Usefulness of frequent arrhythmias after epicardial recanalization in anterior wall acute myocardial infarction as a marker of cellular injury leading to poor recovery of left ventricular function

doi:10.1016/j.amjcard.2003.07.020

The American Journal of Cardiology

Volume 92, Issue 10, 15 November 2003, Pages 1143-1149

https://doi.org/10.1016/j.amjcard.2003.07.020 Get rights and content

Abstract

Ventricular arrhythmias are associated with epicardial reperfusion but may also be a sign of cellular injury, which affects recovery of left ventricular (LV) function. To assess the correlation between reperfusion arrhythmias and the change in LV function after the acute phase in reperfused acute myocardial infarction (AMI), 62 patients with reperfused anterior wall AMI were studied. All patients underwent 24-hour Holter recording, echocardiography, and coronary angiography during the acute phase of AMI. Echocardiography was repeated at 1 to 2 months after AMI. Correlations between ventricular arrhythmias in the reperfusion phase and the change in LV wall motion score (WMS) during follow-up were studied. The number of reperfusion arrhythmias was significantly higher in patients with further deterioration of LV function; there were 5-, 14-, 131-, and 11-fold increases in isolated premature ventricular complexes (PVCs), PVCs in couplets, PVCs in bigeminy, and total PVCs, respectively, in patients with further increases in WMS after the acute phase. The incidence of repetitive, frequent, and early accelerated idioventricular rhythms (AIVRs) was correlated significantly with the change in LV function, with 129- and 105-fold increases in numbers of early AIVRs and total AIVRs, respectively, in patients with further worsening of LV function during follow-up. The incidence and the number of long-lasting nonsustained ventricular tachycardias as well as the number of rapid ventricular tachycardias and total ventricular tachycardia episodes were also correlated significantly with further deterioration. Thus, frequent arrhythmias associated with epicardial reperfusion strongly correlate with further worsening of LV function after the acute phase of AMI. This supports the hypothesis that these reperfusion arrhythmias are probably a noninvasive marker of cellular injury.

Section snippets

Study population

Sixty-six consecutive patients admitted to the coronary unit of the University Hospital Maastricht with a diagnosis of anterior wall AMI (defined as chest pain lasting >30 minutes and ST-segment elevation ≥0.1 mV in ≥2 adjacent precordial leads [V₁ to V₄]) were included in the study. Patients with complete left bundle branch block, previous AMI, and/or previous cardiac surgery were excluded. Four patients were excluded from further analysis (3 early deaths and 1 lost to follow-up). The relation

Major clinical events

Five patients presented with pulmonary edema and 1 with cardiogenic shock. Five patients were cardioverted for primary ventricular fibrillation, 2 patients for secondary ventricular fibrillation, and 1 patient for both (an episode of primary ventricular fibrillation occurred in the hospital during Holter recording in only 1 patient). Three patients showed complete right bundle branch block with left anterior hemiblock in the acute phase; 2 of the 3 patients experienced complete recovery. Two

Discussion

To our knowledge, this study is the first to correlate electrical activity with mechanical recovery of the left ventricle in the setting of infarct artery recanalization. This study shows a significant relation between incidence and frequency of reperfusion arrhythmias, using an accurate quantitative assessment from continuous Holter monitoring, and serial echocardiographic assessments of LV functional recovery. The results suggest that frequent ventricular arrhythmias in the setting of

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Cited by (25)

