Predictors of ventricular tachyarrhythmia in high-risk myocardial infarction patients treated with primary coronary intervention

Background. We investigated the association between clinical characteristics, angiographic data and ventricular arrhythmia in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI) Methods. In patients with STEMI (n=225), a Holter analysis was performed the first 12 hours after primary PCI. Results. A total of 151 (66%) patients had ≥1 episode of ventricular tachycardia (VT). Age <70 years (RR 4.9, 95% CI 1.8 to 12.7), TIMI 0-1 pre-PCI (RR 2.6, 95% CI 1.1 to 6.1) and peak CK (RR 3.5, 95% CI 1.9 to 5.8) were independent predictors of VT. One-year mortality was 7%, no association between mortality and presence of early VT was found. Conclusion. Ventricular tachycardia is common in the first 12 hours after primary PCI for STEMI. Independent predictors of VT are younger age, TIMI 0-1 flow prior to PCI and larger infarct size. The presence of early VT was not significantly associated with one-year mortality. (Neth Heart J 2010;18:122-8.)     

Troponin elevation in patients with various tachycardias and normal epicardial coronaries

Troponin elevation is usually synonymous with acute coronary syndrome (ACS). Although sensitive for ACS, the elevation of serum troponin, in the absence of clinical evidence of ischemia, should prompt a search for other etiologies of myocardial necrosis. In fact, elevated values of troponin are correlated with myocardial necrosis even though it does not discriminate the mechanism involved. We report a series of seven patients (age range 18-67 years), who presented with complaints of chest discomfort and were found to have regular supraventricular tachycardia (5 patients) and one patient each with atrial fibrillation and ventricular tachycardia. All these patients had elevated troponin I and underwent coronary angiography that revealed normal epicardial coronary arteries. This is first case series in which all patients underwent coronary angiography and none of the patients was hemodynamically unstable at the time of presentation. Patients with elevated troponin due to conditions other than ACS can receive inappropriate and delayed definitive diagnosis and treatment.     

Catheter ablation of recurrent polymorphic tachycardia: Use of sodium channel blockade to organize the tachycardia: A case report

A 55 year old male presented with recurrent implantable cardioverter defibrillator (ICD) shocks due to polymorphic ventricular tachycardia (PMVT). He had undergone prior catheter ablation for VT three years ago. During the prior attempt he underwent voltage guided substrate ablation. With programmed ventricular extrastimulation (PVES), PMVT was repeatedly induced requiring DC shock. Intravenous procainamide was administered and PVES was repeated which induced sustained monomorphic ventricular tachycardia (MMVT). This VT had pseudo delta waves with maximum deflection index of 0.68, suggestive of epicardial origin. Activation mapping was performed epicardially. Presystolic potentials were recorded in mid anterolateral wall of left ventricular epicardial region. Radiofrequency (RF) ablation at this site terminated the VT. Post ablation there was no inducible tachycardia and patient is free of arrhythmias during 2 years of follow-up.     

Dronedarone for Recurrent Ventricular Tachycardia: A Real Alternative?

Sustained ventricular tachycardia (VT) is an important cause of morbidity and sudden death in patients with dilated cardiomyopathy. Although ICD effectively terminate VT episodes and improve survival, shocks reduce quality of life, and episodes of VT predict increased risk of heart failure and death despite effective therapy. Patients suffering recurrent VT episodes remain a challenge. Antiarrhytmic therapy reduces VT episodes, but it is associated with serious adverse events, and disappointing efficacy. Catheter ablation has emerged as an important option to control recurrent VT, but major procedure-related complications, and even death, are still issues to concern. And even with these armamentaria, some patients still have recurrent VT episodes and ICD shocks. We report on a patient with non-ischemic dilated cardiomyopathy and recurrent ventricular tachycardia resistant to multiple antiarrhytmic agents, in whom dronedarone was effective in completely suppressing ventricular tachycardia episodes.     

