Medical Policies - Medicine
Non-Invasive Measurement of Central Blood Pressure (cBP)
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Non-invasive measurement of central blood pressure (cBP) is considered experimental, investigational and/or unproven.
Pressure measured with a cuff and sphygmomanometer in the brachial artery is accepted as an important predictor of future cardiovascular risk. However, systolic pressure varies throughout the arterial tree, such that central aortic blood pressure (cBP) is actually lower than corresponding brachial values, although this difference is highly variable between individuals. Some evidence suggests that central pressure is better related to future cardiovascular events than is brachial pressure. Moreover, anti-hypertensive drugs can exert differential effects on brachial and central pressure.
Several devices and techniques, each purporting to estimate cBP, have entered commercial use. These devices may allow the noninvasive recording of the arterial waveform and the generation of a proximal aorta pressure profile. The devices when clinically validated in catheterization laboratories and when accurately calibrated have been shown to be within 1 mm Hg to 2 mm Hg of the actual pressure in the proximal aorta. Pulse waveforms can be obtained either using a tonometer (handheld or stationary), which captures the radial artery waveform, or by oscillometric methods, which use a cuff encircling the limb. Both methods produce a waveform, either from the brachial (oscillometric) or radial (tonometric) arteries, which is usually subjected to a general transfer algorithm to produce a central pressure profile. A typical duration of waveform capture is on the order of 10 seconds.
SphygmoCor XCEL System (AtCor Medical) was cleared by the U.S. Food and Drug Administration (FDA) in November 2012 (K122129). Several additional 510(k) clearances had been granted earlier by the FDA. The predicate device was the SphygmoCor CVMS, cleared in August 2007 (K070795).
This policy was originally developed in 2016 and has been updated with searches of scientific literature through July 2017. The following is a summary of the key literature to date.
Sharman et al. noted that several methodological issues remain to be addressed before measurement of central pressure is fully integrated into clinical decision making and of practical benefit for patients. (1) Firstly, although a number of simple-to-use reliable devices are now on the market, a standard approach to validation of new devices is required. This approach can sometimes produce higher central pressure estimates than the measured brachial cuff pressure, which may seem unphysiological, but is due to the brachial cuff giving a falsely low estimate of brachial systolic pressure. The alternative approach calculates central pressure relative to the measured brachial cuff pressure, which tends to under-estimate the ‘true’ aortic pressure, but may be more intuitive. The authors also commented that there is a need to adopt a standard method for calibrating peripheral waveforms, using either systolic/diastolic or mean arterial pressure/diastolic pressure, and to better understand the impact of brachial-radial and aortic-carotid amplification.
In a 2014 clinical update review the European Heart Journal (2) noted: “There is now a substantial body of evidence that antihypertensive drugs, and particularly beta-blockers, exert differential effects on brachial and central pressure. As a result, the pharmaceutical industry is becoming increasingly convinced that basing treatment decisions on central, rather than brachial pressure, is likely to have important implications for the future diagnosis and management of hypertension. However, cuff measurements of brachial systolic and diastolic pressure continue to remain the accepted surrogates by drug regulatory authorities. This means that new therapies will continue to be assessed on the basis of brachial measurements, which may ultimately serve as a potential barrier to novel drug development. Therefore, appropriately powered clinical trials demonstrating that preferential lowering of central pressure improves outcome, will ultimately be required before central pressure becomes an accepted surrogate of cardiovascular risk. Nitrovasodilating drugs may be particularly useful in this respect. Before such trials are completed, smaller studies based on established surrogates for cardiovascular disease, such as carotid intima media thickness (IMT) and left ventricular mass (LVM) will be important in providing proof of principle that reduction in central rather than brachial pressure is a more effective therapeutic strategy.”
Narayan et al. (3) performed a systematic meta-analysis of studies reporting cBP between 2000 and 2012. Studies were included if both central and brachial blood pressure (cBP and bBP) were reported. Studies were categorized by technique and according to the prevalent disease state with the bBP?-?cBP difference calculated. Random-effects modeling (inverse variance weighted approach) was used to estimate the pooled mean difference associated with each technique. Of the 164 eligible studies, the SphygmoCor device was most commonly reported (110 studies); with direct carotid applanation second-most utilized (31 studies). In 30 included invasive cohorts, the measured cBP did not differ significantly from the oscillometric bBP recorded [mean difference 4.19 ?mmHg, 95% confidence interval (CI) -4.13 to 12.51], whereas mean differences of 12.77 ?mmHg (95% CI 11.93, 13.60) and 8.83 ?mmHg (95% CI 7.86, 9.79) were obtained with the SphygmoCor and carotid applanation estimates of cBP, respectively (both P?<?0.05). Conversely, the reported mean cBP-to-bBP differences measured across various disease states with SphygmoCor did not differ significantly. This meta-analysis suggests that noninvasive cBP estimation is device/technique-dependent. Consequently, caution is advisable in applying these devices and techniques across clinical studies.
