Orthostatic hypertension and strokes

That's right you read the title correctly- it reads orthostatic hypertension and not hypotension.  Ordering orthostatics on patients is quite common.   Most of the time the clinical query is in regards to the latter (hypotension).  My mentor, Dr. Andreoli, would often refer to performing orthostatics in the hospital as the "death provocation test".  He reasoned that a great majority of hospitalized patients with acute illness will have a significant drop in blood pressure after rising from a seated position.  He felt this was likely not always indicative of volume depletion, but rather from a global sympathetectomy from their acute illness.  If we asked a patient to quickly rise and they did in fact have a robust drop in blood pressure a topple to the floor with resulting head trauma could occur.  Always makes me want to have a couple of extra hands on deck when performing this maneuver.  But, what about performing orthostatic blood pressure measurements on stable outpatients with no complaints. 

I read an interesting editorial in Hypertension this week in regards to orthostatic hypertension.  It took a few glances to read that correctly.  Occasionally I check orthostatic blood pressures on patients in the clinic and get a surprising result.  A huge increase in blood pressure of 40 mmHg from sitting to standing.  I never really thought about the long term consequences of this until I read this editorial and accompanying article by Yatsuya et al.  

Yatsuya et al. prospectively followed 12,817 patients (in the ARIC study) who had baseline orthostatic blood pressure measurements.  They further grouped theses patient into several baseline categories depending on their BP changes from sitting to 2 min after standing.

1. Decline in BP- Major (-63 to -20), 547 subjects or Minor (-20 to -10), 1507 subjects 
2. Stable BP- (-10 to +10), 8981 subjects 
3. Increase in BP- Major (+65 to +20), 303 subjects or Minor (+20 to +10), 1479 subjects

Data was obtained in regards to ischemic stroke incidence and type for a median of 18.7 years.  They report:

• Little change in BP after standing in the entire cohort.  SBP increased 0.4 mmHg and DBP increased by 3mmHg. 
• Patients with orthostatic SBP and DBP decreases of greater than 20mmHg had an increased incidence of thrombotic and cardioembolic strokes. 
• Patients with orthostatic SBP decreases and increases of greater than 20mmHg had an increased incidence of lacunar strokes.  

The authors conclude that these findings are consistent with previous studies showing silent strokes in elderly hypertensive patients with orthostatic hypo- or hypertension.  They speculate that this BP elevation from sitting to standing could be due to excessive sympathetic nervous system activation, which could in turn lead to endothelial dysfunction.  Another theory discussed in the editorial and by these authors is that elderly patients with orthostatic hypertension have been shown have excessive BP dipping at night with greater than a 25mmHg drop in BP (referred to as "extreme dipping").  These "extreme dippers" had an increased risk of silent stroke as well.  Several limitations are present.  Only a baseline orthostatic value is present.  How would these values change over time or would they hold true?  Second, not every participant had an MRI to look for silent strokes.  However, this study was prospective and contains a large sample size.  


How will this change practice? Hard to say.  This could merely serve as a marker for autonomic dysfunction and might not be a modifiable risk factor.  Simple measures such as compression stockings have been used to control both orthostatic hypo- and hypertension.  Beta blockers could be useful in controlling orthostatic hypertension.  Further clinical trials to directly examine these relationships could help in answering these questions.