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Effects of Interrupting Precordial Compressions on the Calculated Probability of Defibrillation Success During Out-of-Hospital Cardiac Arrest
- Trygve Eftestøl,
- Kjetil Sunde and
- Petter Andreas Steen
Circulation Volume 105, Issue 1914 May 2002

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Background— Cardiopulmonary resuscitation (CPR) creates artifacts on the ECG and, with automated defibrillators, a pause in CPR is mandatory during rhythm analysis. The rate of return of spontaneous circulation (ROSC) is reduced with increased duration of this hands-off interval in rats. We analyzed whether similar hands-off intervals in humans with ventricular fibrillation causes changes in the ECG predicting a lower probability of ROSC.Methods and Results— The probability of ROSC after a shock was continually determined from ECG signal characteristics for up to 20 seconds of 634 such hands-off intervals in patients with ventricular fibrillation. In hands-off intervals with an initially high (40% to 100%) or median (25% to 40%) probability for ROSC, the probability was gradually reduced with time to a median of 8% to 11% after 20 seconds (P<0.001). In episodes with a low initial probability (0% to 25%; median, 5%), there was no further reduction with time.Conclusions— The interval between discontinuation of chest compressions and delivery of a shock should be kept as short as possible.
Mechanism of Syncope in Patients With Heart Disease and Negative Electrophysiologic Test
- Carlo Menozzi,
- Michele Brignole,
- Roberto Garcia-Civera,
- Angel Moya,
- Gianluca Botto,
- Luis Tercedor,
- Roberta Migliorini,
- Xavier Navarro
Circulation Volume 105, Issue 2311 June 2002

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Background— In patients with syncope and structural heart disease, syncope is suspected to be attributable to a primary cardiac arrhythmia, but little is known of its mechanism when electrophysiologic study is unremarkable.Methods and Results— We applied an implantable loop recorder in 35 patients with overt heart disease at risk of ventricular arrhythmia, because these were patients with previous myocardial infarction or cardiomyopathy with depressed ejection fraction or nonsustained ventricular tachycardia in whom an electrophysiologic study was unremarkable. During a follow-up of 3 to 15 months, syncope recurred in 6 patients (17%) after a mean of 6±5 months; in 3 patients, the mechanism of syncope was bradycardia with long pauses (sudden-onset AV block in 2 cases and sinus arrest in 1 case); in 1 patient, there was stable sinus tachycardia; and in 2 patients, who had chronic atrial fibrillation, there was an increase in ventricular rate. A total of 23 episodes of presyncope were documented in 8 patients (23%): no rhythm variation or mild tachycardia in 12 cases, paroxysmal atrial fibrillation or atrial tachycardia in 10 cases, and sustained ventricular tachycardia in 1 case. No patient died during the study period nor suffered from injury attributable to syncopal relapse.Conclusions— The patients with unexplained syncope, structural heart disease, and negative electrophysiologic study had a favorable medium-term outcome with no case of death and a low recurrence rate of syncope without related injury. The mechanism of syncope was heterogeneous, and ventricular tachyarrhythmia was unlikely.
Change in Systolic Left Ventricular Performance After 3 Years of Antihypertensive Treatment: The Losartan Intervention for Endpoint (LIFE) Study
- Kristian Wachtell,
- Vittorio Palmieri,
- Michael H. Olsen,
- Eva Gerdts,
- Vasilios Papademetriou,
- Markku S. Nieminen,
- Gunnar Smith,
- Björn Dahlöf,
- Gerard P. Aurigemma and
- Richard B. Devereux
Circulation Volume 106, Issue 29 July 2002

