Clinical implications of persistent ST segment depression after admission in patients with non-ST segment elevation acute coronary syndrome.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Kosuge.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Patients with occlusion of the left anterior descending coronary artery (LAD) proximal to both the first septal branch and the first diagonal branch may benefit most from early reperfusion therapy due to extensive area at risk. HYPOTHESIS: The aim of the study was to examine whether 12-lead electrocardiograms (ECGs) in the acute phase of acute myocardial infarction (AMI) could identify total occlusion of the LAD proximal to both the first septal and the first diagonal branch. METHODS: A 12-lead electrocardiogram was recorded on admission in 128 patients with anterior AMI within 12 h from symptom onset. Patients were divided into three groups according to the culprit lesion: 33 patients had total occlusion of the LAD proximal to both the first septal perforator and the first diagonal branch (Group P), in 51 it was proximal to either the first septal perforator or the first diagonal branch (Group D-a), and in 44 it was distal to both the first septal perforator and the first diagonal branch (Group D-b). RESULTS: Sensitivity and specificity of a greater degree of ST-segment depression in lead III than that of ST-segment elevation in lead aVL were 85 and 95%, respectively, which was better than the results derived by all other ECG criteria (p< 0.001). CONCLUSIONS: We conclude that a greater degree of ST-segment depression in lead III than that of ST-segment elevation in lead aVL is a useful predictor of proximal LAD occlusion in patients with anterior AMI.
BACKGROUND: ST-segment elevation of > or = 1.0 mm in lead V4R has been shown to be a reliable marker of right ventricular involvement (RVI), a strong predictor of a poor outcome in patients with inferior acute myocardial infarction (IMI). However, patients with no ST-segment elevation in lead V4R despite the presence of RVI have received little attention. HYPOTHESIS: The study was undertaken to study the clinical features of patients with no ST-segment elevation in lead V4R despite the presence of RVI, which means false negative, as such patients have received little attention in the past. METHODS: We studied 62 patients with a first IMI, who had total occlusion of the right coronary artery (RCA) proximal to the first right ventricular branch and successful reperfusion within 6 h from symptom onset, to examine the implications of the absence of ST-segment elevation in lead V4R despite the presence of RVI. RESULTS: A standard 12-lead electrocardiogram (ECG) and right precordial ECG (lead V4R) were recorded on admission, and three posterior chest ECGs (leads V7 to V9) were additionally recorded in 34 patients. Patients were classified according to the absence (Group 1, n = 18) or presence (Group 2, n = 44) of ST-segment elevation of > or = 1.0 mm in lead V4R on admission. Patients in Group 1 had a greater ST-segment elevation in leads V7 to V9 (2.9+/-2.4 vs. 1.4+/-3.0 mm. p < 0.05), a higher frequency of a dominant RCA (defined as the distribution score > or = 0.7) (72 vs. 11%, p < 0.001), and a higher peak creatine kinase level (3760+/-1548 vs. 2809+/-1824 mU/ml, p < 0.05) than those in Group 2. CONCLUSIONS: In patients with IMI caused by the occlusion of the RCA proximal to the first right ventricular branch, no ST-segment elevation in lead V4R can occur because of concomitant posterior involvement. In such patients, the incidence of RVI may be underestimated on the basis of ST-segment elevation in lead V4R.