Ventricular tachycardia in the absence of structural heart disease

In up to 10% of patients who present with ventricular tachycardia (VT), obvious structural heart disease is not identified. In such patients, causes of ventricular arrhythmia include right ventricular outflow tract (RVOT) VT, extrasystoles, idiopathic left ventricular tachycardia (ILVT), idiopathic propranolol-sensitive VT (IPVT), catecholaminergic polymorphic VT (CPVT), Brugada syndrome, and long QT syndrome (LQTS). RVOT VT, ILVT, and IPVT are referred to as idiopathic VT and generally do not have a familial basis. RVOT VT and ILVT are monomorphic, whereas IPVT may be monomorphic or polymorphic. The idiopathic VTs are classified by the ventricle of origin, the response to pharmacologic agents, catecholamine dependence, and the specific morphologic features of the arrhythmia. CPVT, Brugada syndrome, and LQTS are inherited ion channelopathies. CPVT may present as bidirectional VT, polymorphic VT, or catecholaminergic ventricular fibrillation. Syncope and sudden death in Brugada syndrome are usually due to polymorphic VT. The characteristic arrhythmia of LQTS is torsades de pointes. Overall, patients with idiopathic VT have a better prognosis than do patients with ventricular arrhythmias and structural heart disease. Initial treatment approach is pharmacologic and radiofrequency ablation is curative in most patients. However, radiofrequency ablation is not useful in the management of inherited ion channelopathies. Prognosis for patients with VT secondary to ion channelopathies is variable. High-risk patients (recurrent syncope and sudden cardiac death survivors) with inherited ion channelopathies benefit from implantable cardioverter-defibrillator placement. This paper reviews the mechanism, clinical presentation, and management of VT in the absence of structural heart disease.     

Interaction between left ventricular wall motion and intraventricular flow propagation in acute and chronic ischemia

Myocardial ischemia has been associated with left ventricular (LV) postsystolic shortening. The combination of tissue Doppler imaging and high frame-rate acquisition of two-dimensional color flow makes it possible to study the interaction between LV wall motion and intraventricular flow propagation. The aim of this study was to examine in a clinical model the impact that acute myocardial ischemia and prior myocardial infarct might have on LV flow patterns and to explain the underlying mechanisms from the tissue Doppler data. LV flow propagation and tissue velocities during early diastole were studied in 18 healthy individuals, 17 patients with prior anterior myocardial infarct, and 16 patients before and during percutaneous coronary intervention (PCI) of the left anterior descending artery. Normal individuals had intraventricular flow propagation toward the apex during isovolumic relaxation. During this early diastolic time phase, myocardial velocities measured at mid- and apical septal segment were directed away from the apex. Before PCI, patients without myocardial infarction had similar findings as in normal individuals. In contrast, each patient with either prior myocardial infarction or PCI-induced acute ischemia had flow propagation opposite to normal individuals, and tissue velocities reversed toward the apex during early diastole. Reversal of early diastolic LV flow propagation in acute and chronic anterior myocardial ischemia reflects postsystolic shortening in the dyskinetic apical and septal myocardial segments.     

Cholera toxin enhances ischemia-induced arrhythmias in the isolated rat heart--involvement of a guanine nucleotide binding protein (Gs)

Cholera toxin (CTX) at a dose, which disturbed the intestinal functions, was administered into the rat via the tail vein. At 3 hr after injection, the heart was removed and perfused or subject to global ischemia in the Langendorff isolated heart preparation. Electrocardiogram (ECG) was recorded throughout the experiment. The myocardial cAMP content was measured in the intact non-ischemic heart, and in the isolated ischemic heart at 2.5, 5 and 10 min after ischemia. It was found that the incidence and severity of malignant ventricular arrhythmias including ventricular tachycardia (VT) and ventricular fibrillation (VF) was significantly increased during ischemia in the CTX treated group. The cAMP content was also significantly increased in the CTX treated group in both intact non-ischemic and ischemic hearts, indicating an activation of the guanine nucleotide regulatory protein (Gs). The results of the present study provide evidence that activation of Gs during ischemia may also contribute to the genesis of arrhythmia.     

Cardiac spinal deafferentation reduces the susceptibility to sustained ventricular tachycardia in conscious rats

The response to myocardial ischemia is complex and involves the cardio-cardiac sympathetic reflex. Specifically, cardiac spinal (sympathetic) afferents are excited by ischemic metabolites and elicit an excitatory sympathetic reflex, which plays a major role in the genesis of ventricular arrhythmias. For example, brief myocardial ischemia leads to ATP release, which activates cardiac spinal afferents through stimulation of P2 receptors. Clinical work with patients and preclinical work with animals document that disruption of this reflex protects against ischemia-induced ventricular arrhythmias. However, the role of afferent signals in the initiation of sustained ventricular tachycardia has not been investigated. Therefore, we tested the hypothesis that cardiac spinal deafferentation reduces the susceptibility to sustained ventricular tachycardia in adult (12-15 wk of age), conscious, male Sprague-Dawley rats. To test this hypothesis, the susceptibility to ventricular tachyarrhythmias produced by occlusion of the left main coronary artery was determined in two groups of conscious rats: 1) deafferentation (bilateral excision of the T1-T5 dorsal root ganglia) and 2) control (sham deafferentation). The ventricular arrhythmia threshold (VAT) was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. Results document a significantly higher VAT in the deafferentation group (7.0 ± 0.7 min) relative to control (4.3 ± 0.3 min) rats. The decreased susceptibility to tachyarrhythmias with deafferentation was associated with a reduced cardiac metabolic demand (lower rate-pressure product and ST segment elevation) during ischemia.     