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Background— We have shown that hypertensive patients with left ventricular (LV) hypertrophy have decreased LV midwall mechanics, but the effect of antihypertensive therapy remains unclear.Methods and Results— Echocardiograms were recorded at baseline in 679 hypertensive patients and ECG LV hypertrophy and repeated yearly during 3 years of blinded treatment to achieve target blood pressures (BPs) of 140/90 mm Hg. On average, BP was reduced from 174±21 to 147±19 over 95±11 to 82±10 mm Hg and LV mass from 234±56 to 194±50 g. Endocardial fractional shortening (FS) decreased slightly, whereas midwall FS increased from 15.4±2.0% to 16.8±2.1% and stress-corrected midwall FS increased from 97±13 to 105±12% (all P<0.001). Change in midwall FS was related inversely to change in LV mass (LVM), relative wall thickness (RWT), and diastolic BP and directly to change in Doppler stroke volume (SV, all P<0.001). Multivariate analysis showed that change in MWS was independently inversely related to changes in LVM (β=−0.211), RWT (β=−0.334, all P<0.001), and diastolic BP (β=−0.088, P<0.05) and directly related to SV (β=0.192, P<0.001) with control for blinded therapy. Change in stress-corrected midwall shortening was inversely independently associated with changes in LVM (β=−0.153) and RWT (β=−0.562) and directly with changes in SV (β=0.145) and systolic BP (β=0.s221, all P<0.001) with control for blinded therapy.Conclusions— Antihypertensive therapy reduced LVM and increased LV midwall shortening and contractility with a small decrease in LV chamber function and significant increase in SV. Change in systolic LV performance was independently associated inversely with change in LVM, RWT, and BP and directly with change in SV.
Early Resolution of ST-Segment Elevation Correlates With Myocardial Salvage Assessed by Tc-99m Sestamibi Scintigraphy in Patients With Acute Myocardial Infarction After Mechanical or Thrombolytic Reperfusion Therapy
- Jun Dong,
- Gjin Ndrepepa,
- Claus Schmitt,
- Julinda Mehilli,
- Sebastian Schmieder,
- Markus Schwaiger,
- Albert Schömig and
- Adnan Kastrati
Circulation Volume 105, Issue 2525 June 2002

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Background— Early resolution of ST-segment elevation is an indicator of final infarct size and clinical outcomes. Whether this correlation is an expression of initial infarct characteristics or degree of myocardial salvage achieved with reperfusion therapy is unclear.Methods and Results— We prospectively included 243 patients with acute myocardial infarction (AMI) treated with either coronary stenting (122 patients) or thrombolysis (121 patients). Serial 12-lead electrocardiograms (ECG) were performed at baseline and 90 minutes after initiation of therapy. ST-segment resolution was defined as complete (≥70%), partial (<70% to 30%), or no resolution (<30%). Paired technetium-99m sestamibi scintigraphic studies were performed to calculate the initial perfusion defect, final infarct size, and the proportion of initial defect salvaged with reperfusion (salvage index). ST-segment resolution correlated significantly with salvage index (P=0.008), final infarct size (P<0.001), and 6-month mortality (P=0.03). In the groups with complete, partial, and no resolution, salvage index was 0.54±0.32, 0.39±0.36, and 0.33±0.60; final infarct size was 12.5±12.0%, 20.0±13.9%, and 22.7±19.4% of the left ventricle; 6-month mortality was 2.4%, 6.2%, and 12.8%, respectively. After adjustment for baseline characteristics, ST-segment resolution was the second strongest predictor of salvage index (P=0.007) after the type of reperfusion, stenting, or thrombolysis (P=0.001); it was greater after stenting than after thrombolysis (P<0.001).Conclusion— Early resolution of ST-segment elevation in surface ECG correlates with myocardial salvage as assessed by scintigraphy in patients with AMI after reperfusion therapy. These data provide an explanation for the favorable prognostic value of the ST-segment resolution and support the use of this parameter to compare the efficacy of different reperfusion strategies.
ACC/AHA 2002 Guideline Update for Exercise Testing: Summary Article: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines)
- ,
- Raymond J. Gibbons,
- Gary J. Balady,
- J. Timothy Bricker,
- Bernard R. Chaitman,
- Gerald F. Fletcher,
- Victor F. Froelicher,
- Daniel B. Mark,
- Ben D. McCallister,
- Aryan N. Mooss,
- Michael G. O’Reilly,
- William L. Winters,
- Raymond J. Gibbons,
- Elliott M. Antman,
- Joseph S. Alpert,
- David P. Faxon,
- Valentin Fuster,
- Gabriel Gregoratos,
- Loren F. Hiratzka,
- Alice K. Jacobs,
- Richard O. Russell and
- Sidney C. Smith
Circulation Volume 106, Issue 141 October 2002

