Prognostic value of early sustained ventricular arrhythmias in ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: A substudy of VALIDATE-SWEDEHEART trial.

Background: Prognostic assessment of ventricular tachycardia (VT) or ventricular fibrillation (VF) in ST-segment elevation myocardial infarction (STEMI) is based mainly on distinguishing between early (<48 hours) and late arrhythmias, and does not take into account its time distribution with regard to reperfusion, or type of arrhythmia. Objective: We analyzed the prognostic value of early ventricular arrhythmias (VAs) in STEMI with regard to their type and timing. Methods: The prespecified analysis of the multicenter prospective Bivalirudin versus Heparin in ST-Segment and Non-ST-Segment Elevation Myocardial Infarctionin Patients on Modern Antiplatelet Therapy in the Swedish Web System for Enhancement and Development of Evidence-based Care in Heart Disease evaluated according to Recommended Therapies Registry Trial included 2886 STEMI patients undergoing primary percutaneous coronary intervention (PCI). VA episodes were characterized regarding their type and timing. Survival status at 180 days was assessed through the population registry. Results: Nonmonomorphic VT or VF was observed in 97 (3.4%) and monomorphic VT in 16 (0.5%) patients. Only 3 (2.7%) early VA episodes occurred after 24 hours from symptom onset. VA was associated with higher risk of death (hazard ratio 3.59; 95% confidence interval [CI] 2.01-6.42) after adjustment for age, sex, and STEMI localization. VA after PCI was associated with an increased mortality compared with VA before PCI (hazard ratio 6.68; 95% CI 2.90-15.41). Early VA was associated with in-hospital mortality (odds ratio 7.39; 95% CI 3.68-14.83) but not with long-term prognosis in patients discharged alive. The type of VA was not associated with mortality. Conclusion: VA after PCI was associated with an increased mortality compared with VA before PCI. Long-term prognosis did not differ between patients with monomorphic VT and nonmonomorphic VT or VF, but events were few. VA incidence during 24 to 48 hours of STEMI is negligibly low, thus precluding assessment of its prognostic importance.

Prolonged repolarization in the early phase of ischemia is associated with ventricular fibrillation development in a porcine model.

Background: Repolarization prolongation can be the earliest electrophysiological change in ischemia, but its role in arrhythmogenesis is unclear. The aim of the present study was to evaluate the early ischemic action potential duration (APD) prolongation concerning its causes, expression in ECG and association with early ischemic ventricular fibrillation (phase 1A VF). Methods: Coronary occlusion was induced in 18 anesthetized pigs, and standard 12 lead ECG along with epicardial electrograms were recorded. Local activation time (AT), end of repolarization time (RT), and activation-repolarization interval (ARIc) were determined as dV/dt minimum during QRS-complex, dV/dt maximum during T-wave, and rate-corrected RT-AT differences, respectively. Patch-clamp studies were done in enzymatically isolated porcine cardiomyocytes. IK(ATP) activation and Ito1 inhibition were tested as possible causes of the APD change. Results: During the initial period of ischemia, a total of 11 pigs demonstrated maximal ARIc prolongation >10 ms at 1 and/or 2.5 min of occlusion (8 and 6 cases at 1 and 2.5 min, respectively) followed by typical ischemic ARIc shortening. The maximal ARIc across all leads was associated with VF development (OR 1.024 95% CI 1.003-1.046, p = 0.025) and maximal rate-corrected QT interval (QTc) (B 0.562 95% CI 0.346-0.775, p < 0.001) in logistic and linear regression analyses, respectively. Phase 1A VF incidence was associated with maximal QTc at the 2.5 min of occlusion in ROC curve analysis (AUC 0.867, p = 0.028) with optimal cut-off 456 ms (sensitivity 1.00, specificity 0.778). The pigs having maximal QTc at 2.5 min more and less than 450 ms significantly differed in phase 1A VF incidence in Kaplan-Meier analysis (log-rank p = 0.007). In the patch-clamp experiments, 4-aminopyridine did not produce any effects on the APD; however, pinacidil activated IK(ATP) and caused a biphasic change in the APD with initial prolongation and subsequent shortening. Conclusion: The transiently prolonged repolarization during the initial period of acute ischemia was expressed in the prolongation of the maximal QTc interval in the body surface ECG and was associated with phase 1A VF. IK(ATP) activation in the isolated cardiomyocytes reproduced the biphasic repolarization dynamics observed in vivo, which suggests the probable role of IK(ATP) in early ischemic arrhythmogenesis.