Bursts of reperfusion arrhythmias occur independently of area at risk size and are the first marker of reperfusion injury
2018, International Journal of Cardiology
Citation Excerpt :
Historically ventricular arrhythmias (VA) after thrombolytic therapy were considered a favorable non-invasive marker of reperfusion [1]. More recent studies in the era of primary percutaneous intervention (PCI) have shown that reperfusion VA bursts are related to larger infarct size (IS) and worse left ventricular function (Fig. 1) [2–8]. Such VA bursts include mostly ventricular premature beats with long coupling intervals and accelerated idioventricular rhythms.
The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger infarct size (IS). However it is unclear whether the initial area at risk (AAR), also a determining factor for IS, is responsible for this correlation. We hypothesized that IS would be significantly larger in the presence of VA, while AAR would not differ.
68 STEMI patients from the MAST study with 24-hour, continuous, 12‑lead Holter monitoring initiated prior to primary percutaneous coronary intervention (PCI) resulting in TIMI 3 flow post PCI were included. VA bursts were identified against subject-specific background VA rates using a previously validated statistical outlier method. IS, and infarct endocardial surface area (ESA) were obtained using CMR at mean 4.9 days after admission. Holter and CMR results were determined in core laboratories blinded to all other data.
VA bursts were present in 69% (45/65) of patients. No significant differences were found for demographic characteristics, comorbidities, infarct location, number of diseased coronary vessels, or duration of ischemia between groups with and without VA burst. IS was significantly smaller in the group without VA bursts (median 9.3% vs 17.0%; p = 0.025). Infarct ESA did not significantly differ between the population with and without VA burst; median 24.3% vs 20.0%; p = 0.15.
VA bursts are a marker for larger IS independent of AAR, assessed by surrogate markers. These findings support the hypothesis that VA bursts are a marker of reperfusion damage occurring downstream at myocellular level.
Ventricular arrhythmia burst is an independent indicator of larger infarct size even in optimal reperfusion in STEMI
2016, Journal of Electrocardiology
We hypothesized that ventricular arrhythmia (VA) bursts during reperfusion phase are a marker of larger infarct size despite optimal epicardial and microvascular perfusion.
126 STEMI patients were studied with 24 h continuous, 12-lead Holter monitoring. Myocardial blush grade (MBG) was determined and VA bursts were identified against subject-specific background VA rates in core laboratories. Delayed-enhancement cardiovascular magnetic resonance imaging was used to determine infarct size.
In the group with MBG 3 no significant differences were found for baseline characteristics between burst versus no burst (102 vs. 24). In those with optimal epicardial and microvascular reperfusion (TIMI 3, stable ST-recovery, and MBG 3), VA burst was associated with larger infarct size (N = 102/126; median 11.0 vs. 5.1%; p = 0.004).
In the event of MBG 3, VA bursts were associated with significantly larger infarct size even if optimal epicardial and microvascular reperfusion was present.
Impact of n-3 polyunsaturated fatty acids in predicting ischemia/reperfusion injury and progression of myocardial damage after reperfusion in patients with ST-segment elevation acute myocardial infarction
2015, Journal of Cardiology
Citation Excerpt :
Although the restoration of blood flow to the jeopardized myocardium is a prerequisite for myocardial salvage, reperfusion itself may either directly accelerate ischemia or additionally injure the myocardium, a phenomenon referred to as “myocardial reperfusion injury” [1], which is reported to account for up to 50% of final infarct size in acute myocardial infarction (AMI) [2]. Ventricular arrhythmias and additional ST-segment elevation after coronary reperfusion, signs of additional cellular injury caused directly by the reperfusion process, have previously been shown to result in a larger extent of myocardial infarct [3–8]. Demonstration of the beneficial ischemic preconditioning induced by pharmacological agents or noninvasive devices has regenerated interest in reperfusion phase as a target for cardioprotection [9–11].