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Ambulatory Electrocardiographic Evidence of Transmural Dispersion of Repolarization in Patients With Long-QT Syndrome Type 1 and 2
- Matti Viitasalo,
- Lasse Oikarinen,
- Heikki Swan,
- Heikki Väänänen,
- Kathy Glatter,
- Päivi J. Laitinen,
- Kimmo Kontula,
- Hal V. Barron,
- Lauri Toivonen and
- Melvin M. Scheinman
Circulation Volume 106, Issue 195 November 2002

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Background— Transmural dispersion of repolarization (TDR) may be related to the genesis of torsade de pointes (TdP) in patients with the long-QT (LQT) syndrome. Experimentally, LQT2 models show increased TDR compared with LQT1, and β-adrenergic stimulation increases TDR in both models. Clinically, LQT1 patients experience symptoms at elevated heart rates, but LQT2 patients do so at lower rates. The interval from T-wave peak to T-wave end (TPE interval) is the clinical counterpart of TDR. We explored the relationship of TPE interval to heart rate and to the presence of symptoms in patients with LQT1 and LQT2.Methods and Results— We reviewed Holter recordings from 90 genotyped subjects, 31 with LQT1, 28 with LQT2, and 31 from unaffected family members, to record TPE intervals by use of an automated computerized program. The median TPE interval was greater in LQT2 (112±5 ms) than LQT1 (91±2 ms) or unaffected (86±3 ms) patients (P<0.001 for all group comparisons), and the maximal TPE values differed as well. LQT1 patients showed abrupt increases in TPE values at RR intervals from 600 to 900 ms, but LQT2 patients did so at RR intervals from 600 to 1400 ms (longest RR studied). Asymptomatic and symptomatic patients showed similar TDRs.Conclusions— TDR is greater in LQT2 than in LQT1 patients. LQT1 patients showed a capacity to increase TDR at elevated heart rates, but LQT2 patients did so at a much wider rate range. The magnitude of TDR is not related to a history of TdP.
Exercise Stress Test Amplifies Genotype-Phenotype Correlation in the LQT1 and LQT2 Forms of the Long-QT Syndrome
- Kotoe Takenaka,
- Tomohiko Ai,
- Wataru Shimizu,
- Atsushi Kobori,
- Tomonori Ninomiya,
- Hideo Otani,
- Tomoyuki Kubota,
- Hiroshi Takaki,
- Shiro Kamakura and
- Minoru Horie
Circulation Volume 107, Issue 618 February 2003

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Background— Experimental studies suggest that the interval between peak and end of T wave (Tpe) in transmural ECGs reflects transmural dispersion of repolarization (TDR), which is amplified by β-adrenergic stimulation in the LQT1 model. In 82 patients with genetically identified long-QT syndrome (LQTS) and 33 control subjects, we examined T-wave morphology and various parameters for repolarization in 12-lead ECGs including corrected QT (QTc; QT/R-R^1/2) and corrected Tpe (Tpec; Tpe/R-R^1/2) before and during exercise stress tests.Methods and Results— Under baseline conditions, LQT1 (n=51) showed 3 cardinal T-wave patterns (broad-based, normal-appearing, late-onset) and LQT2 (n=31) 3 patterns (broad-based, bifid with a small or large notch). The QTc and Tpec were 510±68 ms and 143±53 ms in LQT1 and 520±61 ms and 195±69 ms in LQT2, respectively, which were both significantly larger than those in control subjects (402±36 ms and 99±36 ms). Both QTc and Tpec were significantly prolonged during exercise in LQT1 (599±54 ms and 215±46 ms) with morphological change into a broad-based T-wave pattern. In contrast, exercise produced a prominent notch on the descending limb of the T wave, with no significant changes in the QTc and Tpec (502±82 ms and 163±86 ms: n=19) in LQT2.Conclusions— Tpe interval increases during exercise in LQT1 but not in LQT2, which may partially account for the finding that fatal cardiac events in LQT1 are more often associated with exercise.
Effects of Antiarrhythmic Drugs on Fibrillation in the Remodeled Atrium: Insights Into the Mechanism of the Superior Efficacy of Amiodarone
- Kaori Shinagawa,
- Akiko Shiroshita-Takeshita,
- Gernot Schram and
- Stanley Nattel
Circulation Volume 107, Issue 1018 March 2003

