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
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
References (30)
- et al.
Holter recording of ventricular arrhythmias during intravenous thrombolysis for acute myocardial infarction
Am J Cardiol
(1992) - et al.
Usefulness of the accelerated idioventricular rhythm as a marker for myocardial necrosis and reperfusion during thrombolytic therapy in acute myocardial infarction
Am J Cardiol
(1988) - et al.
Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction
Am J Cardiol
(1995) - et al.
Ventricular rhythms with intermediate rates in acute myocardial infarction
Chest
(1978) - et al.
Assessment of coronary artery patency after thrombolytic therapyaccurate prediction utilizing the combined analysis of three noninvasive markers
J Am Coll Cardiol
(1991) - et al.
Angiographic validation of bedside markers of reperfusion
J Am Coll Cardiol
(1993) - et al.
Time course and interrelation of reperfusion-induced ST changes and ventricular arrhythmias in acute myocardial infarction
Am J Cardiol
(1991) - et al.
Status of the myocardium and infarct-related coronary artery in 19 necropsy patients with acute recanalization using pharmacologic (streptokinase, r-tissue plasminogen activator), mechanical (percutaneous transluminal coronary angioplasty) or combined types of reperfusion therapy
J Am Coll Cardiol
(1987) - et al.
Tissue-type plasminogen activator therapy versus primary coronary angioplastyimpact on myocardial tissue perfusion and regional function 1 month after uncomplicated myocardial infarction
J Am Coll Cardiol
(1998) - et al.
Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction. Zwolle Myocardial infarction Study Group
Lancet
(1997)
Relation between ST-segment changes and myocardial perfusion evaluated by myocardial contrast echocardiography in patients with acute myocardial infarction treated with direct angioplasty
Am J Cardiol
Shifting the open-artery hypothesis downstreamthe quest for optimal reperfusion
J Am Coll Cardiol
Reperfusion-induced arrhythmiasmechanisms and prevention
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
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 CardiologyCitation 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.
Ventricular arrhythmia burst is an independent indicator of larger infarct size even in optimal reperfusion in STEMI
2016, Journal of ElectrocardiologyImpact 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 CardiologyCitation 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].
Prospective evaluation of where reperfusion ventricular arrhythmia "bursts" fit into optimal reperfusion in STEMI
2015, International Journal of CardiologyCitation 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.
Transient post-reperfusion left bundle branch block and accelerated idioventricular rhythm with paradoxical QRS narrowing
2014, Journal of ElectrocardiologyCitation 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.
Feasibility and safety of combined percutaneous coronary intervention and therapeutic hypothermia following cardiac arrest
2010, ResuscitationCitation 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