High-resolution and signal-averaged electrocardiography to separate post-myocardial infarction patients with and without ventricular tachycardia

High-resolution and signal-averaged ECG, 24 h Holter recordingand ejection fraction were used to separate post-myocardialinfarction patients with and without ventricular tachycardia(VT) among 150 individuals: 26 patients with an old myocardialinfarction and documented sustained VT, 104 patients with anacute myocardial infarction without sustained VT, who were followed-upfor 2 years, and 20 healthy volunteers. Bipolar orthogonal XYZleads were recorded, high-pass filtered at cut-off frequenciesof 25, 40, 60, 80 and 100 Hz, and combined to vector magnitudex² + Y²+ Z². The filtered QRS duration, the root-mean-squarevoltages of different time intervals and the durations of lowamplitude signals under different thresholds, both from theinitial and terminal QRS, were calculated. The sensitivity andspecificity of each parameter alone and in every combinationof two, three and four parameters (17 million different combinations)were computed both from non-averaged and averaged data. Thebest separation was achieved by 12 combinations all includingfour signal-averaged ECG parameters, with a sensitivity of 81%and a specificity of 79%. The parameters represented most were:filtered QRS duration at 25 Hz, RMS voltage of the last 50 msat 25 Hz, terminal LAS duration at 80 Hz, and RMS voltage ofthe last 20 ms at 80 Hz. Parameters of the initial QRS complexdid not improve either the sensitivity or the specificity ofthe method. In logistic regression analysis, the best combinationsof four signal-averaged ECG parameters separated VT patientsbetter (P<0·001) than non-sustained ventricular tachycardiaat Holter (P=0·001); left ventricular ejection fraction(P=0·01) or age (P=0·006). Parameters calculatedfrom averaged data gave better results than parameters calculatedfrom non-averaged data.     

Time domain analysis of the signal averaged electrocardiogram in patients with a conduction defect or a bundle branch block

Doubts have been expressed about the clinical usefulness oftime domain analysis of the signal averaged electrocardiogramin patients with prolonged QRS complex duration. We studied147 patients using a signal averaged ECG (40–250 Hz) whoseQRS complex was longer than 100 ms. A baseline electrophysiologystudy was also performed in 128 of these patients. Seventy-sevenpatients had a minor (QRS <120 and >100 ms) conductiondefect. Thirty-seven of these 77 had either induced or spontaneoussustained ventricular tachycardia (group I) and 40 had no sustainedventricular tachycardia (group II). Seventy patients had a major(QRS120 and >100 ms) conduction defect, 44 of whom had sustainedventricular tachycardia (group A). The remaining 26 withoutthis condition formed Group B. Group I compared to group IIpatients had a longer filtered QRS duration (120.8 ±14 vs 104.5 ± 9.5 ms, P<0.001), a longer low amplitudesignal duration (41 ± 12.1 vs 31 ± 12.6 ms, P<0.0001)and a lower root mean square of the last 40 ms of the filteredQRS complex (27 ± 29.8 vs 35 ± 25.3 µV,P=ns). Group A compared to group B had a longer filtered QRSduration (157.7±20.2 vs 140.7± 15.7 ms, P<0.001),a longer low amplitude signal duration (57.3 ±24.9 vs37.8 ± 20.3 ms P<0.001) and a lower root mean squareof the last 40 ms of the filtered QRS complex (14.3 ±11.2 vs 22.0 ± 10.5 1 P<0.01). Using conventionallate potential criteria, the sensitivity and specificity ofthe signal averaged ECG for the detection of sustained ventriculartachycardia patients with a minor conduction defect were 89%and 75%, respectively. The same criteria applied to patientswith a major conduction defect were sensitive (sensitivity:87%) but non-specific (specificity: 50%). However, by usingmodified late potential criteria, such as the presence of twoof any of the following three signal averaged parameters: filteredQRS duration 145 ms, low amplitude signal duration 50 ms,root mean square of the last 40 ms of the filtered QRS complex17.5µV, we derived a non-optimal but still acceptablecombination of sensitivity (68%) and specificity (73%). We concludethat traditional late potential criteria can be applied in patientswith a minor conduction defect, but modification of these criteriais necessary to derive useful clinical information for riskstratification of patients with a QRS complex duration 120ms.     

