Science topic

Myocardial Infarction - Science topic

NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
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Hello, I am a postgrad student currently working on my dissertation. I am running a meta-analysis on R and I am looking at the effect of ACEI and ARBs on cardiovascular outcomes such as myocardial infarction, heart failure, and stroke, and renal outcomes such as doubling of serum creatinine and end-stage renal disease. Each outcome has several studies supporting it and so I would like to group those studies together to show an overall result. For example, heart failure outcome has 5 articles that support it, I would like to pool them together if possible. I am using a generic inverse variance meta-analysis (function on R is metagen). Thank you for your help!
The R code I used is: studymeta <- metagen(Log_of_HR, Standard_error, Outcome, data=dat, sm= "HR", random = gs("random"), method.tau = "DL", tau.common= TRUE)
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Not really sure what is the problem. There are different R packages available that can make you compare the different treatments and give the overall effects for treatments by inserting either the number of events or the overall effect.
I usually use the package "metafor" for metanalyses with the frequentist approach.
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Interested to know if there is any relationship between
1. Tuberculosis and Myocardial Infarction
2. Tuberculosis and COVID-related mortality cases?
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I have found some literature there may be increased risk but, as we all know, this is not necessarily a causal relationship.
For example, this was in the Lancet in July 2021:
Risk of acute myocardial infarction and ischaemic stroke following COVID-19 in Sweden: a self-controlled case series and matched cohort study
The first author was Katsoularis, if you need.
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hi my thesis is about detection of myocardial infarction from ECG signals and i want to know is there any database for it?
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hi,
i hope you are fine. is there any research or literature review available on the comparative analysis of different ensemble method used for misdiagnosis of cancer patient against xgboost method?
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Hello everyone,
I would like to evaluate if my treatment has en effect on apoptosis and necrosis in myocardial infarction heart tissue.
Which markers should I use for western blot analysis and on heart sections ?
Thank you in advance
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Ischaemia modified albumin ( IMA) is the earliest biomarker for ACS...other being CKMB, Trop T ,Trop I, LDH , AST, Heart type fatty acid binding protein
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hi my thesis is about myocardial infarction detection. do you know how to import entire database for simulation of research papers?
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Hello!
I am also working on this database (PTB ECG database v 1.0.0)
when i download the database from here:
the file's extension is .dat and i can't open this file in Matlab because it gives me like this:
Error using load
Unknown text on line number 1 of ASCII file
s0484_re.dat
"�����\�".
Error in signal2image (line 8)
load('s0484_re.dat');
how can i open this file correctly?
Any help would be appreciated
📷
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I am working on Isoproterenol induced myocardial infarction model
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Yes, Dear Alok Kumar Bharti. YES ECG is specifically reliable when there are typical changes in serial ECG. So doing ECH IN serial is of importance.
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I will perform Evans Blue staining to measure vascular permeability in cardiac tissue following MI. In the protocols, I read that they usually fix tissues with PFA after collecting them.
I was wondering whether I could skip the PFA fixation step. Do you think skipping the PFA step would affect the staining?
Thank you so much in advance,
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لا علم لنا بهذا الامر وينبغي مراجعة المختصين في هذا المجال
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Blockage of arteries is a common problem during theses days, which may lead to myocardial infraction or heart attack. Once the plaque is formed, it cant be removed. The problem can be overcome either through bye-pass surgery of heart or by putting a stent at blocked portion of the arteries. So my request is to know that is there any chemical individually or in combination in Allopathy / Ayurveda that can reverse the plaque formation.
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Thanks, dear Mahesh Golla for your kind suggestion.
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Example 1: i want to test if Diabetes is a predictor of myocardial infarction. The result is this:
Covariate    b         SE        Wald       P      Exp(b) 95% CI of Exp(b)
Diabetes 1,1624 0,3164 13,4996 0,0002 3,1976 1,7254 to 5,9257
How can i interpret this result? the p is less than 0,05 but i don't understand if it is in favor of patients with diabetes or without diabetes.
Example 2: And with continuos variables, for example:
Covariate      b       SE        Wald        P       Exp(b) 95% CI of Exp(b)
RVD      -1,0549 0,1800 34,3351 <0,0001 0,3482 0,2451 to 0,4947
how can interpret the results?
Could someone help me, please?
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Thanks for gracious participation respected Dr deepay Bause
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Heart attack has become the common problem during these day because of our life style and dietary habits which lead to the clogging of the arteries either due to deposition of calcium or cholesterol. In this context my humble request is to know that is there any proof regarding the removal of the plaque/ reversal of plaque in the arteries by the use of apple cider vinegar.
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Apple cider vinegar will not unclog your arteries or cure atherosclerosis on its own. Making long-term lifestyle adjustments, such as stopping smoking, decreasing weight, and keeping physically active, is crucial.
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The patient's pulse suddenly dropped to 40 ÷ 42 beats per minute, and this for two weeks. Blood pressure did not decrease, and is at the level of 120/140 x 65/80. All biochemical blood analysis parameters are within normal limits, including platelets, AST, ALT, direct bilirubin. Indirect bilirubin - 34 µmol / l. No signs of a heart attack or ischemia were detected. What could it be? Intoxication?
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Dear O. P. Strakhova,
I still believe that Gilbert's syndrome has to be excluded as a causes for the mildly elevated indirect hyperbilrubinaema and bradycardia.
Regards.
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Heart attack is an medical emergency. Treatment received by the patient in the first
' Golden Hour ' is crucial in limiting the damage. However, many heart attacks are " Silent ", i.e.does not cause any symptoms. In other cases, patients attributes symptoms to other less serious ailments like acidity or overwork, delaying treatment and risking lives.
Current AI models and blood/imaging tests detect heart attack risk only as prediction, which spread over a period of 5 to 10 years. I believe that if we can detect impending heart attack 24 - 72 hours before, we are able to save 99 % lives, if not 100 % .
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I realise that heart attacks have a beginning, and that symptoms such as chest tightness, shortness of breath, shoulder and/or arm pain, and weakness might indicate an imminent heart attack. These symptoms might appear hours or weeks before a heart attack.
