Reciprocal ST segment changes in acute inferior myocardial infarction: clinical, haemodynamic and angiographic implications

Reciprocal ST segment changes are frequent during acute inferiormyocardial infarction, yet their significance remains controversial. In order to investigate the implications of these changes, theECG obtained on admission for 83 patients with acute inferiormyocardial infarction was compared with the clinical courseand the results of angiographic and coronary arteriographicstudies performed an average of 3 weeks after the onset of symptoms. Group 1 consisted of 59 patients with at least 1 mm of horizontalon downsloping ST segment depression in at least 1 of leadsV₁ to V₄. Group 2 consisted of 24 patients without precordialST depression in this area. Group 1 patients were generally older than group 2 patients(59.6 ± 6.4 versus 54 ± 5.3 yr, P<0.01) hadhigher total creatine kinase (CK) levels and MB fractions (1835± 940 versus 875 ± 305, P < 001, 269 ±102 versus 95 ± 35 for MB fraction) and more complicationsduring the hospital course (80% versus 38% P<0.01) and greaterleft ventricular dysfunction (ejection fraction 52.2 ±6% for group I versus 59.2±7% for group 2; cardiac index2.75±0.41min^–1 m^–2 for group 1 versus 3.25± 0.3 lmin^–1 m^–2 for group 2 P<0.005). No difference was observed on biplane angiography as far asleft ventricular wall kinesis was concerned. By contrast, coronaryarteriography revealed more frequent left coronary artery diseasein group 1 patients (84%) than in group 2 patients (37%) P<0.005,the left anterior descending and circumflex arteries being equallyoften affected. Finally, the persistence of ST segment depression for more than48 hours was associated with a more severe depression of theejection fraction than transient depression (less than 48 hours). In summary, the presence of ST segment depression in the precordialleads during the acute phase of inferior myocardial infarctionwas associated with greater myocardial necrosis and more frequentleft coronary artery disease, thus identifying a subset of highrisk patients.     

Coronary reserve, extent of coronary disease, recurrent angina and ECG changes during pain in the in-hospital prognosis of acute coronary syndromes

The prognostic value of recurrent angina, severity of coronarydisease, ECG changes during pain and coronary reserve (ischaemicthreshold measured by atrial pacing: heart rate with ST segmentshift = 1 mm), was evaluated in 383 consecutive patients withacute coronary syndromes. Univariate analysis showed a significantrelationship between occurrence of complications (death, infarctionor coronary surgery) and number of anginal episodes, extentof coronary disease, ischaemic threshold and ST depression withpain. A multivariate analysis indicated that the first threeparameters were the main independent predictors. Coronary reservewas reduced (threshold 150 beats. min^–1) in 83% of patientswho had a myocardial infarction (40), in 91% of those who died(11), in 87% of those who underwent coronary surgery (52) andin 47% of uncomplicated cases (301). Also, a low ischaemic thresholdwas associated with a larger number of anginal episodes thana high threshold ( 130 beats. min^–1, 6.1 ± 5.6vs > 150 beats. min^–1, 2.9± 4.1, P<0.0001),and in complicated patients with one-, two- or three-vesseldisease ischaemic threshold (137.3± 21.2, 133.3 ±18.9, and 135.1 ± 21.2 beats. min^–1, respectively)was lower than in the uncomplicated ones (153.4±20.1,P < 0.005; 148.2± 19.1 P < 0.005; and 139.2 ±23.0 ns, beats, min^–1). A threshold <150 beats. min^–1and ECG changes during pain identified the subset with the highestrisk for complications (59/137, 45%), whereas a threshold >150 beats. Min^–1 and absence of pain or ECG changes duringpain identified those with the lowest risk (5/109, 5%, p <0.001). Thus, our findings document the prognostic significance of coronaryreserve for in-hospital complications in patients with acutecoronary syndromes and confirm the prognostic value of previouslyknown risk markers. They also indicate that some of them maybe significantly influenced by the status of coronary reserve.     

