As we are settled in the Middle East now. I feel it is important to know about how good are dates for cardiovascular disease.
The concept of “predisease” arose in 1914 when Dr. William Rodman came up with the idea of intervening early on those patients having signs of a precancerous state. However, Rodman acknowledged that his thesis would be controversial when noted: “I am aware that the term precancerous can be objected by at least two reasons: first, not always there will be a precancerous state; second, if this state existed, it does not mean that cancer will develop”.
Nevertheless, with the goal in preventing the appearance of morbid events, predisease as category makes sense if the following three conditions are met: 1) individuals who fall into this category should be more likely to develop disease; 2) There must be a an intervention that when directed towards this individuals at risk be effective in reducing the risk of evolution to disease, and 3) the benefits of intervening on the pre-disease must exceed the risks. Currently, the state of predisease applies for various conditions: pre-diabetes, pre-hypertension, subclinical thyroid dysfunction or even individuals tested positive for human immunodeficiency virus. All these clinical situations involve an increased risk of developing the disease. Although the lapse of time for this to happen might be uncertain in most cases, lots of studies have shown that there can be several damages at molecular and cellular levels that might be impairing tissues and at the same time fueling the occurrence of the disease.
Then, I wonder, are the current and most used cut-off points in medical practice really reliable to advise a patient on whether he or she has an unhealthy condition?
In the author’s opinion, a fundamental limitation of the cut-off points is that their use on biological variables might be biased since there is not any reliable foundation to do so. However, we keep labeling individuals as healthy or sick based on them and it has been this way since a long time and probably will be until we consider the problem more comprehensibly and stop staying on shallow waters instead of going into the deep end.
I acknowledge that currently the decision-making process would be very weak without cut-off point to make decisions but we must be very cautious when giving an opinion based on them.
In addition, it is valid to say that most of the cut-off points we use in our day to day practice with patient are not autochthonous but they have been taken from guidelines, pathways, etc that have nothing to do with the population of patient we deal with.
Can you imagine what would it be like to use a cut-off points to determine if one individual living in the middle east had any health condition using cut-off points offered by health institutions based in Canada, USA or Asia? It sounds like nonsense, however we do it every day. Why? because we have never thought on it. Some time we simply use what we have been given or taught as the best evidence, but this evidence is far away from us in terms of ethnicity, genetics or socioeconomic status and these factors indeed could have been a significant statistical impact in the countries they were used when where pooled to yield certain cut-off figures, but it does not mean that can be widely used across regions and continents.
Accordingly, I think that each country’s medical society must dig deep and pull out its own cut-off points, otherwise we will continue to miss key elements when it comes to diagnosing in medicine.
In the end my dear colleagues, the autochthonous is and always will be the most consistent and reliable. To be enticed by names of medical associations with a well gained fame in terms of taking all they offered as the absolute truth can be deceptive. So, never fall into the “Band Wagon“ fallacy (if most people like them, then they must be okay)
On one next post, I will expose some examples of some steps taken on this.
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A post from a good blog I want to share with you.
by Rebecca Briant, Student and Receptionist, London, UK
The average life expectancy of humans is increasing at an unprecedented rate. Seen as one of the great achievements of the century, in the last 40 years alone it has risen by 10 years, and in 2011 life expectancy at birth was almost double what it was in 1841(1). But what will happen if our life span continues to increase, and how can we address the issues we will face?
As most people know, with age there comes a natural deterioration of the body. However, what we are already witnessing, and will see more of should trends continue to increase, is an unmanageable presence of chronic, multi-symptomatic conditions in our elderly and increasingly in younger people, which create a huge economic strain on the NHS. The annual cost of health and social care is far higher for elderly people, with more than…
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This is an excerpt of an article written by me submitted recently to be assessed for publication in a scientific journal that I would like to share with you.
In medical practice is common to find situations that might call into question any practitioner on the epidemiological component of cardiovascular disease (CVD).
How many times we assess patients with multiple cardiovascular risk factors (CRF) and poor adherence to the treatment and they never develop one expected disease resulting from these CRF. While at the other extreme, there are individuals without CRF and with an appropriate lifestyle who begin suffering from an “unexpected” acute or chronic heart disease.
