The data is accumulating to show the adverse outcomes in critically
sick patients with persistently elevated troponins. An elegant study by
Amman et al (1) in 58 critically ill patients without acute coronary
syndromes concluded "Positive troponin levels were associated with higher
mortality (22.4% vs. 5.2%, p < 0.018) and a lower LVEF (p = 0.0006).
Troponin-positive patients had significantly high...
The data is accumulating to show the adverse outcomes in critically
sick patients with persistently elevated troponins. An elegant study by
Amman et al (1) in 58 critically ill patients without acute coronary
syndromes concluded "Positive troponin levels were associated with higher
mortality (22.4% vs. 5.2%, p < 0.018) and a lower LVEF (p = 0.0006).
Troponin-positive patients had significantly higher median levels of tumor
necrosis factor (TNF)-alpha, its soluble receptor, and interleukin (IL)-6.
A subgroup of 10 aplastic patients was troponin-negative at study entry.
Three became troponin-positive during leukocyte recovery and subsequently
died, whereas all the others stayed troponin-negative and survived. Flow-
limiting coronary artery disease was not demonstrable at autopsy or stress
echocardiography in 72% of troponin-positive patients".
The results of the present study ( 2), if reproduced in larger
studies in patients with acute exacerbation of chronic obstructive
pulmonary disease; the future guidelines will include estimation and
trajectory of troponin for such patients to assess prognosis. Presently,
there is no way to influence the poor natural history of such patients
.However the future is to explore possible interventions to favourably
influence the natural history. The authors deserve congratulations for
their thought-provoking work.
References:
1.Amman P ,Maggiorini M, Bertel O, et al.Troponin as a risk factor
for mortality in critically ill patients without acute coronary
syndromes.J Am Coll Cardiol .2003;41:2004-2009.
2.Arne Didrik Hoiseth, Anke Neukamm, Tor-Arne Hagve, Torbjorn Omland,
Pol H Brekke, and Vidar Soyseth.
The clinical value of serial measurement of high-sensitivity cardiac
troponin T in acute exacerbations of chronic obstructive pulmonary
disease. Open Heart 2014 1:e000001; doi:10.1136/openhrt-2013-000001
The current dietary guidelines are strongly associated (at least
temporally) with an exponential growth in obesity and Type 2 diabetes.
These unintended consequences may have arisen due to increased consumption
of carbohydrate in order to reduce fat in the diet.
If the guidelines cannot rely on a solid basis of science then they
should be withdrawn and re-written. There is a precedent - we no longer
have limits...
The current dietary guidelines are strongly associated (at least
temporally) with an exponential growth in obesity and Type 2 diabetes.
These unintended consequences may have arisen due to increased consumption
of carbohydrate in order to reduce fat in the diet.
If the guidelines cannot rely on a solid basis of science then they
should be withdrawn and re-written. There is a precedent - we no longer
have limits on dietary cholesterol.
As a layman I feel I have been deceived by "lipophobic cardiologists"
and my food supply has been altered on the basis of false or missing
evidence. I am confronted by red traffic light labels on foods we have
eaten for centuries and I feel the establishment has lost the plot on this
one.
As Professor David Haslam said, it's time for the demonisation of
saturated fat to stop - https://www.youtube.com/watch?v=kf8m04Gu4X0
I beg to differ from the authors about the etiology of CVD and
hypertension related to sugar and salt. Both high carbohydrate diets
(sugar) and salt (1-5) activates the sympathetic nervous system as well
stress, ageing, air pollution, salt, smoke, hypertension, diabetes,
etc...;
The sympathetic activation may represent the true cause of coronary artery
disease according our acidity theory of atherosclerosis developed in...
I beg to differ from the authors about the etiology of CVD and
hypertension related to sugar and salt. Both high carbohydrate diets
(sugar) and salt (1-5) activates the sympathetic nervous system as well
stress, ageing, air pollution, salt, smoke, hypertension, diabetes,
etc...;
The sympathetic activation may represent the true cause of coronary artery
disease according our acidity theory of atherosclerosis developed in 2006.
For more information please see the Powerpoint slides (6) presented by us
in November 2012 at the Fourth International Conference of Advanced
Cardiac Sciences - "The King of Organs Conference, 2012", held in Saudi
Arabia Kingdom.
I'm the author of the book "Acidity Theory of Atherosclerosis - New
Evidences", 2012 available at Amazon.com and other bookstores.
1. 'Volume-expanded' hypertension: the effect of fluid overload and the
role of the sympathetic nervous system in salt-dependent
hypertension,Journal of Hypertension, V30; N1: January 2012
doi:10.1097/HJH.0b013e32834f6de1
2. de Champlain J, Farley L, Cousineau D, van Ameringen MR. Circulating
catecholamine levels in human and experimental hypertension. Circ Res
1976; 38:109-114.
3. 6. Louis WJ, Doyle AE, Anavekar S. Plasma norepinephrine levels in
essential hypertension. N Engl J Med 1973; 288:599-601.
4. Sever PS, Osikowska B, Birch M, Tunbridge RD. Plasma noradrenaline in
essential hypertension. Lancet 1977; 1:1078-1081.
5. Lake CR, Kopin IJ, Ziegler MG, Coleman MD. Plasma catecholamines and
neurogenic hypertension. N Engl J Med 1977; 297:53-54.
6. Powerpoint presentation at
http://www.infarctcombat.org/AcidityTheory.pptx
Dear Sir:
The data is accumulating to show the adverse outcomes in critically sick patients with persistently elevated troponins. An elegant study by Amman et al (1) in 58 critically ill patients without acute coronary syndromes concluded "Positive troponin levels were associated with higher mortality (22.4% vs. 5.2%, p < 0.018) and a lower LVEF (p = 0.0006). Troponin-positive patients had significantly high...
The current dietary guidelines are strongly associated (at least temporally) with an exponential growth in obesity and Type 2 diabetes. These unintended consequences may have arisen due to increased consumption of carbohydrate in order to reduce fat in the diet.
If the guidelines cannot rely on a solid basis of science then they should be withdrawn and re-written. There is a precedent - we no longer have limits...
I beg to differ from the authors about the etiology of CVD and hypertension related to sugar and salt. Both high carbohydrate diets (sugar) and salt (1-5) activates the sympathetic nervous system as well stress, ageing, air pollution, salt, smoke, hypertension, diabetes, etc...; The sympathetic activation may represent the true cause of coronary artery disease according our acidity theory of atherosclerosis developed in...
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