ECG Markers of Acute Melatonin Treatment in a Porcine Model of Acute Myocardial Ischemia.

In myocardial ischemia, melatonin confers antiarrhythmic action, but its electrocardiographic expression is unclear. We aimed to evaluate the effects of melatonin treatment on electrocardiogram (ECG) parameters reflecting major arrhythmogenic factors and to test the association of these parameters with ventricular fibrillation (VF) incidence. Myocardial ischemia was induced by 40 min coronary artery occlusion in 25 anesthetized pigs. After induction of ischemia, 12 and 13 animals were given melatonin or placebo, respectively. Twelve-lead ECGs were recorded and durations of QRS, QT, Tpeak-Tend intervals and extrasystolic burden were measured at baseline and during occlusion. During ischemia, VF episodes clustered into early and delayed phases (<10 and >20 min, respectively), and QRS duration was associated with VF incidence. QT interval and extrasystolic burden did not differ between the groups. The Tpeak-Tend interval was progressively prolonged, and the prolongation was less pronounced in the treated animals. QRS duration increased, demonstrating two maxima (5−10 and 25 min, respectively). In the melatonin group, the earlier maximum was blunted, and VF development in this period was prevented. Thus, acute melatonin treatment prevented excessive prolongation of the QRS and Tpeak-Tend intervals in the porcine myocardial infarction model, and QRS duration can be used for the assessment of antiarrhythmic action of melatonin.

Terminal T-wave inversion predicts reperfusion tachyarrhythmias in STEMI.

INTRODUCTION: A reliable electrocardiographic predictor of ventricular fibrillation (VF) in patients with ST elevation myocardial infarction (STEMI) is lacking so far. Previous experimental/simulation study suggested a terminal T-wave inversion (TTWI) in ischemia-related ECG leads corresponding to anterior infarct localization as an independent predictor of reperfusion VF (rVF). This T-wave characteristic has never been tested as a rVF predictor in clinical settings. The aim of this study was to test if terminal T-wave inversion (TTWI) at admission ECG (before reperfusion) can serve as a predictor of ventricular fibrillation during reperfusion (rVF) in patients with anterior STEMI undergoing primary PCI. METHODS AND RESULTS: Study population included consecutive patients with anterior infarct localization admitted for primary PCI (n = 181, age 65 [57; 76] years, 66% male). Of those, 14 patients had rVF (rVF group, age 59 [47; 76] years, 64% male) and patients without rVF comprised the No-rVF group (n = 167, age 65 [57; 76] years, 66% male). Association of TTWI with rVF was analyzed using logistic regression analysis adjusted for relevant clinical and electrocardiographic covariates. The prevalence of TTWI in rVF group was 62% comparing to 23% in the No-rVF group, p = 0.005. TTWI was associated with increased risk of rVF (OR 5.51; 95% CI 1.70-17.89; p = 0.004) and remained a significant predictor after adjustment for age, gender, history of MI prior to index admission, VF before reperfusion, Tpeak-Tend, maximal ST elevation, and QRS duration (OR 23.49; 95% CI 3.14-175.91; p = 0.002). CONCLUSIONS: The terminal T-wave inversion in anterior leads before PCI independently predicted rVF in patients with anterior MI thus confirming the previous experimental/simulation findings.

Relation of Early Monomorphic Ventricular Tachycardia to Long-Term Mortality in ST-Elevation Myocardial Infarction.