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Background— The basis of the unique effectiveness of amiodarone for atrial fibrillation (AF) is poorly understood. The present study tested the hypothesis that amiodarone blocks electrical remodeling induced by atrial tachycardia.Methods and Results— Mongrel dogs were subjected to atrial tachycardia (400 bpm for 7 days) in the absence and presence of therapy with amiodarone, the class III cardiac antiarrhythmic drug dofetilide, or the class I agent flecainide begun 3 days before the onset of tachypacing and maintained until a final electrophysiological study. AF vulnerability (percentage of sites with AF induction by single premature extrastimuli), mean AF duration, atrial effective refractory period (ERP), and conduction velocity were compared among these dogs and in unpaced dogs in the absence or presence of treatment with the same agents. Only amiodarone prevented promotion of AF duration and vulnerability by atrial tachycardia. Furthermore, only amiodarone eliminated tachycardia-induced ERP abbreviation and loss of ERP rate adaptation while obviating L-type Ca²⁺-current α_1c-subunit downregulation as determined by Western blot. In an additional series of dogs monitored with repeated electrophysiological studies, amiodarone administered after the induction of atrial tachycardia remodeling reversed remodeling within several days, despite continued atrial tachypacing during amiodarone therapy.Conclusions— Amiodarone is uniquely effective against AF promotion by atrial tachycardia remodeling in this experimental model and prevents electrophysiological and biochemical consequences of remodeling. Amiodarone also reversed remodeling established by 4 days of atrial tachycardia. The inhibition of atrial tachycardia remodeling may therefore contribute to the superior efficacy of amiodarone in AF.
Imaging Electrocardiographic Dispersion of Depolarization and Repolarization During Ischemia: Simultaneous Body Surface and Epicardial Mapping
- Martyn P. Nash,
- Chris P. Bradley and
- David J. Paterson
Circulation Volume 107, Issue 176 May 2003

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Background— Myocardial ischemia creates abnormal electrophysiological substrates that result in life-threatening ventricular arrhythmias. Identifying patients at risk of such abnormalities by use of body surface electrical measures is controversial. We investigated the sensitivity of torso measures, recorded simultaneously with epicardial electrograms, to changes in dispersion of depolarization and repolarization during localized ventricular ischemia.Methods and Results— Ventricular epicardial electrograms were recorded from 5 anesthetized pigs with a 127-electrode sock. A controllable suture snare was used to ligate the left anterior descending coronary artery (LAD). The chest was reclosed, and a vest with 256 ECG electrodes was fitted to the torso. Simultaneous arrays of epicardial electrograms and torso ECGs were recorded during LAD occlusion and reperfusion. Activation-recovery intervals (ARIs), QT_u and RT_u dispersion (where u indicates upstroke), and QRST integrals were calculated, and these data were fitted to anatomically customized computational models of the swine ventricular epicardium and torso. LAD occlusion caused the epicardial ARI dispersion to steadily increase, whereas the location of shortest ARI shifted from the posterobasal ventricular tissue (control) to the anteroapical myocardium, distal to the suture snare. These changes were associated with a steady increase in the torso RT_u dispersion as the shortest RT_u interval moved from the right shoulder (control) to the sternum. QT_u and RT_u dispersion determined from the 12-lead ECG did not consistently reflect the myocardial changes.Conclusions— Although changes in myocardial repolarization dispersion resulting from localized ischemia are not reliably reflected in temporal indices derived from the 12-lead ECG, they can be readily identified with high-resolution torso ECG mapping.
Role of L-Type Calcium Channels in Pacing-Induced Short-Term and Long-Term Cardiac Memory in Canine Heart
- Alexei N. Plotnikov,
- Hangang Yu,
- J. Christoph Geller,
- Ravil Z. Gainullin,
- Parag Chandra,
- Kornelis W. Patberg,
- Steven Friezema,
- Peter Danilo,
- Ira S. Cohen,
- Steven J. Feinmark and
- Michael R. Rosen
Circulation Volume 107, Issue 2210 June 2003