Time domain analysis of the signal averaged electrocardiogram in patients with a conduction defect or a bundle branch block

Doubts have been expressed about the clinical usefulness oftime domain analysis of the signal averaged electrocardiogramin patients with prolonged QRS complex duration. We studied147 patients using a signal averaged ECG (40–250 Hz) whoseQRS complex was longer than 100 ms. A baseline electrophysiologystudy was also performed in 128 of these patients. Seventy-sevenpatients had a minor (QRS <120 and >100 ms) conductiondefect. Thirty-seven of these 77 had either induced or spontaneoussustained ventricular tachycardia (group I) and 40 had no sustainedventricular tachycardia (group II). Seventy patients had a major(QRS120 and >100 ms) conduction defect, 44 of whom had sustainedventricular tachycardia (group A). The remaining 26 withoutthis condition formed Group B. Group I compared to group IIpatients had a longer filtered QRS duration (120·8 ±14 vs 104·5 ± 9·5 ms, P<0·001),a longer low amplitude signal duration (41 ± 12·1vs 31 ± 12·6 ms, P<0·0001) and a lowerroot mean square of the last 40 ms of the filtered QRS complex(27 ± 29·8 vs 35 ± 25·3 µV,P=ns). Group A compared to group B had a longer filtered QRSduration (157·7±20·2 vs 140·7±15·7 ms, P<0·001), a longer low amplitude signalduration (57·3 ±24·9 vs 37·8 ±20·3 ms P<0·001) and a lower root mean squareof the last 40 ms of the filtered QRS complex (14·3 ±11·2 vs 22·0 ± 10·5 1 P<0·01).Using conventional late potential criteria, the sensitivityand specificity of the signal averaged ECG for the detectionof sustained ventricular tachycardia patients with a minor conductiondefect were 89% and 75%, respectively. The same criteria appliedto patients with a major conduction defect were sensitive (sensitivity:87%) but non-specific (specificity: 50%). However, by usingmodified late potential criteria, such as the presence of twoof any of the following three signal averaged parameters: filteredQRS duration 145 ms, low amplitude signal duration 50 ms,root mean square of the last 40 ms of the filtered QRS complex17·5µV, we derived a non-optimal but still acceptablecombination of sensitivity (68%) and specificity (73%). We concludethat traditional late potential criteria can be applied in patientswith a minor conduction defect, but modification of these criteriais necessary to derive useful clinical information for riskstratification of patients with a QRS complex duration 120ms.     

Echocardiographic wall motion abnormalities and the signal averaged electrocardiogram in the acute phase of a first myocardial infarction

We studied the relationship between wall motion abnormalitiesdetermined by echocardiography and the signal-averaged electrocardiogramin 82 consecutive patients during the acute phase of a firstmyocardial infarction. An abnormal signal-averaged electrocardiogramwas defined as the presence of two of the following criteria:a QRS duration 114 ms, a root mean square voltage (RMS) ofthe last 40 ms 25 µV and an amplitude signal lower than40µV lasting 39 ms. The left ventricle was divided into13 segments and the contraction pattern divided into akinesiaalone (including dyskinesia) (group A), hypokinesia alone (groupB) and both hypokinesia and akinesia (group C). An abnormal signal-averaged electrocardiogram was found in 14/82patients (17%) and was correlated with the persistence of occlusionof the infarct-related vessel (32% vs 9%. P < 0.02). In patientswith a patent vessel, the incidence of an abnormal signal-averagedelectrocardiogram was 14% in group A, 9% in group B and 0% ingroup C (NS). In patients with an occluded vessel an abnormalsignal-averaged electrocardiogram was found in 10% of groupA patients, in 36% in group B patients and in 75% of group Cpatients (P = 0.05). Our study suggests that the presence of hypokinetic areas duringthe acute phase of a first myocardial infarction and an abnormalsignal-averaged electrocardiogram indicate an occluded infarct-relatedvessel.     

Noise in the signal-averaged electrocardiogram and accuracy for identification of patients with sustained monomorphic ventricular tachycardia after myocardial infarction

Late potentials are detected at various noise levels in clinicalstudies. The aim of this study was, in a case-control design,to assess the effect of residual noise level on the identificationof patients with sustained monomorphic ventncular tachycardiaafter myocardial infarction. Electrocardiograms from 16 patientswith prior myocardial infarction and documented sustained monomorphicventricular tachycardia and 41 patients with prior myocardialinfarction and without ventncular tachycardia, were analysedby two signal averaging procedures to noise level 0·2and 0·4 µV Standard time domain parameters weremeasured. Two definitions of late potential were analysed: (1)if any two of the following criteria were present (signal-averagedQRS duration >120 ms, late potential duration >40 ms,and root-mean-square voltage of the terminal 40 ms of the filteredQRS <25µV); or (2) if the signal-averaged QRS duration120 ms. Overall the signal-averaged electrocardiogram performedbetter at noise level 0·4µV compared to noise level0·2µV with respect to identification of patientswith or without ventricular tachycardia after myocordial infarction.Reducing noise level from 0·4 to 0·2 µVincreased the sensitivity, but the consequence was a substantialdecrease in specificity. Our data indicate that when a highsensitivity is the goal, the definition based only on signal-averagedQRS duration 120 ms should be applied; sensitivity was 88% andspecificity 59% at noise level 0·4 µV. If a highspecificity is the goal, the definition should be based on thedefinition with two abnormal parameters; sensitivity was 69%and specificity 68% at noise level 0·4µV.     

