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Stroke. 2006;37:1968
Published online before print June 22, 2006, doi: 10.1161/01.STR.0000231853.36237.2d
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(Stroke. 2006;37:1968.)
© 2006 American Heart Association, Inc.


Letters to the Editor

Response to Letter by Mysak et al

Ralph L. Sacco, MS, MD, FAAN, FAHA

Stroke and Critical Care Division, Neurological Institute, Columbia University, New York, NY

Larry B. Goldstein, MD, FAAN, FAHA

Duke Center for Cerebrovascular Disease, Center for Clinical Health Policy Research, Duke University Medical Center, Durham, NC

Response:

We appreciate the thoughtful comments from Drs Mysak and Tulloch. We agree that the definition of hypertension used in the PROGRESS trial was a systolic blood pressure ≥160 mm Hg or a diastolic blood pressure ≥90 mm Hg.1 Those with blood pressures below this threshold were classified as nonhypertensive based on older definitions. As correctly pointed out by Drs Mysak and Tulloch, the mean blood pressure in this "non-hypertensive" group of 136/79 mm Hg is in the "pre-hypertension" range (120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic) as defined by JNC-VII.2 Although the standard deviations and range of blood pressures in the "non-hypertensive" group are not given in the PROGRESS trial report, as this is a mean value, the group likely includes subjects who would be classified as having "normal" blood pressures. The recommendation, "Because this benefit extends to persons with and without a history of hypertension, [treatment] should be considered for all ischemic stroke and TIA patients (Class IIa, Level of Evidence B)" is appropriate and reflects the available evidence. This statement, however, needs to be qualified by the recommendation that follows. "An absolute target BP level and reduction are uncertain and should be individualized, but benefit has been associated with an average reduction of 10/5 mm Hg, and normal BP levels have been defined as <120/80 mm Hg by JNC-7 (Class IIa, Level of Evidence B)." Given the stated normal BP of 120/80 mm Hg, we did not mean to imply that stroke patients with normal BP levels would warrant treatment. Unfortunately, most studies still show that the prevalence of under-treated BP in stroke and TIA survivors is still too great.

With regard to hypertension control among diabetics, we agree with the authors that the ALLHAT trial did not show a significant benefit of ACEI over diuretics. Our recommendations, however, were based on the bulk of the evidence from randomized trials and not just this one trial or a consensus statement from the American Diabetes Association. We stated that "ACEI- and ARB-based treatments both have been shown to favorably affect the progression of diabetic nephropathy and reduce albuminuria, and ARBs have been shown to reduce the progression to macroalbuminuria."3–8 We also recommended that "Although all major classes of antihypertensives are suitable for the control of BP, most patients will require more than 1 agent."

We also call the authors attention to our recommendation in the hypertension section where we stated, "The optimal drug regimen remains uncertain; however, the available data support the use of diuretics and the combination of diuretics and an ACEI (Class I, Level of Evidence A). The choice of specific drugs and targets should be individualized on the basis of reviewed data and consideration of specific patient characteristics (eg, extracranial cerebrovascular occlusive disease, renal impairment, cardiac disease, and diabetes; Class IIb, Level of Evidence C)."

We agree with the authors regarding the use of proprietary drug names and apologize for the oversight.

Acknowledgments

Disclosures

None.

References

  1. PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6105 individuals with previous stroke or transient ischaemic attack. Lancet. 2001; 358: 1033–1041.[CrossRef][Medline] [Order article via Infotrieve]
  2. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, Jones DW, Materson BJ, Oparil S, Wright JT, Roccella EJ. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report. JAMA. 2003; 289: 2560–2571.[Abstract/Free Full Text]
  3. Lewis EJ, Hunsicker LG, Bain RP, Rohde RD. The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. The Collaborative Study Group. N Engl J Med. 1993; 329: 1456–1462.[Abstract/Free Full Text]
  4. Laffel LM, McGill JB, Gans DJ. The beneficial effect of angiotensin-converting enzyme inhibition with captopril on diabetic nephropathy in normotensive IDDM patients with microalbuminuria. North American Microalbuminuria Study Group. Am J Med. 1995; 99: 497–504.[CrossRef][Medline] [Order article via Infotrieve]
  5. Lewis EJ, Hunsicker LG, Clarke WR, Berl T, Pohl MA, Lewis JB, Ritz E, Atkins RC, Rohde R, Raz I; Collaborative Study Group. Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes. N Engl J Med. 2001; 345: 851–860.[Abstract/Free Full Text]
  6. Brenner BM, Cooper ME, de Zeeuw D, Keane WF, Mitch WE, Parving HH, Remuzzi G, Snapinn SM, Zhang Z, Shahinfar S; RENAAL Study Investigators. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med. 2001; 345: 861–869.[Abstract/Free Full Text]
  7. Parving HH, Lehnert H, Brochner-Mortensen J, Gomis R, Andersen S, Arner P; Irbesartan in Patients with Type 2 Diabetes and Microalbuminuria Study Group. The effect of irbesartan on the development of diabetic nephropathy in patients with type 2 diabetes. N Engl J Med. 2001; 345: 870–878.[Abstract/Free Full Text]
  8. Julius S, Kjeldsen SE, Weber M, Brunner HR, Ekman S, Hansson L, Hua T, Laragh J, McInnes GT, Mitchell L, Plat F, Schork A, Smith B, Zanchetti A; VALUE trial group. Outcomes in hypertensive patients at high cardiovascular risk treated with regimens based on valsartan or amlodipine: the VALUE randomised trial. Lancet. Jun 19 2004; 363 (9426): 2022–2031.

Related Article:

Addressing the Guidelines
Tania Mysak and Karen Tulloch
Stroke 2006 37: 1967. [Full Text] [PDF]




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