Dobutamine stress test to diagnose the presence and severity of coronary artery lesions in angina

To calculate the accuracy of dobutamine infusion as a stresstest to detect coronary lesions, 90 patients with angina andnine asymptonlatic subjects with nonsignificant coronary lesionswere submitted to a dobutamine test and coronary arteriography.Dobutamine was given in doses of 5, 10, 15 and 20µg kg^–1min^–1 every 5 min; a 12 lead ECG and blood pressure wasmonitored. Pressurexrate product increased from 8240±1667to 14898±3042. The test was negative (neither anginapain, nor ST seginent shift) in 31 patients, and positive in68. The ST segment was depressed in 33 cases and elevated in20. Significant (50%) coronary lesions were seen in 63 patientsand functional (coronary spasm or vasoconstriction) abnormalitiesin six. The sensitivity of the dobutamine test for the detectionof coronary lesions was 95%, specificity 78%, predictive valueof a positive test 88%, of a negative test 90% and diagnosticefficiency 89%. Strongly positive tests predictedsevere lesionsin 91% of the cases, and slightly positive tests ruled out severelesions in 84%. ST segment elevation was induced in 20 casesand corresponded to a severe coronary lesion. In conclusion,the dobutamine stress test is a simple and accurate method ofpredicting coronary artery disease in patients with angina,distinguishing between severe and mild lesions. It can be agood alternative to an exercise test.     

ST段早期恢复反映急性心肌梗死溶栓治疗后心肌再灌注

目的 比较溶栓再通后早期ST段恢复与未恢复者住院期间临床结局的差异，探讨ST段早期恢复在心肌再灌注中的作用。方法 108例溶栓经酶学等指标临床判定再通的急性心肌梗死（AMI）患者，按照有无早期（溶栓后2h)ST段恢复分为两组。连续测定血清肌酸激酶（CK）水平，了解心肌酶峰出现时间及峰值；放射性核素评估左心室功能。观察4周住院期间充血性心力衰竭（CHF）、室壁瘤、心肌梗死后心绞痛发生情况及病死率。结果 无论是前壁MI还是下壁MI，ST段早期恢复组左心室射血分数均高于未恢复组（P＜0．05）；CK峰值则低于未恢复组（P＜0．05）。住院期间ST段恢复组核素心肌显像充盈缺损、CHF及室壁瘤发生率低，心肌梗死后心绞痛发生率高（P值均小于0.05)。结论 同ST段未恢复组相比，溶栓再通后ST段早期恢复者临床预后好。心电图模式可以反映再灌注程度。     

Prognostic value of ambulatory ST segment monitoring compared with exercise testing at 1-3 months after acute myocardial infarction

The relative value of ambulatory ST segment monitoring for assessingprognosis following acute myocardial infarction is currentlyuncertain. Ambulatory monitoring was performed in 177 patientsat a mean of 38 days (range 22–93) post-myocardial infarctionand its prognostic value was compared with exercise treadmilltesting (n=170). Cardiac events (myocardial infarction, cardiacdeath or coronary revascularisation) were noted during at least1 year of follow-up. The presence or absence of ST depressionon ambulatory nonitoring did not predict increased fatal ornon-fatal cardiac events although more severe ST depressionhad some predictive power: after adjusting for clinical variablesand coronary prognostic indices, the duration/24 h (P=0·03)and magnitude (P=0·007) of ST depression had independentvalue. ST deviation on exercise testing was associated (P<0·05)with increased events (19/90; 21% vs 7/80; 9%) and in patientswith a positive exercise test ST depression on ambulatory monitoringdid not identify any additional events (8/41; 20% vs 11/49;22%). No factor available from ambulatory monitoring was predictiveof outcome once variables from exercise testing were taken intoaccount. Ambulatory ST segment monitoring performed in the laterecovery phase (1–3 months) after acute myocardial infarctionis inferior to exercise testing for predicting prognosis anddoes not increase the predictive power of an exercise test.Ambulatory monitoring may only be indicated in patients unableto perform an exercise test.     

Dipyridamole echocardiography evaluation of acute inferior myocardial infarction with concomitant anterior ST segment depression

