Coronary Artery Disease - Science topic

Both cardiac imaging technology are useful for detecting myocardial perfusion and delineating anatomy of coronary in detail but like a every technology there is always pros and cons It will best suited for particular subset of patients

Hello Rodolfo Citro

Apologies for not joining this discussion sooner... Did you eventually get what you were looking for?

Did you want to publish an article on this topic? I am assuming this is what you wanted - for this, I would also keep in mind those journal groups - as mentioned by Yoshihiro J Akashi and Rajkumar Doshi - have a specific one for interventions - and we would, of course, consider MitraClip being a type of intervention...

"JACC: Cardiovascular Interventions"

"Circulation: Cardiovascular Interventions"

"EuroIntervention"

The following RG link is also very useful:

You can download ASCVD risk estimator on mobile app .

Tredamil excercis echocardiographic may be a good choice for detection of CAD. But this test is much operaters skill dependent. The sensitivity and specificity much higher Than DSE.

We keep DSE for patients with Myocardial infarction (post discharge or follow up), for those who can not exercise and for preoperative evaluation.

To us bicycle ergometer echo is preferred when the patients are haveing LVH or if we want to add 2 D strain.

Myocardial contrast echo for detection of CAD is not appealing to us.

I need images

I have already reported the case of a 102 year old lady who was still taking her statin after a heart attack at age 75 years. (She died at age 104 and 1/2 years, having stopped her statin about 6 months earlier.) I am about to report the case of a 100 year old gentleman who is still taking his statin, though he has had a case of heart failure and does have an abdominal aortic aneurysm. My statin-treated patients live a very long time if they stop smoking.

Dear Mukesh Kumar Gupta

Thank you for your reply

Sir, I haven't diluted the plasma after centrifugation

Dear Prof. Ayad Ghany Ismaeel

Thank you for your reply

Sir , I have already gone through that paper. However, I didn't get any answer for my unsual observations

Dear Miaomiao,

For your information, you would may also like to see the HeartFlow company (as a commercial solution for CFD analysis from CT coronary angiography data).

Atherosclerosis is a disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls, by definition you can't induce atherosclerosis in the cell lines but you can induce the marker or components of atherosclerosis in the cell line, in addition there may be some 3D model of atherosclerosis available that you can use to study the lesions.

Check this for example;

See the link below for calculators and detailed answers to your questions:

Best wishes, David Booth

Dear Allen,

Go to the site below.

this paper is not known to me

Please find a paper for your reference

FFR-CT is a novel technology that enables determination of the functional significance of lesions noninvasively, using sophisticated computer algorithms based on computational fluid dynamics applied to coronary CTA . There is evidence from several randomized studies, comparing FFR-CT with invasive FFR (representing the gold standard), that FFR-CT can be helpful in evaluation of hemodynamic significance of stenosis, especially in patients with intermediate severity stenosis.

-B.K. Koo The present and future of fractional flow reserve

Circulation Journal, 78 (2014), pp. 1048–1054

-Noninvasive Fractional Flow Reserve Derived From Coronary CT Angiography Clinical Data and Scientific Principles

James K. Min, Charles A. Taylor, Stephan Achenbach, Bon Kwon Koo, Jonathon Leipsic, Bjarne L. Nørgaard, Nico J. Pijls, Bernard De Bruyne JACC: CARDIOVASCULAR IMAGING, VOL. 8, NO. 10, 2015

Noninvasive Fractional Flow Reserve From CT OCTOBER 2015:1209 – 2 2

-Noninvasive FFR derived from coronary CT angiography in the management of coronary artery disease: Technology and clinical update

Matthew Budoff, Rine Nakansihi, Vascular Health and Risk Management 2016;12:269—278

Genetic marker have some role in predicting risk of stroke in this condition. Spontaneous apoptosis of smooth muscle cell in the atherosclerotic plaque combined with inflammation contribute to thinning of fibrous cap. Polymorphosims of CRP, I L-6,ICMP-1and MMP-3 are studied as a risk factors of stroke in these patients. Genetic Polymorphosims of coagulation factors also have important role. 

Hi Goran,

1. Specify your research question.

2. Identify keywords based on your research question. 

3. Develop a search string using "OR", "AND", and "NOT" boolean operators for the relevant database eg. Pubmed, EMBASE, etc.

