Spontaneous normalization of negative T waves in infarct-related leads reflects improvement in left ventricular wall motion even in patients with persistent abnormal Q waves after anterior wall acute myocardial infarction.

This study aimed to clarify whether spontaneous T-wave normalization (TWN) in infarct-related leads reflects improvement in left ventricular (LV) wall motion even in patients with persistent abnormal Q waves after acute myocardial infarction (AMI). Eighty-five patients were classified into the following 3 groups: patients with Q-wave regression (group A, n = 21), those with persistent abnormal Q waves and TWN (group B, n = 36), and those with persistent abnormal Q waves and absence of TWN (group C, n = 28). Groups A and B had greater improvement in LV ejection fraction and regional wall motion between 1 and 6 months after AMI than group C. In conclusion, spontaneous TWN in the healing stage of anterior AMI reflects functional recovery of viable myocardium in the infarct region even in patients with persistent abnormal Q waves.

Relationship between plasma oxidized low-density lipoprotein and the coronary vasomotor response to acetylcholine in patients with coronary artery disease.

The present study examined the relation of plasma oxidized low-density lipoprotein (LDL) levels to plasma LDL cholesterol levels and the impairment of endothelium-dependent coronary vasorelaxation in patients with coronary artery disease (CAD). In the first study, the relationship between plasma levels of oxidized LDL and LDL cholesterol were investigated in 88 patients with CAD. In the second study, the changes in the diameter of the left anterior descending (LAD) and the left circumflex (LCX) coronary arteries were measured after intracoronary administration of acetylcholine (15 microg) and isosorbide dinitrate (2.5 mg) in 15 patients with CAD. Plasma oxidized LDL levels were determined with a sandwich enzyme-linked immunosorbent assay. Plasma oxidized LDL levels did not correlate with plasma LDL cholesterol levels (r=-0.03, p=NS). The % diameter changes (mean+/-SEM) in the LAD and LCX after intracoronary acetylcholine were -8.3+/-3.5% and -10+/-4.2%, respectively. The % diameter changes in the LAD and LCX after intracoronary isosorbide dinitrate were 23+/-4.8% and 23+/-5.1%, respectively. The % diameter changes in the LAD and LCX inversely correlated with plasma oxidized LDL levels after intracoronary acetylcholine (LAD: r=-0.55, p=0.03; LCX: r=-0.59, p=0.02), but were not after intracoronary isosorbide dinitrate. Plasma LDL cholesterol, triglyceride, and high-density lipoprotein cholesterol levels did not correlate with the coronary vasoreaction to acetylcholine. In conclusion, plasma oxidized LDL levels do not correlate with plasma LDL-cholesterol levels and are related to impairment of endothelium-dependent coronary vasodilation in patients with CAD.

Significance of spontaneous normalization of negative T waves in infarct-related leads during healing of anterior wall acute myocardial infarction.

This study was conducted to elucidate the significance of spontaneous normalization of negative T waves in infarct-related leads during the chronic phase of anterior wall acute myocardial infarction. Results of this study indicate that patients with spontaneous normalization of negative T waves in infarct-related leads between 1 and 6 months after anterior wall acute myocardial infarction have smaller infarct size, decreased left ventricular dysfunction, and greater improvement in left ventricular wall motion in the infarct area, suggesting that T-wave normalization represents functional recovery of viable myocardium in the infarct area.

Angiographic and clinical significance of 'transient' ST-segment depression in the lateral chest leads in anterior wall acute myocardial infarction.