Early ventricular tachycardia (VT) and ventricular fibrillation (VF) are associated with increased in-hospital mortality but do not influence the long-term prognosis in ST-elevation myocardial infarction (STEMI). Recent data advocate a differential approach to the type of arrhythmia and indicate long-term mortality hazard associated with monomorphic VT. We aimed to evaluate the prognostic value of early monomorphic VT compared to nonmonomorphic VT/VF in a nonselected cohort of STEMI patients. Consecutive STEMI patients admitted for primary percutaneous coronary intervention from 2007 to 2010 were included. Clinical characteristics were obtained from the Swedish national SWEDEHEART registry. The occurrence and type of early VT/VF were verified in medical records. All-cause mortality 8 years after STEMI was assessed using the Swedish Cause of Death Register. A total of 2,277 STEMI patients were included (age 66 ± 12 years, 70% male), among them 35 (1.5%) with early monomorphic VT and 115 (5.1%) with nonmonomorphic VT/VF. Patients with monomorphic VT had similar clinical characteristics compared to those with nonmonomorphic VT/VF. In total, 22 patients (63%) with monomorphic VT and 43 (37%) with nonmonomorphic VT/VF died by 8 years of follow-up (p = 0.011). Monomorphic VT was associated with a higher risk of all-cause mortality compared to nonmonomorphic VT/VF in univariate analysis (HR 2.03, 95% CI 1.21 to 3.39, p = 0.007) and after adjustment for age and history of myocardial infarction (MI) (HR 1.74, 95% CI 1.02 to 2.97, p = 0.041). Early monomorphic VT in STEMI is associated with a higher risk of all-cause mortality compared to nonmonomorphic VT/VF and deserves further studies to refine risk stratification strategies.

Contribution of Depolarization and Repolarization Changes to J-Wave Generation and Ventricular Fibrillation in Ischemia.

Background: Activation delay in ischemic myocardium has been found to contribute to J-wave appearance and to predict ventricular fibrillation (VF) in experimental myocardial infarction. However, the role of ischemia-related repolarization abnormalities in J-wave generation remains unclear. Objectives: The objective of our study was to assess a contribution of myocardial repolarization changes to J-wave generation in the body surface ECG and VF in a porcine acute myocardial infarction model. Methods: In 22 anesthetized pigs, myocardial ischemia was induced by occlusion of the left anterior descending coronary artery (LAD, n = 14) and right coronary artery (RCA, n = 8). Body surface ECGs were recorded simultaneously with intramyocardial unipolar electrograms led from flexible electrodes positioned across the left ventricular (LV) wall, interventricular septum (IVS), and right ventricular (RV) wall at apical, middle and basal levels of the ventricles (a total of 48 leads). Local activation times (ATs) and activation-repolarization intervals (ARIs, differences between dV/dt maximum during T-wave and dV/dt minimum during QRS) were measured. Results: J-waves appeared in left precordial leads (in 11 out of 14 animals with LAD occlusion) and right precordial leads (in six out of eight animals with RCA occlusion). During ischemic exposure, ATs prolonged, and the activation delay was associated with J-wave development (OR = 1.108 95% CI 1.072-1.144; p < 0.001) and VF incidence (OR = 1.039 95% CI 1.008-1.072; p = 0.015). ARIs shortened in the ischemic regions (in the IVS under LAD-occlusion and the lateral RV base under RCA-occlusion). The difference between maximal ARI in normal zones and ARI in the ischemic zones (ΔARI) was associated with J-wave appearance (OR = 1.025 95% CI 1.016-1.033, p < 0.001) independently of AT delay in multivariate logistic regression analysis. Conclusions: Both AT delay and increase of ΔARIs contributed to the development of J-wave in body surface ECG. However, only AT delay was associated with VF occurrence.

Melatonin Prevents Early but Not Delayed Ventricular Fibrillation in the Experimental Porcine Model of Acute Ischemia.

