Types of cardiac arrhythmias in patients with myocardial infarction

Full Text

Introduction

Heart rhythm disturbances (HRD) are registered in more than half of the cases among patients with myocardial infarction (MI), and in 25 % of cases arrhythmia appears in the first 24–48 hours from the development of ischemic symptoms [1]. Numerous studies have established a link between the occurrence of HRD and higher mortality in patients with MI [2; 3]. Modern advances in the diagnosis and treatment of patients with MI have led to a significant reduction in hospital mortality and improved long-term survival [4]. It was expected that with the widespread use of reperfusion strategies and the timeliness of percutaneous coronary interventions in patients with MI, it would be possible to reduce the electrophysiological heterogeneity of the myocardium, which significantly determines the occurrence of arrhythmias, and HRDs would not complicate the course of the peri-infarction period. However, the CARISMA and SMART-MI studies showed that patients after percutaneous coronary revascularization still frequently experience arrhythmias, which were recorded using implantable cardiac monitors, and a number of identified HRDs demonstrated an association with adverse cardiovascular outcomes [5; 6].

MI can be accompanied by all known variants of arrhythmia [5; 6]. The formation of areas of acute myocardial ischemia and necrosis, various neurohumoral effects on the myocardium in response to acute coronary hypoperfusion contribute to the progression of electrophysiological inhomogeneity of the myocardium, dispersion of refractoriness and create favorable conditions for the manifestation of electrical instability and the development of various variants of HRD [7–9]. Three main mechanisms are directly involved in the induction and maintenance of arrhythmias: re-entry, abnormal automatism, and trigger activity in patients with acute myocardial infarction (AMI) [9; 10].

As in the general population, all types of arrhythmias in patients with MI can be divided into supraventricular, ventricular, and bradyarrhythmias [7; 9; 11].

Supraventricular Arrhythmias

Supraventricular cardiac rhythm disturbances complicate MI in 2.44 % of cases, and their clinical significance remains controversial [12; 13]. Early studies suggesting that any supraventricular arrhythmia (sinus, atrial, atrioventricular nodal, atrioventricular reciprocating tachycardia) may be associated with adverse outcomes and was performed in the “pre-reperfusion” period [14; 15]. More recent data analyses have not confirmed the prognostic role of supraventricular arrhythmias for cardiovascular mortality [16; 17].

Atrial fibrillation (AF) is the most frequently recorded case of the supraventricular clinically significant arrhythmias that complicate the course of MI [13; 18]. Since the publication of the Framingham Study data, it has been known that MI is a risk factor for newly occurring AF, and further studies have convincingly demonstrated the unfavorable prognostic impact of newly registered AF in patients who have suffered acute coronary events [13]. The incidence of AF complicating MI ranges from 4 to 28 % of cases [18]. AF that first occurs during acute MI (AMI) can lead to acute negative hemodynamic disturbances, including shock, due to tachysystole, loss of atrial pumping contribution and atrioventricular synchrony, and, as a consequence, a decrease in the stroke volume of the left ventricle (LV), which, against the background of suppression of segmental contractility due to impaired coronary blood flow, contributes to a significant reduction in cardiac output, further worsening coronary hypoperfusion [13]. Therefore, the results of the meta-analyses were consistent with expectations: patients with AF have a significantly higher risk of adverse cardiovascular events compared to patients without AF [13; 18; 19]. Even in the absence of structural remodeling of the atria preceding the acute coronary event, which is an indisputable substrate and trigger for changes in the electrophysiological properties of the atrial myocardium and the appearance of re-entry foci in it, the mechanisms responsible for the development of AF accompanying AMI become an increase in pressure in the left atrium due to increased filling pressure of the LV due to its dysfunction (not only systolic, but also diastolic) [20]. An increase in left atrial pressure increases spontaneous ectopic activity at the pulmonary vein orifices, increasing the willingness to generate spontaneous activity [21]. This acutely developed situation in the first 24–48 hours of AMI, changes in intracardiac hemodynamics affect the excitability and refractoriness of atrial cardiomyocytes and can become a trigger for AF [22]. There is experimental evidence of a connection between the reduction of blood flow in the right and circumflex coronary artery basins, responsible for atrial perfusion and activation of re-entry and AF [23]. At later stages from the moment of MI development (48–72 hours), inflammation joins the listed mechanisms (the leading role belongs to cytokines produced by immune, vascular and interstitial tissues), sympathetic and parasympathetic influences are enhanced [22].