This study aimed to clarify the significance of ST-segment depression in the lateral chest leads in anterior wall acute myocardial infarction (AMI) with ST-segment elevation. A total of 196 patients with their first anterior wall AMI (< or =6h) were divided into 2 groups according to the presence (group A, n=39) or absence (group B, n=157) of ST-segment depression > or =0.1 mV in V5 and/or V6 on the admission electrocardiogram. Patients with electrocardiographic confounding factors were excluded. No patients had persistent ST-segment depression in the lateral chest leads. Emergency coronary angiography revealed that group A had higher incidences of occlusion of the left anterior descending coronary artery (LAD) proximal to its first septal branch (77% vs 51%, p<0.01) and good collateral circulation than group B (46% vs 25%, p<0.05). Peak creatine kinase levels were significantly lower in group A than in group B (2060+/-1099 vs 2873+/-2077 IU/L, p<0.01). Left ventricular ejection fraction in the chronic phase was significantly greater in group A than in group B. Regional wall motion in the infarct region in the chronic phase was better in group A than in group B. These results indicate that patients with 'transient' ST-segment depression in the lateral chest leads in anterior wall AMI had a relatively smaller infarct size, despite their higher incidence of occlusion of the LAD proximal to its first septal branch, because of their higher incidence of good collateral circulation.

Relation between negative U waves in precordial leads on the admission electrocardiogram and time course of left ventricular wall motion in anterior wall acute myocardial infarction.

This study indicates that patients with anterior wall acute myocardial infarction showing negative U waves in the precordial leads on the admission electrocardiogram have greater improvement in left ventricular wall motion in the infarct region between 1 and 6 months after acute myocardial infarction. This suggests that these patients have a larger amount of stunned myocardium in the infarct region.

Relation of QT dispersion to infarct size and left ventricular wall motion in anterior wall acute myocardial infarction.

Previous studies have shown that QT dispersion increases during acute myocardial infarction (AMI). However, the relation of QT dispersion to infarct size and left ventricular (LV) function in AMI has not yet been fully clarified. Accordingly, this study was conducted to elucidate this relation at 1 month after anterior wall AMI. We examined 94 patients with first anterior wall AMI (< or = 6 hours) who underwent coronary arteriography at admission, 1 month, and 6 months after AMI, and left ventriculography at 1 and 6 months after AMI. Mean QT dispersion on the chronic phase (about 1 month after AMI) electrocardiogram was 79 +/- 33 ms. There were no significant correlations between QT dispersion and peak creatine phosphokinase levels, LV ejection fraction, and regional wall motion in the infarct region at 1 month after AMI (r = 0.06, p = 0.57; r = 0.11, p = 0.29; r = -0.05, p = 0.63, respectively). In conclusion, the findings of this study suggest that QT dispersion on the resting electrocardiogram at 1 month after anterior wall AMI is unrelated to infarct size estimated by the peak creatine phosphokinase level and the degree of LV dysfunction.

Significance of Q-wave regression after anterior wall acute myocardial infarction.

AIMS: This study was conducted to clarify the significance of abnormal Q-wave regression in anterior wall acute myocardial infarction. METHODS: A total of 74 patients who presented with a first anterior wall acute myocardial infarction within 6 h of onset were divided into two groups according to the presence (group A, n = 29) or absence (group B, n = 45) of regression of abnormal Q waves. Regression of abnormal Q waves was defined as the disappearance of the Q wave and the reappearance of the r wave > or = 0.1 mV in at least one of leads I, aVL, and V1 to V6. RESULTS: Emergency coronary arteriography revealed that group A had a higher incidence of spontaneous recanalization or good collateral circulation than group B (55% vs 31%, P < 0.05). Peak creatine kinase activity tended to be lower in group A than in group B (2358 +/- 1796 vs 3092 +/- 1946 IU.L-1, P = 0.09). Group A had a greater left ventricular ejection fraction and better regional wall motion at 1 and 6 months after acute myocardial infarction than group B. The degree of improvement of left ventricular ejection fraction and regional wall motion between 1 and 6 months after acute myocardial infarction was significantly greater in group A than in group B. CONCLUSION: 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.

Effect of pravastatin (10 mg/day) on progression of coronary atherosclerosis in patients with serum total cholesterol levels from 160 to 220 mg/dl and angiographically documented coronary artery disease. Coronary Artery Regression Study (CARS) Group.

