tag:blogger.com,1999:blog-549949223388475481.post7710538055922605261..comments2024-03-28T14:02:08.119-05:00Comments on Dr. Smith's ECG Blog: Bilateral Arm and Mid Back Pain, BP 250/140, in a 50-somethingUnknownnoreply@blogger.comBlogger7125tag:blogger.com,1999:blog-549949223388475481.post-13277442533587256692014-12-13T13:09:29.167-06:002014-12-13T13:09:29.167-06:00Thanks for correcting that. But this was from ath...Thanks for correcting that. But this was from atheroma. The vast majority of repeated opening and closing of coroanry arteries is due to thrombus, not spasm. And the vast majority of thrombus is due to ruptured plaque. Prinzmetal's angina was a popular diagnosis years ago before the pathophysiology of intracoronary repeated formation and lysis of thrombus was recognized. Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-68146763669326486322014-12-13T03:33:03.699-06:002014-12-13T03:33:03.699-06:00According to UptoDate, it can:
Myocardial infarcti...According to UptoDate, it can:<br />Myocardial infarction (MI) in patients with variant angina is usually due to concurrent obstructive coronary artery disease [83,84]. With variant angina alone, coronary vasospasm may trigger thrombus formation. Lipoprotein(a) may play a role in this setting. It interferes with fibrinolysis by competing with plasminogen binding to molecules and cells, and elevated serum Lp(a) is associated with a history of prior myocardial infarction in patients with coronary vasospasm [85]. Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-19688486013902738632014-12-12T02:48:42.488-06:002014-12-12T02:48:42.488-06:00This is obviously making a bit of a leap, but anot...This is obviously making a bit of a leap, but another reason I believe there was diagnostic confusion is that, by my eye, the first EKG shows subendocardial ischemia (likely secondary to the severe HTN) superimposed on the subtle inferior STEMI.<br /><br />On that first EKG there is ST-depression in V5 and V6 that is not present on the later two EKG's showing clear inferior STEMI (#3 and #5). Also, there frontal ST-vector is right about 180 degrees on the nose, quite a bit superior of the 110–120 degrees we usually see with run-of-the-mill inferior STEMI (and in fact see on EKG's #3 and 5). I'd suggest that this is due to the combination of the diffuse subendocardial ischemia vector, which points in the 240 degree range, averaging with the inferior subepical ischemia vector, pointed at 120 degrees, to yield 180 degrees on-the-nose.<br /><br />Obviously the math's note that simple since the magnitude of the two ST-vectors isn't necessarily equal, nor is their angle guaranteed, but that's the gist of it.<br /><br />Also, the magnitude of the ST-depression in V3 is actually equal between the first EKG (showing subtle STEMI) and the third ECG (showing obvious STEMI), suggesting there is another factor at play increasing the ST-depression on that first ECG. The same could be said for V4, which actually shows MORE ST-depression on the first ECG compared to the third.<br /><br />It's a minor point, but I think it could help explain why that first ECG looks a bit atypical.Vince Dhttps://www.blogger.com/profile/10636259293820649555noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-29343061094766316212014-12-11T20:50:30.941-06:002014-12-11T20:50:30.941-06:00Panagiotis,
I would have just made the diagnosis a...Panagiotis,<br />I would have just made the diagnosis and activated the cath lab. Or if one is uncertain one can either do a bedside ultrasound or just do serial ECGs. They certainly could have been done more quickly. But you can see that any static ECG, or ultrasound, could be normal if obtained between episodes of occlusion.<br />Steve SmithSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-75293434037899200442014-12-11T20:48:30.146-06:002014-12-11T20:48:30.146-06:00No, Prinzmetal's does not cause thrombotic occ...No, Prinzmetal's does not cause thrombotic occlusion. This was from eroded/fissured atheromatous plaque.Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-52615868042102099672014-12-11T02:24:21.739-06:002014-12-11T02:24:21.739-06:00Wouldn't it be safer and faster for the patien...Wouldn't it be safer and faster for the patient to perform a bedside echocardiogram and not wait until the ECG becomes diagnostic?Anonymoushttps://www.blogger.com/profile/02380462350709472931noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-85064272275563582272014-12-11T01:57:23.446-06:002014-12-11T01:57:23.446-06:00Sorry, I wonder If there was only a thrombotic occ...Sorry, I wonder If there was only a thrombotic occlusion or a thrombotic occlusion on atherom plaque.<br /><br />Could Prinzmetal angina induce a thrombotic occlusion , especially If a patient has a prothrombotic and procoagulant status?<br /><br /><br /><br />Anonymousnoreply@blogger.com