Data presented by J. Schmitt et al. showed that the occurrence of AF for the first time after AMI was an independent predictor of both in-hospital and long-term mortality [24]. New-onset AF after primary percutaneous coronary intervention (PCI) for ST-segment elevation acute coronary syndrome was a strong independent predictor of major bleeding (DR 1.74; 95 % CI 1.30–2.34; p = 0.0002) and other serious complications such as mortality (11.9 vs. 6.3 %; p = = 0.01), recurrent MI (16.4 vs. 7.0 %; p < 0.0001), stroke (5.8 vs. 1.5 %; p < 0.0001 [25]. Patients with AMI and AF, even in cases of successful restoration of sinus rhythm at the hospital stage, are at higher risk of stroke both in hospital and during subsequent observation [24; 25].

In contrast to the data on the fairly common occurrence of new-onset AF as a complication of AMI, isolated typical atrial flutter is rarely recorded (0.4% of cases), and is more often associated with MI involving the right ventricle [26]. However, in terms of its impact on outcomes, typical atrial flutter is apparently close to those in AF [16; 18].

Ventricular Arrhythmias

Sudden cardiac death (SCD) due to ventricular tachyarrhythmias remains a significant cause of death in patients with AMI, with highest rates in the first 30 days after the index event (1,4 %) [27]. Ventricular tachycardia (VT) and ventricular fibrillation (VF) most often occur in the early stages of ischemia. Approximately half of patients with AMI who died before hospitalization die precisely because of ventricular HRD [7]. In a study by N. Karam et. al. it was shown that one in 20 patients with acute coronary syndrome with ST elevation experiences SCD at the prehospital stage, which is associated with a 10-fold increase in mortality during the subsequent hospital period [28]. Ventricular HRD develops in 3.4–6 % of patients in the first 48 hours after the development of AMI [29]. Thus, patients with AMI who have registered potentially life-threatening variants of arrhythmia represent a special group with a significantly increased risk of mortality during the year of observation (from 7 to 20 %), and SCD due to VT or VF is the cause of death in 25–50 % of patients who have had AMI [30]. However, the substrate for ventricular arrhythmogenesis during and after acute coronary events has structural differences [31].

The main mechanisms of arrhythmogenesis that occur immediately after disruption / cessation (thrombosis) of blood flow in an infarct-related coronary artery include inhibition of oxidative phosphorylation in mitochondria, adenosine triphosphate deficiency, increased production of reactive oxygen species, anaerobic glycolysis and acidosis of the ischemic myocardium, increased concentrations of extracellular potassium, intracellular calcium, and accumulation of lysophosphatidylcholine, which leads to ionic imbalance, shorter duration of the action potential, preservation of residual membrane potential, decreased conduction velocity due to less functional gap junctions [31; 32]. An additional factor that aggravates the ionic imbalance of cardiomyocytes is an increase in the sympathoadrenal effect on the myocardium due to the activation of pain receptors and increased local release of catecholamines in the ischemic zone as a result of depolarization of afferent nerve endings caused by a decrease in oxygen delivery and the accumulation of K+ ions in the extracellular space, which reduces the effective electromechanical coupling of cardiomyocytes [33]. Reperfusion injury results in additional oxidative stress and calcium overload of myocardial cells [34]. All these mechanisms increase the likelihood of developing ventricular arrhythmias. The vast majority (about 75 %) of life-threatening arrhythmias (VT and VF) in acute ischemia occur via the re-entry mechanism, and the main trigger for re-entry arrhythmias is ventricular extrasystoles, primarily early ones, of the “R on T” type [31]. In addition, heart rate, QT interval duration, and transmural dispersion of repolarization are important for the induction of ventricular arrhythmias in patients with AMI [31; 34]. The electrophysiological features of ischemic tissue are quite complex, and the pathway for the implementation of the re-entry mechanism includes areas of myocardium with normal perfusion, with partially depolarized cardiomyocytes and with completely non-excitable areas that lead to conduction block [35]. The mechanisms of development of ventricular arrhythmias are presented in more detail in the works of V. Gorenek, S.M. Sattler, M. Oknińska, V.E. Oleynikov et al [31; 33–35].

Unsustained monomorphic VT is the most common form of prehospital ventricular arrhythmia, occurring in 1–7 % of cases, while sustained VT does not exceed 2–3 %, but its occurrence is more associated with the immediate and remote outcome of treatment of patients with AMI [4]. The prevalence of prehospital polymorphic VT is not precisely established, but its registration is associated with higher hospital mortality in patients with acute coronary syndrome [4]. Hemodynamic instability, cardiogenic shock, left ventricular (LV) ejection fraction (EF) below 40 %, and total ST segment deviation (in microvolts in all leads) are independent predictors of VT and VF development in patients with AMI [4].