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And what is the role of mechanical ventilator in this surgery?
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Hello
I have read over the years multiple good publications not using a ventilator (that is mechanical pressure or volume based ventilator). Here is one e.g. in mouse
that uses TTE guided approach.
This approach might be later standardized for larger rodent species.
If you are after non opening animal's chest (thoracotomy), I can cite this publication that was also performed using mouse model
I have also read in the past publications that you can search where the surgeon used fast chest opening and pre-sutured the chest for a quick suture closure. There is quite extensive body of literature when you also search for "hanging weights and induction of myocardial infarct". https://www.jove.com/t/52197/minimal-invasive-surgical-procedure-inducing-myocardial-infarction
However both of these publications has a ventilator that is listed.
Hope this list helps you with an initial search, good luck Filip
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Any body doing MI in mice and staining heart slices with tetrazolium at @37°C?
Most often I am facing problem, heart slices distort / contract in tetrazolium incubation @37°C. Staining itself has no problem, but the tissue structure.
Briefly:
  1. Heart is harvested from mouse
  2. To have smooth cutting / slices, heart is wrapped in plastic bag (sealed) in -20°C for around 20-25min, it becomes semi solid.
  3. Slicing of heart (1mm thick) - At this point slices are flat and smooth
  4. Incubate slices in pre-warmed tetrazolium at 37°C at hot plate / heating pad for 20 minutes
  5. (this step distorts the tissue structure (not any more flat)
  6. Incubate in Pre-warmed 10% formalin for 20min on heating pad.
  7. Photos.
Can any body suggest the remedy for this.
Note: This does not matter whether MI was performed or not.
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Hello Ihsan,
I have done TTC staining for multiple studies with similar success. Here is the paper, you might have read already using interesting guidance: "The sections are then removed from the vial, and excess moisture is blotted; a possible distortion can be mended by gently flattening the sections between the index finger and the thumb. Here is the PMID 19820193
Please read carefully whole method section whether you perform it similar way, there might be still some guidance for you.
Hope this helps,
Filip
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Myocardial infarction usually affect heart function. I wish to know if this pathological condition can affect the level of gastric acid production in the body and hence the digestive process.
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1.Stess incited by myocardial infarction can have dual effect. Increase in acid secretion in response to the stress induced increase norepinephrine. The other is protective by reducing the prostaglandins. 2.The haemodynamic changes that may occur following myocardial infarction can also increase the acid secretion.
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Hello,
We tried different techniques and kits to quantify cell apoptosis on cardiac tissue slide from rats or mice with chronic heart failure (after a myocardial infarction). Unfortunately, none of them worked. Do you have any methods or kits to recommend ? Thanks a lot !
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TUNEL(Terminal transferase dUTP Nick end labelling) staining and DNA laddering assay and Annexin-V based apoptosis detection can be useful for detection of apoptosis of cardiac tissue
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Research shows how stress can lead to heart attacks and stroke . your valuable comments are highly appreciated. Thanks
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There are reports that decreased serum albumin level on admission is associated with increased long term mortality in hospital survivors of AMI. What is /are the reasons behind this increased mortality?
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Thanks Eliana Charalambous, Abdul-Aziz Ahmed Aziz, and Mohamed Laimoud for their interest in the topic and their valued addition to the discussion.
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Hi everybody,
looking at the current literature I found different ways to define not resident cardiac macrophages that are found at different time points after myocardial infarction (MI).
While somebody in 2020 still uses the "old fashion" M1/M2 definition (M1 inflammatory in the first days after MI and M2 reparative after 5-7 days after MI), in other articles authors claim that this is not correct nowadays, but without proposing a consensus alternative.
In line with the foregoing, which is the correct definition to use in a scientific article?
Thanks to everybody who will help me with this intricate topic.
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Would the best strategy after acute myocardial infarction be aspirin + NOAC instead of P2Y12 + NOAC in patients with non-valve atrial fibrillation?
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I agree
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How is the process of introducing myocardial infarction in laboratory rats and what are the materials required for this and what are the details of that in order to be sure of that?
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All the information you need is included in my research published in the reseach gate in atitle myocardial infraction Also, I can help you in this field a lot because I worked previously on this model
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Heart burn is close to heart attack ,but there is differences,
heart attack is often masked by pain in the stomach, esophagus and other symptoms of diseases of the digestive system. Confusion creates additional risks. Although 100% without a medical examination it is impossible to say about the diagnosis, there are a number of signs that distinguish heartburn or reflux from angina (a harbinger of a heart attack)
Heartburn Against Angina Pectoris
When you ate, there was a burning sensation in your chest - how can you determine if it is heartburn, or angina (chest pain that can signal a heart attack)?
"The truth is that even in the emergency room, the doctor will not be able to accurately tell what is happening until he sees the results of the tests," writes Health.Harvard.
Heartburn
Heartburn is caused by acid reflux. This usually starts with a burning sensation in the upper abdomen, slowly rising to the chest. A sensation occurs when you bend down, lie down, or immediately after eating. Sometimes reflux wakes up at night if you ate right before bedtime.
Unlike angina pectoris, heartburn can be treated with antacids ,so do you have more remarks?
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Heartburn is the sensation, usually of burning pain, caused by acid reflux. Thus, heartburn is a symptom, not a disease. Heart attack on the other hand side is an event caused by disease in the coronary arteries.
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Hello everyone. I would like to perform a regression analysis to find the time trend of age at onset of myocardial infarction (MI) in a decade with the year of incident MI as continues independent variable and mean age at onset as dependent variable. Is Poisson regression a suitable method for this question?
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This RG link for incidence I hope it is usefull
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According to the article from Siddiqui et al. (2016) entitled "ISOPRENALINE: A TOOL FOR INDUCING MYOCARDIAL INFARCTION IN EXPERIMENTAL ANIMALS" published in the International Journal of Pharmacy 6(2): 138-144, tehere are several ways to induce myocaridal infarction using isoprenaline/isoproterenol, which vary in dose, administration route and exposure time:
• Low doses of isoproterenol (0.3–6 mg/kg body weight) administered acutely or repeatedly during 1–3 weeks
• Medium doses of isoproterenol (10–85 mg/kg body weight) applied in a single dose
• High doses of isoproterenol (150–300 mg/kg body weight) applied in a single dose or in two consecutive doses.