Townsend and colleagues were part of a panel of clinical researchers and clinicians who study and clinically use pulse wave analysis. (4) This panel was assembled to discuss strategies for using pulse wave analysis in the clinical encounter. The article presents an approach to the clinical application of pulse waveform analysis, how to interpret central pressure waveforms, and how to use existing knowledge about the pharmacodynamic effect of antihypertensive drug classes in combination with brachial and central pressure profiles in clinical practice. The discussion in the article was supplemented by case-based examples provided by panel members, which the authors hope will provoke discussion on how to understand and incorporate pulse wave analysis into clinical practice. The intent was not to recommend replacing brachial pressure with central pressure in the management of BP. The authors go on to note: “such a replacement is not yet supported by sufficient evidence from randomized clinical trials. Our intent was to determine how information from the central pressure and the analysis of the central pressure waveform provides additional information to physicians managing BP beyond current brachial BP goals.”
Rinaldi et al. (5) noted in a 2015 article that emerging evidences now suggest that central pressure may predict cardiovascular diseases better than brachial BP; moreover, it may differently respond to certain antihypertensive drugs. The potential effects beyond peripheral BP control may be due to specific protective properties of different antihypertensive drugs in affecting central aortic pressure and arterial stiffness. Although data on direct cardiovascular benefit impact of central blood pressure treatment in randomized clinical trials are still lacking, it is likely that the improvement of quality of care and the individualized assessment of the hypertension-associated cardiovascular risk are achievable with the use of central hemodynamics. Therefore, basing antihypertensive treatment guidance on central pressures rather than on peripheral blood pressure may be the key for future antihypertensive strategies.
Borlaug et al. (6) sought to determine whether aggressive titration of vasoactive medicines beyond goal?directed heart failure medical therapy (GDMT) based upon aortic pressure improves exercise capacity and cardiovascular structure?function. Subjects with chronic heart failure (HF) (n=50) underwent cardiopulmonary exercise testing, echocardiography, and arterial tonometry to measure aortic pressure and augmentation index, and were then randomized to aortic pressure?guided treatment (active, n=23) or conventional therapy (control, n=27). Subjects returned for 6 monthly visits wherein GDMT was first optimized. Additional vasoactive therapies were then sequentially added with the goal to reduce aortic augmentation index to 0% (active) or if brachial pressure remained elevated (control). Subjects randomized to active treatment experienced greater improvement in peak oxygen consumption compared with controls (1.37±3.76 versus −0.65±2.21 mL min−1 kg−1, P=0.025) though reductions in aortic augmentation index were similar (−7±9% versus −5±6%, P=0.46). Forward stroke volume increased while arterial elastance and left ventricular volumes decreased in all participants, with no between?group difference. Subjects randomized to active treatment were more likely to receive additional vasoactive therapies including nitrates, aldosterone antagonists and hydralazine, with no increased risk of hypotension or worsening renal function. Maximization of goal?directed medical therapy in heart failure patients may enhance afterload reduction and lead to reverse remodeling, while additional medicine titration based upon aortic pressure data improves exercise capacity in patients with heart failure.
