Questions related to Acute Coronary Syndrome
Which is preferred for nasopharangeal swabs and Coronavirus RT-PCR testing
VTM or RPMI
Is there instructions for VTM centrifugation before proceeding RNA extraction?
Since the VTM swabs contains 2-3ml and commercial Coronavirus PCR kits LOD about 100 copy/ml What is the best preparation for VTM before extraction?
I want to sterilise some items covered safely in dry cotton cloth packings. For what duration, should I blow hot air so that the cloth is free from lethal Coronavirus?
My dear Cat Kajsa died Friday because of ( wet) FIP. It all went so fast, we noticed she hat respiratory problems in the night before Thursday and Friday, for a while I thought she was doing better but it turned out to be a false expectation. We sat down in the truck and headed for the hospital. Our cat had always been nervous and she panicked in the truck and died on route. My question is; Is there any cure on the horizon? We took in 5 cats from the shelter and I suspect we have FIP in the population. What can be done? Best regards Henrik
What GIS tools can be used to analyze the global transmission and prediction of a novel coronavirus pandemic (COVID-19)? What methods and formulas can be used and what kind of geospatial tools can be used to estimate the spread of COVID-19 disease across the globe ?.
Thank you so much for all your contributions.
Acute coronary syndrome is quite chalanging to diagnose when clinical appearance or ECG pattern is not spesific and cardiac marker is not available.
So, I wonder if we could use non spesific laboratory findings (leukocyte, ALT/AST, etc) to help or to give more confincing data that this is a case of ACS.
is there any previous study that make score or something using non spesific lab in ACS?
or I am still confuse what type of research could accomodate my research question.
I really do hope to get some help.
I need a validated questionnaire to measure cardiac symptom abnormalities either before or after an incidence of any heart disease problem!!
I am searching for information about the first in world 24-hour duty for acute coronary syndromes. Where and when was it opened?
In order to constitute the criteria of "ST segment deviation" during calculation of the GRACE Risk Score, , Is it EITHER the presence of ST segment elevation or ST segment depression that is necessaryy? SO if either of the two is present,does it fulfil a criteria? What about LBBB?
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?
What are methods used clinically to differentiate between esophageal spasm and angina?
What preliminary investigations could help?
A 43-year-old woman was admitted to our hospital with acute coronary syndrome. Coronary angiography showed significant stenosis in LAD. The lesion was crossed with a soft guidewire and a drug-eluting stent(2.75X32 DES) was implanted. Subsequent angiography showed an extravasation of moderate amounts of contrast material clearing into the right ventricle. The patient remained stable and the shunt volume was moderate.
How can we manage this situation ?
When a stent is placed in a STEMI patient, and a pre-dilation balloon is used to facilitate crossing the lesion, what is regarded as balloon time in the door to balloon time profile? I have had 2 indicators suggested. For me I see it as pre-dilation balloon catheter withdrawal time, as this now facilitates flow through the lesion, but others have said its the device deployed time, as a result, stent balloon catheter withdrawal time. I need to be uniform in my research variable, so would like to ask what is generally accepted as balloon time?
I have young cad affected subjects with the mean age of 42 years, which I have matched to 5 years older subjects with the mean age of 47 years. Is it the right way of doing it or do we need to do an exact age matching?
Is it only applicable in genetic biomarker studies, but not in protein biomarker studies?
And while matching the samples age should I consider current age or age at onset of the disease?
Is this a pretty standard way to divide the time interval groups?
Symptom onset to balloon (less than 180 minutes, 180-360, greater than 360)
Door to balloon (less than 90 minutes, 90-180, greater than 180)
I understand the D2B intervals rationale, but is it specified anywhere that you know of (AHA etc), that symptom onset to balloon is best stratified according to the above 3 time groups?
A new post hoc analysis of the VIVIDD study with the dipeptidyl peptidase 4 (DPP-4) inhibitor vildagliptin (Galvus, Novartis) in patients with type 2 diabetes and heart failure has shown that the drug is not associated with an increase in hospitalizations for HF.
The findings were reported in a poster at the American Diabetes Association (ADA) 2014 Scientific Sessions last week by Wolfgang Kothny, MD, therapeutic area head for diabetes at Novartis Pharma, Basel, Switzerland.
This new analysis of VIVIDD was performed in the wake of a signal of possible heart failure associated with saxagliptin (Onglyza or Kombiglyze XR, Bristol-Myers Squibb/AstraZeneca) from the SAVOR-TIMI 53 trial in patients with type 2 diabetes at high risk for or with a history of cardiovascular events. In this, a significant 27% increased risk for hospitalizations for heart failure came seemingly out of the blue last autumn, and the US Food and Drug Administration (FDA) is currently reviewing this risk.
