Are Central BP Readings the “Waves” of the Future?

I was taught how to take blood pressures early in medical school. If a few “dos and don’ts” were respected, things seemed to proceed uneventfully (with attention to cuff placement and size, Korotkoff sounds, etc).

In the past year or so, more has been written about the differences between brachial cuff pressures and central blood pressures. Is the dialogue merely a fad? I suspect not. Much of the criticism of atenolol for blood pressure control revolves around the disparity between cuff and central pressures when this agent is used to treat hypertension. Let’s look at the controversy in more detail.^1,2
 
The underlying theory goes something like this: brachial cuff pressures are not equivalent to central pressures, that is, the pressure as experienced by the heart, brain, and kidneys. The value we use to define and treat hypertension, the office or home sphygmomanometer reading, reflects not only the blood pressure per se, but propagation of waveforms in arteries (contingent on size and location), the character of those waves, their reflection back, and a host of physical variables consequent to the degree of arterial distensibility or “stiffness.”³ If central pressure could only be measured invasively, the debate would be moot. That is not the case.

Central blood pressure can be measured accurately by applanation technique (placing a noninvasive, innocuous probe over the radial artery) coupled with equations that quantify and characterize wave behaviors as they move from one vessel to another (yuck, but bear with me).³ Analysis of radial artery systolic-diastolic waveforms by noninvasive transducers provides a relative assessment of blood pressure backwards where it counts-in the vessels supplying the brain, heart, and kidneys. The early debate regarding the differences between brachial and central pressures was generated by atenolol-induced declines in cuff pressures with simultaneous rises in central pressures during treatment.^4,5
 
The atenolol data standing alone may seem provocative, but nonetheless are insufficient. The story has recently gotten more complex. For example, a study in cognitively deficient patients with hypertension demonstrated that carotid intimal-media thickness, a tangible marker for cerebrovascular disease, correlated most strongly with elevated central, not cuff, blood pressures.⁶ Other studies have verified the same pattern for cerebrovascular and aortic diseases.⁶ Short-term cold exposure quickly raised the central blood pressure of hypertensive men from an average of 130/93 to 162/107 mm Hg and could be appreciated quickly.⁷
 
JNC 2013 (or JNC 8) is slated for release at the end of this year. The poster child for central pressure pathology is the blood pressure response to atenolol. Increases in central blood pressure seen in patients taking this drug are the primary reasons why beta-blockers have steadily fallen out of favor. Atenolol does not lower important cardiovascular risks in hypertensive patients treated with this agent. Atenolol use may cause augmentation of pressure waves in the central circulation. Why? The drug slows the heart and may permit initiation of a second pressure pulse wave before the first has completely finished its peripheral course. That pattern leads to a higher central blood pressure, not revealed by cuff values.

Don’t panic; your busy practice will not be derailed by time-consuming central blood pressure measurements. But, ongoing research with central blood pressure will identify those medications and circumstances that predispose to vascular complications better than sphygmomanometers do.

Let’s see if JNC 2013 kicks off the central blood pressure era by addressing the problems with atenolol.    

   
1. Rutecki GW. A future of beta-blockers “plus” to treat hypertension? Consultantlive.com. May 20, 2013. Available at: http://www.consultantlive.com/conference-reports/ash2013/content/article/10162/2143139. Accessed October 3, 2013.
2. Rutecki GW. A requiem for beta-blockers to treat hypertension? Consultantlive.com. Available at: http://www.consultantlive.com/conference-reports/ash2013/content/article/10162/2143207. Accessed September 30, 2013.
3. O’Rourke MF, Adji A. Noninvasive studies of central aortic pressure. Curr Hypertens Rep. 2012;14:8-20.
4. Boutouyrie P, Achouba A, Trunet P, et al. Amlodipine-valsartan combination decreases central systolic blood pressure more effectively than the amlodipine-atenolol combination: the EXPLOR Study. Hypertension. 2010;55:1314-1322.
5. Shah NK, Smith SM, Nichols WW, et al. Carvedilol reduces aortic wave reflection and improves left ventricular/vascular coupling: a comparison with atenolol (CENTRAL Study). J Clin Hypertens. 2011;13:917-924.
6. Da Mota DE, Giollo LT, Martinelli DD, et al. Carotid intima-media thickness is associated with cognitive deficiency in hypertensive patients with elevated central systolic blood pressure. Cardiovasc Ultrasound. 2012;10:41-52.
7. Hinssala H, Kandelberg A, Herzig K-H, et al. Central aortic blood pressure of hypertensive men during short-term cold exposure. Am J Hypertens. 2013 Aug 20; [Epub ahead of print].