Ventricular noncompaction and long QT syndrome – A deadly double hit for the foetus

Congenital long QT syndrome [LQTS] is a channelopathy characterized by QT prolongation and polymorphic VT. LQTS however need not be a purely electrical disease. Defects in ion channels may cause myocardial architectural disruption leading to ventricular non compaction [VNC]. It is defined as the presence of prominent ventricular trabeculations and deep intertrabecular recesses within the endomyocardium. We describe the in-utero management of a foetus who was later found to have LQTS with VNC. The detection of ventricular tachycardia and complete heart block in utero should arouse the suspicion of LQTS. It would be wise to avoid QT prolonging antiarrhythmics in this subset of patients.     

Indications for admission to a coronary care unit in patients with unstable angina.

One hundred cases with an admission diagnosis of acute coronary insufficiency or unstable angina were reviewed to establish criteria for admission to a coronary care unit. Myocardial infarction was subsequently diagnosed in 20 of the patients. Ventricular tachycardia occurred in 16 patients and ventricular fibrillation in 1 patient. Clinical features found to predict an increased risk of myocardial infarction included chest pain for more than 30 minutes within 24 hours prior to admission, new nonspecific electrocardiographic abnormalities consistent with ischemia, and diaphoresis. All patients with ventricular tachydysrhythmias had presented with both prolonged chest pain prior to admission and new electrocardiographic changes. The sensitivity, specificity and predictive value of various clinical criteria for identifying patients likely to have a myocardial infarction were calculated, and criteria with very high (greater than 90%) sensitivity were identified. These could be used to establish which patients are at increased risk of myocardial infarction and therefore require admission to a coronary care unit.     

The role of prostaglandins in the antiarrhythmic effect of ischemic preconditioning

The role of prostaglandins in the antiarrhythmic effect of ischemic preconditioning (IP) was investigated in pentobarbital-anesthetized rats. In 5 unpreconditioned control rats, 30 min of occlusion of the left coronary artery elicited ventricular tachycardia (VT) and fibrillation (VF), with an average duration of VT and VF of 51 +/- 6 and 43 +/- 4 s, respectively. Frequent ventricular premature beats (VPBs; average 1,249 +/- 145) were also documented in these animals. Thirty minutes of reperfusion after the prolonged coronary occlusion in these animals caused more severe arrhythmias, including irreversible VF. In animals pretreated with IP (n = 5), which was achieved by 3 cycles of 3 min of occlusion followed by 5 min of reperfusion, 30 min of coronary artery occlusion caused neither VT nor VF, but occasional VPBs (average 2 +/- 1, p < 0.001 vs. control). Only occasional VPBs were observed during 30 min of reperfusion in this group. In animals pretreated with indomethacin (1 mg/kg i.v., n = 5) followed by IP, prolonged ischemia and reperfusion led to frequent VPBs but no VT or VF. The average number of VPBs during ischemia and reperfusion in this indomethacin-treated group was less than that of the controls but greater than the IP-only group (p < 0.01). In conclusion, prostaglandins appear to play a role in the protective effect of IP against VPBs during acute ischemia and reperfusion.     

定量组织速度成像预测心肌梗死PCI 术后心功能不全的研究

目的:应用定量组织速度成像技术(QTVI)检测经皮冠状动脉介入治疗(PCI)后的ST段抬高的急性心肌梗死(STEMI)患者左心室收缩功能的改变;评价QTVI指标对该类患者未来发生心力衰竭的预测价值。方法:选择行急诊PCI术治疗的冠状动脉单支病变的急性心肌梗死患者,术后一周测量患者的左心室射血分数(LVEF),LVEF<50%者排除,LVEF≥50%者入选。共38例。并设正常对照组30例。入选者继续测二尖瓣环室间隔侧和左室侧壁侧QTVI曲线上心室收缩期速度峰值(Sa),并计算左室平均收缩期速度峰值(mean Sa)。术后12个月随访,查LVEF。结果:PCI术12个月后有17位患者LEVF<50%,21位患者LEVF≥50%。入选的STEMI者术后7天的左室平均Sa波峰值低于正常对照组。术后12个月出现LVEF减低(<50%)的患者,其术后7天的左室平均Sa波峰值低于PCI术12个月后LVEF正常的患者(P<0.01)。结论:通过QTVI检测二尖瓣环的运动速度能够早期发现单支病变所致的急性心肌梗死患者在急诊PCI术后的左心室功能受损;PCI术后LVEF正常的STEMI患者,术后7天QTVI测得的左室平均Sa波峰值减低可能预示着将来发展为LVEF减低的左心室收缩功能不全。     

