Ischemic arrhythmias

Article written and reviewed by Dr Luca Moretti

Ischemic arrhythmias comprise rhythm and conduction disorders that arise in the setting of acute myocardial ischemia, necrosis, reperfusion, or the structural consequences of a previous infarction. The term does not identify a single arrhythmia and does not imply a necessarily chronic or progressive course. The electrophysiological substrate changes profoundly over time: during coronary occlusion, rapidly reversible or evolving metabolic and ionic abnormalities predominate, whereas after the infarction heals, the fibrous scar may create stable reentry circuits that remain present for years.

The distinction between acute-phase arrhythmias and scar-related arrhythmias is clinically essential. Ventricular fibrillation occurring during an evolving infarction may be caused directly by ischemia and requires defibrillation and reperfusion first. Sustained monomorphic ventricular tachycardia occurring months or years after an infarction is instead frequently an expression of reentry through channels of surviving myocardium within the scar. Both mechanisms may coexist in the same patient, and new ischemia can destabilize an already predisposed scar substrate.

Electrophysiological mechanisms

Acute ischemia rapidly reduces ATP production and alters the function of membrane ion pumps. Extracellular potassium accumulation, acidosis, reduced membrane potential, changes in sodium and calcium currents, and nonuniform shortening of the action potential produce heterogeneity of conduction and refractoriness. Adjacent regions may therefore recover excitability at different times and conduct the impulse at different velocities, conditions that favor unidirectional block and reentry circuit formation.
In the early phases of coronary occlusion, electrical instability may manifest as premature ventricular beats, polymorphic ventricular tachycardia, or ventricular fibrillation. Increased sympathetic activity, pain, hypoxemia, and electrolyte abnormalities may amplify the risk. Ventricular fibrillation does not necessarily require a preexisting scar: it can be generated by the marked electrical nonuniformity of acutely ischemic myocardium and is one of the principal mechanisms of cardiac arrest in the early phases of infarction.

Reperfusion again alters the electrophysiological milieu. Rapid restoration of flow may be associated with premature beats, accelerated idioventricular rhythm, nonsustained ventricular tachycardia, and, more rarely, sustained arrhythmias. Accelerated idioventricular rhythm is classically observed after reperfusion and, in the absence of hemodynamic compromise, does not itself require aggressive antiarrhythmic therapy. Sustained ventricular arrhythmias instead require the same severity assessment used in other settings.
As the infarction heals, necrotic tissue is replaced by fibrosis. The scar is not electrically uniform: bundles of viable cardiomyocytes may persist between areas of collagen and create slow-conduction channels. If conduction time allows previously refractory tissue to recover excitability, a reentry circuit capable of sustaining monomorphic ventricular tachycardia is created. QRS morphology during tachycardia reflects the circuit exit site, whereas the critical circuit may lie deep within the scar or at its margins.

The ischemic substrate may also promote atrial arrhythmias and bradyarrhythmias, but the causal relationship is less specific than for ventricular arrhythmias. Ischemia and heart failure increase atrial pressure and neurohormonal activation, promoting atrial fibrillation; an inferior infarction may involve the blood supply to the atrioventricular node and cause often transient nodal block, whereas a large anterior infarction may damage the His-Purkinje system and produce more distal conduction disorders with a less favorable prognosis.

Clinical phenotypes

Premature ventricular beats are common during ischemia and after infarction, but their significance depends on the context. Pharmacological suppression of ectopy alone is not a prognostic goal. The Cardiac Arrhythmia Suppression Trial demonstrated that eliminating premature beats with encainide or flecainide in infarction survivors increased mortality, establishing a fundamental principle: improving an electrocardiographic endpoint is not equivalent to reducing sudden death, and class Ic drugs must not be used for this purpose in structural ischemic heart disease.
Nonsustained ventricular tachycardia may reflect acute electrical irritability or a scar substrate. In a patient with previous infarction, its presence requires assessment of ventricular function, residual ischemia, therapy, and the overall clinical picture. It is not by itself an automatic indication for chronic antiarrhythmic therapy or an ICD, but may contribute to risk stratification in specific algorithms, especially when associated with ventricular dysfunction.

Late sustained monomorphic ventricular tachycardia after infarction is the phenotype most typical of scar-related reentry. It may be hemodynamically tolerated, cause syncope, or degenerate into ventricular fibrillation. Apparent stability must not be interpreted as benignity because recurrence is frequent and risk depends on ventricular function, scar burden, and the possibility of treating the substrate.
Polymorphic ventricular tachycardia and ventricular fibrillation should prompt rapid investigation for ongoing ischemia, electrolyte abnormalities, hypoxia, QT prolongation, and proarrhythmic drugs. During an acute coronary syndrome, treatment of the ischemic cause is an integral part of arrhythmia control. Repeated recurrence of ventricular arrhythmias within a short period constitutes an electrical storm and requires multidisciplinary intensive management, reduction of adrenergic activation, appropriate drugs, correction of triggers, and, when indicated, urgent ablation or neuromodulation strategies.

Ischemic bradyarrhythmias have different characteristics. In inferior infarction, atrioventricular block is often nodal, associated with a relatively stable escape rhythm, and may regress after reperfusion. In anterior infarction, an infranodal block indicates more extensive damage to the conduction system and may be associated with hemodynamic instability. Atropine, transcutaneous or transvenous pacing, and treatment of the cause are selected according to the level of block, heart rate, perfusion, and clinical response.