A second study, EXAMINE, in type 2 patients with acute coronary syndrome, showed a signal for HF with a second DPP-4 inhibitor, alogliptin (Nesina, Takeda Pharmaceuticals), albeit not significant. Doctors have been concerned about this potential side effect with this class of oral type 2 diabetes drugs ever since.
"This is obviously a much smaller study, but the advantage is it's in a dedicated HF [population], and we didn't see any relevant differences between new HF events or HF hospitalizations [between vildagliptin and placebo]," Dr. Kothny told Medscape Medical News.
Asked to comment, Per-Henrik Groop, MD, DMSc, from Helsinki University Central Hospital, Finland, said he thought the new VIVIDD analysis was "very important because you know there are 2 big studies showing that we have a signal, which is of course worrying. This is good news."
But Benjamin M. Scirica, MD, MPH, from Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, a primary investigator of SAVOR-TIMI 53, disagrees. He told Medscape Medical News: "The VIVIDD study by itself was not powered for clinical end points, and any conclusions regarding safety of vildagliptin are statistically unjustified and cannot be supported by this trial."
He added: "Almost by chance, the VIVIDD study may have provided a mechanistic insight into the unexpected finding of an increased risk of hospitalization for heart failure observed in the SAVOR-TIMI 53 and the EXAMINE trials." And, in fact, "the 20% to 25% higher rate of adjudicated hospitalizations for heart failure in patients treated with vildagliptin is consistent with the findings of the larger cardiovascular-outcomes trials of DPP-4 inhibitors," he said.
Many eyes are therefore on the ongoing TECOS study, a cardiovascular-outcomes trial with sitagliptin (Januvia, Merck), which is due to complete in December 2014 and will yield more information on this subject with this drug, which is perhaps the most widely used gliptin in the United States, at least, due to it being the first in class to reach the market there.
VIVIDD Data: Numbers Are Small
In the new VIVIDD poster, Dr. Kothny reported that 13 of 128 (10.2%) patients with diabetes and heart failure randomized to vildagliptin in VIVIDD were hospitalized for heart failure compared with 10 (8%) of those in the trial who received placebo (P = .552).
"We looked in particular at the safety of vildagliptin in patients with heart failure, and that's one of the big differences here with the published big outcomes studies, SAVOR-TIMI and EXAMINE — where they had patients with high CV risk — whereas here, it's established heart failure," he said.
"This is obviously a much smaller study," he conceded, "but the advantage is it's in a dedicated HF [population], and we didn't see any relevant differences between new HF events or HF hospitalizations."
He said, to his mind, doctors should feel confident to treat patients with NYHA class 1 or 2 heart failure with vildagliptin (there are few data on use of the drug in more severe heart failure).
Dr. Groop said: "We need to make sure the signal is there or not....This is of course not proven yet, but [this new analysis] is suggesting there is no big hazard."
But he conceded that the TECOS results will be key. "There is a third big study coming out — TECOS — and if that shows a signal again, then you will have, [for all] gliptins, a warning. If that [study] is neutral, it will be fine."
In acute coronary syndrome (ACS) patients, those with MS were more likely to be female, have a history of percutaneous coronary intervention, and have a lower left ventricular ejection fraction and higher Thrombolysis in Myocardial Infarction (TIMI) score. Since the MS has a negative long-term impact on cardiovascular mortality and reinfarction in patients with ACS, it can be used as a marker of cardiovascular mortality in patients with ACS and aggressively targeted.
I wonder what would be best way to evaluate the role of inflammatory cytokines in outpatient clinical trials in acute myocardial infraction?
Part of my research is an open ended response to why ST Elevation Acute Myocardial Infarction (STEMI) patients did not opt to call Emergency Services and instead chose private transport. Responses were widely varied (I did not think symptoms warranted an ambulance, did not know how to access EMS, did not think it was cardiac etc), but I wanted to ask about two common responses: "private transport was easier", and "private transport was faster". Is there similarity in the responses? Should they be kept separate or combined as one response for the purposes of analysis?
Seeking to develop a dysrhythmic heart failure model specifically for an EP corrective method.
As part of my research, I am collecting blood work from ACS admissions, particularly STEMI. I have found that along with the main labs, Creat, K+, CKMB etc., I am also collecting BNP, but have found that only about 50% of admissions are having this done as routine lab. Does anyone have more info on the rationale as a Yes/No required on admission for STEMI? Why are some patients having it done and some not?