Certainly, the frequency of ventricular arrhythmias associated with AMI has significantly decreased in recent years against the background of timely adequate reperfusion in the infarction-related artery basin, but VT and VF are still associated with increased mortality both during hospitalization with AMI and in the post-infarction period [30; 31]. According to modern studies, long-term mortality rates vary depending on the type of acute coronary syndrome (with or without ST elevation), the type of VT, the time from the onset of pain syndrome to hospitalization, the timeliness of reperfusion measures and the adequacy of drug therapy for AMI [31]. In addition, the area of ​​ischemic myocardial damage and the severity of acute heart failure also affect the frequency of ventricular arrhythmias and determine their impact on the short-term and long-term prognosis [36; 37; 38].

Despite the above data on the association of ventricular arrhythmias with a decrease in immediate and long-term survival, VT and VF that develop during acute coronary syndrome and require intensive care and resuscitation measures are not considered to be associated with an increase in the long-term risk of SCD, since the cause of these arrhythmias lies in acute myocardial ischemia, which is potentially reversible in the era of availability of early reperfusion strategies [39]. Furthermore, among patients with AMI and reduced LV EF, implantation of a cardioverter-defibrillator as a strategy for preventing SCD has not demonstrated a benefit in reducing mortality when implanted within the first 40 days after the index event [40]. However, modern data show a change in the vector of assessing the prognostic positions of ventricular arrhythmias recorded during AMI. A retrospective study including 8062 patients without significant heart failure after acute coronary events (patients with acute coronary syndrome with LV EF above 40 % were included, and the frequency of percutaneous coronary revascularization in the group of patients with life-threatening arrhythmias was 79.1 %, surgical revascularization – 10 %) showed that in patients with potentially fatal ventricular arrhythmias recorded during hospitalization for AMI, the risk of SCD in the long term is three times higher, compared with that in patients without ventricular НРС [41]. Certainly, additional studies are required to revise approaches to implantation of cardioverter-defibrillators in such patients for secondary prevention of SCD, including taking into account the principles of modern drug therapy used in patients who have had an AMI. However, it is already becoming clear that not only the massiveness of the scar field and the decrease in EF determine the likelihood of recurrence of ventricular arrhythmias in patients who have previously suffered an acute coronary event complicated by potentially fatal ventricular НРС [42].

Currently, there is an active search for additional criteria for more accurate risk stratification of adverse outcomes associated with ventricular НРС developing during acute coronary events [43]. Thus, the REFINE study identified patients with LV EF below 40 % in the first 48 hours from the onset of myocardial ischemia symptoms or with reduced LVEF of less than 50 % after 48 hours from the onset of AMI, with impaired baroreflex sensitivity, with higher QT interval dispersion, with significant T-wave alternans with suppressed rhythm variability and turbulence according to ECG monitoring data [44]. Further research in this direction will help to improve the identification of patients at risk of sudden arrhythmic events after AMI [43].

Ventricular Extrasystole

The incidence of ventricular extrasystoles (VES) reaches 93 % in patients with AMI [4]. The occurrence of VES may be a marker of electrical instability of the myocardium. VES has the potential to degenerate into sustained ventricular arrhythmias, including VF, and therefore VES has been identified as a possible risk factor for SCD in patients after MI [5; 7; 15; 17]. However, there is evidence that VES occurring in the first hours of AMI are not always associated with short-term and long-term outcomes [4]. The main difficulty is to identify potentially “malignant” VES. More than thirty years ago, J. Mukharji et al. conducted a study and found that frequent VES (more than 10 VES per hour) were associated with significantly higher mortality during a two-year follow-up after MI, especially in patients with reduced LV EF [45]. The GISSI-2 study also showed that VES were an independent risk factor for SCD in the first six months after AMI, particularly in patients with a frequency of more than 10 VES per hour, with polytopic, polymorphic, early (R on T), and paired extrasystoles [46].