Moreover, searching the literature, I realized that are still other protocols, with the exception of the mentioned above.
Can any research collegue with experience in this model of myocardial injury justify which protocol is better?
Thanks in advance,
Patrick Türck
PhD in Physiology
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ٍSeveral mechanisms proposed to explain the isoproterenol-induced myocardial harm, one might say: an unbalance between oxygen supply to and demand from cardiomyocytes inwardly, which is related to myocardial hyperfunction due to increase both in chronotropism and inotropism as well as to hypotension in the coronary bed [4]. Secondly, it is also claimed that there is an elevation of Ca++ overcharge inside the cell [5]. In addition, that ion is related to the activation of the adenylate cyclase enzyme and the depletion of ATP levels on the course of the events [6]. Eventually, there is an oxidative stress augmentation because of several metabolic products originated from isoproterenol, not to mention free radicals genesis
for more information see this link
regards
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Hello.
I´ve been practicing myocardial infarction induction in mice for three months approximately, but just a few of them has been left alive since I can check the infarcted area using Evan´s blue. Now we´re performing this protocol in the mice that we´re interested on, we have realized that some of the mice dead a few days (3-5 days) after the surgery. When we opened the dead mice, we observed a blood clot in the thoracic cavity around the lungs and the heart, although I didn´t break any near vessel and there were no bleed out when we closed and finished the surgery. So my question is ¿is this bleeding the cause of the death or there can be another reason?
Thank you
Cristina
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Cristina,
Which model of MI are you using? Are you performing a full open chest procedure or the newer method of "popping" the heart out of the intercostal space? Are you sure you are evacuating all of the air out of the chest cavity before finalizing suturing? If any air is left in the chest cavity or the lung is damaged by tool or pressure it can lead to a pneumothorax which will ultimately lead to death. Pulmonary embolism could also develop in small number of animals. The normal morbidity after MI is greatest in mice from 3-7 days after surgery. This is usually the result of direct cardiac rupture and you should be able to see this upon dissection.
More information of your method would be helpful to answer your question efficiently.
Renee
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Recently, one of the leading democratic hopefuls to clinch the drmocratic ticket for the White Huse, Mr. Bernie Sanders, had a heart attack and subsequent heart surgery. Will he pull out of the race eventually and if he does, what impact will it have on the chances of the rest of the candidates?
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Dear John,
if he can convince the public that he has fully recovered he can still run successfully. He appeared in good health during the debate last Tuesday. Could even be a plus for him to recover quite fast from a serious condition without making a fuzz. Also interesting - the (hidden) medical conditions of past presidents:
Regards
Boris
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Here I give two examples:
One is asked by Dr Alka Rani in the thread:
Another is "Why then do experimental animals not survive on diets lacking essential amino or fatty acids?", asked by Dr C.A. (Kees) Kan in the thread:
These questions have helped me to understand the importance of microbiome to our health.
Do you have encountered any good questions in researchGate that inspires and enlightens you?
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Dear Prof Rodolfo Vega Candelario,
Thank you very much for contributing an important question to this discussion. I myself is not specialised in any medical specialties. So it will be good if we could invite some experts to this question.
What percentage of microcirculation in the coronary can be revealed by Coronary Angiography, Electrocardiogram, Echocardiography and Cardiac PET?
Is there any preventative measures to reduce the risk?
Best regards
Ligen
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U.S. Food and Drug Administration opined that biotin interference (from supplemental biotin) cause a falsely low result in a troponin test. Low level of troponin may lead to a misdiagnosis diagnosis of a heart attack that might be disastrous in some situations. We should be cautious about Biotin supplementation in patient who have cardiac risk factors. What is your opinion?
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Thanks Chakrapani Seshachar for your valuable comment.
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We mostly concern ourselves with the cause of death. Rarely do we try to determine the mechanism of death even in qualitative terms let alone semi quantitative. So one would say heart attack (infarction) led to decompensated failure which eventually resulted in death (qualitative). There is no attempt made to quantify the infacrtion and subsequent deterioration of different parameters over time resulting in death (Quantitative).
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سؤال مثير للاهتمام شكرا لكم
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Medscape
" A review of the evidence for use of aspirin in primary prevention was last looked at 5 or 6 years ago but now we have additional data from three new trials published last year — ARRIVE in people at higher CV risk, ASCEND in people with diabetes, and ASPREE in older individuals,"
These trials did not find compelling evidence for using aspirin for primary prevention.
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Aspirin expands arteries that create more space and allow blood to flow more. Doctors often repeat this medical recommendation, "If you are at increased risk of having a heart attack or stroke
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Using a mouse model, I will be collecting atrial and ventricular tissues at various ages. I will block the tissues in gelatin and generate 10um sections for immunohistochemistry.
Does anyone have suggestions for what is typically used in the field to identify cardiac dysfunction/ischemia immunohistologically?
I have seen reports that increased levels of Inosine and hypoxanthine occur following acute ischemia preceding increased troponin levels. Additionally, I have seen reports that proNGF increases in ateriols following myocardial infarct. I am new to this area of research and want to proceed properly.
Thank you everyone,
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you are welcome
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The first person who reach the site of trauma, or to see a heart attack patient or everybody living with a possibility of facing a major disaster anywhere and anytime is inevitable. Poor primary care i.e., first aid at the site of trauma in the shape of wrong method of evacuation, inability to assess a collapsing patient with heart attack usually doesn't allow many patient to reach hospital alive. Definitely majority of such patients do not reach hospital alive or if they do so major damage has been done. So i believe basic life support and first aid like training courses be made mandatory from early schooling. How do you feel about that?
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I am very sure that teachings on first aid are taught by teachers from the elementary schools in Nigeria.
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Hi...
How to stain Myofibroblasts in myocardial infarcted hearts? What about Alpha- Smooth muscle actin in the detection of myofibroblasts? Is there any other specific markers for the detection?
Thank you.
