Of the 99 patients studied, 3 had an ineffective angioplasty at the day of the considered procedure total chronic occlusion. Restenosis was discovered between 23 and days after the procedure median, days. Of the 11 subjects with restenosis, 2 did not have a stent implantation on the day of angioplasty.
All subjects were treated during the procedure and took an antiplatelet combination of aspirin and clopidogrel for 1 month. There was no acute stent thrombosis. These associations were observed after adjustment on age and gender. Restenosis had no significant association with central or peripheral PP. No significant association was observed between aortic or brachial PP and restenosis after angioplasty.
Sphygmomanometer-measured brachial BP has many limitations; DBP measured by this method is substantially less accurate than SBP, compared to invasive measurements. In addition it is closer to the heart, coronary vessels, and carotid arteries and it allows an accurate measurement of mean arterial pressure by direct integration of BP curve. Previous studies 12 , 15 , 16 have shown a significant association between CAD and reduced aortic or carotid compliance.
Because, in most of them, brachial, but not aortic, BP are measured 14 and because brachial PP is significantly higher than aortic PP for the same mean arterial pressure, 6 these studies did not show that aortic PP, and not aortic stiffness, was the main parameter significantly associated with the presence of CAD. Using invasive procedures, Nakayama et al 9 were the first to show a close association between aortic PP and the presence of CAD qualitatively evaluated.
To our knowledge, the present study is the first to relate an independent and significant association between aortic PP, a robust parameter poorly sensitive to placebo, 17 and the extent of CAD quantitatively assessed from the number of diseased coronary vessels. Nakayama et al 9 investigated 53 patients with stable angina pectoris or silent myocardial ischemia who underwent coronary angiography 3 months after PTCA. They found an independent association between restenosis after PTCA and pulsatility of the ascending aorta pulsatile to mean aortic pressure.
It should be mentioned that these patients were investigated between January and December , and, at this period, underwent balloon angioplasty without stent.
It should be noted that stent can mechanically protect the artery wall from pulsatile forces, and, on the other hand, stent implantation has recently been shown to increase the expression of matrix metalloproteinases. Aging changes in PP or arterial stiffness have been suggested to be possibly modulated by different gene polymorphisms. The present study clearly indicates for the first time that structural alterations of the coronary arterial wall are also directly and quantitatively involved.
Further studies are needed to explore this potential cause—effect relationship. Safar ME : Systolic blood pressure, pulse pressure and arterial stiffness as cardiovascular risk factors. Curr Opin Nephrol Hypertens ; 10 : — Google Scholar. Hypertension ; 33 : — J Hypertens ; 19 : — Hypertension ; 37 : — Circulation ; 99 : — Google Preview.
Hypertension ; 39 : — Am J Hypertens ; 14 : — Nakayama Y , Tsumura K , Yamashita N , Yoshimaru K , Hayashi T : Pulsatility of ascending aortic pressure waveform is a powerful predictor of restenosis after percutaneous transluminal coronary angioplasty. Circulation ; : — JAMA ; : — Fuster V : Mechanisms leading to myocardial infarction: insights from studies of vascular biology. Circulation ; 90 : — Hirai T , Sasayama S , Kawasaki T , Yagi S-I : Stiffness of systemic arteries in patients with myocardial infarction: A noninvasive method to predict severity of coronary atherosclerosis.
Circulation ; 80 : 78 — British Standard Institution. Precision of test methods, 1: guide for the determination of reproducibility for a standard test method. Am J Hypertens ; 3 : — Hypertension ; 32 : — Am J Cardiol ; 59 : — Asmar R , Safar M , Queneau P : Evaluation of the placebo effect and reproducibility of blood pressure measurement in hypertension.
Hypertension ; 38 : — N Engl J Med ; : — Circulation ; 94 : — Blood Vessels ; 24 : — Atherosclerosis ; : — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Despite the similarity of the aortic and carotid pulse wave, the amplitude of the augmented pressure wave in the ascending aorta is much higher than that in the carotid artery [ 19 ], which affects the calculation accuracy of some cardiovascular parameters like the augmentation index AI.
This relationship is modeled by a generalized transfer function. This generalized transfer function is employed to reconstruct the central pressure waveform from brachial or radial pressure waveform [ 26 , 27 ]. This is the most well validated [ 28 ] and the most widely used method so far. Figure 1 demonstrates the generalized transfer function produced from 26 subjects.
The transfer function is a low-pass filter that compensates for the boost in high frequency components of the pressure waveform as it travels from central aorta to the periphery. This method can provide not only quantitative CAP but also central aortic pressure waveform, allowing further analysis to access more cardiovascular parameters and predict cardiovascular status.
The transfer error by the GTF depends on heart rate and BP levels, which should be taken into account when applying GTF to populations with different hemodynamic conditions [ 30 ].
The validity of the GTF method in estimating central arterial pressures was evaluated [ 28 ]. The generalizability of GTF has been questioned [ 31 ], especially in some special hemodynamic conditions chronic kidney disease or arterial stiffness [ 32 ].
