This site uses cookies to improve your experience. To help us insure we adhere to various privacy regulations, please select your country/region of residence. If you do not select a country, we will assume you are from the United States. Select your Cookie Settings or view our Privacy Policy and Terms of Use.
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Used for the proper function of the website
Used for monitoring website traffic and interactions
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Strictly Necessary: Used for the proper function of the website
Performance/Analytics: Used for monitoring website traffic and interactions
This usually represents posterior OMI, but in tachycardia and especially after cardiac arrest, this could simply be demand ischemia, residual subendocardial ischemia due to the low flow state of the cardiac arrest. This rules out subendocardial ischemia and is diagnostic of posterior OMI. V4-5 continue to show STD. TIMI-0 flow.
Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion. and repeat the ECG, to see if the apparent ischemia persists. A third ECG was done about 25 minutes after the first: This shows resolution of all apparent ischemia.
Likelihood of truth : High The flamboyant genius of Andreas Roland Gruntzig, from Zurich gifted us the path-breaking treatment modality for coronary stenosis five decades ago. There seems to be a non-academic indication for doing this study to undo the damage done by ORBITA-1. Transluminal dilatation of coronary-artery stenosis.
The culprit lesion was a complex calcified mid LAD stenosis involving the first and second diagonal branches. Smith : the profound persistent STE suggests either persistent occlusion or " no reflow " with persistent downstream ischemia. It makes you think you have done something for the ischemia when you have not! Abstract 556.
FAME 2 Purpose FAME 2 sought to evaluate whether FFR-guided PCI plus optimal medical therapy (OMT) was superior to OMT alone in patients with stable CAD and at least one functionally significant stenosis (FFR 0.80).
Angiography : LMCA — 90-99% osteal stenosis. LCx — 50-69% stenosis of the 1st marginal branch; with 100% distal LCx occlusion. There is no definite evidence of acute ischemia. (ie, Distinction of PMVT vs VFib is an academic one in this case ). Some residual ischemia in the infarct border might still be present.
Marked differences can be seen in the prevalence of coronary artery stenosis at autopsy by age and gender. In 30-39 year old women the rate of coronary stenosis at autopsy was 5/1,545 (0.3%) while 60-69 year old men had a prevalence of 12%, almost 40 times higher. The results of this dataset by age and gender follow. This happens.
Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade. Evidence of acute ischemia (may be subtle) vii. heart auscultation (aortic stenosis); c. Academic Emergency Medicine., 2nd or 3rd degree AV blocks or sinus pause of at least 2 seconds iv. Left BBB vi. Pathologic Q-waves viii. LVH or RV d. Sivilotti, M.,
The therapeutics of coronary stenosis has become a technogical wonder, interwoven with statistical wordplay in the last few decades. It is a strange academic habit among cardiologists, that they have subdivided medical management into optimal and suboptimal. (My Academic lessons from this patient. 2016 Dec;9(12):e003726.
We organize all of the trending information in your field so you don't have to. Join thousands of users and stay up to date on the latest articles your peers are reading.
You know about us, now we want to get to know you!
Let's personalize your content
Let's get even more personalized
We recognize your account from another site in our network, please click 'Send Email' below to continue with verifying your account and setting a password.
Let's personalize your content