In animal models of acute myocardial infarction, n-3 polyunsaturated fatty acids (PUFAs) administered before coronary occlusion have been suggested to prevent induction of ventricular arrhythmia and limit infarct size. However, the relation between the serum levels of n-3 PUFAs and ischemia/reperfusion (I/R) injury remains unclear.
211 patients with ST-segment elevation acute myocardial infarction received emergency percutaneous coronary intervention (PCI) within 6 h from the onset. The patients were divided into two groups according to the sum of serum eicosapentaenoic acid (EPA) levels and docosahexaenoic acid (DHA) levels before PCI: group L (n = 106), EPA + DHA <155 μg/ml and group H (n = 105), EPA + DHA ≥155 μg/ml. The Selvester QRS-scoring system was used to estimate the serial change in infarct size.
Time to reperfusion was similar between the 2 groups. The QRS score before PCI was higher in group L than in group H (2.42 ± 2.00 vs 1.85 ± 2.01, p = 0.015). The proportion of patients with I/R injury immediately after reperfusion, defined as reperfusion ventricular arrhythmias (25% vs 11%, p = 0.006) and ST-segment re-elevation (44% vs 22%, p < 0.001), was also higher in group L than in group H, followed by a greater increment in the QRS score during PCI (3.51 ± 2.51 vs 2.54 ± 1.91, p = 0.006) and higher peak levels of creatinine phosphokinase (3552 ± 241 U/L vs 2660 ± 242 U/L, p < 0.01). On multivariate analysis, serum level of EPA + DHA was an independent predictor of reperfusion injury (odds ratio 0.985, p = 0.032).
Serum level of n-3 PUFAs before PCI may be a predictor of I/R injury and the resultant extent of myocardial damage. These findings suggest a protective effect of serum n-3 PUFAs on ischemic myocardium.
Prospective evaluation of where reperfusion ventricular arrhythmia "bursts" fit into optimal reperfusion in STEMI
2015, International Journal of Cardiology
Citation Excerpt :
In conjunction with thrombolytic therapy, reperfusion VAs were considered a positive event as a non-invasive marker of infarct artery recanalization [2]. In the more contemporary era of direct percutaneous coronary intervention (PCI), where TIMI 3 epicardial flow is restored in > 90% of STEMIs and mortality has been reduced to less than 5% [3], the hypothesis that VA “bursts” are associated with larger infarct size (IS) and worsened outcomes in the setting of anterior MI has been proposed by our group, based on retrospective modeling [4–7]. Over the last years, it has become clear that clinically beneficial reperfusion in STEMI is dependent on both the clinical context and on a series of key mechanistic steps defining “optimal” reperfusion per se.
Early reperfusion of ischemic myocytes is essential for optimal salvage in acute myocardial infarction. VA (ventricular arrhythmia) bursts after recanalization of the culprit vessel have been found to be related to larger infarct size (IS), using SPECT.
The hypothesis was tested that this finding could be confirmed in an independent cohort using a more accurate technique, i.e. delayed-enhancement cardiovascular magnetic resonance imaging (DE-CMR).
All 196 patients from the PREPARE and MAST studies who had 24-hour, continuous, 12-lead Holter, started before primary percutaneous coronary intervention resulting in brisk TIMI (thrombolysis in myocardial infarction) 3 flow and stable ST-recovery were included. VA bursts were identified against subject-specific background VA rates using a previously published statistical outlier method. IS was assessed using DE-CMR. Angiography, Holter and DE-CMR results were assessed in core laboratories, blinded to all other data.
VA bursts were present in 154/196 (79%) of patients. Baseline characteristics between the groups with and without bursts were similar. VA burst was associated with significantly larger infarct size in the population as a whole (median 11.3% vs 5.3%; p = 0.001) and also when divided in non-anterior (median 9.9% vs 4.9%; p = 0.003) and anterior myocardial infarction (median 21.4% vs 12.0%; p = 0.48), the latter not reaching statistical significance due to the small subset of patients.
Beyond the classical markers of “optimal” reperfusion such as TIMI 3 flow and stable ST-segment recovery, VA bursts occurring during the reperfusion phase are an early electrobiomarker of larger IS. Clinical trial registration: PREPARE: ISRCTN71104460 http://www.controlled-trials.com/ISRCTN71104460.