In addition, not all methods that generate GTFs are equally accurate [ 33 ]. Central SBP can be estimated directly from the properly calibrated brachial or radial pressure waveform. The evidences indicate that the reflected wave peak recorded in the periphery approximates to central SBP, since pressure gradients in the arterial system are relatively small during late systole and the late systolic shoulder represents the dominant peak in most adults from midlife onward [ 34 , 35 ].
Therefore, for older adults, central aortic systolic blood pressure can be calculated [ 28 ] via a regression equation employing the second systolic peak as an independent variable [ 36 , 37 ]. For example, central aortic SBP may be inaccurate in younger individuals with early, non-augmented peak systolic pressure [ 39 ].
Besides, this method also suffers the calibration error. A simplified approach for assessing CAP is the N-point moving average NPMA method, which is a kind of first-order low-pass filter, removing all higher frequency-related pulse wave features, which are typically related to wave reflections, and, therefore, providing only central aortic SBP instead of aortic blood pressure waveform.
This method is also a generalized method as the GTF method does; it suffers the intersubject and intra-subject variability. It does not provide an estimated central aortic blood pressure waveform. Several adaptive transfer function methods were proposed trying to tune the generalized transfer function and derive more reliable CAP [ 29 , 40 ].
For example, in our previous work, using aortic and brachial pulse waves derived from 26 patients who underwent cardiac catheterization, generalized transfer functions GTF were derived based on the autoregressive exogenous model.
Then for each individual, the GTF was tuned by its peak resonance frequency, as shown in Figure 2. The optional peak resonance frequency for an individual was determined by regression formulas using brachial systolic blood pressure. Another work by Swamy [ 40 ] used similar method and validated the method in dogs during multiple interventions. The GTF method does not account for intersubject or intra-subject variability of the transfer function. Individualized or quasi-individualized methods were proposed in recent years [ 41 , 42 , 43 ].
These methods primarily employ a physical transmission line model and focus on the individualization of pulse transit time, which is the main determinant of the aorta-brachial and aorta-radial model. Till now, none of the ITF methods are fully validated by invasive data and unfortunately rarely used in clinical practice [ 44 ].
The blind system identification BSI method reconstructs the input from two or more outputs. In the estimation of central aortic pressure waveform, BSI reconstructs the central aortic pressure waveform based on two peripheral pressure waveforms [ 45 , 46 , 47 , 48 , 49 , 50 ].
This method is fully individualized, without the need of measuring or estimating pulse transit time. The main drawback of this method is that it requires extra measurement of peripheral pressure waveforms. The two aorta-periphery models should not be similar in order to provide enough information, which added the inconvenience of clinical application.
The tonometry waveforms in carotid artery are calibrated to MAP and DBP which are similar throughout the arterial system, whereas SBP varies from the proximal artery to the periphery [ 1 , 2 , 3 ]. Because of variable amplification of the pressure waveform as it travels from the brachial to the radial recording site, the calibration of the radial waveform with brachial SBP and DBP leads to neglect of brachial-to-radial amplification, which may be sufficiently high to be of practical importance [ 51 , 52 , 53 , 54 ].
This results in underestimation of radial systolic, mean, and pulse pressure, whereas diastolic pressure is comparable between brachial and radial sites [ 53 , 55 ]. Since the radial waveform is improperly calibrated, the derived aortic pressure waveform will have systolic, mean, and pulse pressures underestimated.
And the difference between central and brachial pressures is overestimated. Thus, incorrect calibration simultaneously underestimates central pressure and overestimates central-to-brachial pressure amplification. In order to decrease calibration errors, the calibration of tonometry waveforms in radial artery with brachial MAP and DBP may be preferable.
One error is the inexact MAP obtained. Using brachial blood pressure and a formula to estimate brachial mean pressure is not acceptable because of high variation in the form factor of the brachial pressure waveform which can affect the accuracy of calibration. The maximum amplitude algorithm, which is commonly employed in oscillometric devices to estimate mean arterial pressure, is susceptible to errors that are related to arterial stiffness [ 56 , 57 , 58 ].
Another error is related to the inaccuracy of brachial cuff blood pressure used to calibrate which will be inevitably transferred to the resulting CAP. To sum up, all current methods for estimating CAP are critically dependent on concurrent assessment of conventional peripheral blood pressure for calibration.
The brachial blood pressure is used as the source of calibration in all the techniques of estimating CAP. The noninvasive oscillometric blood pressure devices are known to underestimate systolic and overestimate brachial diastolic blood pressure [ 59 , 60 ]. Estimates of central pressure based on these incorrect estimates of brachial blood pressure will be proportionally confounded.
The auscultatory blood pressure, which represents the gold standard measure of peripheral blood pressure, also has error similar to the oscillometric device [ 61 ]. Till now, all the available noninvasive methods and devices suffer the calibration error in the estimation of CAP. This means that the performance of these noninvasive methods largely depends on the measurement of peripheral blood pressures [ 53 , 62 ]. That is why measurements from various methods or devices vary widely.