The significance of anterior ST segment depression in inferioracute myocardial infarction (AMI) remains controversial. Theaim of this study was to relate precordial ST segment depressionto the topography of residual myocardial ischaemia, with myocardialmapping of the asynergic area and coronary anatomy. Twenty-fivepatients with first inferior AMI (15 patients with anteriorST segment depression: group A and 10 patients without anteriorST segment shift: group B), all underwent: (1) electrocardiographicevaluation on admission to the Coronary Care Unit and at 24h intervals thereafter; (2) 2D-echocardiographic study within3 h of CCU admission: (3) dipyridamole echocardiographic test(DET) (doses of dipyridamole up to 0.84 mg.kg^–1 i.v. over10 min) 4 days after AMI; (4) coronary arteriography within14 days from AMI. To assess regional left ventricular wall motion,a 16 segment model was used and a wall motion score index (WMSI)was derived. The results of DET were correlated to the anatomyof the infarct-related vessel. Compared to group B, group Apatients showed a significantly greater maximal ST segment elevationin inferior limb leads (lead III: 3.9±1.9 mm vs 2.2±1.1mm, P<0.05; aVF: 3.5±13 mm vs 1.7±0.8 mm, P<0.001).Group A patients showed greater WMSI (1.35±0.22 vs 117±0.12,P<0.05), with more frequent postero-lateral wall involvement(72% vs 20%, P<0.05). No patient of either group showed asynergyof the anterior, anterolateral or anteroseptal segments. Nodifferences in the distribution of coronary artery disease wereobserved. Left anterior descending coronary artery disease waspresent in only three patients (20%) in group A and in one patientin group B. DET was positive in eight patients (53%) in groupA and in three (30%) in group B (P = statistically not significant).In all patients DET induced new wall motion abnormalities locatedin the territory of the infarct-related artery. None of thepatients developed new wall motion abnormalities remote fromthe infarct zone or adjacent to the infarct zone, but locatedin different vascular regions. In conclusion, anterior ST segmentdepression in inferior A MI appears to indicate a more extensivearea of asynergy, with frequent involvement of the posterolateralwall. The topography of DET-induced residual myocardial ischaemiadoes not support the hypothesis of concomitant anterior ischaemia.     

Pathophysiology and prognostic significance of Holter-detected ST segment depression after myocardial infarction. The Tissue Plasminogen Activator: Toronto (TPAT) Study Group.

OBJECTIVES: We performed Holter monitoring on days 4 and 7 after acute myocardial infarction in 109 patients to assess whether ST segment shift would identify those with more severe coronary artery disease, left ventricular dysfunction and unfavorable prognosis. BACKGROUND. Silent myocardial ischemia is a frequent and prognostically significant event after acute myocardial infarction. However, the specific pathophysiologic mechanisms and the impact of thrombolytic therapy are uncertain. METHODS. In addition to Holter monitoring, patients underwent exercise testing, radionuclide angiography on days 1 and 9 and quantitative coronary angiography on day 9. RESULTS. Thirty-five patients (32%) had ST segment depression and had similar recombinant tissue-type plasminogen activator (rt-PA) treatment assignment and a reduced cross-sectional area of the infarct-related artery (0.59 +/- 0.57 vs. 1.04 +/- 1.26 mm2, p < 0.05). Global left ventricular function improved from day 1 to day 9 in patients without (4% +/- 11%, p < 0.001) but not in those with (0% +/- 7%) ST segment depression. In-hospital event rates were similar; however, follow-up 18 +/- 11 months after hospital discharge revealed a greater frequency of death and recurrent myocardial infarction in patients with compared with those without ST segment depression (27% vs. 6%, p = 0.03). CONCLUSIONS. After acute myocardial infarction, approximately one third of patients have ST segment depression on Holter monitoring, independent of the use of thrombolytic therapy. The unfavorable prognosis observed in these patients may be related to greater lumen obstruction in the infarct-related artery and lack of improvement in left ventricular function.     

11例急性单纯后壁心肌梗死心电图及梗死相关动脉特点分析

目的 分析急性单纯后壁心肌梗死（不包括同时合并下壁及右室心肌梗死）的心电图及冠状动脉造影特点。方法 总结自2001年至2006年门、急诊收治的急性单纯后壁心肌梗死患者11例,随访心电图特点,并行冠状动脉造影确定梗死相关动脉。结果 11例患者除了V7-V9导联ST段有典型的弓背向上抬高1．0—2．0mm外,9例（81．8％）V1-V2导联R／S≥1,5例（45．5％）V1-V4导联ST段压低1．0—2．0mm,4例（36．4％）Ⅰ、aVL导联ST段抬高0．5-1．5mm,5例（45．5％）V5-V6导联ST段抬高0．5—1．5mm。冠状动脉造影显示梗死相关动脉均为左回旋支（LCX）。梗死部位1例在第一钝缘支（OM1）发出前,为95％管状狭窄;6例（54．5％）在OM1发出后,其中4例为100％闭塞,1例为99％次全闭塞,1例为90％长段狭窄;4例（36．4％）在OM1,其中2例为100％闭塞,1例为99％次全闭塞,1例为95％局限性狭窄。单支病变3例（27．3％）,合并左前降支（LAD）病变4例（36．4％）,合并右冠状动脉（RCA）病变2例（18．2％）,同时合并LAD及RCA病变2例（18．2％）。结论12导联心电图,如有V1-V2导联R／S≥1,V1-V4导联ST段压低等特点时,结合临床与心肌酶学改变,高度怀疑急性后壁心肌梗死,需做后壁导联和冠状动脉造影加以证实,而梗死相关动脉多为左回旋支。     