Taking into account the above mentioned, this article attempts to answer the following question: which would be the wiser perspective to address the issue of cardiovascular risk in relation to causation in CVD? Continue reading “Why some people with very risky lifestyle and lots of risk factors can live longer than others free of risks? A long-standing question in medical practice.”
Those who has drunk the energy beverage called Red Bull might be aware that its slogan since 1984 when it was first introduced into the Market is “Red Bull gives you wings”, meaning somehow that by consuming it you are freer.
To start with, briefly, I will tell you something that happened to me at my hospital in Cuba. It was a very exhausting day, and the last patient was a 16-aged male teenager who came in along with his parents which seemed to be very concerned for the lack of control of their child´s blood pressure despite the right measurements ordered to him over the past month when the diagnosis was made.
It was a moderate high blood pressure without known cardiovascular risk factors and all the tests indicated so far were within the normal range. The patient and his parents assured me that the non-pharmacological and pharmacological measurements are being carried out in good terms.
After a long chat where I could not find any insights related with this lack of blood pressure control, at last I asked him the following: Continue reading “Red Bull beverage and high blood pressure in adolescents. Watch out ¡¡¡¡¡.”
Since the publication in 1977 of the First American Task Force for the diagnosis, evaluation and treatment of high blood pressure (BP) in children and adolescents, updated in 1987, 1996 and more comprehensibly in 2004 (as Fourth Report) has been stressed out the importance of HTN related organ damage being, in this context, LVH a paradigm. Likewise, the latest European Society of HTN guidelines for the management of HTN in children and adolescents published in 2016 has highlighted the assessment of subclinical organ damage as an intermediate stage in the continuum of vascular disease as well, targeting predominantly LVH (2) Woroniecki and colleagues’ article (1) exposed the somehow puzzling issue when it comes to defining LVH in pediatric population on the basis of the existence of diverse criteria with pros and cons. These arguments are not new and have made very difficult over years to ascertain a reliable standardization of LVH definition at the early stages of life in children and adolescents suffering from HTN. Although, the authors of the article do not mention the connection of prehypertension with LVH, this association exists (3) and can trouble even more the things to decipher a definition of LVH for prehypertensive patients since the long-established studies that have reported the different formulas to define LVH in children and adolescents have been conducted on hypertensive individuals (2)
Unquestionably, the search for a definition of LVH in the context we are commenting here is complex with multiple answer and a solution far to be beheld to date; even though, the future might unfold some results especially with the American Heart Association’s SHIP-AHOY study, intended to evaluate blood pressure thresholds, ambulatory blood pressure, and metabolic phenotype that predicts hypertensive target organ damage. In addition, it is planned an update of the Fourth Report that would help with the necessary consensus on LVH (3)
In the meantime, according to our opinion, the appraisal of HTN induced LVH must get ahead of the simple quantification of left ventricular mass by focusing on the early diastolic alterations as regional mitral Ea, Aa and the E/Ea ratio by Tissue doppler imaging that precede the onset of LVH since this hypertrophy can be observed with the use of steroid, obesity, athletes, growth hormone use, etc., therefore can be reversible (4)
Those topics are not mentioned in Woroniecki and colleagues’ article (1) and might be key to increase consistency to the assessment of the HTN related cardiac organ damage in children and adolescents.
In the PESESCAD-HTA study we found diastolic abnormalities even in prehypertensive adolescents without LVH which makes it clear the relevance of targeting diastolic alterations on individuals prone to be hypertensive likely in the short term (5)
In short, the issue of LVH in pediatric populations remains challenging. The solution will lie on in undertaking large multinational studies in an attempt to find out a more reliable and matching approach to determine the cardiac organ damage that HTN entails in children and adolescents.
1- Woroniecki, Robert P, Andrew Kahnauth, Laurie E Panesar, and Katarina Supe-Markovina Left Ventricular Hypertrophy in Pediatric Hypertension: A Mini Review. Front. Pediatr (2017) 5:101.doi:10.3389/fped.2017.00101
2- Lurbe E, Agabiti-Rosei E, Cruickshank J, Dominiczak A, Erdine S, Hirth A, et al. 2016 European Society of Hypertension guidelines for the management of high blood pressure in children and adolescents. J Am Soc Hypert (2016); vol: 34 (10) pp: 1887-1920.
