“Comment on optimal treatment for resistant hypertension: The missing data on pulse wave velocity (PWV)” by Drs. Elias and Sullivan raises three points that merit attention regarding uncontrolled apparent treatment resistant hypertension (aTRH).1 aTRH is applied to datasets in which information in unavailable to distinguish between ‘true’ and one or more contributors to pseudo-resistance including home and/or ambulatory blood pressure (BP), patient adherence and adequacy of antihypertensive pharmacotherapy.2,3
First, BP values among patients with and without aTRH in the two reports suggest that uncontrolled systolic hypertension predominates (Table 1). Systolic hypertension is more often associated with TRH.3
Table 1.
Comparison of patients without and with aTRH in our report and MSLS.
| Variable | 0–2 BP medications | ≥3 BP Medications | ||
|---|---|---|---|---|
|
| ||||
| Southeast QUIN N=102,951 |
MSLS N=48 |
Southeast QUIN N=44.684 |
MSLS N=46 |
|
| Age, years | 55.9 (55.8–56.0) | 63.9 (60.5–67.2) | 60.6 (60.5–60.7) | 67.0 (63.7–70.8) |
| SBP, mmHg | 149.0 (149.0–149.1) | 141.3 (136.5–145.9) | 152.1 (152.0–152.3) | 152.2 (146.6–157.7) |
| DBP, mmHg | 86.3 (86.2–86.4) | 85.9 (83.9–88.0) | 83.7 (83.6–83.8) | 84.7 (82.1–87.2) |
| PP, mmHg | 62.7 | 55.4 | 68.4 | 67.5 |
S=Systolic; D=Diastolic, BP=blood pressure, PP=pulse pressure
Second, among subjects in the 7th wave of the Main Syracuse Longitudinal Study (MSLS), relative differences in pulse pressure (PP) and PWV between patients with and without aTRH are comparable (Table 1).1 PP, an indirect index of vascular stiffness, was ~22% higher among uncontrolled patients with than without aTRH ([Table 1] 67.5 mmHg/55.4 mmHg = 1.22),1 whereas PWV, a more direct index of vascular stiffness, was ~25% higher (12.9/10.3=1.25).1
The difference in PP between patients with and without aTRH in our Southeast Quality Improvement Network (QUIN) was only ~9% (68.4 vs 62.7 mmHg), rather than 22% as in MSLS. Systolic, diastolic and PP are remarkably similar among uncontrolled patients with aTRH in our report and MSLS (Table 1). However, systolic BP and PP are greater among patients without aTRH in Southeast QUIN than MSLS. We speculate that if PWV had been measured among patients in Southeast QUIN, the differences between groups with and without aTRH would have been smaller than MSLS. If the proportional relationship between differences of PWV to PP (25%/22% = 1.136) among uncontrolled patients with than without aTRH in MSLS applied to our patients, then PWV would have been ~10.2 higher (9% × 1.136 = 10.2%).
Third, among uncontrolled patients without aTRH, PP was greater in Southeast OQUIN than MSLS patients, despite the fact that the former averaged 8 years younger. While PP values were comparable among uncontrolled patients in the two studies with aTRH, Southeast OQUIN patients were on average more than 6 years younger than MSLS patients. Since increases in PP are linked to age-related vascular stiffening, these data coincide with reports indicating an earlier onset and greater severity of cardiovascular disease in the Southeast than other regions of the U.S.3,4
In summary, greater vascular stiffness among uncontrolled patients with than without ‘true’ TRH1 may help explain increased incident cardiovascular events in the former.5 As suggested by Drs. Elias and Sullivan,1 intervention strategies controlling BP and reducing vascular stiffness may improve outcomes and population health more than strategies controlling only BP.
Footnotes
Disclosures: Dr. Egan receives funding from Medtronic: (1) site co-investigator on Symplicity–3 (2) database analyses on treatment resistant hypertension (3) consultant/advisor on Power Over Pressure, which addresses treatment resistant hypertension. Dr. Egan is funded by NHLBI for a clinical study of treatment resistant hypertension (R34 HL105880).
Dr. Todoran is a site principal investigator for Symplicity–3, funded by Medtronic, which examines the effects of renal denervation on blood pressure in patients with treatment resistant hypertension.
References
- 1.Elias M, Sullivan K. Comment on optimal treatment for resistant hypertension: The missing data on pulse wave velocity. Hypertension. 2013 doi: 10.1161/HYPERTENSIONAHA.113.02742. (in press) [DOI] [PubMed] [Google Scholar]
- 2.Egan BM, Zhao Y, Li J, Brzezinski WA, Todoran TM, Brook RD, Calhoun DA. Prevalence of optimal treatment regimens in patients with apparent treatment resistant hypertension in a community-based practice network. Hypertension. 2013;62:691–697. doi: 10.1161/HYPERTENSIONAHA.113.01448. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Calhoun DA, Jones D, Textor S, Goff DC, Murphy TP, Toto RD, White A, Cushman WC, White W, Sica D, Ferdinand K, Giles TD, Falkner B, Carey RM American Heart Association Professional Education Committee. Resistant hypertension: diagnosis, evaluation, and treatment. Hypertension. 2008;51:1403–1419. doi: 10.1161/HYPERTENSIONAHA.108.189141. [DOI] [PubMed] [Google Scholar]
- 4.Hall WD, Ferrario CM, Moore MA, Hall JE, Flack JM, Cooper W, Simmons JD, Egan BM, Lackland DT, Perry M, Roccella EJ. Hypertension-related morbidity and mortality in the southeastern United States. Am J Med Sci. 1997;313:195–209. doi: 10.1097/00000441-199704000-00002. [DOI] [PubMed] [Google Scholar]
- 5.Salles GF, Cardoso CR, Muxfeldt ES. Prognostic influence of office and ambulatory blood pressures in resistant hypertension. Arch Intern Med. 2008;168:2340–2346. doi: 10.1001/archinte.168.21.2340. [DOI] [PubMed] [Google Scholar]