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Dear Budharaju,
I have used CD140a (PDGFRa) for mouse fibroblasts and I am planning to work with CD90 in human fibroblasts. However this is not sufficient if you need to separate fibroblasts from myofibroblasts, I suppose.
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I am currently assessing the risk of myocardial infarction dependent on daily average values of particulate matter (PM) in mcg/m³. I use a case-crossover design where I generate controls for each patient, with different methods of selecting a referent time where he or she has had no infarction. Then I use a conditional logistic regression model.
My question is now, if it is ok to use average PM values of e.g. two days, one 7 days after the event and one 7 days earlier as control, or if I have to use both days as separate strata in the test? I have read papers that describe the method, but I am uncertain if using average values is appropriate.
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If the times vary for patient- time of year or the patients age, I would be interested to see what the data reveals if you include the time parameter and a time shift factors... I have not tired this but consider y ~ x1(t-7) + x2t+x3(t+7) - I will try to run some simulations to test the model and I will let you know if I find anything interesting
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A heart is a muscle, and it needs a proper blood supply to keep it healthy. Before heart attack it is very important to know the prior symptoms.
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I think these factor is so important deal with heart attack: Family history or heredity, cigarette smoking, high blood pressure, high cholesterol, and diabetes.
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Excessive blood cholesterol implies a future risk for atherosclerotic thromoeboembolic risk diseases like heart attack and stroke and exacerbate problems related to hypertension and diabetes.
While many will argue no screening is needed or cholesterol testing is useless, which may be right in some ways. But on the contrary cholesterol/lipid are the actual things getting on to the vessels clogging our vessels to give the aforementioned disease processes. The clogged vessels demonstrate that on dissection.
Alongside the incidence of lipidemias is increasing and getting them diagnosed earlier may help reduce the ris either through life intervention or drugs.
Kindly have you say on this
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Hi Sikandar,
20 years will be a reasonable age to check lipid profile in most communities. However in those with strong family history of lipid disorders or cardio vascular disease, earlier screening will be advisable. In fact 20 years was the original recommendation of the NCEP ATP guidelines.
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what will be the maximum time when we can do PCI ?
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Thank you Dr.Majumder for posting this question. As you have rightly pointed out, PCI for totally occluded infarct related artery in STEMI beyond 48 hours is a Class III indication. The question is what is the optimal timing to open up the vessel if significant viability can be demonstrated. I think the decision will have to be individualized. Large ecstatic vessel with lot of thrombus should not be attempted early. But if one waits too long, it can interfere with ventricular remodelling and can also lead to recurrent ischemia and even Electrical instability. Moreover, chronic total occlusion will be technically more challenging. I think, 5 to 7 days time will be a reasonable time in most patients to open a totally occluded infarct related artery supplying a viable territory.
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I will make an epidemiological research on Myocardial Infarction, and I want to make the questionnaire, can you help me please, what are the important aspects of MI to ask about it?
Thank you All.
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Dear Margaret
It would be very logical first to state your ideas about your study. Your question is very broad. Myocardial infarction is a big subject. A study on MI could expand to cover incidence, mortality, risk factors, prognostic factors, survival, complications ....etc. Your questionnaire and the questions it contains will depend on the area of interest you like to study. If you are not clear about a specific topic, then go through some literature and keep following this web site to get clear research question. With best success.
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I am going to induce acute myocardial infarction in rats by LAD ligation. I want to know what protocol is most suitable for getting to the heart.
Thoracotomy or lateral thoracotomy?
I would be very grateful if you could give me some advice.
The video of your surgeries will also be very helpful.
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The outcome of coronary artery occlusions is age-, species, severity of occlusion, duration, coronary collateral blood flow during ischemia (compared to baseline), operator and drugs used to support and stabilize hemodynamic.
In experimental models, regional ischemia is complicated by the above-mentioned factors and contributes to lack of reproducibility in the same laboratory and in literature.
It is seldom to see authors report complications, arrhythmia, fibrillation and mortality that why young investigators waste time and resources by following prior publications that do not report pitfalls of their studies. Swine model lacks coronary collateral, that is why pigs die with small risk areas (occlusion close to the apex) from arrhythmia and cardiac arrest not from infarction. Investigators treat all groups with lidocaine to attenuate arrhythmia and ventricular fibrillation, yet some more lidocaine and other inotropic drugs are used to minimize mortality.
Unlike regional ischemia, global ischemia and measuring load-independent indices of cardiac performance and correlating that to myocardial bioenergetics, marker enzymes of ischemia and infarction and the end-point of infarct size.
To obtain reproducible studies and results you must design experiments that have clinical relevance and try to minimize variations within same group and amongst other groups and time. GOOD LUCK
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Dyslipidemia is related to the progression of atherosclerosis. Although treatment of dyslipidemia is beneficial in decreasing the number of coronary events its effect on infarct size and myocardial remodeling are still to be assessed. What is the best strategy in terms of preserve myocardial function after AMI?
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Dear colleagues
Thanks for the informations
I agree with you and we have to use statins in high doses to improve microvascular function and reduce systolic dysfunctio.
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In Third Universal Definition of Myocardial Infarction, it was said that Detection of a rise and/or fall of cardiac biomarker values [preferably cardiac troponin (cTn)] with at least one value above the 99th percentile upper reference limit (URL)
I really can't understand what 99th percentile upper reference limit  is.
Can you give an example, such as High Sensitivity Troponins, to explain it? 
Thank you !!!!
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Hi!
The 99th percentile upper reference limit value of troponin I is given by the manufacturer based upon the results of troponin values obtained from a healthy reference population in that area. The 99th percentile upper reference limit value means that almost every normal person will have a value of troponin below the upper reference range obtained by that sample. So if the value of troponin is above the 99th percentile, that is not normal.
99th percentile values may vary from one ethnicity to the other, even when they come from the same manufacturer.
It is however important to note that level above 99th percentile upper reference limit are not by itself diagnostic of myocardial infarction. If you read the complete definition, it requires presence of clinical signs and symptoms and Electrographic changes in addition to troponin levels to diagnose it as MI.
Mild elevation of troponin enzymes above reference limits may be found in chronic kidney disease, tachycardia, myocarditis, hypertensive heart disease, cardiomyopathies, atrial fibrillation, and many other disorders.
