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The ECG does not show any definite signs of ischemia. IMPRESSION: The finding of sinus bradycardia with 1st-degree AV block + marked sinus arrhythmia + the change in PR interval from beat #5-to-beat #6 — suggests a form of vagotonic block ( See My Comment in the October 9, 2020 post in Dr. Smith's ECG Blog ).
My written interpretation on a tracing such as this one would read, "Marked LVH and 'strain' and/or ischemia — with need for clinical correlation." BOTTOM LINE: ECG changes of LV "strain" and/or ischemia that we see on today's initial ECG — were not present 9 years earlier. Please see ECG Blog #73 for additional details ).
Alternation in ST segment appearance ( or in the amount of ST elevation or depression ) — is often linked to ischemia. The most important clinical entity associated with motion alternans is large pericardial effusion — though motion alternans has also been observed in some cases of hypertrophic cardiomyopathy.
This is a very typical ECG for Hypertrophic Cardiomyopathy. The most recent previous was 4 years prior, and was in the normal range) Elderly patients, and patients with cardiomyopathy (including HOCM), may have troponin values in this range chronically ("chronic myocardial injury").
Are you confident there is no ischemia? Primary VT , and the VT with tachycardia is causing ischemia with chest discomfort (supply-demand mismatch/type 2 MI)? Ischemia from ACS causing the chest discomfort, with VT another consequence (or coincidence)? Do you agree with this strategy? How can you better assess the ST segments?
A 50-something male with unspecified history of cardiomyopathy presented in diabetic ketoacidosis (without significant hyperkalemia) with a wide complex tachycardia and hypotension. The fact that he has a cardiomyopathy argues for a more typical ventricular tachycardia, as does the absence of rSR' in lead V1. It is regular.
Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. I have summarized the m ajor e tiologic c ategories of acute myocarditis and inflammatory cardiomyopathies. She was taken to the cath lab and her coronaries were clean!! There was no MRI, but the presumptive diagnosis is myocarditis.
Angiogram No obstructive epicardial coronary artery disease Cannot exclude non-ACS causes of troponin elevation including coronary vasospasm, stress cardiomyopathy, microvascular disease, etc. This suggests further severe ischemia. hours T-wave are getting larger again The patient went for an angiogram at about 7 hours after arrival.
24: Joint American College of Cardiology/Journal of the American College of Cardiology Late-Breaking Clinical Trials (Session 402) Saturday, April 6 9:30 – 10:30 a.m. ET Main Tent (Hall B1) This session offers more insights from key clinical trials presented at ACC.24 24 and find out what it all means for your patients. 12:15 p.m.
Subsequent testing supported the presumption of apical cardiomyopathy as the cause of this patient's sustained VT. CT coronary angiogram showed no obstructive coronary disease. Today's case is illustrative because it shows how high troponin may rise despite the absence of acute coronary occlusion! (
by making it clear to everyone that this is NOT an EKG that one sees with takotsubo cardiomyopathy. Hospital Course The patient was taken emergently to the cath lab which did not reveal any significant coronary artery disease, but she was noted to have reduced EF consistent with Takotsubo cardiomyopathy.
Figure-2: Causes of Low Voltage on ECG ( Figure reproduced from My Comment at the bottom of the page in the November 12, 2020 post in Dr. Smith's ECG Blog ). Figure reproduced from My Comment at the bottom of the page in the September 7, 2020 post in Dr. Smith's ECG Blog ). What is ELECTRICAL ALTERNANS?
Physicians initially attributed symptoms to “panic, anxiety or stress” in half of these patients, with women more likely than men to have their symptoms attributed to psychiatric causes (65% vs. 32%; P < 04). == MY Comment by K EN G RAUER, MD ( 9/7/2020 ): == Interesting case with thorough discussion by Dr. Smith on arrhythmia management.
Weren't you taught that "new tall T wave in V1" is concerning for ischemia, and so this is the opposite? As always, Takotsubo stress cardiomyopathy and focal myocarditis are rare possibilities which can only be proven after a negative cath. Weren't you taught that concave morphology favors pericarditis? What do you think?
Arrhythmogenic cardiomyopathy Long QT syndrome Hypertrophic cardiomyopathy. That said — in a patient who develops TdP — the overall ECG appearance of this initial ECG is consistent with low K+ and/or low Mg++ ( See My Comment in the May 9, 2020 post — for more on the ECG diagnosis of hypokalemia and hypomagnesemia ).
Extensive conduction system abnormalities can have various causes (ischemia, genetic, infectious, amyloid, etc). The granulomatous inflammation affects the heart, causing an infiltrative cardiomyopathy The most common manifestations of cardiac sarcoidosis are atrioventricular (AV) block and ventricular tachyarrhythmias (VT).
Clin Chem [Internet] 2020;Available from: [link] Smith mini-review: Troponin in Emergency Department COVID patients Cardiac Troponin (cTn) is a nonspecific marker of myocardial injury. JAMA Cardiol [Internet] 2020;Available from: [link] 4. JAMA Cardiol [Internet] 2020;Available from: [link] 5. Guo T, Fan Y, Chen M, et al.
2020) The un-disputable fact is ischemic DCM has a target to treat, though it is termed as cardiomyopathy. The simple reason could be we can address the ischemia a potential arrhythmic target by some form of revascularization in IDCM. The second reason is, NDCM is a progressive primary muscle disease. Circulation.
There is no evidence of infarction or ischemia. The absence of any wall motion abnormality makes ischemic cardiomyopathy very unlikely. The new onset cardiomyopathy was thought to be due to both drug/alcohol use and to Tachycardia-Induced Cardiomyopathy. There are nonspecific ST-T abnormalities.
Such findings would normally suggest primary ischemia with concomitant surveillance of coronary occlusion, but these ST/T changes might very well be secondary to the Escape mechanism at hand. LBBB is typically the result of preexisting hypertrophy, ischemic heart disease, or cardiomyopathy. 5] Isnard, R. & Pousset, F.
No family history of sudden cardiac death, cardiomyopathy, premature CAD, or other cardiac issues. Pattern consistent with Takotsubo's cardiomyopathy." The wall motion abnormalities of Takotsubo cardiomyopathy and LAD OMI can be similar. No similar symptoms in the past. He denied headache or neck pain associated with exertion.
Occurrence of “J Waves” in 12-Lead ECG as a Marker of Acute Ischemia and Their Cellular Basis. The relationship between J wave and ventricular tachycardia during Takotsubo cardiomyopathy. Internat J Arrhyth 2020 Uesako H, Fukikawa H, Hashimoto S, et al. Acad Emerg Med 1999 Rituparna S, Suresh S, Chandrashekhar M, et al.
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