Antiarrhythmic effects of melatonin have been demonstrated ex vivo and in rodent models, but its action in a clinically relevant large mammalian model remains largely unknown. Objectives of the present study were to evaluate electrophysiological and antiarrhythmic effects of melatonin in a porcine model of acute myocardial infarction. Myocardial ischemia was induced by 40-min coronary occlusion in 25 anesthetized pigs. After ischemia onset, 12 animals received melatonin (4 mg/kg). 48 intramyocardial electrograms were recorded from left ventricular wall and interventricular septum (IVS). In each lead, activation time (AT) and repolarization time (RT) were determined. During ischemia, ATs and dispersion of repolarization (DOR = RTmax - RTmin) increased reaching maximal values by 3-5 and 20-25 min, respectively. Ventricular fibrillation (VF) incidence demonstrated no relations to redox state markers and was associated with increased DOR and delayed ATs (specifically, in an IVS base, an area adjacent to the ischemic zone) (p = 0.031). Melatonin prevented AT increase in the IVS base, (p < 0.001) precluding development of early VF (1-5 min, p = 0.016). VF occurrence in the delayed phase (17-40 min) where DOR was maximal was not modified by melatonin. Thus, melatonin-related enhancement of activation prevented development of early VF in the myocardial infarction model.

Early repolarization pattern on ECG recorded before the acute coronary event does not predict ventricular fibrillation during ST-elevation myocardial infarction.

BACKGROUND: Generally considered benign, electrocardiographic (ECG) early repolarization (ER) pattern was claimed to be an indicator of increased susceptibility to ventricular arrhythmias during acute ischemia. OBJECTIVE: The purpose of this study was to assess in a nonselected population whether ER pattern documented before ST-elevation myocardial infarction (STEMI) is associated with risk of hemodynamically unstable ventricular tachycardia (VT) or ventricular fibrillation (VF) during acute STEMI. METHODS: For STEMI patients admitted for primary percutaneous coronary intervention from 2007-2010, the latest ECGs recorded before STEMI were exported in digital format. After excluding ECGs with paced rhythm and QRS duration ≥120 ms, the remaining ECGs were processed using the Glasgow algorithm allowing automatic ER detection. The association between ER pattern and VT/VF during the first 48 hours of STEMI was tested using logistic regression. RESULTS: ECGs recorded before STEMI were available for 1584 patients. Of these patients, 124 did not meet inclusion criteria, leaving 1460 patients available for analysis (age 68 ± 12 years; 67% male). ER pattern was present in 272 patients (18.6%; ER+ group). ER+ and ER- groups did not differ with regard to clinical characteristics. VT/VF during the first 48 hours of STEMI occurred in 19 ER+ (7.0%) and 105 ER- patients (8.8%; P = .398). ER was not associated with any VT/VF (odds ratio [OR] 0.78; 95% confidence interval [CI] 0.47-1.29; P = .324); VT/VF before reperfusion (OR 0.48; 95% CI 0.23-1.001; P = .051); or reperfusion-related VT/VF (OR 1.28; 95% CI 0.55-3.01; P = .569). CONCLUSION: In a nonselected population of STEMI patients, the ER pattern on ECG recorded before the acute coronary event was not associated with VT/VF during the first 48 hours of STEMI.

Prolongation of The Activation Time in Ischemic Myocardium is Associated with J-wave Generation in ECG and Ventricular Fibrillation.

J-wave pattern has been recognized as an arrhythmic risk marker, particularly in myocardial infarction patients. Mechanisms underlying J-wave development in ischemia remain unknown. In myocardial infarction model, we evaluated activation time delay as a prerequisite of J-wave appearance and predictor of ventricular fibrillation. Body surface ECGs and myocardial unipolar electrograms were recorded in 14 anesthetized pigs. 48 intramural leads were positioned across ventricular free walls and interventricular septum. Myocardial ischemia was induced by ligation of the left anterior descending coronary artery and the recordings were done during 40-minute coronary occlusion. The local activation times were determined as instants of dV/dt minimum during QRS complex in unipolar electrograms. During occlusion, ventricular local activation time prolonged in the middle portion of the left ventricular free wall, and basal and middle portions of septum, while J-waves appeared in precordial leads in 11 animals. In logistic regression and ROC curve analyses, activation time delay at a given time-point was associated with J-wave development, and a longer activation time was associated with ventricular fibrillation appearance. In experimental coronary occlusion, activation delay in ischemic myocardium was associated with generation of the J waves in the body surface ECG and predicted ventricular fibrillation.