Exercise testing for assessment of the significance of ST segment depression observed during episodes of paroxysmal supraventricular tachycardia

Sixteen patients who had manifested ST segment depression duringepisodes of paroxysmal supraventricular tachycardia (PSVT) werestudied with exercise testing in order to detect coronary arterydisease and myocardial ischaemia. No ST segment depression wasobserved during exercise testing in 15 out of the 16 patientstested. Paroxysms of supraventricular tachycardia associatedwith ST segment depression occurred during exercise testingin three cases. The ST segment depression was immediately apparent,remained constant throughout the supraventricular tachycardiaand was almost instantly abolished following conversion to sinusrhythm. Patients with heart rates > 250 beats min^–1during PSVT had marked ST segment depression associated withthe tachycardia. These results suggest that coronary artery disease and myocardialischaemia are not involved in the genesis of ST segment depressionduring PSVT. Tachycardia per se may be the cause of ST segmentdepression by altering the slope of phase 2 of the ventricularaction potential. Retrograde atrial activation may also induceST segment shifts in some of the cases.     

Further elevation of the ST segment during the first hour of thrombolysis: A possible early marker of reperfusion

OBJECTIVES: To evaluate the clinical implications of early electrocardiographicchanges during thrombolysis in a randomized study in patientswith an acute myocardial infarction. BACKGROUND: Re-elevation of a rapidly resolving ST segment during thrombolysisis currently interpreted as a sign of re-occlusion, but a furtherelevation at very early stages of lytic therapy may not necessarilyhave the same implications. METHODS: In 214 patients with a first transmural acute myocardial infarctionof 4 h randomized to fibrinolytic (streptokinase group, n: 110)vs non fibrinolytic medical therapy (control group, n: 104),a standard 12 lead ECG was continuously recorded during thefirst 60 min and at 2, 4, 10, 16 and 24 h. Serial enzymes weremeasured during 72 h, and in 156 patients (73%) a coronary angiogramwas performed at 10–15 days. RESULTS: Within the first 20–40 min there was an additional STsegment elevation in 50 patients (45%) from the streptokinasegroup and in 19 from control group (18%) (P<0.0001) but theincrement was greater in the streptokinase group (1.2 ±1.4 vs 0.3 ± 1.4 mm, P<0.0001). In the streptokinasegroup, the interval from onset of pain to peak creatine kinaseMB was shorter in patients with additional ST segment elevationthan in those without it (699 ± 193 vs 856 ± 299min, P<0.01). Moreover, in-hospital mortality tended to belower in patients whose ST segment was elevated than in thosewithout such elevation (2150, 4%, vs 6160, 10%). Incidence ofrecanalization was high but comparable in these two subsets.In recanalized patients, with or without additional ST segmentelevation, the ST segment declined significantly at 1 h (–1.0 ± 1.7, P<0.001, vs 0.1 ± 1.5 mm, ns). CONCLUSIONS: Additional ST segment elevation is frequently observed duringthe first hour of intravenous thrombolysis with streptokinase.Its association with a subsequent early decline of ST elevation,reduced mortality, a shorter time interval to peak creatinekinase, and a high rate of late recanalization, suggest thatin some patients it is one of the earliest markers of reperfusion.     