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Background— We tested the hypothesis that I_Ca,L is important to the development of cardiac memory.Methods and Results— The effects of L-type Ca²⁺ channel blockade and β-blockade were tested on acutely anesthetized and on chronically instrumented, conscious dogs. Short-term memory (STM) was induced by 2 hours of ventricular pacing and long-term memory (LTM) by ventricular pacing for 21 days. STM dogs received placebo, nifedipine, or propranolol, and LTM dogs received placebo, atenolol, or amlodipine. AT₁ receptor blockade (candesartan) and ACE inhibition (trandolapril) were also tested in LTM. Microelectrodes were used to record transmembrane potentials from isolated epicardial and endocardial slabs using a protocol simulating STM in intact animals. Left ventricular epicardial myocytes from LTM or sham control dogs were dissociated, and I_Ca,L was recorded (whole-cell patch-clamp technique). Evolution of STM and LTM was attenuated by I_Ca,L blockers but not β-blockers. Neither AT₁ receptor blockade nor ACE inhibition suppressed LTM. In microelectrode experiments, pacing induced an epicardial-endocardial gradient change mimicking STM that was suppressed by nifedipine. In patch-clamp experiments, peak I_Ca,L density in LTM and control were equivalent, but activation was more positive and time constants of inactivation longer in LTM (P<0.05).Conclusions—I_Ca,L blockade but not β-adrenergic blockade suppresses cardiac memory. LTM evolution is unaffected by angiotensin II blockade and is associated with altered I_Ca,L kinetics.
Incomplete Resolution of ST-Segment Elevation Is a Marker of Transient Microcirculatory Dysfunction After Stenting for Acute Myocardial Infarction
Circulation Volume 107, Issue 213 June 2003

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Background— Incomplete ST-segment resolution (STR) after successful primary angioplasty for acute myocardial infarction (AMI) is associated with a poor prognosis. We used intracoronary Doppler velocimetry to investigate whether incomplete STR after primary angioplasty is a marker of severe microcirculatory dysfunction.Methods and Results— Fifty patients with ≤12-hour AMI underwent successful primary angioplasty and systematic stenting with a Doppler guidewire. Patients with incomplete (<50%) STR 60 minutes after TIMI 3 flow was restored had flow velocity features suggestive of severe microcirculatory dysfunction, including a higher incidence of early systolic retrograde flow (41% versus 9%, P=0.007) and lower coronary flow velocity reserve (CVR, 1.3 versus 1.6, P<0.001). CVR improved immediately after stenting in patients with ≥50% STR but not in patients with <50% STR. There was a significant correlation between STR and poststent CVR. At 3 months, CVR was similar in patients with <50% and ≥50% STR. However, left ventriculography indicated lower global (42% versus 55%, P=0.001) and regional (16% versus 20%, P=0.03) left ventricular ejection fractions and ²⁰¹Tl rest-redistribution scintigraphy indicated a larger infarct size (34% versus 16% ²⁰¹Tl defect, P=0.007) in patients with <50% STR.Conclusions— After successful primary angioplasty with systematic stenting, <50% STR is a marker of severe albeit transient microcirculatory dysfunction in patients with AMI and is associated with more extensive myocardial damage.
Prognostic Value of QT Interval Parameters for Mortality Risk Stratification in Chagas’ Disease: Results of a Long-Term Follow-Up Study
- Gil Salles,
- Sergio Xavier,
- Andrea Sousa,
- Alejandro Hasslocher-Moreno and
- Claudia Cardoso
Circulation Volume 108, Issue 322 July 2003

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Background— QT interval parameters are potential prognostic markers of arrhythmogenicity risk and cardiovascular mortality and have never been evaluated in Chagas’ disease.Methods and Results— Outpatients (738) in the chronic phase of Chagas’ disease were enrolled in a long-term follow-up study. Maximal heart rate-corrected QT (QTc) and T-wave peak-to-end (TpTe) intervals and QRS, QT, JT, QTapex, and TpTe dispersions and variation coefficients were measured manually and calculated from 12-lead ECGs obtained on admission. Clinical, radiological, and 2-dimensional echocardiographic data were also recorded. Primary end points were all-cause, Chagas’ disease-related, and sudden cardiac mortalities. During a follow-up of 58±39 months, 62 patients died, 54 of Chagas’ disease-related causes and 40 suddenly. Multivariate Cox survival analysis revealed that the QT-interval dispersion (QTd) (hazard ratio, 1.45; 95% confidence interval, 1.29 to 1.63; P<0.001, for 10-ms increments) and left ventricular (LV) end-systolic dimension (hazard ratio, 1.36; 95% confidence interval, 1.21 to 1.53; P<0.001, for 5-mm increments) were the strongest independent predictors for all end points. The maximum QTc interval (QTcmax) could substitute for QTd with a worse predictive performance. Other predictors were heart rate, presence of pathological Q waves, frequent premature ventricular contractions (PVCs), and isolated left anterior fascicular block (LAFB) on the ECGs. Kaplan-Meier survival curves demonstrated that a QTd ≥65 ms or a QTcmax ≥465 ms^1/2 discriminated the 2 groups with significantly different prognoses.Conclusions— Electrocardiographic QTd and echocardiographic LV end-systolic dimension were the most important mortality predictors in patients with Chagas’ disease. Heart rate, the presence on ECG of pathological Q waves, frequent PVCs, and isolated LAFB refined the mortality risk stratification.
Regression of Electrocardiographic Left Ventricular Hypertrophy by Losartan Versus Atenolol: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study
- Peter M. Okin,
- Richard B. Devereux,
- Sverker Jern,
- Sverre E. Kjeldsen,
- Stevo Julius,
- Markku S. Nieminen,
- Steven Snapinn,
- Katherine E. Harris,
- Peter Aurup,
- Jonathan M. Edelman,
- Björn Dahlöf
Circulation Volume 108, Issue 612 August 2003

