01). In individuals with similar brachial systolic pressure, BAPWV was higher in normal-weight subjects compared to overweight−obese ones. Conclusions: This conflicting finding is attributed to an overestimation of the degree of arterial stiffness as a measure of CVD risk in individuals with a less 'healthy' BMI. This suggests that BMI may not the appropriate obesity indicator to assess CV risk. Our finding emphasizes the importance of establishing a non-linear relationship between CVD risk, age, and BMI, taking into account apparent sex differences, to predict future CV events. While this finding may suggest a lower degree of stiffness in large arteries of overweight−obese subjects compared to their normal-weight counterparts, the potential implications for individuals with higher BMI need be explored further.

Prediction of cardiovascular events and all-cause mortality with central haemodynamics: a systematic review and meta-analysis.

AIMS: To calculate robust quantitative estimates on the predictive value of central pressures and derived central haemodynamic indices for cardiovascular (CV) outcomes and all-cause mortality by meta-analysis of longitudinal studies. METHODS AND RESULTS: We meta-analysed 11 longitudinal studies that had employed measures of central haemodynamics and had followed 5648 subjects for a mean follow-up of 45 months. The age- and risk-factor-adjusted pooled relative risk (RR) of total CV events was 1.088 (95% CI 1.040-1.139) for a 10 mmHg increase of central systolic pressure, 1.137 (95% CI 1.063-1.215) for a 10 mmHg increase of central pulse pressure (PP), and 1.318 (95% CI 1.093-1.588) for a 10% absolute increase of central augmentation index (AIx). Furthermore, we found that a 10% increase of central AIx was associated with a RR of 1.384 (95% CI 1.192-1.606) for all-cause mortality. When compared with brachial PP, central PP was associated with marginally but not significantly higher RR of clinical events (P = 0.057). CONCLUSION: Central haemodynamic indexes are independent predictors of future CV events and all-cause mortality. Augmentation index predicts clinical events independently of peripheral pressures, while central PP has a marginally but not significantly (P = 0.057) better predictive ability when compared with peripheral PP.

An investigation of the individualized, two-point calibration method for cuffless blood pressure estimation using pulse arrival time: an historical perspective using the Casio BP-100 digital watch.

BACKGROUND: The use of wearable cuffless blood pressure (BP) devices is becoming commercially prevalent with little published validation information. Most devices rely, at least in part, on the relationship between pulse arrival time (PAT) and BP, a theoretical fundamental relationship that was first commercially exploited in 1993 with the release of the Casio BP-100 digital watch. OBJECTIVE: This study explored the PAT method of BP estimation in a commercial device where it first began, the Casio BP-100 (Model No. 900) digital watch, which employs an individualized, two-point calibration method. Device accuracy was determined by comparison to a conventional cuff-based BP device measurements. METHODS: Twenty participants (11 female, 9 male) had BP measured using both devices at rest, during a 5-minute isometric hand-grip exercise and at 1-minute post-exercise. RESULTS: Due to bidirectional scatter of BP estimation by the BP-100 device, there was no significant difference between the reference device and the BP-100. The devices showed poor correlation for both systolic BP (SBP) (R=0.36, p=0.13) and diastolic BP (DBP) (R=0.044, p=0.37). However, on average the watch was able to provide correct directional changes in SBP but not DBP with exercise. CONCLUSIONS: Despite being an industry first, the Casio BP-100 watch employed a method that gives a great chance of accuracy: a two point, individualized calibration method - more detailed than calibration methods in more modern devices. The watch, on average across a cohort, provided some information on BP directional change but was uncorrelated with cuff-based BP measurement. If the utility of beat-by-beat BP estimation is to be utilized, limitations of this method need to be addressed.

A novel method to assess valvulo-arterial load in patients with aortic valve stenosis.

INTRODUCTION: Ventricular function in elderly patients with aortic stenosis is impeded both by restricted aortic flow and arterial stiffening. A number of patients continue to have exertional intolerance after relief of aortic valvular obstruction due to unrecognized ventriculo-arterial coupling mismatch. HYPOTHESIS: Quantification of valvulo-arterial load (VAL), using a simultaneous applanation tonometry/cardiac magnetic resonance (CMR) technique, can accurately assess the relative contributions of aortic stiffness and valve gradient in older patients with aortic stenosis. METHODS: Elderly patients with aortic stenosis underwent a simultaneous applanation tonometry/CMR protocol. CMR provided left ventricular volume and aortic flow simultaneously with radial applanation tonometry pressure acquisition. Central aortic pressure was derived by transformation of the radial applanation tonometry waveform. VAL was determined as the relationship of derived aortic pressure to CMR aortic flow in frequency domain (central illustration). RESULTS: Twenty patients (age 80 ±â€Š9 years; 12 males; blood pressure 140/75 ±â€Š20 mmHg) with aortic stenosis on transthoracic echocardiogram (16 severe; mean gradient 45 ±â€Š16 mmHg; aortic valve area 0.8 ±â€Š0.2 cm2) were enrolled. Derived aortic pressure and flow waveforms correlated well with invasive data. Increased VAL was significantly associated with advanced age (P = 0.04) and raised SBP (P < 0.01), irrespective of aortic stenosis severity. CONCLUSION: Difficulties in the measurement and accuracy of ventriculo-arterial coupling means that it is not routinely measured in patients with aortic stenosis. We describe a new noninvasive index that provides an accurate assessment of valvular and arterial load on the left ventricle. VAL may help detect those at risk of ventriculo-arterial coupling mismatch and assist in selection of those most likely to benefit from an invasive procedure.

