Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemia is traditionally considered a cause of intermittent left bundle-branch block (LBBB), and some patients have right precordial T-wave inversion in the normally conducted beats. Clinical correlates of T-wave abnormalities were examined in 46 consecutive patients with intermittent LBBB. Thirty-three patients (72%) had at least transient right precordial (V-14) T-wave inversion suggesting ischemia in normally conducted beats. Seventeen such patients had no evidence of coronary heart disease, including five with normal arteriograms. During LBBB conduction, T-wave abnormalities (upright T-waves I, aVL, V5-6) were frequent (48%) and more common than among patients with permanent LBBB (p less than 0.005). The T-wave abnormalities during LBBB conduction occurred in the absence of coronary heart disease in nine patients, including two with normal arteriograms. Thus, right precordial T-wave inversion may result from recent LBBB itself, associated with T-wave abnormalities during the LBBB, in the absence of coronary artery disease.
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PMID:T-wave abnormalities of intermittent left bundle-branch block. 67 81

A 64-year-old woman with a history of hypertension for ten years and of syncope 18 month previously visited our Division of Cardiology on 12 June, 1989. The S4 and mitral regurgitation were audible at the apex, and her electrocardiogram showed ST-depression in leads II, aVF, V5-6 and prominent U-wave (PU) in V1-3 when first seen. Then, she was thought to have a posterior myocardial ischemia. PU in V1-3 diminished whereas T-wave increased after nitrate and Ca++ blocker. Ergometer exercise ECG showed ST-depression in II, III, aVF, V4-6 and PU with decreased T-wave in V2-3 with no apparent symptoms. Simultaneously, Tl-201 myocardial imaging demonstrated a transient posterior defect. A silent posterior myocardial ischemia was, therefore, confirmed. Coronary arteriograms demonstrated subtotal obstruction of the proximal left circumflex artery, and the peripheral site was filled by collaterals from the right coronary artery. Angina-induced PU in the right precordial leads proved to be useful in detection of posterior myocardial ischemia, and this marker may also improve the possibility of detection of silent posterior ischemia.
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PMID:[A case of silent posterior myocardial ischemia/left circumflex artery obstruction detected by prominent U-wave in right precordial leads]. 228 23

By using our database of continuous 18-lead electrocardiographic (ECG) recordings (standard + V3-5R + V7-9) during coronary angioplasty, we selected 68 patients with left circumflex balloon occlusions (posterior ischemia model) or proximal right coronary artery balloon occlusions (right ventricular IRV] ischemia model). ST-segment amplitudes (J + 60 ms) at preangioplasty baseline were subtracted from maximal ST amplitudes during balloon inflation to create a positive or negative change score (deltaST) for each of the 18 leads. DeltaST elevation was used to describe a change in the ST level in the positive direction from baseline, whether or not actual ST elevation from the isoelectric line was present. DeltaST depression was used to describe a change in the ST level in the negative direction from baseline, whether or not actual ST depression from the isoelectric line was present. ST amplitudes from 8 of the 12 standard leads were then used to estimate ST amplitudes at 192 body surface sites spanning the entire anterior and posterior thorax using the transformation technique of Lux. Thoracic distributions of the DeltaST values were displayed on a torso figure, including locations of the 18 lead locations and points of maximal ST elevation and depression. The 192 estimated body surface unipolar leads were compared with 18-lead ECGs (bipolar and unipolar). During 53 left circumflex occlusions, the maximal deltaST elevation was always located in the 18-lead ECG, with the most frequent locations at leads III, II (41%), V7-8 (34%), and V5-6 (25%). The maximal deltaST depression was located outside the 18-lead ECG (89%), with the most frequent locations above standard lead V2 (67%) and V3 (14%). During 16 proximal right coronary artery occlusions, the maximal deltaST elevation was always located in the 18-lead ECG, with the most frequent locations at leads III (81%) and V2-3R (13%). The maximal deltaST depression was located outside the 18-lead ECG (93%), with the most frequent locations above standard lead V2 (50%), V3 (14%), and V4 (14%). We conclude that maximal deltaST elevation is always located in the 18-lead ECG and maximal deltaST depression is frequently located outside of 18-lead ECG during left circumflex and proximal right coronary artery occlusions. Future studies are required to determine the bipolar leads for the 192 estimated body surface potential mapping leads.
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PMID:Thoracic location of the lead with maximal ST-segment deviation during posterior and right ventricular ischemia: comparison of 18-lead ECG with 192 estimated body surface leads. 1126 18