Cardiac function is improved by optimizing the atrioventricular (AV) delay. An automatic optimizing function of AV delay may be necessary to achieve the most favourable haemodynamic state in paced patients. The QT interval may change when cardiac function is improved by optimizing the AV delay. The QT or stimulus-T interval is used as a sensor for rate-responsive pacemakers. Evoked (e) QT interval is measured as the time duration from the ventricular pace pulse (stimulus) and the T-sense point that is the steepest point of the intracardiac T wave (stimulus-T interval). The relationship between AV delay, eQT interval and cardiac function was studied in 10 patients (73 +/- 10 (SD) years old) with an implanted stimulus-T-driven DDDR pacemaker. Cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) were measured by Swan-Ganz catheter. The AV delay was prolonged stepwise by 30 ms. Electrocardiogram event markers which indicated ventricular spike and sensed T wave were recorded, and the interval between two event markers was measured as eQT interval. When AV delay was changed from 240 ms to the AV delay at which CO was maximal (172 +/- 33 ms), eQT interval prolonged from 346 +/- 60 to 353 +/- 62 ms (P < 0.01). There was a significant positive correlation between the optimal AV delay at which CO was maximal (172 +/- 33 ms) and the optimal AV delay which was predicted from the maximum eQT interval (179 +/- 37 ms, r = 0.92, P < 0.001). When AV delay was changed from 240 ms to the predicted optimal AV delay, CO increased from 4.2 +/- 0.7 to 4.5 +/- 0.81.min-1 (P < 0.001) and PCWP was decreased from 7.1 +/- 4.0 to 5.7 +/- 3.1 mmHg (P < 0.05). In conclusion, the optimal AV delay can be predicted from the eQT interval which is sensed by an implanted pacemaker. Automatic setting of the optimal AV delay may be achieved by the QT sensor of an implanted pacemaker.
BACKGROUND: Although early peak creatine kinase activity (peak CK) is considered a reliable marker of coronary reperfusion in patients with acute myocardial infarction (AMI), whether early peak CK indicates good myocardial salvage is unclear. Moreover, some patients have late peak CK despite successful reperfusion, and its clinical implication remains to be elucidated. METHODS AND RESULTS: We examined the association of the time to peak CK with predischarge left ventricular function in 124 patients with a first AMI who had successful reperfusion within 6 hours from symptom onset. Patients were classified according to the time from reperfusion to peak CK: group A, 61 patients with peak CK < 6 hours; group B, 42 with peak CK from 6 to 12 hours; and group C, 21 with peak CK > 12 hours. There were no differences among the 3 groups in age, sex, method of reperfusion, time from symptom onset to reperfusion, collateral circulation, or the extent of risk area estimated by number of leads with ST-segment elevation. Left ventricular ejection fraction measured by predischarge left ventriculography was lowest in group A, followed by group B, and highest in group C (median values, 43%, 52%, and 60%, P < .01). Left ventricular dysfunction (left ventricular ejection fraction < or = 40%) occurred in 26 (43%) patients in group A, 8 (19%) in group B, and none in group C (P < .01). CONCLUSIONS: We conclude that compared with early peak CK, late peak CK consistently reflects good myocardial salvage in patients with anterior AMI who had successful reperfusion within 6 hours from symptom onset.
BACKGROUND: Patients with an anterolateral acute myocardial infarction (AMI) have a worse prognosis, and those with additional inferolateral wall involvement might be higher risk because of more extensive area at risk. Lead -aVR obtained by inversion of images in lead aVR has been reported to provide useful information for inferolateral lesion. METHODS: We examined the relation between ST-segment deviation in lead aVR on admission electrocardiogram (ECG) and left ventricular function in 105 patients with an anterolateral AMI undergoing successful reperfusion < or = 6 hours after onset. Patients were classified according to ST-segment deviation in lead aVR on admission ECG: group A, 23 patients with ST elevation of > or = 0.5 mm; group B, 47 patients without ST deviation; and group C, 35 patients with ST depression of > or = 0.5 mm. RESULTS: There were no differences among the 3 groups in age, sex, or site of the culprit lesion. In groups A, B, and C, the peak creatine kinase level was 3661 +/- 1428, 4440 +/- 1889, and 6959 +/- 2712 mU/mL, and the left ventricular ejection fraction (LVEF) measured by predischarge left ventriculography was 54% +/- 9%, 48% +/- 7%, and 37% +/- 9%, respectively(P < .01). During hospitalization, congestive heart failure occurred more frequently in group C than in groups A or B (P < .05). ST-segment depression in lead aVR had a higher predictive accuracy than other ECG findings in identifying patients with predischarge LVEF < or = 35%. CONCLUSIONS: We conclude that in patients with an anterolateral AMI, ST-segment depression in lead aVR on admission ECG is useful for predicting larger infarct and left ventricular dysfunction despite successful reperfusion.