3- Sethna CB, Leisman DE. Left Ventricular Hypertrophy in Children with Hypertension: in Search of a Definition. Curr Hypertens Rep (2016) Aug;18(8):65. doi: 10.1007/s11906-016-0672-3.
4- Agu NC, McNiece Redwine K, Bell C, Garcia KM, Martin DS, Poffenbarger TS, et al. Detection of early diastolic alterations by tissue Doppler imaging in untreated childhood-onset essential hypertension. J Am Soc Hypertens (2014);8(5):303–11. Available from: http://www.ncbi.nlm.nih.gov/pubmed/24685005.
5- Perez Fernandez GA, Grau Avalo R. Hypertensive heart disease in adolescence. preliminary results of the PESESCAD-HTA study. Hipertens y Riesgo Vasc (2012) ;29(3):75–85.
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Valentín Fuster, uno de los padres de la cardiología moderna, en la décimo sexta conferencia de Bethesda. EE.UU. en 1996, acerca del papel biológico de los factores de riesgo cardiovascular (FRC), emitió una interesante y no menos jocosa afirmación: “la mejor manera de evitar la aterosclerosis es “escoger” a los progenitores sabiamente”.
Según la literatura, los individuos con antecedentes patológicos familiares (APF) de FRC presentan cifras de presión arterial (PA) mayores que aquellos descendientes de familiares sin este riesgo; aseveración confirmada desde la edad pediátrica con tendencia a adquirir más relevancia posteriormente 1. Se plantea que cuando ambos padres son hipertensos, teóricamente el 50 % de los hijos heredará la condición; si uno solo lo es, la cifra desciende al 20 ó 30 %.
La contribución de la historia familiar de riesgo cardiovascular al exceso de riesgo es independiente del accionar de otros FRC y se ha relacionado con una serie de anormalidades, incluso desde la adolescencia, en individuos con APF de ECV, como son: hiperinsulinismo, resistencia a la insulina, intolerancia a la glucosa, disfunción endotelial, y alteraciones lipídicas y del metabolismo de las mitocondrias 1.
Solini y colaboradores 2, al medir las concentraciones séricas de selectina P, interleucina 6, metaloproteinasas 2 y 9 y el factor tisular inhibidor de las metaloproteinasas en sujetos con APF de ECV y sin este antecedente, llegan a la conclusión de que aquellos con una historia familiar positiva de ECV presentaron niveles de estas sustancias significativamente mayores, lo que sin dudas constituye un elemento indicativo de la presencia de aterosclerosis en los individuos con APF de ECV.
Vercoza y colaboradores 3 midieron por ultrasonografía de alta resolución el grosor de la íntima y la media de la arteria braquial entre niños en edad escolar, y encontraron asociaciones significativas entre dichos parámetros y la presencia de APF de ECV.
En opinión del autor, el presentar APF de ECV es un riesgo para el desarrollo de HTA; la distinción de cuál de los antecedentes es el más notable no es lo más significativo, si se tiene en cuenta que más del 50 % de los individuos poseen más de un APF de ECV; y que el patrón de herencia en este caso no es mendeliano, sino complejo. Lo trascendente aquí sería no dejar de pesquisar la existencia de una historia familiar de FRC.
1- Kones R. Recent advances in the management of chronic stable angina II. Anti-ischemic therapy, options for refractory angina, risk factor reduction, and revascularization. Vasc Health Risk Manag. 2010;6:749-74.
2- A Solini, E Santini, A Passaro, S Madec and E Ferrannini. Family history of hypertension, anthropometric parameters and markers of early atherosclerosis in young healthy individuals. J Hum Hypertens 2009; 23:801–807.
3- Verçoza AM, Baldisserotto M, de Los Santos CA, Poli-de-Figueiredo CE, d’Avila DO. Cardiovascular risk factors and carotid intima-media thickness in asymptomatic children. Pediatr Cardiol. 2009;30(8):1055-60.
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