The problem also arises when one is trying to differentiate between high and low risk chest pain patients.
We have reviewed the low risk chest pain and how the use of troponin I helps is this.
Hope this will be of help to you:
Vivek
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Hi all, I am appreciated if someone could suggest the duration for oxygen glucose deprivation (OGD) to mimic the ischemia/reperfusion injury for H9c2 cell line. Thanks,
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Hi Nghiem Le,
I agree with Tausif and Helene's comments.
Initially, it may be beneficial to undertake some optimisation studies investigating the effect of time on rendering the cells temporarily ischaemic.
My own experience in this area has involved undertaking in-vivo studies, recruiting orthopaedic patients undergoing upper and lower limb surgery, where their limbs  have been rendered temporarily ischaemic for various times, ranging from ~15-95 minutes. 
Refs:
Hughes SF, Hendricks BD, Edwards DR, & Middleton JF, (2010). Tourniquet-applied upper limb orthopaedic surgery results in increased inflammation and changes to leukocyte, coagulation & endothelial markers. PLOS ONE 5(7): e11846. doi:10.1371/journal.pone.0011846.
Stephen F. Hughes, Beverly D. Hendricks, David R. Edwards, Kirsty M. Maclean, Salah S. Bastawrous, & Jim F. Middleton (2010). Total hip and knee replacement surgery results in changes in leukocyte and endothelial markers. Journal of Inflammation [Lond.] 7(2) doi:10.1186/1476-9255-7-2.
Good luck.
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We would like to use the GRACE RISK SCORE in our myocardial infarction registry. Does anybody knows the formula or has a syntax to compute the GRACE SCORE?
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Dear Stephanie,
Sometimes there is a disctepancy between the mannual calculation and thw calculator.
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If field test is not feasible to conduct, how valid is 6-minute walk test on treadmill as an indicator of peak VO2 in myocardial infarction patients?
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Initially, 6MWT was used as field test to monitor the outcomes of therapy specifically in pulmonary conditions, then later was used to assess the exercise tolerance in patients with low work capacity and high risk group for graded maximal exercise testing. Thus, gradually 6MWT was used in cardiac rehab-programs with validation with standard testing protocols.
There are studies  of relationship between 6MWT distance and VO2max in lung transplant candidates due to severe chronic lung diseases (Leonor Meira, Carla Damas, Paula Martins, Luís Gaspar, Emilia Araújo, Ermelinda Eusébio, Isabel Gomes European Respiratory Journal 2015 46: PA750; DOI: 10.1183/13993003.congress-2015.PA750).
Absolutely and fully  I agree with the opinion  of Dr. Conroy. 
I think it is advisable to perform the 6minute walk test as a complement to spirometry but not surrogate for VO2max in your patient population. To determine the 6MWT reliability in assessing maximum aerobic capacity (MAC) can be compared it with the VO2max measured by the cardiopulmonary exercise test (CPET).
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Cisplatin induced myocardial infarction was reported. Radiotherapy will increase the risk of heart disease.
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What was the evidence for the AMI? What did the angio show? What's his LV like now? But this is a curable tumour so the risks of treatment will have to be balanced very carefully against the risks of not treating.
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Coronary artery diseases including myocardial infarction (MI) have been recognized as a major health problem in the world. The patients may experience mental and emotional problems like depression and anxiety at different periods of hospitalization that can negatively affect other important characteristics and medical parameters in patients with myocardial infarction and increase patients’ spiritual needs. Is there any association of spiritual wellbeing with anxiety and depression of patients with myocardial infarction? Coronary artery diseases including myocardial infarction (MI) have been recognized as a major health problem in the world. The patients may experience mental and emotional problems like depression and anxiety at different periods of hospitalization that can negatively affect other important characteristics and medical parameters in patients with myocardial infarction and increase patients’ spiritual needs. Is there any association of spiritual wellbeing with anxiety and depression of patients with myocardial infarction?
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Dear Nader,
These links may interest you:
Religious Involvement, Spirituality, and Medicine: Implications for Clinical Practice
  • Spiritual Well-Being and Depression in Patients with Heart Failure
  • The effect of spiritual care on spiritual health of patients with cardiac ischemia
  • Religion, Spirituality, and Health: The Research and Clinical Implications
  • Spiritual reconfigurations of self after a myocardial infarction: Influence of culture and place
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Hello - I am working on a project when I am doing a LAD ligation in a Rat heart and looking for a stain I can use to mark the spot and distinguish it during sectioning on the cryostat. Anyone have an idea of what to use?
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Thank you for the replies, I can explain the situation more.
After LAD ligations, we will be explanting the heart and using a probe to measure some of the heart's characteristics. Following this, the hearts will be briefly frozen (-20 for 10 minutes) and sectioned using a heart slicer matrix, then stained. I would like to mark the spots on heart where I probed so that I can correlate the readings from the probe with images of the stained sections. We will not be doing OCT perfusion / cryosectioning.
I am looking for the best way to do this marking of the heart. I have considered using different inorganic dyes, Coumasie stain, or even a marker, but I was wondering if anyone has experience in doing this type of marking.
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Risk models for the inhospital-mortality of the acute myocardial infarction show in many investigations also "protective" variables, like hypertension or dyslipidaemia. These results are not only presented in the literature, but also used (in my opinion) for the public hospital benchmarking. For example: 2015 Condition-Specific Measures updates and Specifications report hospital level 30-Day Risk-Standardized Mortality Measures (version 9.0).
Some different attempts for explanation (Hypertension):
"Observational and modeling studies of the ischemic heart disease mortality decline in the United States found that the decline was due to a combination of improved risk factor patterns (primary prevention due presumably in part to dietary changes but also to dyslipidemia and hypertension treatment) and improved acute myocardial infarction treatments." Moran A, Odden MC. Trends in Myocardial Infarction Mortality in Spain and the United States: A Downhill or Uphill Race in the Twenty-first Century? Revista Española de Cardiología (English Edition). 2012; 65(12): 1069–71.
