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Does that normal troponin and ECG obviate the need for cardiology consultation for my patient with a concerning story for acute coronary syndrome? Coming into triage, I see a young man—Georgian-speaking—bracing himself with a hand against the wall and holding his lower abdomen.
He reported a history of ischemic cardiomyopathy with coronary stent placement approximately 10 years prior, but could not recall the specific artery involved. So, when I first began teaching ECGs and writing my books (in the early 1980s) — I decided to synthesize my impressions of the literature into what I felt (e.g. Figure 1-2.
The ECG below show a very clean and text book example of triangular QRST waveform also know "Shark Fin". Other coronaries were normal. ECG#1 There is a regular tachycardia with a ventricular rate of about 180 bpm. Smith comment : When there is a regular wide complex tachycardia, first assess whether it is sinus or not. Is there OMI?
I believe that I was the first to represent Wellens as a reperfusion syndrome, in my book , The ECG in Acute MI , pages 22-23 and 51, and in chapter 27 on Reperfusion and Reocclusion. There are also subtly hyperacute T-wave in I, aVL, and V2-V6. The S-wave is reconstituted. The inferior findings are much less pronounced. Lemkes et al.
The above principles are all well illustrated with this figure from my book, The ECG in Acute MI (2002). It is important to recognize that coronary thrombosis is dynamic , with spontaneous opening and lysing of the thrombus in the infarct-related artery (we all have endogenous tPA and plasmin to lyse thrombi). Akkerhuis KM, et al.
Since then, I’ve developed a habit for outdoor recreation and light versions of mountaineering, which led me to realize that altitude illness can occur in much less extreme conditions than I’d previously thought and that these pathophysiologies might actually be relevant to those of us not living in Nepal.
Note 2 other similar cases at the bottom that come from my book, The ECG in Acute MI. See similar cases below from my book, The ECG in Acute MI New 4-Variable Formula I have published a new formula for Early Repolarization vs. Subtle LAD Occlusion that solves the problem of false positives due to LVH by adding a 4th variable, QRS in V2.
IF the clinical scenario for ECG #1 , was that this tracing was recorded in an ambulatory care setting from an otherwise stable patient with longstanding coronary disease but no new chest pain — then I would interpret this ECG as showing "nonspecific" ST-T wave abnormalities that are probably not acute. The lesion was of course Stented.
Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. de Zwaan C et al. Am Ht J 117(3): 657-665; March 1989. Wehrens XH, Doevendans PA, Ophuis TJ, Wellens HJ.
There is a body of literature from the thrombolytic era showing that high ST score correlates with high mortality (see annotated bibliography below, from my book The ECG in Acute MI ). This comes from chapter 28 of my book The ECG in Acute MI ). J Am Coll Cardiol 1995; 25:1084-1088. 0 0 1 36 207 MMRF 1 1 242 14.0
LVH can mimic an acute anterior coronary occlusion (ACO) on the ECG. LVH usually has concave-upwards ST segments, but conVEX-upwards can also be seen, e.g. in these cases from Dr Smith’s book: The ECG in Acute MI : Case 22-1. ECG #4, 24 hours later Anterior T-wave inversion, indicating reperfusion. 3 Is the STE concave or convex?
Identifying patients with low risk for acute coronary syndrome without troponin testing: validation of the HEAR score. High-sensitivity cardiac troponin I at presentation in patients with suspected acute coronary syndrome: a cohort study. Specifying the level is more accurate, evidence-based and safe 3. Int J Cardiol 2013 2.
From Smith's book: Learning Points: 1. Complete, bubble contrast echo is excellent: if there is no wall motion abnormality then it is very unlikely that there is a large epicardial coronary occlusion. There is STE from V3-V6 (more than 1 mm in V4-V6), and a tiny hint in I and II. There is no STE or STD in III an aVF.
Specifically in today's case, as a direct result of overlooking an obvious acute coronary occlusion ( an infarct that was initially STEMI(-) but clearly OMI(+) ) the necessary cardiac cath with PCI was delayed for more than a day. A recent meta-analysis by Stone et al.
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