Case report: alternating exit sites in reentry circuit of ventricular tachycardia with nonischemic cardiomyopathy - relationship between ablation site and inner loop.

We present a patient with nonischemic cardiomyopathy who had ventricular tachycardia (VT) with QRS morphology alternans. VTs of two QRS morphologies (VT1 and VT2) exhibiting a right bundle branch block pattern with inferior axis was induced by ventricular pacing. The morphology of the QRS complex during VT1 exhibited more distinctively inferior axis than those during VT2. Induced VTs had similar morphologies to clinically the documented VTs. Pacemapping at anterolateral site of the left ventricle during sinus rhythm produced the same QRS complex of VT1 in a surface 12-lead electrocardiogram. A mapping study was performed with an electrode catheter located at the same site of LV during sustained VT1. The analysis of the local electrograms and postpacing interval during concealed entrainment at the catheter mapping revealed this pacing site was at the inner loop of the reentry circuit. Radiofrequency catheter ablation was performed at this site. The morphology of VT1 changed to different QRS morphology (VT2) during the first delivery of radiofrequency energy and was terminated after 20 seconds of the application. Then VT with alternans of QRS morphology and cycle length of VT1 and VT2 was induced by ventricular pacing, and was abolished by the second application of radiofrequency energy at this same site, suggesting that this site was located in the exit site close to inner loop of the reentry circuit and the alternans of QRS morphology was linked to the change of exit site.

Polymorphic ventricular tachycardia in patients with vasospastic angina--clinical and electrocardiographic characteristics and long-term outcome.

There have been few clinical studies exploring the characteristics of spontaneous polymorphic ventricular tachycardia (VT) during a vasospastic angina attack. During a 4-year recruitment period, Holter ECG recordings were monitored for 42+/-24 h during a drug-free period in 60 consecutive patients with vasospastic angina (VSA) and of these, 8 patients had at least one episode of polymorphic VT during monitoring. Ischemic ST segment elevation was immediately preceded the spontaneous polymorphic VT in all 8 patients, 4 of whom had silent coronary vasospasm. Immediately before the onset of polymorphic VT, both R-on-T and long-short sequences were observed in 4 of the 8 patients and ST wave alternans were recorded in 2 patients. VT exhibited a pattern of torsade de pointes in 4 of the 8 patients. Five patients underwent electrophysiologic testing during a drug-free asymptomatic phase, and polymorphic VT was induced in 2 of the 5 patients, with one developing ventricular fibrillation. During a follow-up period of 73+/-17 months, there was a significant difference in the incidence of sudden death between patients with and without VT (2/8 cases [25%] vs 0/52 [0%]; p<0.01). Thus, vasospastic attacks, even if asymptomatic, that immediately precede the development of polymorphic VT may be associated with a repolarization abnormality and an increased risk of sudden death.

Coronary artery spasm induced by carotid sinus massage.

A 60 year old man with a history of frequent episodes of chest pain and dizziness was referred for evaluation of coronary artery disease. He had no significant coronary artery stenosis at baseline coronary angiography. A carotid sinus massage was performed for evaluation of carotid sinus hypersensitivity in the patient. Both heart rate and blood pressure decreased a little, and returned to baseline level immediately after carotid sinus massage. However, 2.5 minutes after carotid sinus massage, ECG showed ST segment elevation in leads II, III, and aVF. Four minutes after carotid sinus massage, he had chest pain with a progressive elevation in the ST segment in the same leads, when he had 99% focal spasm in the right coronary artery. The vasospasm induced by carotid sinus massage was reproducible over several minutes and resolved spontaneously. Coronary artery spasm may be provoked by the enhanced vagal activation due to carotid sinus massage.

Effect of dipyridamole on QT dispersion in vasospastic angina pectoris.