Results of signal-averaged electrocardiography and electrophysiologic study in patients with nonsustained ventricular tachycardia after healing of acute myocardial infarction

Programmed stimulation and signal-averaged electrocardiography were performed in 43 consecutive patients with nonsustained ventricular tachycardia (VT) after healing of inferior (29 patients) or anterior wall (14 patients) acute myocardial infarction. Twenty-two patients had inducible sustained VT. Patients with inferior infarction and inducible sustained VT had significantly longer filtered QRS durations (125 +/- 19 vs 112 +/- 15 ms, p less than 0.01) and significantly lower voltage in the last 40 ms of the filtered QRS complex (19 +/- 5 vs 30 +/- 14 microV, p less than 0.05) than those without inducible sustained VT. In contrast, the signal-averaged electrocardiographic measurements in patients with anterior infarction and inducible sustained VT did not differ significantly from those without inducible sustained VT. The results of these studies were compared with those of 2 control groups: 45 patients without ventricular arrhythmias after myocardial infarction and 95 patients with spontaneous and inducible sustained VT after myocardial infarction. The signal-averaged electrocardiographic measurements in patients with spontaneous nonsustained VT after inferior infarction were intermediate between the control group without arrhythmias and the control group with sustained VT. The signal-averaged electrocardiograms in patients with nonsustained VT after anterior infarction were not significantly different from those in patients without ventricular arrhythmias. The study shows that the site of infarction influences the signal-averaged electrocardiogram in patients with VT after myocardial infarction. The signal-averaged electrocardiogram may be useful in identifying patients with nonsustained VT after a remote inferior myocardial infarction who have inducible sustained VT.     

Absence of change of signal-averaged electrocardiogram identifies patients with ventricular arrhythmias who are non-responders to amiodarone

OBJECTIVES: The aim of this study was to assess the ability of a non-invasive study, the signal-averaged ECG (SAECG), to predict the effect of amiodarone at ventricular level. BACKGROUND: Amiodarone is the main drug drug used in the treatment of ventricular arrhythmias. Standard ECG does not detect any change in QRS complex resulting from amiodarone therapy. SAECG is more sensitive than ECG for detecting changes in QRS complex. METHODS: The study examined the effects of amiodarone on SAECG in relation to the results of programmed ventricular stimulation in 68 patients with old myocardial infarction, spontaneous and inducible sustained ventricular tachycardia (VT). RESULTS: Amiodarone prolonged the total QRS duration (dur) (129+/-28 vs. 140+/-30 ms, P<0.05) and low amplitude signal (LAS) dur (45+/-20 vs. 51+/-20 ms, P<0.1), whereas the root-mean-square voltage of the last 40 ms of QRS complex (RMS 40) was significantly reduced (20+/-16 vs. 14+/-9 microV, P<0.05). Changes in SAECG parameters did not differ significantly in patients in whom amiodarone prevented the inducibility of VT (n=15) and those in whom VT remained inducible with amiodarone (n=53), but in baseline QRS duration was significantly shorter in patients in whom amiodarone prevented the VT induction (118+/-26 vs. 133+/-28 ms, P<0.05). In patients in whom amiodarone did not prolong the cycle length of VT (n=15), SAECG did not change significantly (QRS dur 131+/-29 vs. 132+/-27 ms, LAS 42+/-20 vs. 42+/-19 ms, RMS 40 22+/-14 vs. 19+/-11 microV). Comparison of the SAECG data in patients with no inducible VT and those with slowed VT differed significantly (P<0.05) between the control state and the recording with amiodarone. CONCLUSIONS: The effects of amiodarone on VT inducibility are predicted by a shorter baseline QRS duration and the degree of drug-induced prolongation of filtered QRS duration. Amiodarone prolonged the QRS duration, LAS duration and decreased RMS 40; this effect was more important in patients with no inducible VT and in those with only slowed VT, than in patients with unchanged or accelerated VT. The absence of changes of QRS duration predicted the induction of a more rapid or not slowed VT with amiodarone with a sensitivity of 87% and a specificity of 83%. Therefore, SAECG appears as an useful and simple means to predict the effects of amiodarone in patients with myocardial infarction and VT.     

