Objectives-To clarify the genesis and clinical significance of inferior ST elevation during acute anterior myocardial infarction. Patients and design-A total of 106 patients with first acute anterior myocardial infarction (< 6 h) were divided into two groups according to the presence (group A, n = 12) or absence (group B, n = 94) of ST elevation of > 1 mm in at least two of the inferior leads on the admission electrocardiogram. Results-On admission electrocardiograms, group A had a smaller summed ST deviation in the lateral limb leads than group B. On emergency coronary arteriograms, the incidence of a wrapped left anterior descending artery was higher in group A than in group B (100% v 27%, P < 0.01). The incidence of occlusion of a left anterior descending artery distal to its first diagonal branch was higher in group A than in group B (100% v 46%, P < 0*01).Peak serum creatine kinase activity and in-hospital mortality tended to be lower in group A than in group B. Group A had better left ventricular ejection fraction and regional wall motion in the anterobasal and anterolateral regions in the chronic phase than group B. In contrast, regional wall motion in the diaphragmatic region was reduced to a greater extent in group A than in group B. Conclusions-Inferior ST elevation during acute anterior myocardial infarction appears only in the presence of a combination of a lesser degree of transmural ischaemic myocardium in the anterobasal and anterolateral wall together with transmural ischaemic myocardium in the inferior wall; in all cases there was occlusion of a wrapped left anterior descending artery distal to its first diagonal branch. Patients with such an ST elevation appear to have a better in-hospital prognosis than those without it. (Br HeartJ' 1995;74
To determine whether or not ST segment deviation on admission electrocardiograms can identify patients with anterior acute myocardial infarction due to proximal left anterior descending artery occlusion, the magnitude and location of ST segment elevation or depression were compared between patients with proximal left anterior descending artery occlusion (group A, n = 47) and those with distal left anterior descending artery occlusion (group B, n = 59). ST segment depression in each of the inferior leads was significantly greater in group A than in group B. The incidence of ST segment depression > or = 1 mm in each of the inferior leads (II; 81% vs 27%, III; 85% vs 54%, aVF; 87% vs 47%, P < 0.01) was significantly higher in group A than in group B. In addition, the incidence of ST segment depression > or = 1 mm in all of the inferior leads was significantly greater in group A than in group B (77% vs 22%, P < 0.01). In group A, maximal ST segment elevation was more frequent in lead V2 alone (43% vs 14%, P < 0.01). Group A had greater ST segment elevation in lead aVL than group B, and the incidence of ST segment elevation > or = 1 mm in lead aVL was significantly higher in group A than in group B (66% vs 47%, P < 0.05). ST segment depression > or = 1 mm in all of the inferior leads was most valuable for identifying group A patients (77% sensitivity and 78% specificity). In contrast, the maximal ST segment elevation in lead V2 alone or ST segment elevation > or = 1 mm in lead aVL had a low diagnostic value (43% sensitivity and 86% specificity, 66% sensitivity and 53% specificity, respectively). In conclusion, this study indicates that analysis of ST segment deviation in the inferior leads is useful for identifying patients with acute anterior myocardial infarction due to proximal left anterior descending occlusion.
Patients with anterior wall acute myocardial infarction showing Q-wave regression had a trend towards a smaller amount of necrotic myocardium and a significantly larger amount of stunned myocardium.
Objective-To examine the association between serum lipoprotein(a) and angiographically assessed coronary artery disease progression without new myocardial infarction. Patients and design-85 patients with coronary artery disease who underwent serial angiography with an interval of at least two years were studied. Progression of coronary artery disease was defined as an increase in diameter stenosis of 15% or more. Vessels on which angioplasty had been performed were excluded from the analysis. The patients were classified into two groups: a progression group without new myocardial infarction (n = 48) and non-progression group (n = 37). Risk factors including lipoprotein(a) were evaluated to see how they were related to progression without myocardial infarction. Results-There were no differences between the two groups in the following factors: age, gender, the time interval between the angiographic studies, the distribution of the analysed coronary arteries, and history of well established coronary risk factors. Univariate analysis showed that serum lipoprotein(a) (P = 0'0002), cigarette smoking between the studies (P = 0.002), serum high density lipoprotein (P = 0.003), and serum low density lipoprotein (P = 0*01) were related to progression without myocardial infarction. Multivariate analysis selected two independent factors for progression without myocardial infarction: serum lipoprotein(a) (P = 0.003) and serum high density lipoprotein (P = 0.03).Conclusions-Serum lipoprotein(a) concentrations are closely related to the progression of coronary artery disease without new myocardial infarction. Lipoprotein(a) lowering treatment may be needed to prevent disease progression in patients with coronary artery disease and high serum lipoprotein(a). (Br Heart_J 1995;74:365-369)
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