I support 'Shamima Akter' suggestion, but she makes it simple. You have to be strict otherwise, you will miss important articles and your conclusion will be biased. 

Statins have pleotropic properties encompassing anti inflammatory effects, countering of smooth muscle proliferation and prothrombosis. It has been reported to also cause some blood pressure reduction. These ameliorate atherosclerosis even if hypolidaemic effect is not great

Dear Nader,

These links may interest you:

Religious Involvement, Spirituality, and Medicine: Implications for Clinical Practice

Yes, That is an option if the surgeon  deems the anatomical correction high risk to the patient. Another option being clamping the arch between BCA and LCC without using distal aortic or LCC antigrade perfusion. The latter is bein practised in paediatric patients with good results. I have reservations about the utilityof the latter technique in the adult patients owing to possible cerebral ischemia and spinal cord injury even though protection strategies are employed.

Step 1 : After training phase,feed the test feature set in  your  system (you can use fuzzy toolbox in matlab for this purpose)

step 2 : compute the confusion matrix using matlab syntax " plotconfusion"..you will get the confusion matrix values of desired vs predicted diagnosis.

step 3 :The confusion matrix contains the values of  TP, TN, FP, FN.

Step 4: Calculate the accuracy,specificity  using  the above TP, TN, FP, FN  values.

( for these calculations, you can use the tutorial attached in my previous response ).

Though reduction of LDL or non-HDL is associated with reduction of atherosclerosis but it is not halted. Raised HDL  was considered protective but it is now termed "chameleon" as in conditions where inflammatory markers are raised, raised HDL is associated with accelerated atherosclerosis. Similarly high TG has adverse effects but yet to be defined. Thus we have to have more understanding about the risk factors.

Dear Dr. Yakala,  You can try to contact the 

You can try to contact the  following groups

1 and 2 for human human ES cells and 3rd is for murine ones

All the best,

Tushar

Hi Aaysha,

There are sometimes problem during/after PCI with thrombus formation (stent thrombosis) probably due to highplatelet reactivity. This problem appear more often in ACS patient. The IDEAL-PCI registry evaluate utility of individualising dual platelet therapy (DAPT) in ACS patients but also in stable CAD. They use prasugrel and ticagrelor in case of high on-treatment platelet reactivity with good clinical outcome. Nevertheless further randomised trials seem warranted.

Best regards,

Marcin 

It makes sense to start a statin if the patient is not already on one, in order to obtain stability, or hopefully remission, of arterial atherosclerotic lesions.  I am not sure about whether the anti-inflammatory effect will reduce myocardial damage because trials of  anti-inflammatory medication during myocardial infarction (e.g., steroids) have not been convincing enough to establish such treatment.

This tells it all: Hemingway H, Philipson P, Chen R, Fitzpatrick NK, Damant J, Shipley M, Abrams KR, Moreno S, McAllister KS, Palmer S, Kaski JC, Timmis AD, Hingorani AD.Evaluating the quality of research into a single prognostic biomarker: a

systematic review and meta-analysis of 83 studies of C-reactive protein in stable

coronary artery disease. PLoS Med. 2010; 7: e1000286.

The  topic  is  worth  investigating.

With  echocardiography  the  epicardial  fat  thickness  can  be  easily  quantified  in  a  reproducible  manner.

Establishing  a  cut  off  value  for  predicting  metabolic  syndrome  and  coronary  arterial  disease  may  need  a  triad  study  involving  epicardial, visceral  and  subcutaneous  adipose  tissue  and  then  correlating  them  individually  with  certain  biomarkers,  in  a  longitudinal  study.

This  triad  study  will  involve  2D  or  3D ultrasound  for  visceral  and  subcutaneous  adiposity  and  echocardiography  for  epicardial  adiposity. It  would  be  reasonable  to  do  it  that  way  to  be  sure  of  the  best  predictor   for  metabolic  syndrome  and  coronary  artery  disease.

We  did  a   little  work  on  visceral  adipose  tissue  quantification  with  ultrasound  which  will  still  be  developed  in  future. 

The  link  below  may  be  helpful.

Thank  you.

Look at myocardial perfusion nuclear or MRI study to resolve the question

Ticagrelor increase adenosine plasma levels, this could be a possible explanation to the increased dyspnea. An alternative hypothesis could be the effect on sensory neurons with an increase of the sensation of dyspnea. 

