Myocardial Infarction Ventricular Arrhythmias Research Articles

The autonomic nervous system and ventricular arrhythmias in myocardial infarction and heart failure

Ventricular arrhythmias (VA) can range in presentation from asymptomatic to cardiac arrest and sudden cardiac death (SCD). Sustained ventricular tachycardias/ventricular fibrillation (VT/VF) are a common cause of SCD in the setting of myocardial infarction (MI) and heart failure. A particularly arrhythmogenic cardiac syncytia in these conditions can be attributed to both sympathetic activation and parasympathetic dysfunction, while appropriate neuromodulation has the potential to reduce occurrence of VT/VF. In this review, we outline the components of the autonomic nervous system that play an important role in normal cardiac electrophysiology and function. In addition, we discuss changes that occur in the setting of cardiac disease including adverse neural remodeling and neurohormonal activation which significantly contribute to propensity for VT/VF. Finally, we review neuromodulation strategies to mitigate VT/VF which predominantly rely on increasing parasympathetic drive and blockade of sympathetic neurotransmission.

P6593Comparison of the termination effects between multi-segment continuous illumination and anti-tachycardia pacing on myocardial infarction ventricular arrhythmia

Abstract Introduction Anti-tachycardia pacing (ATP) therapy is an important treatment for current ICD termination of ventricular arrhythmia (VA). But there was concern about excessive frequency and voltage can cause arrhythmia, pain and damage. Optogenetic allowed modulation of electrical excitation with light in myocardium over-expressing light-sensitive protein, and optical illumination developed a non-contact and pain-free approach to research and treatment of cardiac disorder. Purpose Explore the effects of optogenetic termination and electric termination of myocardial infarction VA in vivo. Methods Rats (N=10) accepted jugular vein injection with 1×1012 vector genomes of (AAV-CAG-hChR2(H134R)-mcherry) to achieve cardiac transgenic expression of light sensitive protein Channelrhodopsin-2 (ChR2). After thoracotomy, myocardial infarction was induced by ligation of the left anterior descending coronary artery, and then VA was induced by electrical burst stimulation (10 v, 50 Hz, 2 s). Before the myocardial infarction operation, every heart was illuminated by 473 nm laser or electrical stimulated on the right ventricle in a train of 30 pulses at 8 HZ to test the threshold of light intensity or electrical pacing voltage. The VA termination process during 20 s after burst stimulation was investigated in different performance: optical termination, 1 s constant illumination repeated in 4 episodes with 1 s interval (470 nm, 20 times threshold intensity); electrical termination, ATP in 8 pulses of 8hz with 2ms duration in 4 times pacing threshold; natural recovery from VA, without optical or electrical intervention. Recovery time was defined as the time from the end of the burst stimulation to the recovery of sinus rhythm, and the termination rate was the percentage of sinus rhythm recovery among 11s after the end of burst stimulation with or without any intervention. Results We analyzed the recovery time and the termination rate (N=10, n=127 episodes per mode). The sequence of recovery time was optical termination (7.328±0.3623 s) < electric termination (10.31±0.4482 s) < natural recovery (12.97±0.3834 s) (figure D). We confirmed that the termination rate of optical illumination (86.14±4.145%) was higher than those of ATP (63.5±6.371%) and natural recovery (47.71±5.476%) (figure E), and there was no significant difference between the last two process (one-way of ANOVA; p=0.124). Comparison of three modes Conclusions Optogenetic manipulation shortened the recovery time and increased the termination rate in myocardial infarction ventricular arrhythmia, which may provide a potential approach for translational arrhythmia therapy. Acknowledgement/Funding The national natural science foundation of China (81772044)

THE RISK OF PREMATURE VENTRICULAR CONTRACTIONS DEPENDING ON PARAMETERS OF THE LEFT VENTRICULAR SYSTOLIC FUNCTION AMONG PATIENTS WITH ACUTE MYOCARDIAL INFARCTION

