rss
  1. Overnight dehydration increases the risk of a morning infarct

    Dear Sir, It was with great interest that I read the recent article by A. Suarez- Barrientos and colleagues (1). However, I think there is one very important aspect left out of this very good clinical investigation and that is blood volume. One of the principal problems of heart pumping is having enough blood volume to do this with. If there is insufficient volume then the heart has to alter its rate of contraction, which can change filling time, or the force of contraction, which will depend on the overall peripheral resistance and the viscosity of the blood which will increase rates of cardiac hypertrophy and remodelling. It would appear then to be a problem of physiological fluid (haemo-) dynamics.

    In the study reported here the authors wrote that "the infarct size was found to be significantly larger with STEMI onset in the dark-to-light transition period (6:00 to noon)". This is the first section of the day after an overnight period of sleep. Fluid consumption is not usually recommended during this period yet there is substantial loss of water which leads to overnight dehydration of both the intra and extracellular compartments (2). Therefore, at the end of the sleep period there would be an overall decreased blood volume, which would imply reduced perfusion throughout the vascular system, with perhaps an increase in viscosity, and thus extra work for the heart. It would therefore not be surprising to see an increased number of infarcts occuring in this period. One of the indicators of insufficient blood volume is an increase in plasma levels of the hormones making up the renin-angiotensin-aldosterone system (RAS) (3). Although none of these hormones are treated in the current article I imagine if they were measured they would be increased in the period 6.00 to noon. Furthermore, antagonists of the RAS are used extensively in the treatment of heart failure (4). It could be suggested therefore that one way to reduce the risk of myocardial infarction in the morning would be improved tissue perfusion through increased water intake, perhaps before going to bed and at intervals during sleep.

    References.

    1. Su?rez-Barrientos A, L?pez-Romero P, Vivas D, Castro-Ferreira F, N??ez-Gil I, Franco E, Ruiz-Mateos B, Garc?a-Rubira JC, Fern?ndez-Ortiz A, Macaya C, Ibanez B. Circadian variations of infarct size in acute myocardial infarction. Heart. 2011 Apr 27. [Epub ahead of print] 2. Colwell CS. Preventing dehydration during sleep. Nat Neurosci. 2010;13:467-74. 3. Thornton SN. Thirst and hydration: physiology and consequences of dysfunction. Physiol Behav. 2010;100:15-21. 4. Zannad F, McMurray JJ, Krum H, van Veldhuisen DJ, Swedberg K, Shi H, Vincent J, Pocock SJ, Pitt B; EMPHASIS-HF Study Group. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med. 2011;364:11-21.

    Conflict of Interest:

    None declared

    Submit response
  2. CIRCADIAN VARIATIONS AND MELATONIN IN THE ACUTE MYOCARDIAL INFARCTION: STILL A FORGOTTEN EXTRACARDIAC FACTOR.

    To the Editor:

    We read with great interest the article by Su?rez-Barrientos et al (1) regarding circadian oscillations on infarct size. Although the article is both exhaustive and clinically relevant, we felt that the authors failed in the recognition of the potential value of melatonin in the association between cardiovascular events and circadian variation.

    Synchrony between external and internal circadian rhythms and harmony among molecular fluctuations within cells are essential for normal organ biology. Circadian clocks exist within multiple components of the cardiovascular system. These clocks have the potential of affecting multiple cellular processes and, therefore, they hold the promise of modulating various aspects of cardiovascular function over the course the 24-hr cycle (2). Many aspects of cardiovascular physiology are subject to diurnal variations, and serious adverse cardiovascular events appear to be conditioned by the time of day. The internal oscillator, or control station regulating the body's circadian clock, is the suprachiasmatic nucleus, a tiny structure located in the hypothalamus above the optic chiasm. The circadian pacemaker within the suprachiasmatic nucleus stimulates the pineal gland to produce circadian melatonin with high serum levels during the night (2). The results of many publications suggest a decrease in circulating melatonin concentration at different stages of the coronary heart disease in humans. Furthermore, experimental and clinical data suggest that melatonin is involved in normal cardiovascular physiology (3).

    Melatonin is known to be a powerful radical scavenger of the hydroxyl radical and to protect against cardiac tissue damage mediated by oxidative stress (2). A recent study from our group showed, in patients with ST- elevation myocardial infarction undergoing primary percutaneous coronary intervention, a relationship between melatonin concentrations and ischemia -modified albumin, a marker of myocardial ischemia. Our data suggest that melatonin acts as a potent antioxidant agent, reducing myocardial damage induced by ischemia/reperfusion (4). Furthermore, melatonin rhythmicity appears to have crucial roles in various cardiovascular functions as an antioxidant, an anti-inflammatory agent chronobiotic and possibly as an epigenetic regulator (2).

    We recognize that melatonin is of special interest, beging an endogenous molecule that can be used in humans, and which is also safe. The omission in the articles, such as that of Suarez-Barrientos et al (1), could deprive at the medical community of potentially useful information.

    REFERENCES 1. Suarez-Barrientos A, Lopez-Romero P, Vivas D, et al. Circadian variations of infarct size in acute myocardial infarction. Heart 2011 doi:10.1136/hrt.2010.212621. 2. Dominguez-Rodriguez A, Abreu-Gonzalez P, Sanchez-Sanchez JJ, Kaski JC, Reiter RJ. Melatonin and circadian biology in human cardiovascular disease. J Pineal Res 2010;49:14-22. 3. Reiter RJ, Tan DX. Melatonin: a novel protective agent against oxidative injury of the ischemic/reperfused heart. Cardiovasc Res 2003;58:10-9. 4. Dominguez-Rodriguez A, Abreu-Gonzalez P, Garcia-Gonzalez MJ, Samimi- Fard S, Reiter RJ, Kaski JC. Association of ischemia-modified albumin and melatonin in patients with ST-elevation myocardial infarction. Atherosclerosis 2008;199:73-78.

    Conflict of Interest:

    None declared

    Submit response
« Parent article

Free sample
This recent issue is free to all users to allow everyone the opportunity to see the full scope and typical content of Heart.
View free sample issue >>

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.