Why you might avoid beta blockade in severe aortic insufficiency

It comes down to coronary perfusion.

Heart muscle needs blood and oxygen like any other muscle. In the case of the myocardium, coronary perfusion occurs during diastole, when the muscle relaxes. The pressure gradient between the aortic and left ventricular pressures drives blood forward through the coronaries. The coronary perfusion pressure, in the context of chest compressions, is that difference between at end-diastole, for example.

In a normal heart, the gradient is present throughout diastole, so the myocardium gets lots of good, oxygenated blood throughout that part of the cycle (Figure 1). In severe aortic insufficiency, though, the blood from the aorta quickly rushes back into the ventricle during diastole, dropping the gradient between aortic and ventricular pressures to zero (Figure 2). The myocardium, therefore, only has a short period of time, in early diastole, to get that oxygenated blood.

Beta blockade prolongs diastole and therefore prolongs the time that the coronaries aren’t being perfused. Based on that, some cardiologists (including where I trained) avoid beta blockers with the thought that they decrease coronary perfusion in severe AI and therefore promote ischemia. However, beta blockers also decrease myocardial oxygen demand.

So, as with most things in medicine, it’s a balance, and there are few good clinical studies.

Figure 1: Coronary perfusion in a normal heart

Figure 2: Coronary perfusion in severe aortic insufficiency

Read more: Aortic Regurgitation in Chapter 283: Aortic Valve Disease, Harrison’s Principles of Internal Medicine 19e.

The above Wiggers diagrams are modifications of: adh30 revised work by DanielChangMD who revised original work of DestinyQx; Redrawn as SVG by xavax – Wikimedia Commons: Wiggers Diagram.svg, CC BY-SA 4.0

Measuring BNP

If atrial natriuretic peptide (ANP) is released by distension of the atria, then brain natriuretic peptide (BNP) must be released by distension of the… ventricles? Don’t think about it too hard.

BNP and the N-terminal fragment of proBNP (NT-proBNP) are useful for diagnosing heart failure, especially when there’s uncertainty. In fact, at least one trial1 has suggested that it should be used for screening of high-risk patients to identify those who have preclinical heart failure (if such a thing can be said to exist).

Measurements of BNP and NT-proBNP can be used interchangeably, but have different cutoffs. The cutoffs stratify people into three categories: low likelihood of having heart failure (good LR-), high likelihood (good LR+), and intermediate (not terribly helpful).

Besides diagnosis, it can also be used for prognosis as well as for tracking response to treatment. That last one hasn’t made it into the guidelines yet.

Read more:

Works cited:

  1. Ledwidge M, Gallagher J, Conlon C, et al. Natriuretic Peptide–Based Screening and Collaborative Care for Heart Failure: The STOP-HF Randomized Trial. JAMA. 2013;310(1):66-74. doi:10.1001/jama.2013.7588.

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