Despite the preventive measures taken to reduce the incidence of coronary heart disease, cardiovascular diseases remain the leading cause of death. In patients with acute myocardial infarction ventricular arrhythmias can be an important prognostic factor. Identifying of premature ventricular contractions (PVCs) predictors and stratifying the risk of life-threatening arrhythmias development are a complex clinical task.
 Purpose of the study. To determine the relative risk of premature ventricular contractions depending depending on the parameters of the left ventricular systolic function among patients with acute myocardial infarction.
 Material and methods. The results of the study are based on the data obtained from a comprehensive examination of 120 patients after STEMI: with premature ventricular contractions (86 patients) and without premature ventricular contractions (34 patients). Screening of patients was carried out at the base of Municipal institution «Regional medical center of cardiovascular diseases» of Zaporizhzhia Regional Council in the period from 2016 to 2017. All examined persons were comparable by age, social status and sex (the ratio of men to women was 4 to 1).
 Results and discussion. The largest area under the ROC curve (AUC = 0,76, 95% CI 0,668 to 0,829) among the analyzed parameters of systolic heart function had an indicator of the left ventricle ejection fraction (LF EF). At the cut-off point < 54,2% sensitivity was 57,0% and specificity 85,3%. In the group with STEMI and PVCs were 50 patients with LF EF below 54,2% and 36 ones above 54,2%, in the group STEMI without PVCs, 6 patients had LF EF below 54,2% and 28 ones had LF EF above 54,2% respectively. Relative risk was 1,59, 95% CI 1,26–2,01.

Exercise training reduces ventricular arrhythmias through restoring calcium handling and sympathetic tone in myocardial infarction mice.

Exercise can improve morbidity and mortality in heart failure patients; however, the underlying mechanisms remain to be fully investigated. Thus, we investigated the effects of exercise on cardiac function and ventricular arrhythmias in myocardial infarction (MI) induced heart failure mice. Wild‐type male mice underwent sham‐operation or permanent left coronary artery ligation to induce MI. MI mice were divided into a sedentary (MI‐Sed) and two intervention groups: MI‐Ex (underwent 6‐week treadmill exercise training) and MI‐βb (oral bisoprolol treatment (1 mg/kg/d) without exercise). Cardiac function and structure were assessed by echocardiography and histology. Exercise capacity and cardiopulmonary function was accepted as oxygen consumption at peak exercise (peak VO2). Autonomic nervous system function and the incidence of spontaneous ventricular arrhythmia were evaluated via telemetry recording. mRNA and protein expressions in the left ventricle (LV) were investigated by real‐time PCR and Western blotting. There were no differences in survival rate, MI size, cardiac function and structure, while exercise training improved peak VO2. Compared with MI‐Sed, MI‐Ex, and MI‐βb showed decreased sympathetic tone and lower incidence of spontaneous ventricular arrhythmia. By Western blot, the hyperphosphorylation of CaMKII and RyR2 were restored by exercise and β‐blocker treatment. Furthermore, elevated expression of miR‐1 and decreased expression of its target protein PP2A were recovered by exercise and β‐blocker treatment. Continuous intensive exercise training can suppress ventricular arrhythmias in subacute to chronic phase of MI through restoring autonomic imbalance and impaired calcium handling, similarly to that for β‐blockers.

Troponin and CRP as Indicators of Possible Ventricular Arrhythmias in Myocardial Infarction of the Anterior and Inferior Walls of the Heart.

Introduction:Heart rhythm disorders are quite common in the clinical course of acute myocardial infarction and have a significant influence on the prognosis of the disease.Aim:To investigate the type and frequency of ventricular arrhythmias in patients with acute myocardial infarction (AMI) by sex and age, according to localization of myocardial infarction, and correlated with troponin and C reactive protein (CRP).Material and Methods:A prospective, analytical, comparative clinical study was performed. A total of 100 patients was included who were hospitalized at the Clinic for Heart Disease and Rheumatism at the Clinical Center University of Sarajevo for a period of 6 months, of both sexes, aged from 20 to 90 years. The occurrence of ventricular arrhythmias, CRP and troponin, were observed in relation to the localization (anterior and inferior myocardial wall).Results:It was found that men are more represented in comparison to women and that the largest number of males were in the age group of 51-60 years of life and women in the age group of 71-80 years. It has been established that there is no significant difference between ventricular arrhythmia according to localization of AMI. By determining the mean CRP and troponin levels, a positive correlation was found between CRP and troponin values and recorded ventricular arrhythmias.Conclusion:There is a positive correlation between the troponin and CRP values and ventricular arrhythmias, not related to the localization of AMI, which is important in prevention and planning the treatment of complications of potentially malignant ventricular arrhythmias and fatal outcome at AMI.