Lipid peroxidation and antioxidant status following thrombolytic therapy for acute myocardial infarction

We have investigated the timescale of increased lipid peroxidationfollowing successful early thrombolytic therapy for acute myocardialinfarction and report for the first time reciprocal changesin plasma chain-breaking antioxidants. Sixty-seven patientswere recruited following a first acute myocardial infarctionwithin 6 h of the onset of symptoms and received 70 or 100 mgof recombinant tissue plasminogen activator (Actilyse) as twointravenous bolus injections 30 min apart. Serial blood sampleswere taken before administration of thrombolytic therapy andafter 30 min, 60 min, 90 min, 6 h and 24 h. Coronary arterypatency was assessed at 90 min by coronary angiography. Malondialdehyde(MDA), a marker of lipid peroxidation, and the chain-breakingantioxidants alpha-tocopherol, retinol and ascorbate were measuredby high performance liquid chromatography. When the coronaryartery was patent there was an early rise in plasma MDA (time0.091 ± 0.05 µmol.l^–1) with levels peakingat 90 min (1.02 ± 0.06, P<0.05) and returning to baselineby 6 h (0.85 ± 0.06), accompanied by reciprocal decreasesin alpha-tocopherol (time 0 7.13 ± 0.34 µmol.mmol^–1cholesterol, 90 min 6.64±0.33, P<0.05) and retinol(time 0 1.99±0.10 µmol.l^–1, 90 min 1.81 ±0.08, P<0.05). Ascorbate levels did not change significantlyuntil 24 h (time 0 29.5 ± 4.9 µmol.l^–1, 24h 22.6 ± 4.4, P<0.05). Where the coronary artery wasoccluded no changes in these parameters were found except fora late (24 h) fall in ascorbate (time 0 18.5 ± 2.0 mol.l^–1,24 h 12.2 ± 2.2, P<0.05). The timescale of changesin MDA and antioxidants supports a role for increased free radicalproduction following successful early thrombolytic therapy foracute myocardial infarction.     

The de winter electrocardiogram pattern is a transient electrocardiographic phenomenon that presents at the early stage of ST‐segment elevation myocardial infarction

Background

The de Winter electrocardiogram (EKG) pattern is a novel sign that indicates left anterior descending coronary artery (LAD) occlusion in patients with chest pain. This study aimed to assess the prevalence and clinical characteristics of patients with this pattern.

Hypothesis

The de Winter EKG pattern is an special anterior ST‐segment elevation myocardial infarction (STEMI) equivalents without obvious ST‐segment elevation.

Methods

This retrospective study included all patients with anterior myocardial infarction admitted between January 2011 and December 2017. Patients were categorized into two groups: those with the de Winter EKG pattern and those with typical STEMI.

Results

Of 441 patients, 15 (3.4%) with anterior myocardial infarction had the de Winter EKG pattern. Similar to those with typical STEMI, the majority of patients with the de Winter EKG pattern had ST‐segment elevation, pathologic Q wave, and absence of R wave at follow‐up. The median time from recognition of this pattern until its evolution was 114 minutes. The ST‐segment in leads V3R to V5R and leads V7 to V9 were normal or slightly depressed when a typical de Winter EKG pattern was noted in leads V1 to V6. The culprit lesion was mainly in the proximal LAD or the diagonal branch. Patients with this EKG pattern responded poorly to thrombolytic therapy.

Conclusions

We believe that the de Winter EKG pattern may be a sign of ischemia and presents at the early stage of STEMI rather than being an independent pattern. In patients with this pattern, a percutaneous coronary intervention rather than follow‐up and thrombolytic strategy should be performed.     

Intracoronary ST segment evolution during primary coronary stenting predicts infarct zone recovery

In patients with acute myocardial infarction (AMI), early ST segment elevation resolution on ECG predicts myocardial reperfusion and LV recovery. Intracoronary ECG is more sensitive than surface ECG to detect regional ischemia. In patients undergoing primary percutaneous coronary intervention (PCI), we investigated if failed myocardial reperfusion, despite successful infarct vessel recanalization, could be rapidly and easily identified by intracoronary ST segment monitoring from guidewire recording. We recorded intracoronary and standard ECG during primary coronary stenting (PCI) in 50 patients with AMI (59 ± 11 years; anterior AMI in 66%). All patients had a successful PCI and underwent 2D echocardiography soon after PCI and 6 months later. Following PCI, intracoronary ST resolution ≥ 50% from baseline was documented in 39 patients (78%; group A; from 11 ± 8 to 1 ± 2 mm) but not in 11 (22%; group B; from 11 ± 8 to 8 ± 5 mm). Group A had slightly shorter ischemic time (202 ± 94 vs. 238 ± 112 min in B; P = 0.2) and smaller peak CK values (2,752 ± 2,038 vs. 4,802 ± 3,671 U/L in B; P = 0.02). After PCI, ST resolution was found on standard ECG in 34 (87%) group A and in 3 (27%) group B patients. At 6‐month follow‐up, left ventricular ejection fraction was greater in group A (47% ± 8% vs. 39% ± 8% in B; P < 0.001) with improved wall motion score index (from 2.2 ± 0.3 to 1.7 ± 0.3 in A; from 2.3 ± 0.4 to 2.1 ± 0.4 in B; P < 0.001). There were no significant differences between intracoronary and standard ECG for sensitivity (92% vs. 86%) and specificity (62% vs. 57%) to predict improved infarct zone recovery after 6 months. ST elevation resolution on intracoronary recording during PCI predicts infarct zone recovery. Monitoring ST segment evolution by intracoronary ECG allows prompt and inexpensive identification in the catheterization laboratory of those patients without myocardial reperfusion, who may require adjunctive therapeutic interventions after successful infarct vessel recanalization. Catheter Cardiovasc Interv 2005;64:53–60. © 2004 Wiley‐Liss, Inc.     