Life-threatening ventricular arrhythmias have frequently been documented in patients with vasospastic angina. Moreover, the incidence of ventricular arrhythmias has been closely associated with increased QT dispersion. However, the underlying mechanism responsible for this arrhythmogenesis has not been clarified. The effects of dipyridamole and subsequent aminophylline administration on QT dispersion were examined in 35 patients with vasospastic angina and 30 patients with atypical chest pain. None of the patients enrolled in this study revealed any significant stenosis in coronary angiography. QT dispersion during dipyridamole followed by aminophylline administration was compared between the 2 groups. The baseline QT dispersion was similar in both groups (vasospastic angina: 27 +/- 8 ms; atypical chest pain: 28 +/- 7 ms). No significant changes in QT dispersion were observed in patients with atypical chest pain by dipyridamole (23 +/- 9 ms) and subsequent aminophylline administration (23 +/- 5 ms). However, the QT dispersion in patients with vasospastic angina increased significantly by dipyridamole administration (53 +/- 14 ms, p <0.0001) and returned to baseline by subsequent aminophylline administration (26 +/- 10 ms). Our data suggest that the disparity of ventricular repolarization in vasospastic angina may be mediated by increased endogenous adenosine.

Increased QTc dispersion predicts lethal ventricular arrhythmias complicating coronary angioplasty.

This study found that increased QT dispersion just before angioplasty is an useful marker to predict the risk for lethal ventricular arrhythmias during angioplasty. The fact that successful coronary revascularization decreased QT dispersion suggested that a part of increased QT dispersion is related to myocardial ischemia.

Increased QT dispersion in patients with vasospastic angina.

BACKGROUND: The risk factors for ventricular arrhythmias in patients with coronary vasospasm have not been identified. We evaluated QT dispersion in patients with vasospastic angina and its relation to susceptibility to ventricular arrhythmias during myocardial ischemia and reperfusion. METHODS AND RESULTS: We assessed the corrected QT (QTc) dispersion before induction of coronary artery spasm by intracoronary injection of acetylcholine (baseline) and 30 minutes after administration of isosorbide dinitrate in 50 patients with vasospastic angina and 50 patients with atypical chest pain. The baseline QTc dispersion was significantly greater in patients with vasospastic angina than in patients with atypical chest pain (mean+/-SD: 69+/-24 versus 44+/-19 ms, 95% confidence interval of mean difference [CI]: 16 to 33 ms; P<0.001). QTc dispersion decreased significantly, to 48+/-15 ms (CI: 15 to 26 ms; P<0.001 versus baseline), after administration of isosorbide dinitrate in patients with vasospastic angina but did not change significantly in patients with atypical chest pain (mean+/-SD: 41+/-17 ms, CI: -3 to 9 ms). During the provocation test, 24 of 50 patients with vasospastic angina experienced ventricular arrhythmias. The baseline QTc dispersion was significantly greater in patients with than without ventricular arrhythmias (mean+/-SD: 77+/-23 versus 61+/-19 ms, CI: 4 to 26 ms; P<0.05). CONCLUSIONS: Patients with vasospastic angina exhibited an increased baseline QTc dispersion compared with patients with atypical chest pain, which suggests that inhomogeneity of repolarization and susceptibility to ventricular arrhythmias are increased in patients with vasospastic angina, even when asymptomatic. The association between increased QTc dispersion and ventricular arrhythmias during the provocation test suggests that measurement of QT dispersion may help predict which patients with vasospastic angina are at high risk for ventricular arrhythmias during ischemia.

Adrenocorticotropic hormone-secreting pheochromocytoma.

A 41-year-old female had pheochromocytoma which secreted adrenocorticotropic hormone (ACTH). She was admitted to our hospital because of weight loss and excessive sweating. Not only urinary metanephrine but also plasma ACTH was extremely high. An abdominal echogram showed a cystic tumor in the left adrenal gland. An abdominal magnetic resonance imaging scan showed a hyperintense T2-weighted abnormality inside the tumor. Left adrenalectomy was done. The tumor consisted of benign pheochromocytoma cells diffusely stained with anti-ACTH antibody. The present case did not show any typical Cushingoid symptoms which are common in ACTH-secreting pheochromocytomas.

Demonstration of Purkinje potential during idiopathic left ventricular tachycardia: a marker for ablation site by transient entrainment.