As shown by the study conducted by L.M. Tsybikova et al., in patients with AMI who had rare, monotopic, late VES, the incidence of VF (primary and secondary) was about 4.1 %; in the presence of similar, but more frequent (more than one per minute) extrasystoles, VF was observed in 8 % of cases. VF was recorded somewhat more often in patients with polytopic (11.5 %), allorhythmic (13.7 %), group (15.6 %) and early (20 %) extrasystoles. However, with combinations of the above types of extrasystole, the incidence of VF increased sharply, reaching 34.9 % with a combination of two types, 65.6 % with three types, and 90 % with four types [47]. VES that persist for more than 48–72 hours after the onset of AMI symptoms may be associated with an increased risk of long-term complications [4].

Bradyarhythmias

Various bradyarrhythmias complicate the course of AMI in 1.78 % of cases [12]. Sinoatrial block occurs in 1.2–4 % of AMI cases and is often associated with damage to the right coronary artery [48]. High-degree atrioventricular (AV) block is of greatest interest from the point of view of the impact on the immediate and long-term prognosis (2nd degree, Mobitz 2 and complete AV block), detected in AMI in an average of 5 % of patients [19; 49; 50]. Patients who develop complete AV block are usually older and have a higher risk of cardiogenic shock, ventricular arrhythmias, and in-hospital mortality than patients without AV block [51; 52]. The frequency of detection of AV block in AMI of the inferior localization is 7.3–13 %, while in the case of anterior localization it is 3.6–4.9 % [53]. In cases where there is AMI with involvement of the right ventricle, the association of AV block and adverse hospital outcomes is most obvious [19].

A study of 4,799 patients with acute coronary syndrome with ST-segment elevation showed that the presence of AV block was associated with higher 30-day mortality, but there was no significant difference in mortality during one year of observation [54].

The mechanism of development of AV block differs depending on the localization of AMI.

The AV node is supplied with blood by the distal branches of the right coronary artery in 90 % of patients and by the distal parts of the left circumflex artery basin in 10 %. In general, conduction disturbances associated with myocardial damage to the inferior wall of the LV are primarily associated with ischemia or increased activity of the vagus nerve at the level of the AV node, and often these conduction disturbances are transient, especially when timely percutaneous coronary interventions are performed. In patients with left coronary artery disease and anterior AMI, AV block occurs below the AV node [55]. The listed features of the localization of ischemic myocardial damage are closely related to the negative immediate results of AMI treatment in patients with complete AV block: with anterior AMI, patients with AV block died 4 times more often during 30 days of observation than with AMI of inferior localization with AV block [55]. Complete AV block in anterior AMI, compared with inferior AMI, is associated with a more negative prognosis due to more massive myocardial damage, since it requires fairly extensive anterior septal necrosis involving the His bundle or its distal branches, which is possible with thrombotic occlusion of the left coronary artery [56]. This is why early reperfusion is of paramount importance in preventing the development of AV block in patients with AMI.

Conclusions

НРС complicates the course of AMI quite often. Improvement of electrical stability of the myocardium after timely and complete reperfusion reduces the number of potentially life-threatening ventricular and supraventricular arrhythmias. However, some of the variants of НРС have implications for both short- and long-term prognosis: AF, VT, VF, high-grade AV block requiring pacemaker implantation. In all cases, the ability to recognize these rhythms, understand their likelihood, and assess their associated risks improves preparedness and, hopefully, outcomes for a given cohort of patients.

About the authors

Ye. N. Orekhova

Ye.A. Vagner Perm State Medical University

Email: roman_rod2@mail.ru
ORCID iD: 0000-0002-7097-8771

DSc (Medicine), Associate Professor of the Department of Hospital Therapy and Cardiology

Russian Federation, Perm

Roman A. Rodionov

Ye.A. Vagner Perm State Medical University

Email: roman_rod2@mail.ru
ORCID iD: 0009-0009-3224-4628
SPIN-code: 8815-3190

Assistant of the Department of Hospital Therapy and Cardiology

Russian Federation, Perm

Olga V. Khlynova

Ye.A. Vagner Perm State Medical University

Email: olgakhlynova@mail.ru
ORCID iD: 0000-0003-4860-0112
SPIN-code: 2713-9138

DSc (Medicine), Professor, Corresponding Member of the Russian Academy of Sciences, Head of the Department of Hospital Therapy and Cardiology

Russian Federation, Perm

Natalya S. Karpunina

Ye.A. Vagner Perm State Medical University

Author for correspondence.
Email: karpuninapsma@mail.ru
ORCID iD: 0000-0003-3127-1797
SPIN-code: 6562-9930

DSc (Medicine), Associate Professor, Professor of the Department of Hospital Therapy and Cardiology

Russian Federation, Perm

References

Supplementary files