Change of the main parameters of 24-hour ekg monitoring in patients with myocardial infarction associated with ventricular arrhythmias

Aim. To study the change of the main parameters of 24-hour EKG monitoring over time in patients with myocardial infarction associated with ventricular arrhythmias of different grades. Methods. The change of the echocardiography parameters, heart rhythm variability, corrected QT interval duration and dispersion, late ventricular potentials, heart rhythm turbulence were examined in 70 adult men (mean age 52.6±1.3 years) with primary Q-wave myocardial infarction on 10-14th day of the disease and after 6 months. Patients were assigned into 3 groups depending on ventricular arrhythmias severity (according to Lown classification modified by Ryan): А1 (n=29) - grade 1-2, А2 (n=23) - grade 3-4, А3 (n=18) - patients with paroxysmal ventricular tachycardia. Results. Presence of late ventricular potentials and pathologic heart rhythm turbulence in patients in acute period of myocardial infarction suggested high grade of ventricular arrhythmia. Ventricular arrhythmias were associated with severe sympathicotonia, prolongation of corrected QT interval and QT dispersion. 6 months after Q-wave myocardial infarction an autonomic imbalance increased and no positive changes of myocardial homogenicity parameters, late ventricular potentials and pathologic heart rhythm turbulence were observed with increasing ventricular arrhythmia grading and heart rate frequency. A relationship between left ventricle ejection fraction, myocardium mass and myocardial electric non-stability values was revealed. In patients with Q-wave myocardial infarction ventricular arrhythmias are mediated by several mechanisms: systolic and autonomic disorder, repolarization abnormalities, late ventricular potentials pathologic heart rhythm turbulence. The severity of abnormalities is marked by the ventricular arrhythmias grade. Conclusion. 6 months after myocardial infarction (in healing stage) the significant positive changes are found only in patients with 1-2 grades ventricular arrhythmias. The significant non-homogeneity of myocardial electrophysiological features still persists in patients with life-threatening ventricular arrhythmias.

Electrophysiologic effects of volatile anesthetics, sevoflurane and halothane, in a canine myocardial infarction model.

The effects of sevoflurane and halothane on the effective refractory period (ERP) and ventricular activation were examined in a canine myocardial infarction model. Sevoflurane (1 MAC) reduced the heart rate and prolonged ERP in both normal and infarcted zones. A prolongation of ERP with sevoflurane was observed also during atrial pacing at a fixed rate, but the effect was less than during sinus rhythm. Sevoflurane either further delayed or blocked the delayed activation entirely in the infarcted zones with only slight effects on the activation of the normal zones. Halothane (1 MAC) prolonged ERP during sinus rhythm and atrial pacing, but to a lesser extent during the latter. Halothane also depressed ventricular activation in the infarcted zone during atrial pacing. In conclusion, sevoflurane as well as halothane selectively depresed the delayed activation and the prolongation of ERP in myocardial infarction, which may inhibit ventricular arrhythmias in myocardial infarction.

Effects of volatile anesthetics, enflurane, isoflurane, and halothane on ventricular delayed activation in a canine myocardial infarction model

The authors examined the effects of volatile anesthetics (enflurane, isoflurane, and halothane) on ventricular activation in a canine myocardial infarction model. Enflurane at 1 minimum aveolar concentration further delayed or blocked delayed activation in the infarcted zones with only slight effects on activation of the normal zones. Halothane showed similar and comparable effects on ventricular activation to those of enflurane. Although isoflurane also showed similar effects, they were of a lesser extent. Enflurane and halothane, but not isoflurane, inhibited ventricular stimulation-induced arrhythmias. Thus, enflurane and halothane produced marked depression of delayed activation in myocardial infarction, which may affect, that is, inhibit or provoke, ventricular arrhythmias in myocardial infarction.

Effects of intravenous anesthetics, thiopental, fentanyl, and morphine on ventricular delayed activation in a canine myocardial infarction model.

We examined the effects of intravenous anesthetics (thiopental, fentanyl and morphine) on the ventricular activation in a canine myocardial infarction model. Thiopental at 5 and 10 mg/kg delayed or abolished the delayed activation in the infarcted zones with slight delay of activation of the normal zones. Fentanyl at 30 micrograms/kg slightly but significantly prolonged the activation time in both normal and infarcted zones. Morphine at 1 mg/kg did not produce any significant effect. Thiopental, but neither fentanyl nor morphine, inhibited ventricular stimulation-induced arrhythmias. Thus, thiopental, but not fentanyl nor morphine, markedly depressed the delayed activation in myocardial infarction, which may affect and probably inhibits the ventricular arrhythmias in myocardial infarction. It also should be kept in mind that thiopental may have arrhythmogenic effects in myocardial infarction.