No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Valoración global del enfermo hipertenso. Hiponatremia inducida por carbamazepina y diuréticos
Abstract
We present the case of a 70-year-old patient with histories of arterial hypertension (HTN), electrocardiographic left ventricular hypertrophy (LVH), trigeminal neuralgia, and with controlled blood pressure. In the last year, she has undergone several changes in her hypertensive treatment in response to gradual BP elevations. She attends the consult for reasons of physical weakness, stress intolerance, malaise, paresthesias and muscular cramps of several months evolution which had been becoming worse. After a detailed study, it becomes evident that we are dealing with beta-blocker side effects, together with a secondary hyponatremia resulting from the use of diuretics and carbamazepine. We also note that the assumption of “good blood pressure control” was incorrect. A simple home self-measurement with a validated automatic device revealed continued morning rises in BP. After appropriate treatment modifications and a later follow-up, symptoms are observed to disappear and ionic alterations are normalized.
The use of oxcarbazepine as anti-seizure treatments has been related with many cases of hyponatremia (serum sodium
To determine whether diurnal variation occurs in the onset of stroke.
Community based study over four years.
Oxfordshire, United Kingdom.
105,000 people, of whom 675 had a first ever stroke. 545 had a cerebral infarction, 66 had primary intracerebral haemorrhage, 33 had subarachnoid haemorrhage, and in 31 the type of stroke was not known.
Time of stroke and degree of activity at onset.
In the 578 patients for whom it was known whether onset occurred while asleep or awake, the proportion with onset during sleep was 25% (135/545) for cerebral infarction, 17% (11/66) for primary intracerebral haemorrhage, and 0% (0/33) for subarachnoid haemorrhage. This difference persisted if patients in whom it was not known whether they were asleep or awake at onset were classed as asleep. For all stroke types together there was a significant (chi 2 = 218.7, p less than 0.001) diurnal variation with a morning peak between 0800 and 1000, which persisted even after allowing for strokes first noted on waking by redistributing the hour of onset through the preceding eight hours (chi 2 = 47, p less than 0.001). A significant diurnal variation was also found in the onset of cerebral infarction (peak 0800-1000, chi 2 = 208.4, p less than 0.001). Fewer patients had other forms of stroke and the diurnal variations for primary intracerebral haemorrhage (peak 1000-1200) and subarachnoid haemorrhage (peaks 0800-1000 and 1800-2000) were not significant. There seemed to be a second smaller peak for all types of stroke.
All types of stroke are most likely to occur after waking in the morning. The cause of the circadian variation requires further study.
The time of acute myocardial infarction was determined in all 1,741 patients of the ISAM (Intravenous Streptokinase in Acute Myocardial Infarction) Study, based on onset of clinical symptoms and evaluation of plasma CK-MB enzyme time-activity curves. The incidence of myocardial infarction was markedly increased between 6:00 AM and 12:00 noon compared with other times of day (p less than 0.001). Myocardial infarction occurred 3.8 times more frequently between 8:00 and 9:00 AM (hour of maximum incidence) than between 12:00 midnight and 1:00 AM (hour of minimum incidence). Time of myocardial infarction based on clinical and enzymatic methods correlated well (r = 0.95). Patients with higher or lower left ventricular ejection fraction, higher or lower degree of wall motion abnormalities and residual stenosis of the coronary arteries, and one-, two-, or three-vessel disease exhibited a similar circadian pattern, suggesting that the morning is a risk period for patients with mild as well as severe coronary artery disease. Only the group of patients receiving beta-adrenergic blocking therapy before the event did not show an increased morning incidence of myocardial infarction. This observation may contribute to an understanding of the mechanisms by which beta-blockers reduce the incidence of myocardial infarction. Further investigation of physiologic changes occurring during the morning period of increased risk of myocardial infarction may lead to better understanding of the disorder. Design and timing of cardioprotective medication may play a crucial role in improving prevention 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.
Evidence obtained over the past decade indicates that myocardial infarction (MI) and sudden death are not random events but rather, in many cases, may be triggered by the daily activities of the subject. The importance of physical or mental stresses as triggers is suggested by the parallel morning increased onsets of MI, sudden cardiac death, and stroke.
Unstable angina and MI are usually precipitated by thrombus formation over a disrupted plaque that causes partial or complete obstruction of coronary artery blood flow. This process may be caused by physiologic factors that lead to rupture of a vulnerable plaque and subsequent thrombosis. β-Blockers and aspirin, which can diminish these physiologic processes, have been shown to blunt or abolish the morning peak of onset of acute MI.