In 2016, Cheng et al. (7) evaluated the prognostic value and clinical utilities of pulse wave analysis (PWA) derived mechanical biomarkers in two independent population based cohorts. PWA on central arterial pressure waveforms were obtained from subjects without a prior history of cardiovascular diseases. The two studies were the Kinmen study (1272 individuals, a median follow-up of 19.8 years); and the Cardiovascular Disease Risk Factors Two-Township Study (CVDFACTS) (2221 individuals, median follow-up of 10 years). In the Kinmen study, right carotid artery pressure waveforms, which have been demonstrated to closely resemble central aortic pressure waveforms, were registered noninvasively with a tonometer. In the CVDFACTS study, central aortic pressure waveforms were obtained with a SphygmoCor device using radial arterial pressure waveforms. The associations between all mechanical biomarkers derived from pulse wave analysis and cardiovascular mortality were then examined in the multivariate Cox proportional hazards models that took into account cardiovascular risk factors including age, sex, systolic BP, body mass index, fasting glucose, triglycerides, low-density-lipoprotein cholesterol, and high-density-lipoprotein cholesterol, and smoking. Only systolic (SC) and diastolic rate constant (DC) of reservoir pressure could independently and consistently predict cardiovascular mortality in both cohorts. Cardiovascular mortality was higher in the Kinmen study due to higher hypertension prevalence and more male participants. During a median follow-up of 19.8 years, 315 (26.9%) deaths occurred (84 of cardiovascular origin). In the CVDFACTS study, a total of 171 deaths occurred (34 of cardiovascular origin) during a median follow-up of 10 years. Increased brachial systolic BP, pulse pressure, backward wave amplitudes (Pb), and augmentation index (AI) were significantly associated with increased cardiovascular mortality in both studies. Biomarkers derived from reservoir pressure-wave analysis were positively associated with cardiovascular mortality in the Kinmen study, and in the CVDFACTS study, only peak of reservoir pressure and DC remained significant in predicting cardiovascular mortality. The authors concluded that these findings suggested that mechanical biomarkers derived from pulse wave analysis could not only independently predict the long-term cardiovascular risks beyond the traditional risk factors, but also provide more accurate risk stratification by incorporating these mechanical biomarkers into the risk prediction models. It is not clear how this information will affect patient management and outcomes.
Summary of Evidence
Evidence is required to clarify the interchangeability of central blood pressure (cBP) measurements between noninvasive devices and the influence of disease states on central to brachial pulse pressure amplification. The clinical evidence from multi-center clinical trials demonstrating the use of this technology alters patient management and improves clinical outcomes is lacking. Additional research involving larger, well-designed studies is needed to establish the role of cBP in the early identification, prevention and management of cardio vascular disease (CVD).
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1. Sharman, J. E., Marwick, T.H., et al. Randomized Trial of Guiding Hypertension Management Using Central Aortic Blood Pressure Compared with Best-Practice Care: Principal Findings of the BP GUIDE Study. Hypertension. 2013; 62:1138-1145. PMID: 24060891
2. McEniery, C.M., et al. Central blood pressure: current evidence and clinical importance. European Heart Journal. January 2014. PMID: 24459197
3. Narayan O1, Casan J, et al. Estimation of central aortic blood pressure: a systematic meta-analysis of available techniques. J Hypertens. 2014 Sep; 32(9):1727-40. PMID: 24937639
4. Townsend, R.R., Black, H, R., et al. Clinical Use of Pulse Wave Analysis: Proceedings from a Symposium Sponsored by North American Artery J Clin Hypertens (Greenwich). 2015; 17: 503–513. PMID: 26010834
5. Rinaldi E.R., Yannoutsos A., et al. Central hemodynamics for risk reduction strategies: additive value over and above brachial blood pressure. Curr Pharm Des. 2015; 21(6):730-6. PMID: 25341860
6. Borlaug, BA et al. A randomized pilot study of aortic waveform guided therapy in chronic heart failure. J Am Heart Assoc. 2014 Mar 20; 3(2): e000745. PMID: 24650926
7. Cheng, Hao-Min, Chuang, Shao-Yuan, Wang, J, et al. Prognostic significance of mechanical biomarkers derived from pulse wave analysis for predicting long-term cardiovascular mortality in two population-based cohorts. International Journal of Cardiology (2016) 388–395. PMID: 27128568
|7/15/2018||Reviewed. No changes.|
|10/15/2017||Document updated with literature review. Coverage unchanged .|
|12/1/2016||Reviewed. No changes.|
|5/1/2016||New medical document. Non-invasive measurement of central blood pressure is considered experimental, investigational and/or unproven.|
|Title:||Effective Date:||End Date:|
|Non-Invasive Measurement of Central Blood Pressure (cBP)||10-15-2017||07-14-2018|
|Non-Invasive Measurement of Central Blood Pressure (cBP)||12-01-2016||10-14-2017|
|Non-Invasive Measurement of Central Blood Pressure (cBP)||05-01-2016||11-30-2016|