It has been reported that cardiac function can be improved by implanting a DDD pacemaker (PM) and setting a short atrioventricular (AV) delay in patients with impaired cardiac function. A previous report found that the critical AV delay that induces diastolic mitral regurgitation (MR) may represent the upper limit of the optimal AV delay. The optimal AV delay can be predicted by a simple method: slightly prolonged AV delay minus the interval between the end of the atrial kick and complete closure of the mitral valve (duration of diastolic MR) at the AV delay setting. The patient was a 84-year-old man with an old myocardial infarction. He had repeated admissions to hospital for congestive heart failure. ECG showed prolongation of the PQ interval (0.28 s) and complete left bundle branch block. Cardiac function was improved by AV sequential pacing when the AV delay was set at 120ms. After DDD-PM implantation, the cardiothoracic ratio decreased from 57 to 45% and cardiac function was improved from New York Heart Association class III to I. The AV delay was optimized during follow-up. Four years after PM implantation, the patient was in good condition without further hospital admission.
The present study investigated the relationship between myocardial damage and C-reactive protein (CRP) levels, with no increase in creatine kinase (CK) activity, immediately after the onset of acute myocardial infarction (AMI) in 85 patients with their first reperfused anterior AMI without CK elevation on admission and no ischemic events during hospitalization. Patients were classified into those with low levels (<0.3 mg/dl) of CRP (Group L; n=67) and those with high levels (> or =0.3 mg/dl) of CRP (Group H; n=18). Group H had a higher proportion of patients with a history of preinfarction angina (89 vs 55%, p<0.01), especially unstable angina. SigmaST in leads V1-6 on admission ECG was lower in Group H than in Group L (14+/-7 vs 21+/-13 mm, p<0.05). Predischarge left ventriculography showed that the left ventricular global ejection fraction (55+/-11 vs 48+/-10%, p<0.01) and SD/chord at the left anterior descending artery lesion (-1.7+/-0.9 vs -2.3+/-0.9, p<0.01) were better in Group H. Multivariate analysis demonstrated that both CRP on admission (p=0.011) and preinfarction angina (p=0.002) were independently associated with better regional wall motion (SD/chord >-2.0) before discharge. These results suggest that the clinical situation of elevated CRP immediately after onset is associated with less myocardial damage and better left ventricular function in reperfused anterior AMI.
It is unknown whether the pathogenetic mechanisms underlying acute myocardial infarction (AMI) differ according to the clinical presentation of preinfarction angina, so the present study measured plasma levels of C-reactive protein (CRP) in 280 patients with AMI in whom serum creatine kinase levels were normal on admission and increased subsequently. Patients were classified into 3 groups according to the type of preinfarction angina: no angina (n=95), stable angina (n=48), and unstable angina (n= 137). Patients with unstable angina were subdivided according to the Braunwald classification: class IB (n=39), class IIB (n=22), and class RIB (n=76). There were no differences among the 5 groups in baseline characteristics. CRP on admission was significantly higher and the level of physical activity at symptom onset was significantly lower in the Braunwald class RIB group than in the other groups, but no differences were observed among the other groups. Patients with preinfarction Braunwald class IIB unstable angina had higher CRP levels on admission and symptom onset at a lower level of physical activity. In such patients, the pathogenetic mechanisms may differ from those in other subsets of patients with AMI and active inflammation may play a more important role in AMI onset.