Ventricular tachycardia due to cardiac ischaemia: assessment by exercise electrocardiography

Although ventricular tachycardia is a well-known complication of myocardial ischaemia and may be provoked by exercise, many patients may appreciate only the angina and be unaware of the unduly rapid heart rate that precipitates it. Exercise testing is needed to show this arrhythmia and to enable treatment to be started.Twenty-three patients were found to have chronic ischaemic heart disease complicated by ventricular tachycardia. Six patients with old myocardial infarction had ventricular tachycardia at rest which required conversion to sinus rhythm; 17 patients developed ventricular tachycardia only when they exercised. In 12 of these 17 patients coronary angiography showed disease of the anterior descending branch of the left coronary artery; other vessels were usually also affected. Although beta-adrenergic blocking drugs increased exercise tolerance, ventricular tachycardia still occurred when the heart rate on exercise reached a level similar to that before treatment. In five patients coronary artery bypass surgery was performed because of angina and exercise-induced ventricular tachycardia. Exercise tolerance was increased in all three patients who underwent exercise tests after operation, and in two of these patients, both of whom were known to have patent grafts, ventricular tachycardia was abolished.If part of the beneficial effect of coronary bypass surgery is preventing life-threatening ventricular arrhythmias it is essential to detect these, and ambulatory monitoring and stress testing have a complementary role.     

Radiofrequency ablation for post infarction ventricular tachycardia

Radiofrequency ablation has an important role in the management of post infarction ventricular tachycardia. The mapping and ablation of ventricular tachycardia (VT) is complex and technically challenging. In the era of implantable cardioverter defibrillators, the role of radiofrequency ablation is most commonly reserved as an adjunctive treatment for patients with frequent, symptomatic episodes of ventricular tachycardia. In this setting the procedure has a success rate of around 70-80% and a low complication rate. With improved ability to predict recurrent VT and improvements in mapping and ablation techniques and technologies, the role of radiofrequency ablation should expand further.     

Mechanically induced electrical storm as a complication of cardiac resynchronization therapy: A case report

BackgroundCardiac resynchronization therapy (CRT) has been shown to improve both the functional status and mortality of heart failure patients with left bundle branch block. Multiple recent studies suggest several mechanisms for proarrhythmia associated with CRT device.Case summaryA 51-year-old male with symptomatic non-ischemic cardiomyopathy and no previous history of ventricular arrhythmias underwent placement of a biventricular cardioverter-defibrillator. The patient developed sustained monomorphic ventricular tachycardia (VT) soon after implantation. The VT recurred despite reprogramming to right ventricular only pacing. The electrical storm resolved only after a subsequent discharge from the defibrillator caused inadvertent dislodgement of the coronary sinus lead. No recurrent VT occurred throughout 10-years follow up after urgent coronary sinus lead revision.DiscussionWe describe the first reported case of mechanically induced electrical storm due to the physical presence of the CS lead in a patient with a new CRT-D device. It is important to recognize mechanical proarrhythmia as a potential mechanism of electrical storm, as it may be intractable to device reprogramming. Urgent coronary sinus lead revision should be considered. Further studies on this mechanism of proarrhythmia are needed.     

Effect of 6-wk estrogen withdrawal or replacement on myocardial ischemic tolerance in rats

Menopausal status is a risk factor for coronary artery disease death, but the mechanism underlying this association is uncertain. To test whether estrogen ameliorates the effects of acute myocardial ischemia in ways likely to translate into a mortality difference, we compared the response to brief (6-min) and prolonged (45-min) coronary occlusion in vivo in five groups (each n = 16) of rats: ovariectomized females; ovariectomized females after 6 wk 17beta-estradiol replacement; male rats supplemented with estradiol for 6 wk; normal males; and normal females. Coronary occlusion produced a uniform ischemic risk area averaging 53 +/- 3% of left ventricular volume. After a brief occlusion, reperfusion ventricular tachycardia/fibrillation occurred with >85% frequency in all groups. During a prolonged occlusion, ischemic ventricular tachycardia occurred in 100% and sustained tachycardia requiring cardioversion in >75% of rats in all groups. Myocardial infarct size averaged 52 +/- 4% of the ischemic risk area and was similarly unaffected by gender or estrogen status. We conclude that neither short-term estrogen withdrawal, replacement, nor supplementation significantly affects the potentially lethal outcomes from acute coronary occlusion in this species.     

