30
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Morning Surge in Blood Pressure as a Predictor of Silent and Clinical Cerebrovascular Disease in Elderly Hypertensives : A Prospective Study

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Cardiovascular events occur most frequently in the morning hours. We prospectively studied the association between the morning blood pressure (BP) surge and stroke in elderly hypertensives. We studied stroke prognosis in 519 older hypertensives in whom ambulatory BP monitoring was performed and silent cerebral infarct was assessed by brain MRI and who were followed up prospectively. The morning BP surge (MS) was calculated as follows: mean systolic BP during the 2 hours after awakening minus mean systolic BP during the 1 hour that included the lowest sleep BP. During an average duration of 41 months (range 1 to 68 months), 44 stroke events occurred. When the patients were divided into 2 groups according to MS, those in the top decile (MS group; MS > or =55 mm Hg, n=53) had a higher baseline prevalence of multiple infarcts (57% versus 33%, P=0.001) and a higher stroke incidence (19% versus 7.3%, P=0.004) during the follow-up period than the others (non-MS group; MS <55 mm Hg, n=466). After they were matched for age and 24-hour BP, the relative risk of the MS group versus the non-MS group remained significant (relative risk=2.7, P=0.04). The MS was associated with stroke events independently of 24-hour BP, nocturnal BP dipping status, and baseline prevalence of silent infarct (P=0.008). In older hypertensives, a higher morning BP surge is associated with stroke risk independently of ambulatory BP, nocturnal BP falls, and silent infarct. Reduction of the MS could thus be a new therapeutic target for preventing target organ damage and subsequent cardiovascular events in hypertensive patients.

          Related collections

          Most cited references11

          • Record: found
          • Abstract: found
          • Article: not found

          Circadian variation in the frequency of onset of acute myocardial infarction.

          To determine whether the onset of myocardial infarction occurs randomly throughout the day, we analyzed the time of onset of pain in 2999 patients admitted with myocardial infarction. A marked circadian rhythm in the frequency of onset was detected, with a peak from 6 a.m. to noon (P less than 0.01). In 703 of the patients, the time of the first elevation in the plasma creatine kinase MB (CK-MB) level could be used to time the onset of myocardial infarction objectively. CK-MB-estimated timing confirmed the existence of a circadian rhythm, with a three-fold increase in the frequency of onset of myocardial infarction at peak (9 a.m.) as compared with trough (11 p.m.) periods. The circadian rhythm was not detected in patients receiving beta-adrenergic blocking agents before myocardial infarction but was present in those not receiving such therapy. If coronary arteries become vulnerable to occlusion when the intima covering an atherosclerotic plaque is disrupted, the circadian timing of myocardial infarction may result from a variation in the tendency to thrombosis. If the rhythmic processes that drive the circadian rhythm of myocardial-infarction onset can be identified, their modification may delay or prevent the occurrence of infarction.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Circadian variation in vascular tone and its relation to alpha-sympathetic vasoconstrictor activity.

            The frequency of several cardiovascular events, such as myocardial infarction, sudden death, and stroke, is increased during the early morning hours. There is also a similar circadian pattern in several physiologic variables, including blood pressure, suggesting that certain dynamic processes may contribute to the circadian distribution and onset of acute events. To determine whether there are circadian variations in vascular tone and to investigate their underlying mechanisms, we measured blood flow and vascular resistance in the forearm and their responses to phentolamine (an alpha-adrenergic-antagonist drug) and sodium nitroprusside (a direct vasodilator) in 12 normal subjects (7 men and 5 women; mean age [+/- SD], 44 +/- 9 years) at three different times of day (7 a.m., 2. p.m., and 9 p.m.). The drugs were infused into the brachial artery, and the responses were measured by strain-gauge plethysmography. The basal forearm vascular resistance was significantly higher, and the blood flow significantly lower, in the morning than in the afternoon and evening (mean vascular resistance, 31 +/- 8, 25 +/- 6, and 22 +/- 7 mm Hg per milliliter per minute per 100 ml of forearm volume, respectively; P less than 0.01). The vasodilator effect of phentolamine was also significantly greater in the morning (mean decrease in vascular resistance, 38 +/- 6 percent) than in the afternoon (26 +/- 6 percent) and evening (21 +/- 7 percent) (P less than 0.05). Consequently, there was no circadian variation in vascular resistance or blood flow after the infusion of this drug. In contrast, the vasodilation in response to sodium nitroprusside was similar at all three times of day. There is a circadian rhythm in basal vascular tone, due either partly or entirely to increased alpha-sympathetic vasoconstrictor activity during the morning. This variation may contribute to higher blood pressure and the increased incidence of cardiovascular events at this time of day.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Circadian variation in the incidence of sudden cardiac death in the Framingham Heart Study population.

              To determine if sudden cardiac death shows circadian variation, the time of day of sudden cardiac deaths in the Framingham Heart Study was analyzed. Analysis was based on mortality data collected in a standardized manner for the past 38 years for each death among the 5,209 persons in the original cohort. The necessary assumptions about the cause and timing of unwitnessed deaths were made in a manner likely to diminish the possibility of detecting an increased incidence of sudden cardiac death during the morning. In the Framingham study, analyses using these assumptions reveal a significant circadian variation (p less than 0.01) in occurrence of sudden cardiac death (n = 429), with a peak incidence from 7 to 9 AM and a decreased incidence from 9 AM to 1 PM. Risk of sudden cardiac death was at least 70% higher during the peak period than was the average risk during other times of the day. Further studies are needed to confirm this finding in other populations, to collect data regarding medications and to determine activity immediately before sudden cardiac death. Investigation of physiologic changes occurring during the period of increased incidence of sudden cardiac death may provide increased insight into its causes and suggest possible means of prevention.
                Bookmark

                Author and article information

                Journal
                Circulation
                Circulation
                Ovid Technologies (Wolters Kluwer Health)
                0009-7322
                1524-4539
                March 18 2003
                March 18 2003
                : 107
                : 10
                : 1401-1406
                Affiliations
                [1 ]From the Department of Cardiology (K.K., Y.U., S.H., Y.H., K.E., M. Morinari, M. Murata, T.K., K.S.), Jichi Medical School, Tochigi, Japan; The Zena and Michael A. Wiener Cardiovascular Center (K.K., T.G.P.), Mount Sinai School of Medicine; and the Department of Psychiatry and Behavioral Science, State University of New York at Stony Brook, NY (J.E.S), Stony Brook, NY.
                Article
                10.1161/01.CIR.0000056521.67546.AA
                12642361
                19efce7d-6081-4dcf-8673-bf552b2a8687
                © 2003
                History

                Comments

                Comment on this article