Spectral turbulence analysis of the signal-averaged electrocardiogram for predicting inducible sustained monomorphic ventricular tachycardia in patients with and without bundle branch block

Spectral turbulence analysis of the signal-averaged electrocardiogramis a new method for identifying patients prone to sustainedmonomorphic ventricular tachycardia. In contrast to analysisin the time domain, it has been claimed to be applicable inpatients with bundle branch block. The aim of this study wasto assess the predictive value of spectral turbulence analysis,in relation to the inducibility of sustained monomorphic ventriculartachycardia, in patients with and without bundle branch block.One hundred and sixty nine patients, of whom 120 had a QRS duration 120 ms, were studied Forty-seven patients had inducible sustainedmononwrphic ventricular tachycardia and were compared to 122control patients. The overall sensitivity of the spectral turbulenceanalysis for predicting inducible ventricular tachycardia was77%, the spectficity 35% and the total predictive accuracy 47%.The limited predictive accuracy was mainly due to a lack ofd between patients with and without ventricular tachycardiain patients with a QRS duration 120 ms. In patients with QRS 120 ms, however, there were significant differences in allspectral turbulence parameters and the method had a sensitivityof 75%, a specificity of 72% and a total predictive accuracyof 73%. The diagnostic usefulness of spectral turbulence analysis isdependent upon normal QRS duration and the method is applicableonly to patients without bundle branch block.     

Spectral turbulence analysis of the signal-averaged electrocardiogram for predicfing inducible sustained monomorphic ventricular tachycardia in patients with and without bundle branch block

Spectral turbulence analysis of the signal-averaged electrocardiogramis a new method for identifying patients prone to sustainedmonomorphic ventricular tachycardia. In contrast to analysisin the time domain, it has been claimed to be applicable inpatients with bundle branch block. The aim of this study wasto assess the predictive value of spectral turbulence analysis,in relation to the inducibility of sustained monomorphic ventriculartachycardia, in patients with and without bundle branch block.One hundred and sixty nine patients, of whom 120 had a QRS duration 120 ms, were studied Forty-seven patients had inducible sustainedmononwrphic ventricular tachycardia and were compared to 122control patients. The overall sensitivity of the spectral turbulenceanalysis for predicting inducible ventricular tachycardia was77%, the spectficity 35% and the total predictive accuracy 47%.The limited predictive accuracy was mainly due to a lack ofd between patients with and without ventricular tachycardiain patients with a QRS duration 120 ms. In patients with QRS 120 ms, however, there were significant differences in allspectral turbulence parameters and the method had a sensitivityof 75%, a specificity of 72% and a total predictive accuracyof 73%. The diagnostic usefulness of spectral turbulence analysis isdependent upon normal QRS duration and the method is applicableonly to patients without bundle branch block.     

When should we diagnose incomplete right bundle branch block?

An rSr' pattern with QRS duration of less than 0.12 s in theright precordial leads can be due to incomplete right bundlebranch block (which may progress to complete right bundle branchblock) or can be a normal electrophysiological variant. To identifyother ECG features that may help to distinguish between thesetwo possibilities, ECGs of 15 patients who progressed from normalto complete right bundle branch block through an intermediaterSr' pattern of incomplete right bundle branch block were analysed.The following features in the right precordial leads (V₁, V₂)that preceded or accompanied the appearance of the rSr' wereidentified: diminution of the S wave depth (100%), inversionof ratio of the S wave depth to SV₁,/SV₂ (93%), slurring ofthe downstroke or upstroke of the S wave (27%) and prolongationof the QRS duration to 0.10 s (73%). When a further 79 subjectswith rSr' pattern in the right precordial leads and QRS durationof <0.12 s were divided into those with SV₁/SV₂ ratio >1.0 and those with SV₁/SV₂ < 1.0, compared with the latterthe subjects with SV₁/SV₂ ratio > 1.0 were found to be significantlyolder (59.8±18.4 years vs 32.8±18.1 years, P<0.001),to exclusively show S wave slurring (37% vs 0%), and to morelikely have a QRS duration 0.10s (74% vs 7%). The findings indicatethat when faced with a single ECG showing an rSr' pattern inthe right precordial leads and QRS duration 0.12 s, severalother features, and in particular the relative sizes of theS waves in V₁ and V₂, may be useful in distinguishing rSr' dueto incomplete right bundle branch block from ‘normal’rSr'.     