To evaluate the effect of pravastatin on progression of coronary atherosclerosis in normocholesterolemic patients with coronary artery disease (CAD), 90 patients with CAD and serum cholesterol levels of 160 to 220 mg/dl were randomized into a pravastatin (10 mg/day) group (n = 45) and control group (n = 45) in a 2-year study. The proportions of patients with progression (an increase of > or = 15% in percent stenosis) and regression (a decrease of > or = 15% in percent stenosis) of coronary atherosclerosis were compared between the 2 groups. Of 90 patients, 80 (89%) had a final angiogram: the pravastatin (n = 39) and control group (n = 41). Percent changes in total cholesterol, low-density lipoprotein cholesterol, and apoprotein B levels were significantly greater in the pravastatin group than in the control group (total cholesterol -11 +/- 12% vs 3 +/- 15%, p < 0.01; low-density lipoprotein cholesterol -18 +/- 16% vs 4 +/- 21%, p < 0.01; apoprotein B -5 +/- 20% vs 6 +/- 20%, p < 0.05). The proportion of patients with progression of coronary atherosclerosis was significantly smaller in the pravastatin group than in the control group (21% vs 49%, p < 0.05). The proportion of patients with disease regression did not differ in the 2 groups (3% vs 2%, p = NS). In conclusion, this study indicates that cholesterol-lowering therapy with pravastatin can prevent the progression of coronary atherosclerosis even in normocholesterolemic patients with established CAD.

Significance of negative U waves in the precordial leads during anterior wall acute myocardial infarction.

This study was conducted to clarify the clinical significance of negative U waves in the precordial leads during anterior wall acute myocardial infarction (AMI). In all, 141 patients with first anterior wall AMI (< or = 6 hours) were classified into 2 groups according to the presence (group A, n = 31) or absence (group B, n = 110) of negative U waves in the precordial leads on the admission electrocardiogram (ECG). The number of leads showing ST elevation > or = 1 mm on the admission ECG was smaller in group A than in group B (5.2 +/- 1.3 vs 6.2 +/- 1.7, p < 0.01). Emergent coronary arteriography revealed that group A had a higher incidence of good collateral circulation than group B (39% vs 19%, p < 0.05). Peak creatine kinase activity was lower in group A than in group B (1,708 +/- 1,271 vs 2,735 +/- 1,865 IU/L, p < 0.01). The number of abnormal Q waves on the predischarge ECG was smaller in group A (2.0 +/- 1.5 vs 3.4 +/- 2.0, p < 0.01). Group A had a greater left ventricular ejection fraction and better regional wall motion in the anterobasal, anterolateral, and apical regions in the chronic phase than group B. In conclusion, patients with anterior wall AMI having negative U waves in the precordial leads on admission had a relatively smaller mass of necrotic myocardium than those without the waves. Therefore, negative U waves during anterior wall AMI may be a useful marker for identifying patients with smaller infarction partly due to better collateral circulation.

Reflection of epicardial U-wave changes in surface inferior electrocardiograms during inferoposterior or anterior wall myocardial ischemia.

The surface inferior electrocardiogram (ECG) has limited value for detecting frequently occurring epicardial U-wave changes over the ischemic inferoposterior wall. Reciprocal U-wave changes could occur in this ECG during anterior wall myocardial ischemia.

How epicardial U-wave changes are reflected in body surface precordial electrocardiograms in anterior or inferoposterior myocardial ischaemia during coronary angioplasty.