- http://content.onlinejacc.org/article.aspx?articleID=1787221

- http://www.ncbi.nlm.nih.gov/pubmed/23070079

Stop researching risk factors and get into prevention. If you want to research risk factors, find a disease we haven't already studied to death. 

Placental imaging, placental dysfunction?

Thanks all. I'm looking for an automated method to define the ROI (left ventricle) for tagged MR images.

To Aymeric Histace, I think the paper you recommended me is useful to me. I'm interested with the mean-std image method which I have personally tried to apply. But I ran into some problem. I've attached the image of the mean-std image below. The mean-std image i generated does not show a a significant contrast between the cavity and the left ventricle wall. I think I'm doing it wrong or missing some steps.

Here are the steps I have taken using Matlab to process the image.

1) compute local mean image using 'conv2' with kernel size N=11

2) compute local std image using 'stdfilt' with kernel size N=11

3) compute uendomap(i,j)=w_m.m_N(i,j) - w_o.O_N(i,j) with w_m=1/3 and w_o=2/3 where wm+wo=1 and wo/wo=2.

Any help is appreciated as I might adopt this method to localize my tagged MR images for my coming paper. Thanks.

I am less and less inclined to believe that lowering heart rate with pharmacological interventions can lower cardiac risk. As you state in your question, higher heart rates are strongly associated with reduced cardiorespiratory fitness. Simply giving a drug can't and won't change that. Recent studies do not suggest beta blockers help much for patients with CAD or recent MI; however, there is still compelling evidence that they help for patients with systolic CHF so I can't write them off completely.

The best guiding cath for RCA are Amplatz series: AR#1 in small size and AR#2 in larger size patients. You can also look for AL#.75 or AL#1 if anterior or high take off, MP#1-2 if anterior and low take of (like SVG). For LAD you want to look for EBU #3.5-4 or Easy Radial (ERAD). For LCx w/ short left main EBU #4.5 and AL#2 are also good.Best!

How to determine if ischemic hearts have irreversible ischemia_And How to treat them? Answer from a Clinical and Physiology investigator

First, assuming that severe ischemia or infarction occur as consequence of coronary obstruction or occlusion (clot) usually shows large number of coronary collateral anastomosis (inter/Intra artery anastomosis) along with precise natural bypass in the site of the major obstruction (Baroldi G et al, Circulation Res. 1956, Cardiovasc. Ultrasound 2005. His book is available from Internet, 2002): Macrovascular CHD. In these patients is better to assume that myocardial in “bypassed artery” has reversible options. In effect, ECG are reversed or returned to normal, under a novel therapeutic approach (Brief discussed at the end).

Second, assuming that severe ischemia or infarction occur in presence of “normal selective coronary arteriogram” (Likoff W et al, NEJM 1967), “a changing Philosophy“(Bugiardini R, Mertz BCN, JAMA 2005) implies that other critical factors, as the microvascular blood flow and O2 delivery are missing: Microvascular CHD.

However, in any scenario the incontrovertible fact is that O2 delivery occurs at the cellular level and involves a critical role of red-cell K-dependent ATP synthesis and release in presence of low pH or low PO2 (Ellsworth ML. Physiology, Bethesda 2009). Therefore, impaired capillary vasodilation instead of blood flow of the conductive coronary arteries) appears to be a major factor in the pathogenesis of CHD (Research Gate: Delgado-Almeida. Am Coll Cardiology Dec 2014, Figure).

This critical role in red-cell K-dependent function includes the K-activation of O2 binding by human hemoglobin (Delgado-Almeida A. FASEB J, 2012), suggesting that an enhanced hemoglobin O2-binding in the lung capillary bed is a required step for anti-anginal effects of nitrates or any other drugs, while explaining the failure of intracoronary administration of nitroglycerin to relieve angina induced by pacing, rapidly reversed by intravenous or sublingual doses (Ganz W, Marcus HS. Circulation 1972).