Absence of ST elevation in ECG leads V7, V8, V9 in ischaemia of non-occlusive aetiologies

BACKGROUND AND OBJECTIVE: Occlusion of the circumflex coronary artery may present with either ST elevation typical of inferior or lateral myocardial infarction, ST depression or a normal 12-lead electrocardiogram (ECG). In patients presenting with ST depression, concomitant ST elevation in the posterior leads V7, V8 and V9 is believed to reflect ST-elevation myocardial infarction of the posterior wall. However, to be confident of this diagnosis, it is necessary to know that posterior ST depression does not occur in acute subendocardial ischaemia. METHODS AND RESULTS: We have prospectively recorded leads V7, V8 and V9 simultaneously with the standard 12-lead ECG in patients who underwent treadmill stress test. Group A consists of 35 patients who showed ischaemic praecordial ST depression in their 12-lead ECGs during treadmill stress test and subsequent angiographic documentation of significant coronary artery disease. Group B consists of 35 subjects who showed normal ECG findings during treadmill stress test. In none of the Group A or B patients was there ST elevation in leads V7, V8 or V9 either at rest or at peak exercise. ST depression was seen in 69% in V7, 31% in V8 and 11% in V9 in the Group A patients at peak exercise. CONCLUSION: ST elevation in leads V7, V8 and V9 is uncommon in patients presenting with subendocardial ischaemia. Therefore, in patients presenting with acute chest pain and ST depression in the 12-lead ECG, concomitant posterior ST elevation may be a reliable indicator of ST elevation posterior MI. This is likely due to circumflex artery occlusion and may require thrombolytic therapy.     

Further elevation of the ST segment during the first hour of thrombolysis: A possible early marker of reperfusion

OBJECTIVES: To evaluate the clinical implications of early electrocardiographicchanges during thrombolysis in a randomized study in patientswith an acute myocardial infarction. BACKGROUND: Re-elevation of a rapidly resolving ST segment during thrombolysisis currently interpreted as a sign of re-occlusion, but a furtherelevation at very early stages of lytic therapy may not necessarilyhave the same implications. METHODS: In 214 patients with a first transmural acute myocardial infarctionof 4 h randomized to fibrinolytic (streptokinase group, n: 110)vs non fibrinolytic medical therapy (control group, n: 104),a standard 12 lead ECG was continuously recorded during thefirst 60 min and at 2, 4, 10, 16 and 24 h. Serial enzymes weremeasured during 72 h, and in 156 patients (73%) a coronary angiogramwas performed at 10–15 days. RESULTS: Within the first 20–40 min there was an additional STsegment elevation in 50 patients (45%) from the streptokinasegroup and in 19 from control group (18%) (P<0·0001)but the increment was greater in the streptokinase group (1·2± 1·4 vs 0·3 ± 1·4 mm, P<0·0001).In the streptokinase group, the interval from onset of painto peak creatine kinase MB was shorter in patients with additionalST segment elevation than in those without it (699 ±193 vs 856 ± 299 min, P<0·01). Moreover, in-hospitalmortality tended to be lower in patients whose ST segment waselevated than in those without such elevation (2150, 4%, vs6160, 10%). Incidence of recanalization was high but comparablein these two subsets. In recanalized patients, with or withoutadditional ST segment elevation, the ST segment declined significantlyat 1 h (– 1·0 ± 1·7, P<0·001,vs 0·1 ± 1·5 mm, ns). CONCLUSIONS: Additional ST segment elevation is frequently observed duringthe first hour of intravenous thrombolysis with streptokinase.Its association with a subsequent early decline of ST elevation,reduced mortality, a shorter time interval to peak creatinekinase, and a high rate of late recanalization, suggest thatin some patients it is one of the earliest markers of reperfusion.     