"With increasing admission blood pressure, long-term mortality decreases, with a systolic blood pressure above 160 mmHg being associated with best outcome. Blood pressure modifying medication at admission had no influence on this effect. This suggests that low, and even low-normal, admission blood pressure should serve as a warning sign in patients with AMI. Admission blood pressure should therefore be interpreted in opposite to the regular, preventive, point of view."Roth D, van Tulder R, Heidinger B et al. Admission blood pressure and 1-year mortality in acute myocardial infarction. Int J Clin Pract. 2015; 69(8): 812–9.
One explanation from the disussion is, that the heart is still able to react in this acute phase.
"...hypertension may be a marker for the absence of low blood pressure, which may be caused by cardiac pump failure and therefore indicate greater cardiac disease severity....paradoxical relationships may reflect coding bias in administrative data, in that patients with serious disease or complications are less likely to have certain common conditions coded, even when present." Vaughan-Sarrazin MS, Lu X, Cram P. The impact of paradoxical comorbidities on risk-adjusted mortality of Medicare beneficiaries with cardiovascular disease. Medicare Medicaid Res Rev. 2011; 1(3): 17.
And finally the GRACE score for in-hospital mortality:
The higher the SBP, the less risk points are given.
What do you think? Are there further statements or experiences?
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Yes, hypotension is a known risk factor for poor outcome not only in cardiovascular diseases. But whats about the hypertension. Were you able to make similar or even inverse experience here, like it shown in nearly all risk models for the mortality after MI?
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I want to assess return to work after myocardial infarction with SAQ
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PFA
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How much time after thrombolysis, is possible start the anticoagulation in patients with stroke, myocardial infarction or pulmonary embolism?
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If you decide to use warfarin for oral anticoagulation in In pulmonary embolism you must start heparin immediately while you also start warfarin. Reason is warfarin binds reversibly to protein C, and protein S; both are natural anticoagulants; this creates a pro - thrombotic state for 3-5 days when you must cover with heparin. Then this binding breaks down and you continue on warfarin only afterwards. Also warfarin will need time to exhaust liver storage of vitamin K.
If you decide on NOAC, you can go for them with no heparin cover.
Thanks
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I have been working on experimental models of heart failure since a year ago. For induction of heart failure we administered 170mg/kg/day of isopretrenol 4 consecutive days to male Wistar rats weighing between 150-180 grams subcutaneously. Beyond high mortality during the treatment days, in best situation only 50% of the remaining animals developed heart failure. Heart failure was defined as having EF below 60% according to echocardiographic study 28 days after the last injection. We used 10 MHz Vivid7 echocardiography probe. 
Here are the things I need your comments about:
1. dosing suitable for inducing HF (Indeed I am bewildered with the variety of protocols used)
2. criteria to define heart failure in experimental rat models
3. expected ratio of the subjects expected to develop HF
4. proper weight range of the subjects for model preparation
5. timing for drug injection and observation of the HF
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I have ever reviewed the CHF rat models before, as mentioned above, such as the models using TAC, LAD banding, RAP, and drug (isoproterenol, ISO) induction. Considering technical difficulty and sternotomy related hemodynamic change, I decided to use isoproterenol to induce CHF and cardiac fibrosis. In addition, I compared the dosing of isoproterenol for the rat model and concluded intraperitoneal administration of ISO at the dose of 2-10 mg/Kg for 5-7 days was suitable for induction of CHF syndrome and cardiac fibrosis with fewer death rates. Therefore, I consider you need to decrease the dose in order to increase the survival rate. This is my lab experience. I kindly share this with you. Please see my article as "Paricalcitol attenuates cardiac fibrosis and expression of endothelial cell transition markers in isoproterenol-induced rats" in press of Critical Care Medicine. 
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I am working on evaluation of cardioprotective activity of a plant extract in my treatment schedule fixed for 28 day pre-treatment with extract and last 2 days we'll induce myocardial infarction. this is routine work by all researchers but what is the necessity of pre-treatment of plant extract?
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Good luck 
Best wishes,
Mehdi
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If patient had an MI in a non-hospital setting, and it was recognized immediately by a medical personnel, can management begin at the scene? In other words if sublingual Isosorbide Dinitrate and Aspirin were available, can they be given at once, or should we wait until hospital is reached?
If so, what doses can be given? and at what interval until hospital is reached? 
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The most important to give at once is a chewable aspirin 300 mg tab.  it has a high mortality benifit.
GTN Spray even better than sublingual GTN but only for symptomatic relief. no mortality benefit.
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please I want the historical reference above 2004,thanks alot
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Hi,
if you mean a history from the patients, then go their charts.
if you mean literature, then search the international data bases...use the advance searching option by limiting the retrieved results to be above 2004
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i have to obtain a standard questionnaire for risk factors of MI,please any one can help me?
thanks alote 
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The suggestion of Dr. Nidal Eshah would be good to follow,
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Does anyone know guideline of questioner on risk factor contibuting myocardial infarction?
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Dear Zhino,
I hope that this publication will be helpful
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Partial heart block - this is when the electrical impulses are delayed or stopped. The heart does not beat regularly.
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Avoid tricyclic antidepressants
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Can sensitivity and specificity tree point be calculated by ROC curve?
I want to be determinate tree point mild, moderate, and severe cutoff point when I use a questionnaire. For example; I gathered data among myocardial infarction patients by Cardiac Depression Scale (CDS). CDS against Beck inventory hasn't any cutoff point to determination of status depression in cardiac patients.  
Can be calculated sensitivity and specificity tree point by ROC curve?
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Some excellent comments and advice given above. I would just add the importance of the number of non-trivial points on the ROC curve being sufficient to allow smooth and continuous curve fitting. This will ensure a reliable measure of d' for the whole curve for the monotonic changes in threshold and reliable measures of partial curve areas at particular values of sens. and spec. Minimum of five non-trivial points preferred.
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LDL and HDL receptors are responsible for uptake of both the Lipoproteins but increased expression is a signature marker of cancer as is the case with Myocardial infarction?
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The guestion  does not lie within my scope.