The time from admission to reperfusion in patients with acute myocardial infarction (AMI) was compared according to the type of hospital and treatment strategy. A total of 164 patients with a first AMI within 12h of onset were enrolled at one tertiary emergency center (TEC) and 6 community hospitals (CHs). The subjects were randomly assigned to receive either primary percutaneous transluminal coronary angioplasty (PTCA) (TEC-primary PTCA and CHs-primary PTCA groups) or 800,000 units of intravenous monteplase, half the standard dose of a mutant tissue plasminogen activator (t-PA), followed by rescue PTCA if the Thrombolysis in Myocardial Infarction (TIMI) flow grade was 2 or less (TEC-monteplase and CHs-monteplase groups) on the first coronary angiogram. Sixty minutes after admission, TIMI flow grade 3 rates of the study groups were as follows, in descending order: TEC-monteplase group, CHs-monteplase group, TEC-primary PTCA group, and CHs-primary PTCA group (56%, 41%, 36%, and 8%, respectively; p<0.01). However, there was no significant difference in the final TIMI flow grade 3 rate among the 4 groups. In the CHs, the peak creatine kinase tended to be lower in the monteplase group than in the primary PTCA group. The results suggest that low-dose monteplase followed by rescue PTCA is an effective strategy for promoting early reperfusion in patients with AMI, especially those who are treated at CHs.
Encephalitozoon spores were isolated in a primary tissue culture of the kidneys from an encephalitozoonosis-suspected rabbit in a municipal zoo in Hokkaido. The isolated spores were morphologically characteristic of microsporidial ones in chromotrope stain, and proven to be E. cuniculi by a polymerase chain reaction (PCR) with a species-specific primer set and by direct DNA sequencing of the PCR products.
Cardiac function is improved by bi-ventricular pacing in patients with severe reduced cardiac function. Atrioventricular (AV) delay optimization is also important in this therapy. However, the AV delay required to achieve the optimal AV synchrony varied from time to time. We have reported that the critical AV delay that induces diastolic mitral regurgitation (MR) may represent the upper limit of the optimal AV delay. The optimal AV delay can be predicted by a simple method; slightly prolonged AV delay-interval between the end of atrial kick and complete closure of the mitral valve (duration of diastolic MR) at the AV delay setting. [Case] 60 year old Japanese male with dilated cardiomyopathy. He was repeatedly admitted to our hospital due to congestive heart failure. Ejection fraction was 14%. ECG showed complete left bundle branch block and his PQ interval was 0.22 sec. He was dependent on intravenous injections of catecolamine and could not be discharged from the hospital for over one year. Optimal AV delay was predicted as 80 msec during bi-ventricular pacing by our formula. Cardiac output was 4.9, 6.0, 5.1 l/min when the AV delay was set at 50, 80, 110 msec. Cardiac function was improved from NYHA class III to II and he has been relieved from the dependency on intravenous catecholamine injections. AV delay was optimized (70-100 msec) by our method during follow-up for one year. This case indicates that AV delay optimization is important in bi-ventricular pacing.
OBJECTIVES: The efficacy of injection of a low-dose mutant tissue-type plasminogen activator (mt-PA), monteplase, followed by planned rescue percutaneous transluminal coronary angioplasty (PTCA) was compared with that of primary PTCA. METHODS: A total of 164 patients with acute myocardial infarction within 12 hr from onset were randomly assigned to a treatment with 80 x 10(4) U bolus of monteplase (Group M) or no administration (Group P) by the envelope method, followed by immediate angiography with angioplasty in patients with Thombolysis in Myocardial Infarction (TIMI) flow grade 0, 1 or 2. RESULTS: There were no differences in baseline characteristics between the two groups. Initial angiography showed a higher reperfusion rate (TIMI 2 + 3: 21% + 38% vs 13% + 9%, p < 0.001) and the median time to TIMI 3 was shorter (63 vs 78 min, p < 0.005) in Group M than in Group P, but the final TIMI 3 rate was similar (93% vs 96%). Peak creatine kinase was lower, and predischarge left ventricular ejection fraction measured in 70% of all patients was higher (59 +/- 9% vs 54 +/- 14%, p = 0.02) in Group M than in Group P. Recurrent ischemia with ST elevation occurred in three patients in Group M, but death, re-acute myocardial infarction or stroke did not occur in either group and the rate of bleeding complication was similar (4.9% vs 3.7%). PTCA was performed less frequently in Group M, but medical expenses were comparable in both groups. CONCLUSIONS: Low-dose mt-PA followed by rescue PTCA is effective for early recanalization and preservation of left ventricular function without increases in bleeding complications or medical expenses. These results suggest that low-dose mt-PA should be given to all patients with acute myocardial infarction who are scheduled to undergo primary PTCA.