Doppler flow and echocardiography in functional cardiac insufficiency: Assessment of nisoldipine therapy: Results of the DEFIANT-II study

Aims A multicentre, double-blind, placebo-controlled trial wasconducted in 542 patients, randomized 7–10 days aftermyocardial infarction, to study the effect of nisoldipine coat-core(nisoldipine-CC) on exercise after 6 months. Secondary endpointsincluded exercise-induced ischaemia, left ventricular functionmeasured by Doppler echocardiography, adverse cardiac eventsand clinical outcome. Methods and results Patients had reduced left ventricular ejectionfraction between 25 and 50%, but no heart failure. Exercisetime was not different in the two groups. Nisoldipine-CC prolongedtime to 1 mm ST deviation (P=0·03). There was an effectof nisoldipine-CC of +3·6cm. s^–1 on early peakvelocity (P=0·01 and of –6·2 ms on isovolumicrelaxation time (P=0·005), but no effects on left ventricularvolumes or ejection fraction. There was a trend towards reducedmortality (one death in the nisoldipine-CC group vs seven inthe placebo group, P0·07) and the combined end-pointof mortality and cardiac events (P0·09). Peripheral oedemaoccurred in 49 patients assigned to nisoldipine-CC and two assignedto placebo (P0·001). There were no differences in non-cardiacevents. Conclusions Nisoldipine-CC did not improve exercise time butincreased time to 1 mm ST deviation, and improved diastolicleft ventricular function. It is safe and well tolerated inpost-infarction patients with impaired left ventricular function.     

Captopril adjuvant therapy to beta-blockers and nitrates improves post-myocardial infarction left ventricular performance

A growing body of data support the beneficial effects of angiotensin-convertingenzyme inhibitors in the prevention of cardiac enlargement andimprovement of left ventricular function in patients with acutemyocardial infarction. However, very little information existsabout the direct effect of increased afterload on cardiac performancein these patients and the possible favourable effects of angiotensin-convertingenzyme inhibitors as adjunctive treatment to thrombolysis, beta-blockersand nitrates. We have, therefore, studied the effects of captoprilas adjuvant therapy to thrombolysis, beta-blockers and nitrates(standard therapy) on left ventricular performance in 77 consecutivepatients with uncomplicated Q-wave acute myocardial infarction,by the measurement of the pre-ejection period/left ventricularejection time ratio before and after (0·25–0·50mg) phenylephrine administration on the 4th and 30th post-infarctiondays. Patients were randomized on day 4 either to continue standardtherapy alone (group 1, 35 patients) or to receive oral captopriltherapy (12·5 mg t.i.d.) in addition to standard therapy(group 2, 42 patients) in a double-blind parallel study. Among the patients of group 1 there was a significant deteriorationof left ventricular function after phenylephrine administration.This was shown by an increase of pre-ejection period/left ventricularejection time ratio only in the subset of patients with ejectionfraction <40%, as measured by contrast ventriculography,on both the 4th and 30th post-infarction days changing from0·435±0·070 to 0·528±0·101,P<0·01 and from 0·404±0·098 to0·515±0·092, P<0·02, respectively.In contrast there were no significant changes in patients withejection fraction 40%. Among patients of group 2, phenylephrineadministration induced a significant increase, only on the 4thday, in pre-ejection period/left ventricular ejection time ratioonly in the subset of patients with ejection fraction <40%changing from 0·410±0·107 to 0·535±0·102,P<0·01. In the remaining patients with ejection fraction>40% there were no significant changes on either the 4thor 30th post-infarction days. Furthermore, a significant improvementwas observed after phenylephrine administration in the pre-ejectionperiod/left ventricular ejection time ratio between the 4thand 30th post-infarction days, which changed from 0·535±0·102on day 4 to 0·368± 0·052 on day 30 (P<0·004).Also, a four-way ANOVA detected a significant reduction of heartrate in patients with ejection fraction <40< from day4 to day 30. The results indicate that: (1) the response of pre-ejectionperiod/left ventricular ejection time ratio after increasingafterload may be a useful non-invasive method for the detectionof left ventricular dysfunction in myocardial infarction patients;and (2) captopril adjuvant therapy as compared to thrombolysis,beta-blockers and nitrates alone, after phenylephrine administration,improves the left ventricular performance response in asymptomaticQ-wave post-infarction patients and beneficially affects heartrate. This effect is most pronounced in patients with ejectionfraction 40% whereas those with ejection fraction 40% do notobtain clear benefit.     