Third, how to determine if ischemia is irreversible or reversible damage? And How to treat them

a) Clinical and ECG serial evaluations and others as Echoc.

b) BOLD analysis (intra capillary levels of deoxyhemoglobin, MRI) documenting that reduced coronary perfusion in CHD does not always implies deoxygenation, opening a new way to assess myocardial ischemia (Karamitsos TD, Circ. Cardiovasc. Imaging 2010).

c) Improving the inherited effect in Red-Blood-Cell Potassium Content recorded in hypertensive and half of their normotensive offspring, as reported by our laboratory, confirmed to be a critical factor in vascular, renal function and total body water and K content (Delgado-Almeida A. Circulation. Abstract, AHA 2013).

d) Preserving the impaired RBC-K uptake related to drugs, particularly Diuretics and β-blockers (Oski FA et al, Science 1972, Agostoni A et al, Science 1973, both with propranolol) inducing abrupt K-efflux from RBC-K and disturbed oxygen affinity to hemoglobin.

e) Finally, a Physiological and Therapeutic approach addressing the defective RBC-K content and functions in CHD, by a novel composition of Amiloride HCl Dihydrate, allowing to improve Central Aortic BP and systolic pulse waveform reflection (type II-IV), reversing ischemic ECG with normal ECG in half of angina patients (in 6-months) and inducing electrical regeneration in previous areas of old infarcts (Delgado-Almeida A et al. Recent Pat on Cardiovasc Drug Discov.2010 and 2012).

Although these paragraphs might support myocytes regeneration of adult human heart by resident or bone marrow stems cells, the fact is that collateral anastomosis recorded by angiography are clear angiogenesis evidences in ischemic hearts. These peripheral and capillary support in CHD may explain innate regeneration of the heart and isolated living cells surrounded by large infarction (Anversa P, Leri A. Mayo Clin Proc. 2013).

Of note, that the role of stem cells in human biology might be recognized and traced as far as two centuries ago in different tissues and organs: Bones (bone reparation in fractures, cited in NEJM 1800’s), Liver (Donor and receptor of hepatic lobule, leading to almost normal anatomy by MRI and function in 3-4 months), Heart (collateral anastomosis and electrical regeneration of the heart in CHD). References for Bone and Liver Regeneration in PubMed.

FIGURE: Erythrocyte K-dependent ATP Synthesis-Function (See Delgado-Almeida A. β-blockers in Angina. J Am Coll Cardiol. Dec 2004; 64:2710-12).

FIGURE LEGEND: Electron microscopy views at the myocardial capillary net, in which diameters and blood flow is tightly controlled by a RBC-K dependent enzyme (pyruvate kinase activity) required for ATP synthesis and ATP release in the presence of low pH or PO2 (See, References 11-13, 38).

In myocardial cell, RBC release 1 mmol of O2 and 0.7 mmol of K from Oxyhemoglobin, in exchange for protons and CO2 from the myocardium; the reverse of K and O2-binding occurs at the lung capillary beds, as documented in our laboratory by in vitro studies in human venous blood samples (FASEB J 2012, Delgado-Almeida A).

An anatomical aspect is well evident in this picture, the larger RBC diameter (7±0.5 µ) versus 3.5-5.0 µ for most microvascular lumen (purple arrows). However, despite narrower capillary diameters, the flow velocity of these cells in healthy subject is 300-400 µ/sec, critically dependent of RBC-K dependent Pyruvate Kinase activity for ATP synthesis and release, the most powerful regulator of capillary vasodilatation and blood flow. Therefore, impaired vasodilatation and longer RBC transit time, instead of arterial vasoconstriction appears to be the most critical factor in essential hypertension and CHD, and probably represent a novel paradigm in the therapeutic management of these cardiovascular diseases.

you are welcome prof shahid  and i agree lowering the viralload would naturally resolve the etiology as in children the etiology is ifferent from that of adults with obesity or children with FH. and one has to modify treatment according to the aetiology.

You should check receptor biology first.

Hi Dirk, there are several links between calcifications and warfarin use. However, not all patients are candidate to switch from VKA to NOAC for cardioembolic risk prevention.

Hi Dr. Cocco I recently finished a cross sectional study of 171 adult patients undergoing echocardiography in our hospital where I measured Epicardial fat pad thickness and correlated them with cardiovascular and metabolic profile. My result showed that increasing age starting at age >40, Dyslipidemia and FBG >100 mg/dl was significantly correlated with EAT thickness. Our mean EAT thickness was just 2.7 mm comparable to some asian studies but much less to the western studies. Also those with BMI < 27 had higher epicardial fat pad although not statistically significant. Our study showed those with age <40 had very minimal fat pad.

Richard just to add we also tape the breasts to the side routinely in an attempt to reduce dose to sensitive tissue.