Utility of the prehospital electrocardiogram in diagnosing acute coronary syndromes: the Myocardial Infarction Triage and Intervention (MITI) project

Objectives. We sought to determine whether the prehospital electrocardiogram (ECG) improves the diagnosis of an acute coronary syndrome.Background. The ECG is the most widely used screening test for evaluating patients with chest pain.Methods. Prehospital and in-hospital ECGs were obtained in 3,027 consecutive patients with symptoms of suspected acute myocardial infarction, 362 of whom were randomized to prehospital versus hospital thrombolysis and 2,665 of whom did not participate in the randomized trial. Prehospital and hospital records were abstracted for clinical characteristics and diagnostic outcome.Results. ST segment and T and Q wave abnormalities suggestive of myocardial ischemia or infarction were more common on both the prehospital and hospital ECGs of patients with as compared with those without acute coronary syndromes (p ≤ 0.00001). Those with prehospital thrombolysis were more likely to show resolution of ST segment elevation by the time of hospital admission (14% vs. 5% in patients treated in the hospital, p = 0.004). In patients not considered for prehospital thrombolysis, both persistent and transient ST segment and T or Q wave abnormalities discriminated those with from those without acute coronary ischemia or infarction. Compared with ST segment elevation on a single ECG, added consideration of dynamic changes in ST segment elevation between serial ECGs improved the sensitivity for an acute coronary syndrome from 34% to 46% and reduced specificity from 96% to 93% (both p < 0.00004). Overall, compared with abnormalities observed on a single ECG, consideration of serial evolution in ST segment, T or Q wave or left bundle branch block (LBBB) abnormalities between the prehospital and initial hospital ECG improved the diagnostic sensitivity for an acute coronary syndrome from 80% to 87%, with a fall in specificity from 60% to 50% (both p < 0.000006).Conclusions. ECG abnormalities are an early manifestation of acute coronary syndromes and can be identified by the prehospital ECG. Compared with a single ECG, the additional effect of evolving ST segment, T or Q waves or LBBB between serially obtained prehospital and hospital ECGs enhanced the diagnosis of acute coronary syndromes, but with a fall in specificity.     

Initial experience with the Endicor X-sizer thrombectomy device in patients with ST segment elevation myocardial infarction

We investigated 16 patients with ST segment elevation myocardial infarction who had an occluded coronary artery (TIMI 0) at initial angiogram. Instead of balloon angioplasty and stenting, patients were subjected to thrombectomy (Endicor X-sizer) and stenting. In 15/16 patients the occlusion could be crossed by the thrombectomy device resulting in TIMI flow 3 in all of them. Thereafter, stenting was performed. At final angiogram all 15 patients continued to show TIMI flow grade 3. Twelve-lead ECG was performed prior to and post-intervention. ST elevation was measured as the sum of eight leads for anterior infarction and of five leads for inferior infarction. In 13/15 patients, ECG analysis was possible (2 developed bundle branch block post-intervention). In all 13 patients, a >50% ST decrease of the initial amount of ST elevation was observed reaching a >70% reduction in 11 patients. Procedural complications were low (one coronary dissection after thrombectomy) and 30 days follow-up was uneventful. Thrombectomy using the Endicor X-Sizer device may become an attractive mechanical reperfusion strategy for patients with acute myocardial infarction.     

Estimates of myocardium at risk and collateral flow in acute myocardial infarction using electrocardiographic indexes with comparison to radionuclide and angiographic measures