The Cardiovascular Continuum extended: aging effects on the aorta and microvasculature.

The 'Cardiovascular Continuum' was described by Dzau and colleagues in 2006 to explain the development over many years of coronary disease with its complications, then end-stage heart failure. The Continuum identified different points along the way where the process could be interrupted by drug therapies or interventions, then described the trials that have been undertaken over the last three decades to establish their value. The approach summarized the major steps in cardiology through modern times, but it had an emphasis on coronary atherosclerosis in prosperous nations, and did not account fully for the problems of aging, which occur in all societies. Aging of the aorta and elastic arteries causes arterial stiffening and leads to development of cardiac failure and microvascular disease in highly perfused organs such as the brain and kidneys. The 'Vascular Aging Continuum' which we introduce, dovetails with the late phases of the Cardiovascular Continuum and provides a more comprehensive explanation, especially for vascular diseases in nations with little atherosclerosis. It will become more common in the Western World where attention to risk factors and widespread use of statins are responsible for a decrease in atherosclerotic disease, prolongation of life, and dominance of macrovascular and microvascular arterial disease, as well as of cardiac failure.

Non-Invasive Quantification of Ventricular Contractility, Arterial Elastic Function and Ventriculo-Arterial Coupling from a Single Diagnostic Encounter Using Simultaneous Arterial Tonometry and Magnetic Resonance Imaging.

PURPOSE: Optimal assessment of cardiovascular performance requires simultaneous measurement of load independent left ventricular (LV) contractility, arterial function and LV/arterial coupling. We aimed to demonstrate feasibility of non-invasive ventricular pressure-volume and aortic pressure-flow-impedance measurements using simultaneous arterial tonometry (AT) and cardiovascular magnetic resonance imaging (CMRI). METHODS: 21 consecutive patients referred for CMRI were enrolled to undergo a simultaneous AT and CMRI protocol. A CMRI compatible AT apparatus provided aortic end-systolic pressure, taken to be equivalent to LV end-systolic pressure in the absence of aortic stenosis. CMRI provided LV volume and aortic flow at the time of pressure acquisition. Pressure-volume relationships were determined and correlated to traditional parameters of LV function including ejection fraction and circumferential strain. Aortic pressure-flow relationships were used to determine aortic characteristic impedance and systemic vascular resistance. RESULTS: Simultaneous AT and CMRI permitted measurement of LV end-systolic elastance, preload recruitable stroke work, arterial elastance, aortic characteristic impedance and systemic vascular resistance. Absolute values were within the expected range for our cohort, were highly reproducible and showed appropriately directed correlation to traditional parameters. CONCLUSION: Non-invasive assessment of LV pressure-volume and aortic pressure-flow relationships are both feasible and reproducible using simultaneous AT and CMRI. Methods permit assessment of load independent LV contractility, arterial function and LV/arterial coupling from a single non-invasive diagnostic encounter.

Different role of wave reflection magnitude and timing on left ventricular mass reduction during antihypertensive treatment.

OBJECTIVE: Regression of left ventricular (LV) mass during antihypertensive treatment has been associated with reduction in aortic augmentation index, a composite measure of peripheral wave reflection. The aim of this study was to clarify which of the two reflection factors, that is magnitude or timing, plays the dominant role in this regression. METHODS: We evaluated the reflection magnitude (RM; the reflected-to-forward pressure wave amplitude ratio), the round-trip travel time of the pressure wave (a parameter for reflection timing), and the aortic pulse wave velocity (PWV) with echocardiographic LV mass in 61 hypertensive patients before and after 1-year standard medical treatment. RESULTS: Antihypertensive therapy significantly (P < 0.01) decreased brachial and aortic blood pressures and aortic PWV, reduced LV mass, and increased travel time. Neither increase in travel time nor decrease in PWV, however, was related to the reduction in LV mass. By contrast, treatment-induced change in RM was significantly correlated with change in LV mass; the correlation was particularly close in patients with LV hypertrophy (r = 0.61, P < 0.001). Only a marginal correlation was observed between the changes in RM and travel time. The association between RM decrease and LV mass reduction was independent of age, sex, changes in travel time and blood pressure, and use of renin-angiotensin system inhibitors (beta = 0.41, P = 0.001). CONCLUSION: Decreased wave RM contributes to LV mass regression more strongly than, and independently of, delayed reflection timing. Peripheral muscular arteries (from which reflection arises) appear to be more important therapeutic targets in regressing LV mass than central elastic arteries.