OBJECTIVES: To examine the epicardial U-wave changes recorded in intracoronary electrocardiograms (ECGs) during anterior or inferoposterior myocardial ischaemia and the corresponding changes in precordial ECGs recorded from the body surface in humans. METHODS: 40 patients undergoing coronary angioplasty of the left anterior descending (LAD) coronary artery (22 patients) or left circumflex (LC) artery (18 patients). Intracoronary and surface precordial ECGs were simultaneously recorded under baseline conditions and during angioplasty. RESULTS: Four different patterns of U-wave change were identified on the intracoronary ECG: change to positivity, no change, change to negativity, and biphasic change. The incidence of each pattern was similar in the two groups (LAD v LC groups, 23% v 39%; 23% v 17%; 41% v 44%; 13% v 0%, respectively). The intracoronary ECG was more sensitive than the surface ECG for detecting U-wave changes (intracoronary v surface ECG: LAD group, 77% v 55%; LC group, 83% v 28%). A study of the correlation between intracoronary and surface precordial ECGs showed that in patients who had U-wave changes in their intracoronary ECG (17 LAD and 15 LC patients) 65% of the LAD group but only 6% of the LC group had primary U-wave changes in the surface precordial ECG, and that 27% of the LC patients had reciprocal U-wave changes in the right to central precordial ECG. CONCLUSIONS: These results provide fundamental information for an understanding of the correlation between U-wave changes in the epicardial and surface pre-cordial ECGs during myocardial ischaemia in humans. As well as the primary U-wave changes seen in many of those with anterior myocardial ischaemia, some of those with posterior myocardial ischaemia had reciprocal U-wave changes in their surface precordial ECGs.

[Projection of epicardial U-wave change to surface precordial electrocardiogram in coronary artery disease].

U-wave changes on the intracoronary electrocardiogram (ECG) during anterior or inferoposterior myocardial ischemia were correlated with the U-wave changes in the precordial leads of the body surface ECG in 28 patients who underwent coronary angioplasty of the left anterior descending (LAD group; 17 patients) or left circumflex (LC group; 11 patients) coronary artery. The intracoronary ECG was recorded simultaneously with the body surface multiple precordial leads at the baseline and during angioplasty. The amplitude of the U-wave on the intracoronary ECG was measured quantitatively, and U-wave changes from baseline to angioplasty were assessed qualitatively on the body surface ECG. Three different patterns of U-wave changes were distinguishable on the intracoronary ECG from baseline to angioplasty: change to positivity; no change; and change to negativity. The incidence of each pattern was similar in the LAD and LC groups (35 vs 36%; 30 vs 18%; 35 vs 46%, respectively). The intracoronary ECG was more sensitive for detecting U-wave changes during angioplasty than body surface precordial ECG (LAD group 71 vs 47%; LC group 82 vs 27%). When compared to the intracoronary ECG, concordant U-wave changes occurred in the surface precordial ECG in 67% (8/12) of the LAD group with accompanying epicardial U-wave changes, and discordant changes in 33% (3/9) of the LC group with epicardial U-wave changes. The present study provides fundamental information for understanding the correlation of U-wave changes between epicardial and surface precordial ECGs during myocardial ischemia in humans. As well as primary U-wave changes in anterior myocardial ischemia, reciprocal U-wave changes may also be prominent in the surface precordial ECGs in some cases of posterior myocardial ischemia.

Electrocardiographic diagnosis of left circumflex artery occlusion and the occlusion site.

In patients with a posteroinferior acute myocardial infarction and both ST depression (in lead V1 or V2) and ST elevation in the inferior leads, it is difficult to differentiate a left circumflex artery occlusion from a right coronary artery occlusion. Furthermore, there is no useful method to identify the obstruction site in the left circumflex artery. In a study of 52 patients with single-vessel left circumflex artery disease, ST elevation in V6 was found to be a useful indicator for left circumflex artery occlusion in such patients. Furthermore, the sum of the ST changes in leads a VF and V2 is useful for identifying the occluded site in the left circumflex artery.

Inferior ST segment depression as a useful marker for identifying proximal left anterior descending artery occlusion during acute anterior myocardial infarction.

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.

Clinical significance of inferior ST elevation during acute anterior myocardial infarction.

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 (< or = 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 > or = 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.

Serum lipoprotein(a) concentrations are related to coronary disease progression without new myocardial infarction.

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).

Emergent coronary angiographic findings of patients with ST depression in the inferior or lateral leads, or both, during anterior wall acute myocardial infarction.