Progressive increase of the Tpeak-Tend interval is associated with ischaemia-induced ventricular fibrillation in a porcine myocardial infarction model.

Aims: Repolarization indices of ECG have been widely assessed as predictors of ventricular arrhythmias. However, little is known of the dynamic changes of these parameters during continuous monitoring in acute ischaemic episodes. The objective of the study was to evaluate repolarization-related predictors of ventricular fibrillation (VF) during progression of experimental myocardial infarction. Methods and results: Myocardial infarction was induced in 27 pigs by 40-min balloon inflation in the left anterior descending coronary artery, and 12-lead ECG was continuously recorded. Rate-corrected durations of the total Tpeak-Tend intervals measured from the earliest T-wave peak to the latest T-wave end in any lead were determined at baseline and at minute 1, 2, 5, and then every 5th minute of occlusion. There were 7 early (1-3 min) and 10 delayed (15-30 min) VFs in 16 pigs. Baseline Tpeak-Tend did not differ between animals with and without VF. Tpeak-Tend interval rapidly increased immediately after balloon inflation and was greater in VF-susceptible animals at 2-15 min compared with the animals that never developed VF (P < 0.05). Tpeak-Tend was tested as a predictor of delayed VFs. Median Tpeak-Tend at 10th min of occlusion was higher in delayed VF group (n = 10) than in animals without VF (n = 11): 138 [IQR 121-148] ms vs. 111 [IQR 106-127] ms, P = 0.02. Tpeak-Tend ≥123 ms (10th min) predicted delayed VF episodes with HR = 4.5 95% CI 1.1-17.8, P = 0.031. Conclusion: Tpeak-Tend prolongation during ischaemia progression predicts VF in the experimental porcine myocardial infarction model and warrants further testing in clinical settings of acute coronary syndromes.

QRS broadening due to terminal distortion is associated with the size of myocardial injury in experimental myocardial infarction.

INTRODUCTION: Not only repolarization, but also depolarization ECG indexes reflect the progression of ischemic injury. The aim was to assess the QRS duration and morphology dynamics during the prolonged coronary occlusion and their association with the myocardial area at risk (MaR) and final infarct size (IS). METHODS: In pigs, myocardial infarction was induced by inflation of an angioplasty balloon in the left descending artery (LAD), and ECG was continuously recorded. QRS duration was calculated on a beat-to-beat basis during the occlusion period. Single photon emission computed tomography (SPECT) was performed for the assessment of MaR, and IS was assessed by magnetic resonance imaging (MRI). RESULTS: All animals developed an anteroseptal infarction with MaR 40±9% and IS 23±7%. Two peaks of QRS widening were found in all animals: the early peak immediately after LAD occlusion and the late one 17.7±4.1min later. No association was found between MaR and IS and either QRS width or the degree of QRS widening at the early peak. QRS duration on the late peak correlated with both MaR (r=0.61; p=0.007) and IS (r=0.55; p=0.018). CONCLUSION: The QRS widening at the late peak, but not at the early peak, is associated with the size of myocardial injury, suggesting different underlying mechanisms.

Predictors of ventricular fibrillation at reperfusion in patients with acute ST-elevation myocardial infarction treated by primary percutaneous coronary intervention.