Transient post-reperfusion left bundle branch block and accelerated idioventricular rhythm with paradoxical QRS narrowing
2014, Journal of Electrocardiology
Citation Excerpt :
In the clinical MI reperfusion setting, it is not established if AIVR is better correlated with complete or partial resolution of obstructed coronary flow. Although AIVR after reperfusion has been reported as identifying a patient subgroup with a favorable prognosis [3], other reports on reperfusion AIVR associate the arrhythmia with both left ventricular systolic and diastolic dysfunction [4,5] especially if the AIVR episodes are frequent. Deterioration of hemodynamic status occurs during AIVR [6], but this is transient and may be partly due to A-V dissociation and loss of pre-load plus ventricular desynchronization secondary to prolonged ventricular excitation.
Accelerated idioventricular rhythm (AIVR) commonly follows coronary reperfusion and has been called a “reperfusion arrhythmia”. Transient left bundle branch block (LBBB) is only rarely seen after interventional reperfusion and is usually considered a procedural complication. We report herein electrocardiograms (ECGs) in a case of acute lateral myocardial infarction which demonstrate both post-perfusion AIVR and a simultaneous transient LBBB with fusion complexes causing paradoxical QRS narrowing.
Feasibility and safety of combined percutaneous coronary intervention and therapeutic hypothermia following cardiac arrest
2010, Resuscitation
Citation Excerpt :
Our results suggest that PCI may be safe and feasible during MTH, and outcomes are comparable to those who undergo isolated MTH. Importantly, both PCI and MTH are associated with the potential for inducing cardiac dysrhythmias.6,16–18 A large randomized trial of MTH versus normothermia demonstrated a 36% rate of serious dysrhythmias in patients treated with MTH.2
Mild therapeautic hypothermia (MTH) has been associated with cardiac dysrhythmias, coagulopathy and infection. After restoration of spontaneous circulation (ROSC), many cardiac arrest patients undergo percutaneous coronary intervention (PCI). The safety and feasibility of combined MTH and PCI remains unclear. This is the first study to evaluate whether PCI increases cardiac risk or compromises functional outcomes in comatose cardiac arrest patients who undergo MTH.
Ninety patients within a 6-h window following cardiac arrest and ROSC were included. Twenty subjects (23%) who underwent PCI following MTH induction were compared to 70 control patients who underwent MTH without PCI. The primary endpoint was the rate of dysrhythmias; secondary endpoints were time-to-MTH induction, rates of adverse events (dysrhythmia, coagulopathy, hypotension and infection) and mortality.
Patients who underwent PCI plus MTH suffered no statistical increase in adverse events (P = .054). No significant difference was found in the rates of dysrhythmias (P = .27), infection (P = .90), coagulopathy (P = .90) or hypotension (P = .08). The PCI plus MTH group achieved similar neurological outcomes (modified Rankin Scale (mRS) ≤3 (P = .42) and survival rates (P = .40). PCI did not affect the speed of MTH induction; the target temperature was reached in both groups without a significant time difference (P = .29).
Percutaneous coronary intervention seems to be feasible when combined with MTH, and is not associated with increased cardiac or neurological risk.

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Coronary artery diseaseUsefulness of frequent arrhythmias after epicardial recanalization in anterior wall acute myocardial infarction as a marker of cellular injury leading to poor recovery of left ventricular function

Abstract

Section snippets

Study population

Major clinical events

Discussion

Am J Cardiol

Am J Cardiol

Am J Cardiol

Chest

J Am Coll Cardiol

J Am Coll Cardiol

Am J Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

Lancet

Am J Cardiol

J Am Coll Cardiol

J Mol Cell Cardiol

Angiographic assessment of prospectively determined noninvasive reperfusion indexes in acute myocardial infarction

Heart

The Thrombolysis In Myocardial Infarction (TIMI) trial. Phase I findings

N Engl J Med

Coronary artery disease
Usefulness of frequent arrhythmias after epicardial recanalization in anterior wall acute myocardial infarction as a marker of cellular injury leading to poor recovery of left ventricular function