In conclusion, the present study indicates that there are several distinctive differences in emergent coronary angiographic findings according to the presence or absence of ST depression in the inferior or lateral leads, or both, and location of the leads showing ST depression on admission electrocardiograms in patients with anterior AMI. The coronary angiographic features of patients with this ECG finding greatly support a poor prognosis. In patients with anterior AMI, analysis of ST depression on an admission electrocardiogram should be routinely performed because it is useful in predicting coronary anatomy, the extent of infarction, and its prognosis.

[Relationship of mitral valve area to hemostatic condition in rheumatic mitral stenosis].

The influence of mitral valve area (MVA) on hemostatic conditions was assessed in patients with rheumatic mitral stenosis (MS) without atrial thrombus who underwent percutaneous mitral valvuloplasty (PMV). The Doppler-derived MVA and hemostatic variables were obtained before and 2-3 months after PMV. Hemostatic tests included measurements of beta-thromboglobulin and platelet factor 4 levels as indexes of platelet activation, fibrinopeptide A and thrombin-antithrombin complex as markers of fibrin generation, and D-dimer and plasmin-alpha 2-plasmin inhibitor complex as indexes of active fibrinolysis. Thirty-three measurements in 17 MS patients were subdivided into three groups: group A, 16 samples when MVA was < 1.5 cm2, group B, 12 samples obtained when MVA was 1.5 - < 2.0 cm2, and group C, 5 samples obtained when MVA was > or = 2.0 cm2. The mean level of beta-thromboglobulin was significantly lower in group C (43.6 +/- 32.4 ng/ml) than in group A (142.5 +/- 132.5 ng/ml) or B (163.8 +/- 179.8 ng/ml) (p < 0.05). The incidence of abnormal beta-thromboglobulin was also significantly lower in group C (20%) than in group A (67%) or B (73%) (p < 0.05). Other mean values or incidence of abnormal values of other hemostatic parameters did not differ between the groups. The hemostatic change induced by PMV was examined in 15 MS patients with no change in cardiac rhythm after PMV therapy. The patients were divided into suboptimal (MVA widening < 0.5 cm2, n = 7) and optimal (> or = 0.5 cm2, n = 8) groups. No favorable hemostatic changes were achieved by PMV in the suboptimal group.(ABSTRACT TRUNCATED AT 250 WORDS)

[Relation of T wave polarity in precordial V1 lead to right coronary pathoanatomy in inferoposterior wall acute myocardial infarction].

To test the hypothesis that right ventricular (RV) involvement may affect precordial T wave polarity, the relationship of T wave polarity in lead V1 to right coronary pathoanatomy was examined in 61 patients with first inferoposterior wall acute myocardial infarction (AMI) due to right coronary occlusion within 5 hours of symptom onset. One hundred healthy subjects served as normal controls. The patients were divided into two major groups based on the site of right coronary occlusion: group A (n = 34) with proximal occlusion and group B (n = 27) with distal occlusion. Each major group was classified into two subgroups according to the direction of the ST segment shift in lead V1. Group A was divided into subgroups A1 (27 patients with isoelectric or ST segment elevation) and A2 (7 patients with ST segment depression), and group B into subgroups B1 (8 patients with isoelectric or ST segment elevation) and B2 (19 patients with ST segment depression). The incidence of upright T wave in lead V1 (> or = 0.15 mV) was higher in the patients with proximal right coronary occlusion (70.6%) than in the controls (27%) (p < 0.001) or the patients with distal right coronary occlusion (18.5%) (p < 0.001). Upright T wave occurred most frequently in subgroup A1 (89%) (p < 0.001 vs controls), and least in subgroup B2 (6%) (p < 0.05 vs controls). T wave polarity agreed with the direction of the ST segment shift in 40 of 61 AMI patients (66%) and disagreed in only one patient (2%).(ABSTRACT TRUNCATED AT 250 WORDS)