Ventricular fibrillation (VF) during reperfusion (rVF) in ST-segment elevation myocardial infarction (STEMI) is an infrequent but serious event that complicates coronary interventions. The aim of this study was to analyze clinical predictors of rVF in an unselected population of patients with STEMI treated with percutaneous coronary intervention (PCI). Consecutive patients with STEMI admitted to a tertiary care hospital for primary PCI from 2007 to 2012 were retrospectively assessed for the presence of rVF. Admission electrocardiograms, stored in a digital format, were analyzed for a maximal ST-segment elevation in a single lead and the sum of ST-segment deviations in all leads. Clinical, electrocardiographic, and angiographic characteristics were tested for associations with rVF using logistic regression analysis. Among 3,724 patients with STEMI admitted from 2007 to 2012, 71 (1.9%) had rVF. In univariate analysis, history of myocardial infarction, aspirin and ß-blocker use, VF before PCI, left main coronary artery disease, inferior myocardial infarction localization, symptom-to-balloon time <360 minutes, maximal ST-segment elevation in a single lead >300 µV, and sum of ST-segment deviations in all leads >1,500 µV were associated with increased risk for rVF. In a multivariate analysis, sum of ST-segment deviations in all leads >1500 µV (odds ratio 3.7, 95% confidence interval 1.45 to 9.41, p = 0.006) before PCI remained an independent predictor of rVF. In-hospital mortality was 18.3% in the rVF group and 3.3% in the group without VF (p <0.001), but rVF was not an independent predictor of in-hospital death. In conclusion, the magnitude of ST-segment elevation before PCI for STEMI independently predicts rVF and should be considered in periprocedural arrhythmic risk assessment. Despite higher in-hospital mortality in patients with rVF, rVF itself has no independent prognostic value for prognosis.

Transient and rapid QRS-widening associated with a J-wave pattern predicts impending ventricular fibrillation in experimental myocardial infarction.

BACKGROUND: Certain types of the early repolarization phenomenon, previously considered to be benign, have been reported to be associated with ventricular fibrillation (VF), both in population-based studies and in the myocardial infarction (MI) settings. OBJECTIVE: To analyze whether QRS widening and appearance of a J-wave pattern in experimental MI settings is predictive of VF. METHODS: MI was induced in 32 pigs by 40-minute inflation of an angioplasty balloon in the left descending artery, and electrocardiogram was continuously recorded. Multilead QRS boundaries were computed, and QRS duration was calculated on a beat-to-beat basis during the occlusion period for each pig. An association between QRS widening and subsequent VF was studied using receiver operating characteristic curve analysis. Electrocardiograms at maximum QRS duration were reviewed for the presence of a J-wave pattern. RESULTS: Sixteen animals had VF episodes during the occlusion period. Two peaks of QRS widening were found in all animals: the first peak immediately on left descending artery occlusion and the second peak 19.1 ± 4.0 minutes later. The magnitude of changes in the QRS width over time had significant interindividual differences. A QRS widening of ≥28 ms during a 3-minute time window was observed in 14 animals and predicted impending VF (selectivity 80%, specificity 73%, positive predictive value 57%, and negative predictive value 89%; P = .008). In 10 of 14 (71%) pigs, a J-wave pattern appeared at maximal QRS duration. The appearance of a J-wave pattern predicted VF with selectivity 80%, specificity 68%, positive predictive value 53%, and negative predictive value 88% (P = .02). CONCLUSION: Transient QRS widening, commonly associated with a J-wave pattern, appears to predict impending VF in acute ischemia settings and motivates further clinical studies for monitoring immediate risk of VF in MI.

T wave alternans in experimental myocardial infarction: time course and predictive value for the assessment of myocardial damage.

BACKGROUND: T-wave alternans (TWA) is associated with prognosis after myocardial infarction (MI), however its link to the extent of ischemic injury has not been clarified. We analyzed the course of TWA and its relation to myocardial damage in experimental myocardial infarction. METHODS: In 21 pigs, infarction was induced by 40-minute long balloon inflation in LAD under continuous 12-lead ECG monitoring. TWA was assessed in a 32-beat sliding window, using periodic component analysis and the Laplacian Likelihood Ratio method. Myocardium at risk (MaR) and infarct size (IS) were evaluated by SPECT and magnetic resonance imaging respectively. RESULTS: TWA appeared at 7.2±4.5minutes of occlusion, reached its maximum at 12.7±6.3 and lasted until 26.5±9.2minutes. The maximal level of TWA was associated with both MaR (r=0.499, p=0.035) and IS (r=0.65, p=0.004). CONCLUSION: TWA magnitude is associated with both MaR and IS in experiment, which encourages further studies in clinical settings.