All of newer generation of DES are available in IRAN (e.g. promus element,xience  V prime xpedition resolute bintegrity and also Absorb) and their cost is  about 400 euros'.

Hi,

The subjects is controversial. Gastroenterologists have looked at the subject with skepticism, and cardiologists has not taken this association as a targeted clinical approach in daily practice. Publications in marginal impact factor journals indicate a potential role of H. pylori in atherosclerosis/atherogenesis. However, other publications in higher impact journals consider that the subject is still debatable. I think that current data accumulated still does not allow one either to prove or to disprove this association.

Actually, I used to teach my medical graduate students about a potential association between H. pylori (and other infective agents such as C. pneumonie) with atherogenesis, and I still do. But this has been taken just in a conceptual background.

Although some amount of data on this subject have accumulated for more than a decade, a definite associate between H. Pylori infection, atherosclerotic plaque formation and development, and further myocardial infarction triggering still needs to be demonstrated in large randomized trials.

These few references may provide some insights into the subject. I hope they can be of aid.

1) Anderson JL, Muhlestein JB, Carlquist J, Allen A, Trehan S, Nielson C, Hall S, Brady J, Egger M, Horne B, Lim T. Randomized secondary prevention trial of azithromycin in patients with coronary artery disease and serological evidence for Chlamydia pneumoniae infection: The Azithromycin in Coronary Artery Disease: Elimination of Myocardial Infection with Chlamydia (ACADEMIC) study. Circulation. 1999 Mar 30;99(12):1540-7.

2) Kowalski M. Helicobacter pylori (H. pylori) infection in coronary artery disease: influence of H. pylori eradication on coronary artery lumen after percutaneous transluminal coronary angioplasty. The detection of H. pylori specific DNA in human coronary atherosclerotic plaque. J Physiol Pharmacol. 2001;52(1 Suppl 1):3-31.

3) Alejandra Martínez Torresa, Miguel Martínez Gaenslyb. Helicobacter pylori: a New Cardiovascular Risk Factor? Rev Esp Cardiol. 2002;55:652-656.

4) Laek B, Szklo M, McClelland RL, Ding J, Tsai MY, Bluemke DA, Tracy R, Matsushita K. The prospective association of Chlamydia pneumoniae and four other pathogens with development of coronary artery calcium: the multi-ethnic study of atherosclerosis (MESA). Atherosclerosis. 2013;230(2):268-274.

Peace and blessings.

ask please the question in refdoc of inist vandoeuvres les nancy france.

EH sidibé tropical epigenetician pobox 5062 DAKAR FANN 99000 SENEGAL

I don't know

Why are you age matching? The difference in mean age between your cases and controls mean that they are not comparable in any event. 

What is your research question?

If you want to look at age and coronary artery disease, then you are better off looking at a sample across the age range. Your design suggests that there is something intrinsically interesting about five years, which I don't think is the case.

Stable CAD never killed anyone. Neither PCI nor ACB prolongs life in patients with stable CAD and are indicated only in patients with intractable symptoms. So any test for diagnosing stable CAD, including 3D stress echo should only be directed at this small group of patients. 

I don't think there are "exact"; dimensions for coronary artery networks, as, even among species (including humans), the dimensions can vary quite a bit.  Age, weight, etc. can affect density.  Even among those individuals with the same ages, etc. there can be variations, so the best you can do is use averages.  Any good college anatomy text can give you an idea of those averages, and show you the basic geometry so you can get an idea of the branching in the network.

Hope this helps.

Dear Aramendi. The problem is not to think or not. This complication is possible and the question is what treatment is the first choice.

Dear Yuan,

I introduce you our studies regarding redo CABG. 1) Dohi et al. The off-pump technique in redo coronary artery bypass grafting reduces mortality and major morbidities: propensity score analysis of data from the Japan Cardiovascular Surgery Database. Eur J Cardiothorac Surg 03/2014. 2) Yaku. Redo coronary artery bypass grafting. Gen Thorac Cardiovasc Surg 06/2014. 3) Dohi et al. Upgrading redo coronary artery bypass grafting by recycling in situ arterial graft. Ann Thorac Surg 07/2014, 98(1), 311-4.

Thank u so much sir... one more doubt 

Hi Paulo,

As you know, miRNA have different functions and target tissues/cells. Depend on the function of miRNA they can be pro-inflammatory, induce cell apoptosis/necrosis (like in cardiomyocytes), influence endothelial and smooth muscle cell function. Ofcourse there are more, I think it is all depend on your research question and targets.