Diagnosis and risk stratification

Diagnosis begins with a 12-lead ECG obtained during symptoms whenever possible. Morphology, rate, regularity, and the relationship between atrial and ventricular activity make it possible to distinguish ventricular tachycardias, supraventricular tachycardias with aberrancy, and conduction disorders. In a patient with structural heart disease and wide-QRS tachycardia, ventricular tachycardia must be considered the leading diagnosis until proved otherwise.
Continuous monitoring is essential in acute infarction and unstable patients. In the outpatient phase, Holter monitoring and prolonged monitoring systems are selected according to symptom frequency. Rare syncopal episodes may require long-term monitoring; the temporal correlation between symptoms and rhythm is especially important when premature beats or nonsustained tachycardia are nonspecific findings.

Echocardiography assesses ejection fraction, volumes, aneurysms, ischemic mitral regurgitation, and other conditions that modify risk. Cardiac magnetic resonance with late gadolinium enhancement can define scar distribution and transmurality and identify heterogeneous tissue at the margins of the infarction. The amount and architecture of fibrosis add information about the arrhythmic substrate, although device indications remain anchored to validated clinical criteria and not to the presence of enhancement alone.
When an arrhythmia occurs together with chest pain, ST-segment changes, increased troponin, or hemodynamic instability, active ischemia must be assessed. CCTA, coronary angiography, and functional tests are used according to the acute or chronic context. Revascularization may eliminate the ischemic trigger, but not necessarily the scar substrate of late monomorphic tachycardia.

The electrophysiological study retains a selective role. It may be used to define the mechanism, plan ablation, and, in specific populations with coronary artery disease, ventricular dysfunction, and nonsustained ventricular tachycardia, contribute to stratification through inducibility of sustained ventricular tachycardia. It is not a universal post-infarction screening test.

Acute treatment and prevention of recurrence

Ventricular tachycardia or a wide-QRS arrhythmia with hemodynamic instability requires synchronized cardioversion; ventricular fibrillation and pulseless ventricular tachycardia require defibrillation and cardiopulmonary resuscitation according to advanced algorithms. In the ischemic setting, electrical therapy must proceed in parallel with correction of the cause, with particular attention to reperfusion, oxygenation when necessary, acid-base balance, and electrolytes.
Amiodarone or lidocaine may be used in specific acute ventricular arrhythmias, including refractory ventricular fibrillation or pulseless ventricular tachycardia according to resuscitation algorithms. Magnesium is not a universal antiarrhythmic drug for ischemia: it is specifically indicated for torsades de pointes and documented hypomagnesemia. Indiscriminate antiarrhythmic prophylaxis after infarction is not recommended.

Beta-blockers, when not contraindicated by shock, severe bradycardia, advanced block, or other conditions, reduce adrenergic activation and are fundamental in the management of many patients with ischemic heart disease and ventricular dysfunction. Sympathetic control is particularly important in electrical storm. The choice and route of administration must, however, be adapted to hemodynamic stability and ventricular function.
Secondary prevention of sudden death with an implantable cardioverter-defibrillator is indicated in many patients who survive ventricular fibrillation or sustained ventricular tachycardia not attributable to a completely reversible cause. An arrhythmia confined to the very early phase of an acute infarction, eliminated by reperfusion without a residual high-risk substrate, requires a different assessment from late scar-related tachycardia. The decision must therefore integrate timing, reversibility, coronary anatomy, ventricular function, and life expectancy.

For primary prevention, ejection fraction remains the most validated clinical parameter. Guidelines recommend an ICD in selected patients with ischemic heart disease at least 40 days after infarction, persistently reduced ejection fraction despite optimized medical therapy, and a reasonable expectation of survival with good functional status. Implantation very early after infarction has not demonstrated a reduction in total mortality because fewer arrhythmic deaths may be offset by nonarrhythmic deaths during the phase of greatest clinical instability.
CRT is not a therapy for ischemic arrhythmia itself. It is indicated in patients with heart failure, reduced ejection fraction, and specific features of electrical dyssynchrony, particularly left bundle branch block with a wide QRS, despite optimal therapy. In patients who also meet criteria for prevention of sudden death, a device with defibrillation capability is often used.

Catheter ablation is central to the treatment of recurrent scar-related monomorphic ventricular tachycardia. Mapping identifies slow-conduction channels, late potentials, and critical isthmuses; ablation aims to interrupt the circuit and modify the substrate. In patients with coronary artery disease and symptomatic recurrences or ICD shocks despite amiodarone, ESC guidelines favor ablation over simply escalating antiarrhythmic therapy.
Optimal treatment ultimately includes therapy for ischemic heart disease: control of atherogenic lipoproteins, antiplatelet therapy when indicated, management of blood pressure and diabetes, smoking cessation, treatment of heart failure, and revascularization of lesions causing ischemia. Reducing ischemic risk decreases future triggers, while heart failure therapy and reverse remodeling may modify arrhythmic risk over time.

Prognosis

Prognosis is heterogeneous and does not follow an obligatory progression from premature beats to tachycardia and then ventricular fibrillation. Many acute-phase arrhythmias disappear after reperfusion; others identify extensive myocardial damage; late scar-related tachycardias may instead recur for years. The risk of sudden death is greatest when severe ventricular dysfunction, heart failure, residual ischemia, or previous sustained ventricular arrhythmias coexist with the scar substrate.
The modern strategy therefore does not consist of suppressing every ectopic beat, but of distinguishing reversible triggers, structural substrate, and prognostic risk. Prompt defibrillation during the acute event, reperfusion when necessary, prognostic medical therapy, an ICD in appropriate patients, and ablation of recurrent tachycardias have transformed the management of ischemic arrhythmias, reducing mortality without exposing patients to indiscriminate and potentially proarrhythmic antiarrhythmic therapy.