It is hypothesized that occlusive coronary thrombosis occurs when an atherosclerotic plaque becomes vulnerable to rupture, and mental or physical stress causes the plaque to rupture. Increases in coagulability or vasoconstriction triggered by daily activities may also contribute to complete occlusion of the coronary artery lumen.
Recognition of the circadian variation of the onset of acute cardiovascular disease suggests the need for pharmacologic protection of patients during the vulnerable periods and provides clues to the mechanism of disease onset, the investigation of which may lead to improved methods of prevention.
Hiponatremia al ingreso en pacientes mayores de 65 años. Relación con la estancia media y mortalidad hospitalaria
- A García
- C Gadea
- Ruiz B R Oliva
- F Antón
- J Pinilla
García A, Gadea C, Oliva B, Ruiz R, Antón F, Pinilla J, et al. Hiponatremia al ingreso en pacientes mayores de 65 años. Relación con la estancia media y mortalidad hospitalaria. Ann Med Interna 1994;10:487-9.
Hiponatremia en el anciano
- Camos P C López
- S Núñez
- Dalfó
Camos P, López C, Núñez S, Dalfó A. Hiponatremia en el anciano. Aten Primaria 1996;17:34-8.
Disorders of fluid balance deydra-tation and hiponatremia Principles of ge-riatrics. Medicine and Gerontology. 3. a ed
- Davis Km Minaker Kl Hazzard Wr
- Bleman El
- Jp
- Ettinger Wh
- Halter
- Jb
Davis KM, Minaker KL. Disorders of fluid balance deydra-tation and hiponatremia. En: Hazzard WR, Bleman EL, Blass JP, Ettinger WH, Halter JB, editores. Principles of ge-riatrics. Medicine and Gerontology. 3. a ed. New Basker-Vi-lle: McGraw-Hill Inc; 1994. p. 1183-90.
Medicina Interna versión electrónica. Capí-tulo 29. Alteraciones del agua y los electrólitos 1997
- Rodés J Guardia
Rodés J, Guardia J. Medicina Interna versión electrónica. Capí-tulo 29. Alteraciones del agua y los electrólitos 1997. p. 243-9.
Fisiología clínica de los trastornos elec-trolíticos y del equilibrio ácido-base Trastornos de los electrólitos y del equilibrio ácido-base. Lippincott. Marbán
- Rose Bd Post Rw Rose Bd
- Black Rm
- Rw Schrider
- T Post
- Narirg
Rose BD, Post RW. Fisiología clínica de los trastornos elec-trolíticos y del equilibrio ácido-base. En: Rose BD, Black RM, Schrider RW, Post T, Narirg RG, editores. Trastornos de los electrólitos y del equilibrio ácido-base. Lippincott. Marbán; 2002. p. 447-76.
Incremento matutino de la pre-sión arterial. Aspectos fisiopatológicos y clínicos. Boherin-ger Ingelheim
- A V Lahera
- Poch
Mora-Maciá J, González-Juanetey R, Redón J, Roca-Cu-sachs A, Lahera V, Poch E. Incremento matutino de la pre-sión arterial. Aspectos fisiopatológicos y clínicos. Boherin-ger Ingelheim. Barcelona: Caronte; 2000. p. 57-112.
A quantitative analisis of the effects of ac-tivity and time of day on the diurnal variations of blood pressure
- Clark La L Denby
- D Pregibon
- Chlirman
- Lawrence Rk Sg
- Pickering
Clark LA, Denby L, Pregibon D, Chlirman SG, Lawrence RK, Pickering TG. A quantitative analisis of the effects of ac-tivity and time of day on the diurnal variations of blood pressure. J Chronic Dis 1987; 40:671-9.
Hormona tirotropa en la población adulta demandante de un centro de atención primaria
- Casas J R Marquet
- E Grifell
- Cortés P Benet Jm
- Lucas
Casas J, Marquet R, Grifell E, Benet JM, Cortés P, Lucas A. Hormona tirotropa en la población adulta demandante de un centro de atención primaria. Med Clin 1990;95: 89-91.
Alteraciones de Líquidos y elec-trólitos Madrid: McGraw-Hill-Intera-mericana
- Singer Gg
- Brenner Bm
- E Braunwald
- Isselbacher
- Kj
- Wilson
- Martin Yb Jd
- Al Kaspe
Singer GG, Brenner BM. Alteraciones de Líquidos y elec-trólitos. En: Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin YB, Kaspe AL, et al, editores. Principios de Me-dicina Interna. Vol I. 14. a ed. Madrid: McGraw-Hill-Intera-mericana; 1998. p. 303-16.