Significance of ST-segment elevation during dobutamine-stress echocardiography in patients with acute myocardial infarction treated with thrombolysis

BACKGROUND: Stress-induced ST-segment elevation in patients with recentmyocardial infarction treated with thrombolysis has not beenextensively investigated. According to the results of previousstudies it may represent residual myocardial ischaemia or dyskinesiain the infarcted region. The aim of the study was to analysethe significance of dobutamine-induced ST-segment elevationin the infarcted area in a consecutive group of patients (n=42,41 men, mean age 53 ± 7 years) with a first acute myocardialinfarction treated with thrombolysis within 6 h from symptomsonset. METHODS AND RESULTS: All patients underwent dobutaminestress echocardiography (upto 40 µg. kg^–1. min^–1+ atropine) 7 ±3 days from the acute event and coronary arteriography within1 month from the test. Significant ST-segment elevation wasdefined as a shift 1 mm during dobutamine compared to baselinein at least two contiguous infarct-related leads; a correlationwas made between the site of ST-segment elevation and wall motionchanges during dobutamine. Dobutamine-induced ST-segment elevationin 23/42(55%) patients (group 1) while no changes were observedin 19/23 (45%) patients (group 2). Compared to group 2, group1 patients showed a higher asynergy score index (1·72± 0·24 vs 1·50 ± 0·32, P<0·02)and a higher number of asynergic segments (5·04 ±1·9 vs 4·11 ± 1·8), at baseline,a higher incidence of baseline and/or stressinduced dyskinesia(39 vs 10%, P<0·05) in the infarct-related regionand a higher percentage of occluded infarct-related arteries(48 vs 0%, P<0·001). In the 42 patients studied, asignificant correlation was found between baseline ST-segmentelevation and baseline asynergy score index (RS=0·56,P<000l) and between ST-segment elevation and asynergy scoreindex at peak stress (RS=0·55, P<0·001). Theincidence of reversible wall motion abnormalities indicativeof myocardial viability and residual myocardial ischaemia wassimilar in the two groups (87 vs 84% and 74 vs 68%, respectively),while the number of segments with irreversible akinesia indicativeof myocardial necrosis was higher in group 1 compared to group2 (1·5 ± 14 vs 0·9 ± 1·4).Among the 23 patients of group 1 with dobutamine-induced ST-segmentelevation, six had no reversible wall motion abnormalities indicativeof myocardial ischaemia; of the 17 patients with myocardialischaemia, 11 had 50% and six had 50% of basally asynergic segmentsshowing reversible wall motion abnormalities. CONCLUSIONS: In patients with recent thrombolyzed myocardial infarction dobutamine-inducedST-segment elevation is associated with a larger akinetic areain basal conditions and either with reversible wall motion abnormalitiesindicative of myocardial ischaemia or with irreversible or minimallyreversible wall motion abnormalities in the infarct area duringthe test. Thus, dobutamine echocardiography provides usefulinformation for the interpretation of stress-induced ST-segmentelevation and clinical management of these patients.     

Left ventricular function after repeated episodes of ventricular fibrillation and defibrillation assessed by transoesophageal echocardiography

Background Investigators studying the effects of cardioverter-defibrillatorson left ventricular systolic function have given only minorattention to the diastolic effects. Objectives The purpose of this study was to investigate theimpact of repeated episodes of ventricular fibrillation anddefibrillation on systolic function and diastolic filling ofthe left ventricle during non-thoracotomy implantation of acardioverter-defibrillator. Methods Systolic function and diastolic filling of the leftventricle were assessed peri-operatively on a beat-by-beat basisusing a transoesophageal echo-Doppler technique in 12 patientsduring 4 episodes of ventricular fibrillation and defibrillation.Systolic function was assessed from the fractional area changeand diastolic filling from the E/A ratio. Arterial blood pressureand the ECG were recorded continuously. Results Blood pressure and heart rate did not change significantlythroughout the procedure. The systolic function, similarly,was not significantly affected; the only changes were seen inthe first two beats after defibrillation when the mean fractionalarea increased from 0·2±0·01 to 0·4±0·02and 0·3±0·02, respectively (P<0·001).Diastolic filling was, however, impaired as reflected by a decreasein the E/A ratio from 2·6±0·5 before to1·6±0·4 (P<0·01) after repeatedthreshold tests. Conclusions. While the combined ischaemic and electrical traumacaused by repeated episodes of ventricular fibrillation anddefibrillation during the implantation of a cardioverter-defibrillatordid not cause any systolic dysfunction, diastolic filling wassignificantly impaired.     