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Background— Electrocardiographic left ventricular hypertrophy (LVH) predicts cardiovascular morbidity and mortality, and regression of ECG LVH may predict improved prognosis in hypertensive patients. However, uncertainty persists as to how best to regress ECG LVH.Methods and Results— Regression of ECG LVH with losartan versus atenolol therapy was assessed in 9193 hypertensive patients with ECG LVH by Sokolow-Lyon voltage or Cornell voltage-duration product criteria enrolled in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study. Patients had ECGs at study baseline and after 6 months, 1, 2, 3, 4, and 5 years of blinded losartan-based or atenolol-based therapy. After 6 months’ follow-up, adjusting for baseline ECG LVH levels, baseline and in-treatment systolic and diastolic pressures, and for diuretic therapy, losartan-based therapy was associated with greater regression of both Cornell product (adjusted means, −200 versus −69 mm · ms, P<0.001) and Sokolow-Lyon voltage (−2.5 versus −0.7 mm, P<0.001) than was atenolol-based therapy. Greater regression of ECG LVH persisted at each subsequent annual evaluation in the losartan-treated group, with between 140 and 164 mm · ms greater mean reductions in Cornell product and from 1.7 to 2.2 mm greater mean reductions in Sokolow-Lyon voltage (all P<0.001). The effect of losartan was consistent across subgroups defined by gender, age, ethnicity, and diabetes.Conclusions— After adjusting for baseline and in-treatment blood pressure and baseline severity of ECG LVH, losartan-based antihypertensive therapy resulted in greater regression of ECG LVH by Cornell voltage-duration product and Sokolow-Lyon voltage criteria than did atenolol-based therapy. These findings support the value of angiotensin receptor blockade with losartan for reversing ECG LVH.
Prognostic Value of Lead aVR in Patients With a First Non–ST-Segment Elevation Acute Myocardial Infarction
- José A. Barrabés,
- Jaume Figueras,
- Cristina Moure,
- Josefa Cortadellas and
- Jordi Soler-Soler
Circulation Volume 108, Issue 719 August 2003

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Background— ST-segment elevation in lead aVR has been associated with severe coronary artery lesions in patients with acute coronary syndromes, but the prognostic significance of this finding is unknown.Methods and Results— We analyzed the initial ECG in 775 consecutive patients admitted to our center with a first acute myocardial infarction without ST-segment elevation in leads other than aVR or V₁. The rates of in-hospital death in patients without (n=525) and with 0.05 to 0.1 mV (n=116) or ≥0.1 mV (n=134) of ST-segment elevation in lead aVR were 1.3%, 8.6%, and 19.4%, respectively (P<0.001). After adjustment for the baseline clinical predictors and for ST-segment depression on admission, the odds ratios for death in the last 2 groups were, respectively, 4.2 (95% CI, 1.5 to 12.2) and 6.6 (95% CI, 2.5 to 17.6). The rates of recurrent ischemic events and heart failure during hospital stay also increased in a stepwise fashion among the groups, whereas creatine kinase–MB levels were similar. Among the 437 patients that were catheterized within 6 months, the prevalence of left main or 3-vessel coronary artery disease in the 3 groups was 22.0%, 42.6%, and 66.3%, respectively (P<0.001).Conclusions— Lead aVR contains important short-term prognostic information in patients with a first non–ST-segment elevation acute myocardial infarction. Because the poorer outcome predicted by ST-segment elevation in lead aVR seems to be related to a more severe coronary artery disease, an early invasive approach might be especially beneficial in patients presenting with this finding.
Prognostic Significance of Corrected QT and Corrected JT Interval for Incident Coronary Heart Disease in a General Population Sample Stratified by Presence or Absence of Wide QRS Complex: The ARIC Study With 13 Years of Follow-Up
- Richard S. Crow,
- Peter J. Hannan and
- Aaron R. Folsom
Circulation Volume 108, Issue 1621 October 2003