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Following ST Elevation Myocardial Infarction (STEMI) the myocardial ischemia causes an inflammatory response, which is a predictor of mortality and myocardial remodeling. Treatment with statins have been shown to be able to reduce the area at risk by reducing inflammation in hypercholesterolemic patients with unstable angina. It is unknown whether the anti-inflammatory effect can really reduce the size of myocardial necrosis in STEMI and if this is due to the anti-inflammatory effect of statins. What would be the best way to advance in the anti-inflammatory strategy for treating STEMI?
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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.
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Meyloperoxidase is one of the biomarkers which will rise in patients with chest pain.
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Thank you for your contribution to my question.
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I wonder what kind of echo stress contributes most to the diagnosis of myocardial viability, and if the addition of the strain can add value to the method.
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I'm assuming by 'strain' you're referring to 2D or 3D speckle-tracking? I'm not sure Tissue Doppler imaging adds much to the assessment (indeed there is published data to support that the incremental benefit is negligable).
Dipyridamole, as a vasodilator, is more useful for perfusion imaging rather than wall motion assessment and in this context is used with microsphere contrast, which is likely to render your strain software useless... While perfusion imaging has been described as a measure of viability, i am less certain of the proven value of Dipyridamole and wall motion assessment in this context.
On the other hand, Dobutamine is well established for viability assessment and can easily provide a measureable substrate for strain imaging. However, in our lab as with many others, this again is used frequently with contrast to improve endocardial definition which unfortunately renders most strain software uselss...
If it were feasible i can certainly see a value for it in patients with very severe systolic dysfunction where improvement may be quite subtle indeed.
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A new class of cholesterol drugs - the PCSK9 inhibitors - might reduce the risk of heart attacks and strokes, and some trials were recently presented demonstrating these evidences, but we do not have large populacional studies really showing it? What do you think?  Is longer the time for regulatory agencies release this group of medications for regular use of the population?
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PCSK9 inhibitors target and inactivate a specific protein in the liver. Knocking out this protein, called proprotein convertase subtilisin kexin 9, dramatically reduces the amount of harmful LDL cholesterol circulating in the bloodstream. The results of three clinical trials involving PCSK9 inhibitors were presented at the annual meeting of the American College of Cardiology, and simultaneously published in the New England Journal of Medicine, suggest that these may be a very useful drug for dyslipidemia. The trials show that PCSK9 inhibitors are extremely powerful cholesterol-lowering agents. In all three trials, all of the participants took a statin. Half got a PCSK9 inhibitor (either evolocumab or alirocumab) every two to four weeks; the other half got a placebo. After a year, LDL levels were 60% lower in the PCSK9 groups.
As with all drugs, there are downsides. At least for now, PCSK9 inhibitors which are basically developed as monoclonal antibodies, must be given by injection every 2 to 4 weeks. Neurocognitive problems, such as mental confusion or trouble paying attention, were seen in some of the study participants. And regarding cost, CVS officials have estimated that a year’s worth of treatment could cost as much as $7,000. 
PCSK9 inhibitors are still experimental drugs. The three trials presented at the American College of Cardiology meeting were designed to look at how well the drugs lowered LDL, not how well they prevent heart attack, stroke, and other cardiovascular problems. Other trials now underway aim to do just that. The FDA can’t begin to evaluate whether PCSK9 inhibitors should become part of the cholesterol-lowering armamentarium until after the results of these trials have been presented and published, and better information is available about the drugs’ side effects.
Among the ongoing phase 3 trials, one is Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk (FOURIER) trial which is basically a double-blind, randomized, placebo-controlled, multicenter study assessing the impact of additional LDL-cholesterol reduction on major cardiovascular events when evolocumab (AMG 145) is used in combination with statin therapy In patients with clinically evident cardiovascular disease. Estimated time for this study completion is February 2018. Another one is Trial Assessing Long Term Use of PCSK9 Inhibition in Subjects With Genetic LDL Disorders (TAUSSIG) trial whose estimated time foe completion is January 2020. 
If approved, these drugs would probably be used first in people who don’t respond to statins or who develop side effects from them. But because it appears that PCSK9 inhibitors reduce the risk of heart attack and other cardiovascular problems in those taking a statin, combining a statin and a PCSK9 inhibitor may be a good option for people at especially high risk for cardiovascular disease. We’ve never before had medications that can reduce LDL cholesterol levels this much. Time will tell if PCSK9 inhibitors safely prevent heart attack and stroke. Thus, let us hope that the trials will eventually come out with promising results, so that regulatory agencies can grant approval as early as possible to control widespread surge of dyslipidemia and associated cardiovascular and cerebrovascular accidents.
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Thanks a lot Kumar. I agree totally with you that an anticoagulant, like heparin, LMWH or fondaparinux, is recommended as Class I for treatment of NSTEMI, this is even in the latest ACC NSTEMI guidelines in 2014.(Amsterdam, et al JACC 2014) However, if you go back to evidence behind it's use, it depends mostly on old trials conduced before the era of newer antiplatelets like GPIIb/IIIa inhibitors and PY12 inhibitors.(Cohen, et al NEJM 1997, Antman, et al Circulation 1999, Oler, et al JAMA 1996) When heparin (which is a non specific anticoagulant) was compared to LMWH, LMWH was found to be superior mainly because of a decreased incidence of bleeding (Ferguson, et al JAMA 2004) and recently when LMWH was compared to an even more specific anticoagulant "fundaparinux" the latter was found be associated with less odds of major bleeding and death. (Szummer et al JAMA 2015) My question is maybe we don't need anticoagulants at all. Up till current date, these is no randomized trial comparing antiplatelets + anticoagulants to antiplatelets alone. No institution would have the courage to do so.
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I came across from several articles that after Myocardial Infarction (MI) and other injuries, there is release of stem cells from bone marrow into circulation. Is there any natural or synthetic compound that also cause a release of bone marrow stem cells into circulation under normal conditions?
