Seeing the Forest, But Not the Trees: Pertinent Considerations for Examining Acute Changes in Pulse Wave Velocity in Response to Pharmaceutical Interventions and Exercise

Gkaliagkousi and colleagues1 examined the effect of 3 months of lowering blood pressure (with 160 mg of the angiotensin II receptor blocker valsartan) on aortic pulse wave velocity at rest and in response to 85% maximum heart rate aerobic exercise (duration was not reported). Aortic stiffness is a powerful tool for predicting cardiovascular mortality and morbidity that incorporates a multitude of physiological information including arteriosclerotic progression, prevailing autonomic balance, and distending pressure.2-4 As such, the implications of Gkaliagkousi's results may allow for better understanding of arterial stiffness responses to both exercise and various pharmaceutical agents. A few salient points would aid in the elucidation of the present data. First, as acknowledged, it is well appreciated that mean arterial pressure (MAP) is the primary factor capable of acutely altering central arterial distensibility secondary to the effect of varying distention on visoelastic components of the arterial wall.4, 5 For example, increased MAP increases the propagation speed of the pulse wave while lower MAP leads to the opposite effect. In light of this major consideration, and the clear effect of exercise and valsartan treatment on blood pressure in this study, it would be salient to consider changes in blood pressure as a possible explanation for the major findings.6 It appears that changes in blood pressure largely mirror the changes in aortic stiffness shown in the present study (Figure 1 and Figure 2), although the most pertinent measure (ie, central blood pressure) is missing the key time point during max exercise (Figure 3), and it is not reported at what duration of exercise these measures were recorded from. Did any significant changes between groups or conditions persist after normalizing for prevailing MAP? This could be rudimentarily completed by simply dividing aortic stiffness by the concurrent MAP. Second, it is not described whether the foot-to-foot technique was used or some other strategy (such as derivative of the upstroke or peak of the systolic waveform) to detect pulse wave arrival. These latter techniques are particularly sensitive to changes in heart rate (while the foot-to-foot technique is not) and therefore may have further confounding influences considering the heart rate responses during and after exercise.5 How was pulse wave arrival detected? Last, no study has examined the relationship between acute changes in aortic stiffness in response to exercise and/or pharmaceuticals and long-term changes in aortic stiffness as a result of long-term analogous interventions. Although the basic understanding of the acute relationships between blood pressure, exercise/pharmacy, and aortic stiffness is of basic-science interest, the long-term implications or potential impact on cardiovascular disease risk remain hypothetical. In order to translate findings from studies such as these into clinical relevancy, a long-term study examining whether the acute vascular changes in response to exercise/pharmacy are related to long-term changes in vascular health is needed, similar to that which has been done for blood pressure itself.7 In summary, although greater clarity is needed in the experimental design, Gkaliagkousi and coworkers provide new insight to better understand the interconnected relationship between blood pressure, aortic stiffness, and exercise. Future studies should attempt to address the mechanisms and interactions of these important variables.

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