Identification of patients with coronary artery disease using magnetocardiographic signal analysis.

INTRODUCTION: Magnetocardiography (MCG), which measures the magnetic component of the heart's electrical activity, offers an alternative approach for analyzing changes induced by coronary artery disease (CAD). This study examines several parameters that quantify spatial and temporal aspects of cardiac magnetic signals in CAD. MATERIALS AND METHODS: MCGs were registered at rest in 144 subjects, aged 58.3 +/- 9.8 years: 50 healthy subjects, 43 CAD patients without myocardial infarction (MI), 36 with MI, and 15 with spontaneous episodes of ventricular tachycardia (VT). Spatial characteristics of magnetic field maps (MFM), quantified using their centers of gravity, included MFM orientation and trajectory plots. Spatio-temporal analysis was performed by determining the spatial distribution of the QT interval. RESULTS: In CAD patients, MFM orientation during the QT interval deviated from normal in 67% of patients without MI and in 85% of patients with MI. Trajectory plots deviated from those of the normal group, with deviation increasing with disease severity. Quantifying the distribution of QT interval duration using a smoothness index demonstrated a significant difference between the values for healthy subjects and non-MI patients, as well as MI patients with and without VT (p < 0.001). CONCLUSION: The results reported demonstrate that disturbances in cardiac electrogenesis resulting from CAD may be assessed using MCG signal analysis.     

Susceptibility to ischemia-induced arrhythmias and the effect of preconditioning in the diabetic rat heart

Diabetic heart is suggested to exhibit either increased or decreased resistance to ischemic injury. Ischemic preconditioning suppresses arrhythmias in the normal heart, whereas relatively little is known about its effects in the diseased myocardium. Our objective was to investigate whether development of diabetes mellitus modifies the susceptibility to ischemia-induced arrhythmias and affects preconditioning in the rat heart. Following 1 and 9 weeks of streptozotocin-induced (45 mg/kg, i.v.) diabetes, the hearts were Langendorff-perfused at constant pressure of 70 mm Hg and subjected to test ischemia induced by 30 min occlusion of the left anterior descending (LAD) coronary artery. Preconditioning consisted of one cycle of 5 min ischemia and 10 min reperfusion, prior to test ischemia. Susceptibility to ischemia-induced arrhythmias was lower in 1-week diabetics: only 42 % of diabetic hearts exhibited ventricular tachycardia (VT) and 16 % had short episodes of ventricular fibrillation (VF) as compared to VT 100 % and VF 70 % (including sustained VF 36 %) in the non-diabetics (P<0.05). Development of the disease was associated with an increased incidence of VT (VT 92 %, not significantly different from non-diabetics) and longer total duration of VT and VF at 9-weeks, as compared to 1-week diabetics. Preconditioning effectively suppressed arrhythmias in the normal hearts (VT 33 %, VF 0 %). However, it did not provide any additional antiarrhythmic protection in the acute diabetes. On the other hand, in the preconditioned 9-weeks diabetic hearts, the incidence of arrhythmias tended to decrease (VT 50 %, transient VF 10 %) and their severity was reduced. Diabetic rat hearts are thus less susceptible to ischemia-induced arrhythmias in the acute phase of the disease. Development of diabetes attenuates increased ischemic tolerance, however, diabetic hearts in the chronic phase can benefit more from ischemic preconditioning, due to its persisting influence.     

Ischemic Ventricular Tachycardia Presenting as a Narrow Complex Tachycardia

This report describes a patient presenting with a narrow complex tachycardia in the context of prior myocardial infarction and impaired ventricular function. Electrophysiological studies confirmed ventricular tachycardia and activation and entrainment mapping demonstrated a critical isthmus within an area of scar involving the His-Purkinje system accounting for the narrow QRS morphology. This very rare case shares some similarities with upper septal ventricular tachycardia seen in patients with structurally normal hearts, but to our knowledge has not been seen previously in patients with ischemic heart disease.