Lipoprotein(a) as a risk predictor for cardiac mortality in patients with acute coronary syndromes

Aims Raised lipoprotein(a) concentrations are considered to be arisk factor for atherothrombotic diseases. We examined whetherbaseline concentrations were a risk factor for an adverse outcomein patients admitted with acute coronary syndromes. Methods and Results Five hundred and nineteen patients admitted with suspected acutecoronary syndromes were studied and followed prospectively fora median of 3 years. The prognostic significance of a baselinelipoprotein(a) concentration of 30mg.dl^–1or lower forsubsequent cardiac death was assessed in patients with myocardialinfarction (266) and unstable angina (197) and compared withother variables in regression models. In patients with myocardialinfarction, a baseline lipoprotein(a) concentration of 30mg.dl^–1wasassociated with a 62% increase in subsequent cardiac death comparedto the lower concentration group (29·8% vs 18·6%,Log rankP=0·04). In a multivariate regression model abaseline lipoprotein(a) concentration of 30mg.dl^–1retainedits significance as an independent predictor of cardiac death(P=0·037). In patients with unstable angina, baselineconcentrations of 7·9mg.dl^–1were found to be significantpredictors of cardiac death in univariate (P=0·021) andmultivariate (P=0·035) regression models. Conclusion Baseline lipoprotein(a) concentrations in patients admittedwith acute coronary syndromes are associated with an increasedrisk of cardiac death. For patients with myocardial infarctiona concentration of 30mg.dl^–1appears appropriate as a riskdiscriminator; for patients admitted with unstable angina, however,much lower concentrations of lipoprotein(a) appear to be prognosticallyimportant.     

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

Aims This study was conducted to clarify the significance of abnormalQ-wave regression in anterior wall acute myocardial infarction. Methods A total of 74 patients who presented with a first anterior wallacute myocardial infarction within 6h of onset were dividedinto two groups according to the presence (group A, n=29) orabsence (group B, n=45) of regression of abnormal Q waves. Regressionof abnormal Q waves was defined as the disappearance of theQ wave and the reappearance of the r wave 0·1mV in atleast one of leads I, aVL, and V₁to V₆. Results Emergency coronary arteriography revealed that group A had ahigher incidence of spontaneous recanalization or good collateralcirculation than group B (55% vs 31%,P<0·05). Peakcreatine kinase activity tended to be lower in group A thanin group B (2358±1796 vs 3092±1946IU.L^–1,P=0·09).Group A had a greater left ventricular ejection fraction andbetter regional wall motion at 1 and 6 months after acute myocardialinfarction than group B. The degree of improvement of left ventricularejection fraction and regional wall motion between 1 and 6 monthsafter acute myocardial infarction was significantly greaterin group A than in group B. Conclusion Patients with anterior wall acute myocardial infarction showingQ-wave regression had a trend towards a smaller amount of necroticmyocardium and a significantly larger amount of stunned myocardium.     

Identification of patients with ventricular tachycardia after myocardial infarction: signal-averaged electrocardiogram, Holter monitoring, and cardiac catheterization

Electrocardiographic signal averaging techniques have demonstrated a low-amplitude late potential and a long filtered QRS complex in patients with ventricular tachycardia (VT) after myocardial infarction. Complex ventricular ectopy and left ventricular aneurysms have also been associated with VT. The purposes of this study were (1) to determine whether the findings from the signal-averaged electrocardiogram (ECG) were independent of those from Holter monitoring and cardiac catheterization and (2) to determine the combination of findings from the signal-averaged ECG, cardiac catheterization, and Holter monitoring that best characterize patients with VT after myocardial infarction. We studied 174 patients after myocardial infarction, 98 of whom had recurrent sustained VT. By multivariate logistic regression only three parameters were found to be independently significant, listed in order of power: positive signal-averaged ECG (presence of a late potential or a long filtered QRS duration), peak premature ventricular contraction greater than 100/hr, and presence of a left ventricular aneurysm (p less than .001). The signal-averaged ECG provides independent information in identifying patients with VT after myocardial infarction.     