Here are two papers about miRNA in CVD.

Good luck.

I agree with Ugo Limbruno

OK Dr. Giuseppe. I agree with you and I think SE has an important contribuition in the evaluation of CAD

Or Mitral Stenosis! Looking at some recent data, its not about the wholesome Metabolic syndrome as a factor, rather individual component of blood pressure, lipid and glycaemia that are stronger determinants of risk and prognosis

We had a similar case (left main TH with TIMI III flow). We tried 48 h of DAPT + GPI + UFH and repeated angio. Unfortunately the TH was still there. We then positioned 1 Filterwire in LAD and 1 in Circumflex before to apply thrombus aspiration. The thrombus then disappeared from left main (in part aspirated, in part retrieved by the LAD filter). The case report is published (is in attachment).

Unfortunately is in italian but pictures are very explicative...

The criteria for evaluation of peri-renal fat is well established?

agree with Dr Hudzik, we should at least be targeted by the evidence. This particular condition should take into account the associated dual antiplatelet therapy with warfarin becomes effective control of thrombotic complications and also enables support in the clinical complications when there is a need to abort the effect of warfarin. The classic example is fracture of neck of femur in the elderly.

Despite the good reliability and relatively easy assessment from standard echo images (apical windows), I would like to add a word of caution when considering longitudinal strain as a parameter. Longitudinal strain is a global measurement that is extremely oversimplified and its great reliability is likely caused by an extreme averaging of many myocardial segments. In my opinion, the exact opposite is required for the detection of coronary artery disease, where segmental analysis may help to detect which area of the myocardium is potentially ischemic. In that case, short-axis images may be a better approach as the velocities / strain rates in these views is equally represented in all segments (which is not the case with longitudinal strain, where apical segments are largely underrepresented).

Rotational atherectomy facilitates percutaneous coronary intervention for complex de novo lesions with severe calcification. A strategy of routine rotational atherectomy has not, however, conferred reduction in restenosis or major adverse cardiac events. As it is techically demanding, rotational atherectomy is also uncommon. At this 25-year anniversary since the introduction of rotational atherectomy, we sought to review the current state-of-the-art in rotational atherectomy technique, safety, and efficacy data in the modern era of drug-eluting stents, strategies to prevent and manage complications, including slow-flow/no-reflow and burr entrapment, and appropriate use in the context of the broader evolution in the management of stable ischemic heart disease. Fundamental elements of optimal technique include use of a single burr with burr-to-artery ratio of 0.5 to 0.6-rotational speed of 140,000 to 150,000 rpm, gradual burr advancement using a pecking motion, short ablation runs of 15 to 20 s, and avoidance of decelerations >5,000 rpm. Combined with meticulous technique, optimal antiplatelet therapy, vasodilators, flush solution, and provisional use of atropine, temporary pacing, vasopressors, and mechanical support may prevent slow-flow/no-reflow, which in contemporary series is reported in 0.0% to 2.6% of cases. On the basis of the results of recent large clinical trials, a subset of patients with complex coronary artery disease previously assigned to rotational atherectomy may be directed instead to medical therapy alone or bypass surgery. For patients with de novo severely calcified lesions for which rotational atherectomy remains appropriate, referral centers of excellence are required.

Controlling hypertension, hyperlipidemia, diabetes and glucose intolerance often is easier than reducing weight, and such metabolic interventions greatly lower excess risk for CAD and stroke associated with overweight and obesity. However, risk unrelated to these mediators is substantial, suggesting that adiposity itself requires more effective interventions.

We use GIK + MgSO4 in all "on pump" cases, starting before opening the chest and we keep the infusion 6 hours pos-operatively.

He ´ve seen a reduction in pos-op. arritmias, including atrial fibrillation, but no difference in mortality.

Smart comment from Alicia,

In effect, these assumed "separated" tissues (SK mass, Nervous system, or Kidneys) are strictly linked to erythrocyte potassium (RBC-K) function and transport, as follows:

a) Tissues and cells survive by in situ microvascular and blood flow tightly regulated for oxygen sensing and delivery according tissue demands; b) This complex event explains how in clinical or experimental Shock states, the "circulatory system and the erythrocytes" provide efficient blood flow to the brain, heart and kidneys in order to sustain the live, and c) the critical role of RBC-K dependent ATP synthesis and release, in the presence of low pH or low PO2 are the basis for this vital control. In brief, the human body is a complex and integrated systems, beyond our current knowledge, and its entirely true!