Objectives. This study sought to determine the accuracy of the initial 12-lead electrocardiogram (ECG) in predicting final infarct size after direct coronary angioplasty for myocardial infarction and to examine which physiologic variables known to be determinants of outcome the ST segment changes most closely reflect.Background. Myocardium at risk, collateral flow and time to reperfusion have been shown to be independent physiologic predictors of infarct size in animal and clinical models. However, such measurements may be difficult to perform on a routine basis in patients with myocardial infarction. The standard 12-lead ECG is inexpensive and readily available.Methods. Sixty-seven patients with acute myocardial infarction, ST segment elevation and duration of chest pain <12 h had an initial injection of technetium-99m sestamibi. Tomographic imaging was performed 1 to 8 h later (after direct coronary angioplasty), and the images were quantified to measure perfusion defect size (myocardium at risk) and severity (a measure of collateral flow). Contrast agent injection and tomographic acquisition were repeated at hospital discharge to measure infarct size. The ST segment elevation score was calculated for each patient according to infarct location and using previously described formulas.Results. ST segment elevation score correlated closest with the radionuclide measure of collateral flow (r = −0.44, p ≤ 0.0001), as well as an angiographic measure of collateral flow (r = −0.38, p = 0.05). Although ST segment elevation score correlated weakly with the magnitude of myocardium at risk by technetium-99m sestamibi, it was not as strong as infarct location alone in predicting myocardium at risk ([mean ± SD] anterior 51 ± 13% left ventricle vs. inferior 17 ± 10% left ventricle, p < 0.0001). ST segment elevation score was weakly associated with final infarct size (r = 0.34, p = 0.005). A multivariate ECG model was constructed with infarct location as a surrogate for myocardium at risk, ST segment elevation score as a surrogate for estimated collateral flow, and elapsed time to reperfusion from onset of chest pain. All three variables were independently associated with infarct size.Conclusions. The initial standard 12-lead ECG can provide insight into myocardium at risk and, to a greater extent, collateral flow and can consequently provide some estimate of subsequent infarct size. However, the confidence limits for such predictors are wide.     

Myocardial Infarction Triage and Intervention Project--phase I: patient characteristics and feasibility of prehospital initiation of thrombolytic therapy

Prehospital initiation of thrombolytic therapy by paramedics, if both feasible and safe, could considerably reduce the time to treatment and possibly decrease the extent of myocardial necrosis in patients with acute coronary thrombosis. Preliminary to a trial of such a treatment strategy, paramedics evaluated the characteristics of 2,472 patients with chest pain of presumed cardiac origin; 677 (27%) had suitable clinical findings consistent with possible acute myocardial infarction and no apparent risk of complication for potential thrombolytic drug treatment. Electrocardiograms (ECGs) of 522 of the 677 patients were transmitted by cellular telephone to a base station physician; 107 (21%) of the tracings showed evidence of ST segment elevation. Of the total 2,472 patients, 453 developed evidence of acute myocardial infarction in the hospital; 163 (36%) of the 453 had met the strict prehospital screening history and examination criteria and 105 (23.9%) showed ST elevation on the ECG and, thus, would have been suitable candidates for prehospital thrombolytic treatment if it had been available. The average time from the onset of chest pain to prehospital diagnosis was 72 +/- 52 min (median 52); this was 73 +/- 44 min (median 62) earlier than the time when thrombolytic treatment was later started in the hospital. Paramedic selection of appropriate patients for potential prehospital initiation of thrombolytic treatment is feasible with use of a directed checklist and cellular-transmitted ECG and saves time. This strategy may reduce the extent and complications of infarction compared with results that can be achieved in a hospital setting.     

Cardiac tamponade early after thrombolysis for acute myocardial infarction: a rare but not reported hemorrhagic complication

Among 392 consecutive patients admitted for acute myocardial infarction and treated with thrombolytic drugs, 4 patients (1%) developed an early hemorrhagic pericardial effusion (without ventricular wall rupture) evolving within 24 h to cardiogenic shock consequent to cardiac tamponade. They all suffered from a large anterior myocardial infarction treated within 4 h after onset of symptoms with intravenous anisoylated plasminogen streptokinase activator complex (one case), recombinant tissue-type plasminogen activator (rt-PA) (two cases) or streptokinase (one case), anticoagulation with heparin (all cases) and aspirin (three cases). As soon as pericardial effusion was established by echocardiography, emergency percutaneous pericardiocentesis was performed at the bedside 20 +/- 6 h after thrombolytic therapy was started. This corrected immediately the clinical and hemodynamic status of each patient and a catheter was left in the pericardial space for 34 +/- 18 h. Thus, in the presence of unexplained clinical and hemodynamic deterioration occurring during the first 24 h after thrombolytic treatment of a large myocardial infarction, cardiac tamponade should be suspected. Immediate percutaneous pericardiocentesis followed by continuous drainage is a simple and definitive treatment for this complication.