In studies that performed direct comparisons of existing devices, agreement between devices is suboptimal [ 59 , 63 , 64 ]. New noninvasive methods should be introduced to get rid of calibration error, and the accuracy of peripheral blood pressure measurement should be improved.
Hamirani YS, et al. As chronic aortic regurgitation worsens, regurgitant volume increases, as does stroke volume in order to maintain forward cardiac output. This results in increased systolic pressures, reduced diastolic pressures and widened pulse pressure. Increased stroke volume leads to a number of unusual peripheral physical examination findings, discussed below in Peripheral Signs. The low diastolic aortic pressures can significantly affect coronary perfusion pressures, as coronary flow occurs during diastole.
Afterload peripheral resistance is an important factor in the degree of aortic regurgitation. All other factors being equal, increased peripheral resistance will be associated with increased regurgitation.
Thus, afterload reduction has become the mainstay of pharmacotherapy in aortic regurgitation. Aortic regurgitation can result from abnormalities of the aortic valve leaflets or dilation of the aortic root, though an increase in afterload is not by itself a cause of aortic regurgitation.
When the aortic leaflets are involved, a destructive process such as infective endocarditis or rheumatic valvular disease is frequently implicated. Any disease process that leads to aortic root dilation eg, Marfan syndrome or aortic dissection may cause enlargement of the aortic valve annulus; this results in failure of the leaflets to coapt close properly in diastole loss of coaptation and aortic regurgitation.
Frequently, repairs to the aortic root and valve are required in these conditions. The most common causes of acute aortic dissection include bacterial endocarditis, aortic dissection and blunt trauma-induced aortic valve damage Hamirani YS, et al.
As chronic aortic regurgitation develops slowly over time, the left ventricle slowly dilates and hypertrophies, as described previously. The disease remains asymptomatic for a long period of time. The later symptoms of chronic AR are mostly due to congestive heart failure.
Left heart failure results in passive elevation of pulmonary pressures with dyspnea. Physical activity may even cause transient pulmonary edema. Right heart failure symptoms include lower extremity-dependent edema and hepatic congestion. At night, when patients are recumbent, the excess extracellular fluid redistributes centrally, causing orthopnea the need to sit up to breathe or paroxysmal nocturnal dyspnea.
The large stroke volumes and forceful left ventricular contractions may cause head bobbing and awareness of the peripheral pulse. Angina may occur in the absence of atherosclerotic coronary disease, as the low diastolic pressures in severe aortic regurgitation compromise coronary filling, and the left ventricular hypertrophy increases oxygen demand. Other symptoms related to low cardiac output include fatigue, weakness and, in extreme cases, cardiac cachexia.
Unlike in chronic aortic regurgitation, almost all patients with significant acute aortic regurgitation are symptomatic. Signs of acute left heart failure — including severe dyspnea, dyspnea at rest, orthopnea and paroxysmal nocturnal dyspnea PND — arise. Patients typically present with symptoms of low cardiac output and systemic vasoconstriction, including pallor and coolness in the distal extremities, peripheral cyanosis and tachycardia with a reduced peripheral pulse.
Hypotension, flash pulmonary edema and shock can also occur. In chronic aortic regurgitation, visible cardiac and arterial pulsations are common due to the large stroke volume.
The carotid pulse can commonly be seen. The point of maximal impulse PMI is displaced laterally and caudally due to the LV dilation and hypertrophy that occurs. This murmur may be difficult to distinguish from the Graham-Steele murmur of pulmonic insufficiency. As aortic regurgitation worsens, the murmur becomes shorter, as less time is needed for left ventricular and aortic pressure equalization. In addition, a systolic ejection murmur may be present at the right upper sternal border, simply due to the large stroke volume passing through the aortic valve with each left ventricular systolic contraction.
An early diastolic rumble the Austin-Flint murmur may also be heard at the apex, due to the regurgitant jet striking the anterior leaflet of the mitral valve and causing it to vibrate. A widened pulse pressure is often present due to increased stroke volume, as previously described. When heart failure develops, the pulse pressure decreases and the peripheral signs of aortic regurgitation, listed below, are lessened.
A fourth heart sound S4 may develop when LV hypertrophy becomes severe and limits diastolic filling. A third heart sound S3 is often present, due to increased early diastolic filling into a compliant, dilated left ventricle.
Acute aortic regurgitation will cause a very short, early diastolic decrescendo murmur with the aortic and left ventricular pressures equalized quickly, as the left ventricle has not had time to dilate or hypertrophy.
The peripheral signs of aortic regurgitation are mostly due to the increased stroke volume and wide pulse pressure seen in aortic regurgitation. In 19th century Europe, syphilis was widespread. Syphilitic aortitis, resulting in aortic root dilation and severe aortic valve regurgitation, was quite common.
With no therapy — medical or surgical — available, the disease was allowed to progress; many individuals developed congestive heart failure from aortic regurgitation. Many physicians described various physical findings of aortic regurgitation. These were often named after the physician who described them; they are listed below.
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