So, " Who may think that female physiology during pregnancy is independently of her newborn since the first day of conception until delivery"?

I agree with Dean. The Stages of Change model is a classic. In fact, it has been used to describe an organization's readiness to make changes (e.g., nursing home culture change). So, the process of change has the following concepts: Precontemplation, contemplation, preparation, action, an maintenance.

Have a look in Health Behavior and Health Education: Theory, Research, and Practice, fourth edition (2008), Glanz, Rimer, Viswanath (editors). If the Stages model doesn't fit the bill, there may be something else more suitable in Glanz et al.

You have to look for the differences in lifestyle, cultural habits, social resources, and screening practices.

thanks a lot for all these pertinent answers.

stenting the wrong lumen is a really risk when we opt of percutaneous angioplasty. If necessary, the procedure can be done under guidance of intravascular ultrasounds. it must make PCI more safe!!

Yes I guess the type of HDL is more important than quantity alone

for 3 vessel disease surgery (CABG) give more good results than STENT especially if the patient is diabetic

Guess will need to wait for sometime before we have a final word on it

Actually the best effettive mode of improving HDL level is the use of pharmacology therapy by CEPTS inhibitors as dalcetrapib or anacetrapib.Ongoing or recent trials and randomized studies will confirm if this effective improvement is efficacious in clinical practice and most medical settiings.

Hi Michelle - the most comprehensive data source for any questions related to cardiothoracic surgery is the Cardiothoracic Surgeons Database - a good background reference for you is Ann Thorac Surg 2011;92:32–9) © 2011 by The Society of Thoracic Surgeons

I suggest texts in the links below. I hope that helps.

Hi Jose,

We now know that chronic inflammation is a contributor to future cardiovascular events. Have a read of this paper which provided some strong evidence that statin therapy administered to persons with 'normal' cholesterol levels but high CRP reduces the risk of CV events and mortality.

Ridker, P. M., et al. (2008) Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein. New England Journal of Medicine 359, 2195-2207.

Dear Lorenzo,

In my opinion I would not send any asymptomatic patients for any tests to detect "cardiac ischaemia", neither non-diabetics nor diabetics. As BARI-2D has shown, there is no benefit of revascularisation over optimal medical treatment for many initially symptomatic patients, let alone for asymptomatic ones! Just get there glycaemia, cholesterol and blood pressure optimally controlled and tell them to stop smoking. Non-invasive tests are often false positive, both imaging and functional tests and I don't find them helpful at all. A good history and optimal primary prevention is far more useful!

You can use a syringe needle-type miniature oxygen electrode. It is convenient to use in animals, and very easy to make it in the lab.

You can use 100 and 80 kV scans with specific calibration , the result are similar to 120 kv, every one must make the own machine calibration, own stratification according results.

There seems to be a lot of confusions as to the role of CAC scanning in clinical practice as noted by the above answers. While there may be a role of calcium scanning in acute chest pain or in planning intervention, that is not where it should be used for clinical decision making. It is best used as a way to assess cardiovascular risk in asymptomatic patients. It is the only way to non-invasively assess the presence of non-obstructive disease in the coronaries. Exercise tests, nuclear and echo all require the presence of an obstructive lesion to be abnormal. Standard risk factors such as lipids, HTN etc. do not tell you what is happening in the coronaries. The majority of MACE events occur in patients with normal cholesterol levels. When assessing a patient for possible lipid lowering therapy the presence or absence of calcium, as well as the total calcium score is extremely helpful in deciding whether or not to treat and how aggressive yo be. The evidence is overwhelming at this point of the added predictive value of CAC scoring to risk assessment. There will probably never be a randomized clinical trial showing the survival benefit from aggressive treatment in patients with high calcium scores given the cost, time and ethical issues that would be involved in not treating patients with high calcium scores, but that does not mean that you should not use the existing data to guide your decision making.

Logistic regression takes one of the categories as baseline. For R that is dependent on the order of the categorical variable. If you want to predefine the 'baseline', then convert the variable to a factor and specify the levels, with first level the one you would like as 'baseline'.

Hope this helps.