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Background— Heart rate-corrected QT interval (QTc) is the traditional method of assessing the duration of repolarization. Prolonged heart rate-corrected QT interval is associated with higher risk of mortality in patients with coronary heart disease (CHD) and in the general population. However, the QTc is typically not evaluated when QRS duration is ≥120 ms, because increased QRS duration (QRSd) contributes to QT interval prolongation. In these circumstances, the JT interval has been proposed as a more valid way to assess ventricular repolarization.Methods and Results— To allow for variation in heart rate, corrected JT interval (JTc) was defined as QTc−QRSd. Using data from the Atherosclerosis Risk in Communities Study, JTc and QTc were compared for their prognostic associations with incident CHD events among 14 696 men and women who were CHD-free at baseline, having either normal conduction or wide QRS complex. Among individuals with normal QRS duration, logistic regression adjusted for age, hypertensive status, diabetes, race, systolic blood pressure, smoking, HDL and LDL cholesterol, R-R interval, and menopausal status in women showed QTc and JTc were nonpredictive of future coronary events in men but significant in women. In individuals with wide QRS complex (QRSd ≥120 ms), similar analyses showed JTc had a significant prognostic advantage compared with QTc in men but not in women, among whom only 11 events occurred.Conclusions— The JTc is a simple measurement that is a significant independent predictor of incident CHD events in men with wide QRS complex.
Determinants of Sudden Cardiac Death in Individuals With the Electrocardiographic Pattern of Brugada Syndrome and No Previous Cardiac Arrest
- Josep Brugada,
- Ramon Brugada and
- Pedro Brugada
Circulation Volume 108, Issue 2523 December 2003

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Background— Patients with Brugada syndrome who were resuscitated from an episode of ventricular fibrillation are at high risk for recurrent sudden death. There is general agreement about the therapeutic strategy for these patients. Conversely, the prognosis and approach in patients with a diagnostic ECG but without a previous history of sudden cardiac death is controversial. We analyzed a large cohort of patients with Brugada syndrome without previous cardiac arrest to understand the determinants of prognosis.Methods and Results— A total of 547 patients with an ECG diagnostic of Brugada syndrome and no previous cardiac arrest were studied. The mean age was 41±15 years, and 408 were male. The diagnostic ECG was present spontaneously in 391 patients. In the remaining 156 individuals, the abnormal ECG was noted only after the administration of an antiarrhythmic drug. One hundred twenty-four patients had suffered from at least 1 episode of syncope. During programmed ventricular stimulation, a sustained ventricular arrhythmia was induced in 163 of 408 patients. During a mean follow-up of 24±32 months, 45 patients (8%) suffered sudden death or documented ventricular fibrillation. Multivariate analysis identified the inducibility of a sustained ventricular arrhythmia (P<0.0001) and a history of syncope (P<0.01) as predictors of events. Logistic regression analysis showed that a patient with a spontaneously abnormal ECG, a previous history of syncope, and inducible sustained ventricular arrhythmias had a probability of 27.2% of suffering an event during follow-up.Conclusions— Individuals with Brugada syndrome and no previous cardiac arrest have a high risk of sudden death. Inducibility of ventricular arrhythmias and a previous history of syncope are markers of a poor prognosis.
Mechanism of ST Elevation and Ventricular Arrhythmias in an Experimental Brugada Syndrome Model
- Masaomi Kimura,
- Takao Kobayashi,
- Shingen Owada,
- Keiichi Ashikaga,
- Takumi Higuma,
- Shingo Sasaki,
- Atsushi Iwasa,
- Shigeru Motomura and
- Ken Okumura
Circulation Volume 109, Issue 16 January 2004