The value of the intracoronary electrogram for the early detection of myocardial ischaemia during coronary angioplasty

The clinical value of intracoronarv electrography for the detectionofmyocardial ischaemia was assessed during coronary angioplastyand compared to a standard technique of surface ECG monitoring.In 73 patients undergoing single lesion angioplasty, an iniracoronarvelectrogram and four representative surface ECG leads were obtained.During angioplasty of the left anterior descending artery leads,I, V₃ V₅ V₆ were recorded. For the circumflex artery leads I,a V_L, a VF, V₆ and for the right coronar artery leads II, III,a VF, V₆ were monitored. Eight patients were excluded due totransient intraventricular conduction disturbances during ballooninflation; 65 patients remained for further analysis. Out ofa total of 154 balloon inflations (35 in the circumflex, 71in the left anterior descending and 48 in the right coronaryartery), the percentage that produced a mm ST segment elevation,the time to the appearance of a mm ST segment elevation andthe maximal ST segment elevation were recorded. During inflationsin the circumflex artery, the respective values of these threeparameters were 20%, 22·6±11·5 and 0·37±0·80mm in V₆ the most sensitive surface lead, versus 70% (P<0·001),14·4±9·6 s (P<0·01 and 5·82±6·35mm (P<0·0001) on the intracoronary electrogram. Forleft anterior descending inflations the corresponding valuesin V₃ the most sensitive surface lead, were 61%, 26·2±13·2s and 2·08±2·32mm versus 74% (NS), 18·3±12·4s(P<0·001) and 5 (P<0·0001) on the intracoronarytracing. For right coronary artery inflations the correspondingvalues in V₃ the most sensitive surface lead, were 77%, 22·2±12·8s and 2·31±1·65mm versus 32% (P<0·0001),29·8±26·3 (NS) and 1·18±2·19mm(P<0·05 Keeping in mind that only four surface leadswere monitored, these data suggest that intracoronary electrographyis helpful for adequate nonitoring of ischaemia during circumflexangioplasty. During left anterior descending angioplasty itadds some additional information, but it appears superfluousduring right coronary angioplasty.     

Effects of sotalol on the signal-averaged electrocardiogram in patients with sustained ventricular tachycardia: relation to suppression of inducibility and changes in tachycardia cycle length.

OBJECTIVES. This study examines the effects of sotalol on the signal-averaged electrocardiogram (ECG) in patients with spontaneous and inducible sustained ventricular tachycardia and correlates these findings with the effect of sotalol on tachycardia inducibility and tachycardia rate. BACKGROUND. Standard electrocardiography generally does not detect any change in the duration of the QRS complex resulting from sotalol therapy. However, the signal-averaged ECG is more sensitive than the standard ECG for detecting changes in QRS duration induced by antiarrhythmic drugs and can also detect changes in late potential duration. METHODS. Signal-averaged electrocardiography was performed before therapy in 30 patients with spontaneous and inducible ventricular tachycardia, and both electrophysiologic study and a signal-averaged ECG were repeated during therapy with d,l-sotalol. RESULTS. During sotalol therapy the signal-averaged QRS duration decreased by 2.6 +/- 6.6 ms in the 11 patients with no inducible tachycardia during therapy, whereas it increased by 3.8 +/- 5.8 ms (p = 0.01) in the 19 patients with inducible tachycardia during therapy. In the latter group there was a significant positive correlation between prolongation of tachycardia cycle length and prolongation of late potential duration by sotalol (r = 0.56, p = 0.01). CONCLUSIONS. Sotalol can alter QRS and late potential duration as measured by the signal-averaged ECG. Prolongation of QRS duration or late potential duration may reflect a slowing of conduction by sotalol that may interfere with this agent's antiarrhythmic efficacy and slow ventricular tachycardia.     

Eligibility for reperfusion therapy and outcome in elderly patients with acute myocardial infarction

Reperfusion therapy by thrombolysis or angioplasty was consideredin 260 unselected patients consecutively admitted within 6 hof the onset of Q wave myocardial infarction. Rates of reperfusionand in-hospital mortality were compared in 206 patients <70years and 54 patients 70 years. Early reperfusion was obtainedin 864% of the patients under 70 years and in 72·2% ofthose over 70 (P<0·01). Thrombolysis was more frequentlyused in the younger group (66·0% vs 31·5%, P<10^–5and primary angioplasty in the older (44·4% vs 29·6%,P<0·05). Overall in-hospital mortality was higherin the older group (22·2% vs 4·4 P<10^–5After successful reperfusion, mortality was 12·8% inthe patients over 70 and 3·9% in those under 70. Afterfailed or unproven reperfusion, mortality was 46·7% inthe patients over 70 and 7·1% in those under 70. Reperfusiontherapy is feasible in the majority of patients over 70 years,but failure to attempt or to achieve reperfusion is associatedwith a poor outcome. Although not controlled, this study providesan incentive for attempting early reperfusion therapy as oftenas possible in the elderly with acute myocardial infarction.