2 Matching Annotations
  1. Jul 2018
    1. On 2017 Jun 13, David Keller commented:

      The above letter to the editor is freely available at the following link, and is posted here to stimulate discussion, and perhaps elicit answers to questions raised in the study:

      http://www.nejm.org/doi/full/10.1056/NEJMc1309586#SA1?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed

      To the Editor:

      Anderson et al. (June 20 issue)[1] describe the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial 2 (INTERACT2), in which patients received alpha-blockers, diuretics, combined alpha- and beta-blockers, calcium-channel blockers, nitrates, hydralazine, and other anti-hypertensive agents. These medications lower blood pressure by means of different mechanisms and therefore have different effects on relevant physiological variables such as vascular smooth-muscle tone, intravascular volume, heart rate, and pulse pressure. For example, the authors indicate that 16.2% of patients in the intensive-treatment group received a calcium-channel blocker “such as nicardipine or nimodipine” versus 8.5% of patients in the standard-treatment group. Nimodipine is known to reduce adverse outcomes associated with arterial vasospasm when administered after subarachnoid hemorrhage.[2] If more of the patients in the intensive-treatment group received nimodipine and benefited from this additional protection, independent of its antihypertensive effect, then this imbalance would tend to inflate the apparent benefit of intensive blood-pressure lowering. How much of the overall benefit seen with intensive treatment was due to lower blood pressure per se, and how much was due to pleiotropic effects of the medications used?

      David L. Keller, M.D. Providence Medical Group, Torrance, CA

      email: davidlouiskeller@gmail.com

      No potential conflict of interest relevant to this letter was reported.

      References

      1: Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med 2013;368:2355-2365

      2: Allen GS, Ahn HS, Preziosi TJ, et al. Cerebral arterial spasm -- a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med 1983;308:619-624


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.

  2. Feb 2018
    1. On 2017 Jun 13, David Keller commented:

      The above letter to the editor is freely available at the following link, and is posted here to stimulate discussion, and perhaps elicit answers to questions raised in the study:

      http://www.nejm.org/doi/full/10.1056/NEJMc1309586#SA1?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed

      To the Editor:

      Anderson et al. (June 20 issue)[1] describe the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial 2 (INTERACT2), in which patients received alpha-blockers, diuretics, combined alpha- and beta-blockers, calcium-channel blockers, nitrates, hydralazine, and other anti-hypertensive agents. These medications lower blood pressure by means of different mechanisms and therefore have different effects on relevant physiological variables such as vascular smooth-muscle tone, intravascular volume, heart rate, and pulse pressure. For example, the authors indicate that 16.2% of patients in the intensive-treatment group received a calcium-channel blocker “such as nicardipine or nimodipine” versus 8.5% of patients in the standard-treatment group. Nimodipine is known to reduce adverse outcomes associated with arterial vasospasm when administered after subarachnoid hemorrhage.[2] If more of the patients in the intensive-treatment group received nimodipine and benefited from this additional protection, independent of its antihypertensive effect, then this imbalance would tend to inflate the apparent benefit of intensive blood-pressure lowering. How much of the overall benefit seen with intensive treatment was due to lower blood pressure per se, and how much was due to pleiotropic effects of the medications used?

      David L. Keller, M.D. Providence Medical Group, Torrance, CA

      email: davidlouiskeller@gmail.com

      No potential conflict of interest relevant to this letter was reported.

      References

      1: Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med 2013;368:2355-2365

      2: Allen GS, Ahn HS, Preziosi TJ, et al. Cerebral arterial spasm -- a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med 1983;308:619-624


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.