To identify ways to decrease the risk of out-of-hospital cardiac arrest (CA) caused by an acute coronary syndrome, we examined factors associated with the development of CA > or = 1 hour after symptom onset. Multivariate analysis revealed that a low level of physical activity, a history of diabetes mellitus, and a history of unstable angina are associated with out-of-hospital CA occurring > or = hour after symptom onset.
Explore the source record for details and available documents.
Although sinus node recovery time (SNRT) assessment by the overdrive suppression test (ODST) is important in detecting sick sinus syndrome (SSS), its sensitivity is still inadequate. We have evaluated the effect of intravenous injection (i.v.) of disopyramide phosphate (DP) in ODST. The subjects were 30 SSS patients (64.9 +/- 10.0 years old). If SNRT was <2,000 ms or the corrected SNRT (CSNRT) was < 1,000 ms, ODST was repeated after DP i.v. (2 mg. kg(-1), < or = 100 mg in total). Eleven normal subjects (59.3 +/- 9.0 years old) were also studied. Although SNRT was <2,000 ms or the CSNRT was < 1,000 ms in 13 of the 30 SSS patients (43%), SNRT was prolonged from 1,510 +/- 300ms to 3,400 +/- 1,160 ms (P<0.01), and CSNRT from 510 +/- 190 to 2,470 +/- 1,470 ms (P<0.01) after DP i.v. in these patients. Thus, SNRT was > or = 2,000 ms and the CSNRT was > or = 1,000 ms in 27 of 30 SSS patients (90%) after DP i.v. Using a combination of overdrive suppression and intravenous injection of disopyramide phosphate, the corrected sinus node recovery time was diagnostic (>525 ms) in 29 of the 30 patients (97%). In contrast, SNRT and CSNRT were shortened in the normal subjects during ODST after DP i.v. (P<0.01). The plasma concentration of DP estimated in nine patients was 4.1 +/- 1.0 microg.ml(-1). No serious side effect occurred. ODST employing DP i.v. is safe and seems to be highly effective in diagnosing SSS.
Atrial flutter (AF) is a troublesome arrhythmia for patients with an implanted pacemaker. Although it has recently become possible to eliminate AF by radiofrequency catheter ablation (RF-CA), the incidence of AF before and after pacemaker implantation has not been clarified. The present study was conducted with 123 consecutive patients (69.3+/-11.6 (SD) years old) implanted with pacemakers, excluding patients who had chronic atrial fibrillation (AFib) when the pacemaker was implanted; 69 patients with atrioventricular (AV) block and 54 patients with sick sinus syndrome (including 29 patients with bradycardia-tachycardia syndrome). All patients were implanted with physiological pacemakers. The follow-up period was 4.7+/-1.9 years. In 11 of the 123 patients (8.9%), AF was observed before pacemaker implantation and the incidence was significantly higher in patients with sick sinus syndrome than in those with AV block (16.7 vs 2.9%, p<0.01). Nine of the 29 patients with bradycardia-tachycardia syndrome (31%) had AF. After physiological pacemaker implantation, AF recurred in 9 of the 11 patients, and AF was newly observed in 1 patient. Thus, 10 of the 123 patients (8.1%) had AF after physiological pacemaker implantation. Recurrence of AF was not suppressed by physiological pacing. Thirty of the 123 patients had AFib before implantation of a pacemaker and its occurrence was reduced by physiological pacing (from 24.4% to 12.2%, p<0.05). The incidence of AFib in patients with AF was significantly higher than in those without AF (90.0 vs 5.3%, p<0.001). In conclusion, the recurrence of AF is not prevented by physiological pacing and is closely related to the occurrence of AFib. RF-CA should be considered in patients who have AF before pacemaker implantation.