Electrocardiographic predictors of proximal left anterior descending coronary artery occlusion

Open Medicine ◽  
2008 ◽  
Vol 3 (3) ◽  
pp. 294-299
Author(s):  
Javad Kojuri ◽  
Amir Vosoughi ◽  
Shahdad Khosropanah ◽  
Amir Aslani
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Coronary Angiography ◽  
Proximal Part ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Control Group ◽  
Lower Sensitivity ◽  
Anterior Myocardial Infarction ◽  
St Depression

AbstractProximal occlusion of the left anterior descending coronary artery (LAD) results in a less favorable prognosis in coronary angiography. Therefore, it is important to determine whether there are significant lesions in LAD by electrocardiography (ECG) before coronary angiography. Twelve-lead ECG was compared in 130 patients with significant lesions (≥70% stenosis) confined to proximal part of the LAD (P LAD group) and 492 patients with normal coronary angiography (control group). Fifty-nine patients in the P LAD group and 18 patients in the control group had signs of anterior myocardial infarction as shown by ST elevation (≥1.0 mV) in two consecutive pericardial leads or the presence of a pathological Q wave. An inverted U wave (biphasic T wave) in leads V1 to V4 had a sensitivity of 49.3% (35/71) in P LAD patients without signs of anterior myocardial infarction (MI) and 96.6 % (57/59; specificity, 66.6%; positive predictive value, 90.9 %) in the P LAD patients with signs of anterior MI. In the P LAD patients with signs of anterior MI, T inversion in V4–V5 had a lower sensitivity (67.0% [40/59]) than an inverted U wave. ST depression in inferior leads and ST depression in V5 were not useful markers of proximal LAD occlusion. In conclusions, an inverted U wave in V1 to V4 (or in each of these leads) and T inversion in V4–V5 are the best predictors of significant proximal LAD lesion, especially in patients with ECG findings of anterior MI.

scholarly journals A Sign to Heaven: aVR Lead Elevation and Myocardial Infarction

2011 ◽  
Vol 11 ◽  
pp. 662-665
Author(s):  
Amir M. Nia ◽  
Natig Gassanov ◽  
Hannes Reuter ◽  
Fikret Er
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Proximal Part ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Correct Treatment ◽  
Total Occlusion ◽  
St Segment Elevation ◽  
St Segment ◽  
Long Time

Isolated ST-segment elevation only in the aVR lead, reflecting an acute myocardial infarction due to a left main coronary artery occlusion, was ignored as part of physicians' training in emergency medicine for a long time. The recognition of aVR lead elevation is becoming more accepted as a mandatory diagnostic tool, in particular for physicians working at emergency departments. We report a typical myocardial infarction with total occlusion of the proximal part of the left anterior coronary artery, presenting with ST-segment elevation in the aVR lead, which was misinterpreted as diffuse ischemia. The lacking mandatory awareness of this entity endangered prompt and correct treatment.

scholarly journals The “Spiked Helmet” Sign Associated with ST-Elevation Myocardial Infarction: A Case Report

2021 ◽  
Vol 2 (5) ◽  
pp. 152-154
Author(s):  
Bruno Minotti ◽  
Jörg Scheler ◽  
Robert Sieber ◽  
Eva Scheler
Keyword(s):  
Myocardial Infarction ◽  
Case Report ◽  
Coronary Artery ◽  
Case Series ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
St Elevation Myocardial Infarction ◽  
St Depression ◽  
Cardiac Illness ◽  
St Elevation

Introduction: The “spiked helmet” sign was first described in 2011 by Littmann and Monroe in a case series of eight patients. This sign is characterized by an ST-elevation atypically with the upward shift starting before the onset of the QRS complex. Nowadays the sign is associated with critical non-cardiac illness. Case Report: An 84-year-old man with a history of three-vessel disease presented to the emergency department with intermittent pain in the upper abdomen. The electrocardiogram revealed the “spiked helmet” sign. After ruling out non-cardiac conditions the catherization lab was activated. The coronary angiography revealed an acute occlusion of the right coronary artery, which was balloon-dilated followed by angioplasty. The first 24 hours went uneventfully with resolution of the “spiked helmet” sign. On the second day, however, the patient died suddenly and unexpectedly. Conclusion: Despite the association with non-cardiac illness, the “spiked helmet” sign can be seen by an acute coronary artery occlusion as an ST-elevation myocardial infarction (STEMI). Reciprocal ST-depression in these cases should raise the suspicion of STEMI.

Some Problems Concerning Coronary Artery Occlusion and Acute Myocardial Infarction

Circulation ◽  
1969 ◽  
Vol 40 (5s4) ◽  
Author(s):  
DONALD B. HACKEL ◽  
E. HARVEY ESTES ◽  
ABE WALSTON ◽  
STEPHEN KOFF ◽  
EUGENE DAY
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion

Abstract 12: EMMPRIN-Targeted Magnetic Nanoparticles for in vivo Visualization and Regression of Acute Myocardial Infarction in a Model of Acute Coronary Artery Occlusion

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Irene Cuadrado ◽  
Maria Jose Garcia Miguel ◽  
Irene Herruzo ◽  
Mari Carmen Turpin ◽  
Ana Martin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Extracellular Matrix ◽  
Coronary Artery ◽  
Left Ventricle ◽  
Infarct Size ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Gadolinium Enhancement

Extracellular matrix metalloproteinase inducer EMMPRIN, is highly expressed in patients with acute myocardial infarction (AMI), and induces activation of several matrix metalloproteinases (MMPs), including MMP-9 and MMP-13. To prevent Extracellular matrix degradation and cardiac cell death we targeted EMMPRIN with paramagnetic/fluorescent micellar nanoparticles with an EMMPRIN binding peptide AP9 conjugated (NAP9), or an AP9 scramble peptide as a negative control (NAPSC). NAP9 binds to endogenous EMMPRIN as detected by confocal microscopy of cardiac myocytes and macrophages incubated with NAP and NAPSC in vitro, and in vivo in mouse hearts subjected to left anterior descending coronary artery occlusion (IV injection 50mγ/Kg NAP9 or NAP9SC). Administration of NAP9 at the same time or 1 hour after AMI reduced infarct size over a 20% respect to untreated and NAPSC injected mice, recovered left ventricle ejection fraction (LVEF) similar to healthy controls, and reduced EMMPRIN downstream MMP9 expression. In magnetic resonance scans of mouse hearts 2 days after AMI and injected with NAP9, we detected a significant gadolinium enhancement in the left ventricle respect to non-injected mice and to mice injected with NAPSC. Late gadolinium enhancement assays exhibited NAP9-mediated left ventricle signal enhancement as early as 30 minutes after nanoprobe injection, in which a close correlation between the MRI signal enhancement and left ventricle infarct size was detected. Taken together, these results point EMMPRIN targeted nanoprobes as a new tool for the treatment of AMI.

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