Association between wasted pressure effort and left ventricular hypertrophy in hypertension: influence of arterial wave reflection.

BACKGROUND: Wave reflection during the systole increases left ventricular (LV) pressure, tension-time index (TTI) and myocardial oxygen requirement. The purpose of this study was to extract that component of extra myocardial oxygen requirement that is due to early systolic wave reflection, define it as wasted effort (DeltaE(w)), and examine its relationship to LV hypertrophy (LVH). METHODS: Radial artery pressure waveforms were recorded using applanation tonometry and central aortic waveforms generated in 98 patients with untreated hypertension. Aortic augmentation index (AI(a)), wave reflection amplitude (i.e., aortic augmented pressure (AG)) and systolic duration (ED-Tr), ejection duration (ED) and round-trip travel time of the pressure wave (Tr) were calculated from the aortic waveform, and DeltaE(w) estimated as 2.09 AG (ED-Tr). Carotid-femoral pulse wave velocity (PWV(e)) was also measured and LV mass index (LVMI) determined by echocardiography. RESULTS: DeltaE(w) was significantly correlated with age, body height, and LVMI. Women had greater DeltaE(w) than men. The correlation between DeltaE(w) and LVMI was independent of age, gender and body height (P = 0.003). Patients with LVH (LVH (+) group) showed greater DeltaE(w) than patients without LVH (LVH (-) group) (P = 0.003), and this difference remained significant when adjusted for confounding factors. Also, AI(a) and AG were higher in the LVH (+) than in the LVH (-) group (both P < 0.01). In contrast, PWV(e) was not different between the groups, and Tr showed only a marginal difference (P = 0.07). CONCLUSIONS: DeltaE(w) appears to be directly and positively associated with LVH in untreated hypertensive patients. The amplitude and duration of the reflected wave, rather than its travel time, are probably responsible for this association.

Effects of arterial stiffness, pulse wave velocity, and wave reflections on the central aortic pressure waveform.

Brachial systolic and pulse blood pressures (BPs) are better predictors of adverse cardiovascular (CV) events than diastolic BP in individuals older than 50 years. The principal cause of increased systolic and pulse BP is increased stiffness of the elastic arteries as a result of degeneration and hyperplasia of the arterial wall. Recent studies have shown that central BP, the pressure exerted on the heart, brain, and kidneys, is a better predictor of CV risk than brachial BP. As stiffness increases, reflected wave amplitude increases and augments pressure in late systole, producing an increase in left ventricular afterload and myocardial oxygen demand. Vasoactive drugs have little direct effect on large human elastic arteries but can markedly modify wave reflection by altering stiffness of the muscular arteries and changing pulse wave velocity of the reflected wave from the periphery to the heart. Vasodilators decrease the amplitude and increase the travel time (or delay) of the reflected wave, causing a generalized decrease in systolic BP. The decrease in systolic BP brought about by this mechanism is grossly underestimated when systolic BP is measured in the brachial artery.

Structure and Function of Systemic Arteries: Reflections on the Arterial Pulse.

"Structure and Function of Arteries"-is a topic of great importance to those who deal with arterial hypertension, since it links the source of flow, the left ventricle of the heart (whose output is pulsatile) to the peripheral tissues (whose flow is near continuous). The arterial tree acts passively as a conduit and cushion, and the interaction of heart, arterial tree, and organs is conventionally gauged on the basis of blood pressure measured by cuff in a conveniently located place (the brachial artery). For any precision and perspective to be gained, measurements of brachial systolic and diastolic pressure need be supplemented by other information. When such information is gained, one can understand how beautifully the arterial tree is tuned to the beat of the heart in animals of different size and shape and in humans at age 30 through the first third of a 3 billion beat lifetime. After age 30, the beats themselves progressively destroy the human arteries and their tuning to the heart, with emergence of clinical syndromes. In this review, the subject is tackled quantitatively on the basis of published numerical, physical, physiological, and pathophysiological basis, with principal focus on the beat of the heart, the pulse of the arteries, and their interaction.