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Hello 
yes i agree with researchers , you can use BM by granulocyte colony-stimulating factor (G-CSF) add , there are Evidence for vasculogenesis and arteriogenesis found after delivery of BM-derived stem cells in transgenic mice with myocytes, endothelial and smooth muscle cells proliferating in the infarcted region .
you can see this artical in attachment
Good Luck
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My understanding is, when the myocadium cells lack of blood supply, the cell will be damaged but to some degree, it's still reversible. When the blood flow recovered, the cell can become alive again. When the ischemia is serious to a certain stage, the cell will die completely. Thus even the blood flow recover, the cell cannot gain live again, call irresversible. (if these are not true, please kindly correct me)
And my question is, for a specific patient, how to judge if his ischemia is reversible, irreversible? E.g. by using some imaging machines??
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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.
See References in RG.net
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Hi,
Since the risk factors of Myocardial infarction are different in different nations, I want to know the risk factors which are more prevalent in Iranian lifestyle especially for NSTEMI which their prevalence in other country aren't  so controversial.
Regards,
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I want know how many genes for responding cardio vascular diseases, diagnosis and what are the genes expressed  myocardial infarction and coronary artery disease can tell me whom are working these relevant working
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Rupture of ventricular septum, Papillary muscle and free ventricular wall after myocardial infarction in the same patient .Did your patient survive? Usually these patients don't survive.
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Post MI ventricular septal rupture is generally managed waiting as long as clinically possible to improve the surgical result. The reason is related to the inconsistency of peri-infarcted tissue in the weeks following the acute phase. Post MI papillary rupture is an acute complication due to the massive mitral regurgitation. Post MI free ventricular wall rupture is a generally a final complication with few exception represented by cases with subtile wall fissuration of the necrotic area with thrombus closing the hole. I remember single patients surviving these distinct complications but no one surviving with the three at the same time. A post MI free wall rupture with pericardial tamponade was successfully treated in my Department with surgeons at bed site and immediate starting of cardiac surgery during resuscitation maneuvers.
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can anybody tell me about the use of Isoproterenol in induction of Myocardial Ischemia in laboratory animal model?
Please send me reference.
thanks
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When using isoproterenol to induce myocardial infarction, one has to consider 2 different methods, namely by direct injection vs osmotic minipump implantation. Both methods are very easy to obtain but dosage will differ. The osmotic minipump method have successfully been done by Heather et al in 2009 and have made use of a much lower dosage for a longer period of time compared to an injectable dosage, which ultimaly are only injected for 2-3 days.
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Most recent guidelines unanimously recommend statin therapy for secondary ischaemic stroke prevention. Ambulatory patients were preferentially included into SPARCL and HPS studies.
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My opinion is that the treatment of each patient suffering from a disabled stroke should be individually decided, although statin therapy in hyperlipidemic patients with stroke could be suggested.
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I am going to isolate T cells from mice hearts after myocardial infarction. However, I do not know how can I get them.  They will go for the flow cytometry analysis later.
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@Julijus Bogomolovas: Thank you very much Julijus. It is exactly what i want!
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We want to determine the concentration of cGMP in ventricular tissue, in order to evaluate the activity of the Soluble Guanylate Cyclase enzyme.
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that will be good if also answer in english
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Inodilators may have a beneficial effect on some patients with septic shock and important myocardial dysfunction
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We use milrinone frequently in pediatric septic shock.  The typical scenario is a child who with tachycardia, cool extremities, delayed capillary refill time and low central venous saturation with normal or elevated blood pressure.  I typically start it at a low dose (0.25 mcg/kg/min) without a loading bolus and watch for hypotension.  If the child becomes hypotensive, I may give additional fluids or stop the milrinone.  If the milrinone is tolerated, I increase it gradually to as high as 1.2 mcg/kg/min.  If the patient has renal dysfunction I use it more carefully and at a lower dose.  I frequently use it in combination with epinephrine.
See also Figure 1 in this article: http://www.ncbi.nlm.nih.gov/pubmed/19325359
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We would like to measure the MPO activity from myocardial tissue from control Vs treated groups. We have the tissue lysate in RIPA buffer. Is it possible to measure the MPO activity from these lysate which was stored in -80 deg C. Many protocol says the tissue should be homogenized in MPO assay buffer and fresh. Is colorometric activity assay is the best assay or any alternative assays (e.g. Immunoblot of MMP 2/9 etc.) available. We do not have the intact tissue so can not perform sectioning and staining now.
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Hi Narendra.
Heart lysates in RIPA buffer should normally work for MPO assay. However, it depends on the kit. We have tried ELISA with tissue lysate in RIPA buffer and it worked always.
Alternative strategies depends on your aim. If you want to measure MPO activity, then MPO assay kits or ELISA are the best option. If you are interested in MPO mass, then immunoblot of MMP2/9 or MPO should be sufficient. 
For activity measurements, I would suggest to go for ELISA than colorimetric assays.
All the best,
Chintan
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Hi, I am working with H9C2 (rat cardiomyoblast) cells and I am looking at the effect of high levels of dopamine on these cells. Addition of dopamine resulted in decreased viability of these cells. However, blocking the specific dopamine receptors (D1like and D2 like) did not reverse this effect, suggesting a receptor independent signaling of dopamine. Does anyone have any experience with this and have literature about this ? or does anyone know if dopamine can bind to other receptors that might explain this ? thanks in advance!
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My first post apparently got lost -- DA binds to adrenergic receptors at high concentrations. You'll need to use adrenergic antagonists. You can often get a useful first look at this at: http://pdsp.med.unc.edu/.
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Test in SPSS
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It sounds like you want a model with ejection fraction as the outcome variable and age, gender and risk factor(s) for MI as explanatory variables.  If so, you want a linear regression model, I think (given that ejection fraction is a percentage -- http://www.mayoclinic.org/ejection-fraction/expert-answers/faq-20058286).  (In the SPSS GUI:  Analyze > Regression > Linear.)
Re age, if you have people's actual ages, I would treat age as a continuous variable rather than carve it into (usually arbitrary) categories.  There are plenty of articles that explain why carving into categories is a bad idea.  You can also view slides from a short conference talk I gave on it a few years ago--see the link below.
Finally, you should be aware of the possibility of over-fitting your model.  See Mike Babyak's nice article for more info (link below).
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In what all ways can magnetic nanoparticles with various biocompatible coatings be used for dealing with cardiovascular disorders? What are the newer imaging modalities which can be incorporated without any side effects?
 
 
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