Prognostic impact of early ventricular fibrillation in patients with ST-elevation myocardial infarction treated with primary PCI.

AIMS: Current guidelines do not advocate implantation of cardioverter-defibrillators (ICD) for survivors of ventricular fibrillation (VF) during the first 48 hours of ST-elevation myocardial infarction (STEMI). However, contemporary studies in a real-life setting with long-term follow-up are lacking. We assessed the prognostic impact of early VF in a non-selected population of STEMI patients treated with primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: Consecutive STEMI patients admitted to a Swedish tertiary care hospital during 2007-2009 were identified from the Register of Information and Knowledge about Swedish Heart Intensive Care Admissions (n=1718, age 66±12 years, 70% male). Patients with VF were identified from the register, and medical records were reviewed to determine the time point of VF. Patients surviving VF in the first 48 hours after symptom onset were compared with patients without VF for one-year mortality and a combined endpoint of death, resuscitated VF or appropriate ICD therapy. VF within 48 hours occurred in 7% of STEMI patients (n=121). In patients alive at 48 hours (n=1663), VF patients (n=101) had higher in-hospital mortality (12% vs. 2%, p<0.001). However, in VF patients discharged alive (n=89), mortality was low (1%) and combined endpoint rate (3%) did not differ compared with patients without VF (n=1538; 4% and 4% respectively). CONCLUSION: In a large non-selected population of STEMI patients treated with primary PCI, VF during the first 48 hours after STEMI is associated with increased in-hospital mortality but does not influence the long-term prognosis for those discharged alive.

ST-segment dynamics during reperfusion period and the size of myocardial injury in experimental myocardial infarction.

BACKGROUND: Exacerbation of ST elevation associated with reperfusion has been reported in patients with myocardial infarction. However, the cause of the "reperfusion peak" and relation of its magnitude to the size of myocardial damage has not been explored. The aim of our study was to assess the correlation between the ST-dynamics during reperfusion, the myocardium at risk (MaR), and the infarct size (IS). METHODS: Infarction was induced in 15 pigs by a 40-minute-long balloon inflation in the left anterior descending coronary artery. Tetrofosmin Tc 99m was given intravenously after 20 minutes of occlusion, and ex vivo single photon emission computed tomography was performed to assess MaR. Maximal ST elevation in a single lead and maximal sum of ST deviations in 12 leads were measured before, during, and after occlusion from continuous 12-lead electrocardiographic monitoring. A gadolinium-based contrast agent was given intravenously 30 minutes before explantation of the heart. Final IS was estimated using ex vivo cardiac magnetic resonance imaging. RESULTS: All pigs developed an anteroseptal infarct with MaR = 42% ± 9% and IS = 26% ± 7% of left ventricle. In all pigs, reperfusion was accompanied by transitory exacerbation of ST elevation that measured 1300 ± 500 µV as maximum in a single lead compared with 570 ± 220 µV at the end of occlusion (P < .001). The transitory exacerbation of ST elevation exceeded the maximal ST elevation during occlusion (920 ± 420 µV, P < .05). The ST elevation resolved by the end of the reperfusion period (90 ± 30 µV, P < .001). Exacerbation of ST elevation after reperfusion correlated with the final IS (r = 0.64, P = .025 for maximal ST elevation in a single lead and r = 0.80, P = .002 for sum of ST deviations) but not with MaR (r = 0.43, P = .17 for maximal ST elevation in a single lead and r = 0.49, P = .11 for sum of ST deviations). The maximal ST elevation in a single lead and the sum of ST deviations during occlusion did not correlate with either MaR or final IS. CONCLUSION: In the experiment, exacerbation of ST elevation is common during restoration of blood flow in the occluded coronary artery. The magnitude of the exacerbation of ST elevation after reperfusion in experimentally induced myocardial infarction in pigs is associated with infarct size but not with MaR.