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Background— Although phase 2 reentry is said to be responsible for initiation of ventricular tachycardia (VT) in Brugada syndrome, information about the activation sequence during VT is limited.Methods and Results— We developed an experimental Brugada syndrome model using a canine isolated right ventricular preparation cross-circulated with arterial blood of a supporter dog and examined the VT mechanism. Two plaque electrodes (35×30 mm) containing 96 bipolar electrodes were attached to the endocardium and epicardium. Saddleback and coved types of ST elevation in transmural ECG were induced by pilsicainide, a pure sodium channel blocker, and pinacidil, a K_ATP channel opener. Eighteen polymorphic VT episodes were recorded in 9 of the 12 preparations associated with ST elevation. Fourteen episodes spontaneously developed in 5 preparations after an extrasystole during basic drive pacing. Analysis of local recovery times revealed increased dispersion especially in epicardium, and the extrasystole originated from a site with a short recovery time, suggesting that phase 2 reentry was its mechanism. The other 4 VTs in 4 preparations were induced by premature stimulation. Analysis of the activation sequences during VT revealed reentry between epicardium and endocardium or reentry around an arc of a functional block confined to epicardium or endocardium with bystander activation of the other.Conclusions— Electrical heterogeneity in the recovery phase was induced in this experimental Brugada syndrome model, which can be a substrate for the development of phase 2 reentry and the subsequent reentry around an arc of the functional block, resulting in sustained VT.
The Electrocardiogram 102 Years After Einthoven
- Hein J.J. Wellens and
- Anton P. Gorgels
Circulation Volume 109, Issue 510 February 2004

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Worrisome Thoughts About the Diagnosis and Treatment of Patients With Brugada Waves and the Brugada Syndrome
- Joon Ahn and
- J. Willis Hurst
Circulation Volume 109, Issue 1230 March 2004

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The Brugadas have made a significant contribution to medicine. Their discovery of a new clinical syndrome and ECG abnormalities has created a great deal of interest and has opened Pandora’s box. Here, we discuss some worrisome thoughts about the condition. We stress the need for improved diagnostic criteria and treatment because it is not always possible to perform coronary arteriography, electrophysiological studies, right ventricular myocardial biopsy, and MRI in all patients in whom ST-segment abnormalities are seen in the ECG, especially in patients who are asymptomatic. Accordingly, further research is needed to guide the clinician in the diagnostic and therapeutic problems of patients who have unusual ST segments in leads V₁ and V₃. We present a patient who illustrates the problem.
Electrocardiographic Recognition of the Epicardial Origin of Ventricular Tachycardias
- Antonio Berruezo,
- Lluis Mont,
- Santiago Nava,
- Enrique Chueca,
- Eduardo Bartholomay and
- Josep Brugada
Circulation Volume 109, Issue 1520 April 2004

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Background— Some ventricular tachycardias (VTs) originating from the epicardium are not suitable for endocardial radiofrequency ablation and require an epicardial approach. The aim of this study was to define the ECG characteristics that may identify an epicardial origin of VTs.Methods and Results— We analyzed the 12-lead ECG recordings during epicardial and endocardial left ventricular pacing in 9 patients to verify the hypothesis that the epicardial origin of the ventricular activation widens the initial part of the QRS complex. Then, we analyzed the ECG pattern in 14 VTs successfully ablated from the epicardium after a failed endocardial approach (group A), in 27 VTs successfully ablated from the endocardium (group B), and in 28 additional VTs that could not be ablated from the endocardium (group C). Four distinct intervals of ventricular activation were defined and measured: (1) the pseudodelta wave, (2) the intrinsicoid deflection time in V2, (3) the shortest RS complex, and (4) the QRS complex. VTs from groups A and C showed a significantly longer pseudodelta wave, intrinsicoid deflection time, and RS complex duration compared with VTs of group B. There was no difference between groups A and C. A pseudodelta wave of ≥34 ms has a sensitivity of 83% and a specificity of 95%, an intrinsicoid deflection time of ≥85 ms has a sensitivity of 87% and a specificity of 90%, and an RS complex duration of ≥121 ms has a sensitivity of 76% and a specificity of 85% in identifying an epicardial origin of the VTs.Conclusions— ECG suggests VTs originating from the epicardium and those with an unsuccessful radiofrequency ablation from the endocardium.

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