During VT of QRS morphology with right bundle branch block and left axis deviation in a patient without obvious structural heart disease, entrainment by pacing from the right ventricular outflow tract and high right atrium was demonstrated. During entrainment of VT, a Purkinje potential preceding the QRS and recorded at the left ventricular mid-septum was activated by orthodromic impulses in the reentry circuit. The interval between the Purkinje potential and the earliest left ventricular activation was decrementally prolonged with shortening of pacing cycle length. Radiofrequency energy was applied to this site, resulting in successful elimination of VT. Therefore, the Purkinje potential represented activation by an orthodromic wavefront in the reentry circuit, while the orthodromically distal site to this potential showed an area of slow conduction with decremental property.

Induction of polymorphic ventricular tachycardia by programmed ventricular stimulation in vasospastic angina pectoris.

This study was designed to examine the ventricular vulnerability of patients with vasospastic angina. Fourteen patients (mean age 57 +/- 9 years) with vasospastic angina underwent electrophysiologic testing during the asymptomatic phase (baseline) and after the relief of acetylcholine-induced spasm with isosorbide dinitrates. Twenty patients without structural heart disease served as a control group. By programmed ventricular stimulation, polymorphic ventricular tachycardia (VT) was induced at baseline in 6 of 14 patients, with 1 patient developing ventricular fibrillation and 7 of 14 patients developing repetitive ventricular responses. After isosorbide dinitrate, polymorphic VT was induced in only 1 patient who had ventricular fibrillation at baseline. Repetitive ventricular responses were induced in 3 of 5 patients who had VT at baseline and in 4 of the 7 patients with repetitive ventricular responses at baseline. There was a significant difference in the incidences and severity of induced ventricular arrhythmias between the 2 phases (p <0.01). Among 20 control subjects, repetitive ventricular responses were induced only in 6 patients, but no VT was induced. There was a significant difference in the incidence of induced ventricular arrhythmias and VT at baseline between the vasospastic angina and control groups (p <0.001 and <0.01, respectively). Thus, patients with vasospastic angina had increased ventricular vulnerability, even during the symptom-free period without ischemic events, which could predispose to the development of life-threatening arrhythmias aggravated by vasospastic attacks.

Long-term follow-up of the reproducibility of carotid sinus hypersensitivity in patients with carotid sinus syndrome.

The reproducibility of carotid sinus hypersensitivity to carotid sinus massage was studied in the long-term follow-up of 8 patients with carotid sinus syndrome. A cardioinhibitory response was induced in 7 patients, while a vasodepressor response was found in the remaining patient. The 7 patients were treated with dual-chamber pacemaker implantation and the remaining patient was treated with propranolol. All of the patients remained asymptomatic during a follow-up period of 48 +/- 11 months. Carotid sinus massage during the follow-up period in patients with a cardioinhibitory response revealed asystolic intervals of 3 s or longer in 4 patients and in 3 patients at the second and third follow-up examinations, respectively, although there were no significant differences in the ventricular asystolic intervals between before, and 34 +/- 11 months and 48 +/- 11 months after treatment. However, each patient showed a wide variation in asystolic intervals. The differences in asystolic intervals between prior to treatment (first) and the third test were significantly greater than those between the first and the second test (2.4 +/- 1.2 s vs 0.7 +/- 0.6 s; p < 0.05). The one patient with a vasodepressor response had a decreased systolic blood pressure greater than 50 mmHg by carotid sinus massage at all three occasions. In conclusion, most patients with carotid sinus syndrome showed abnormal and variable responses to carotid sinus massage during long-term follow-up period although there was no recurrence of symptoms after treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Multiple kinetic effects of beta-adrenergic stimulation on single cardiac L-type Ca channels.

During beta-adrenergic stimulation, several different mechanisms are known to modulate single cardiac L-type Ca channels, such as an increase in the proportion of nonblank sweeps (availability), graded changes in open and closed time constants, and potentiation of "mode 2" gating. To clarify the interrelationships of the above mechanisms in terms of "molecular modulation," we reevaluated the adenosine 3',5'-cyclic monophosphate-dependent increase in single cardiac Ca channel activity under conditions where all of the proposed mechanisms could take place. We observed considerable variations in the kinetic properties of basal channel activity among individual patches, presumably due to the diversity of intracellular metabolic conditions of individual myocytes. This made the contribution by each mechanism as described above variable from one patch to another. Increases in open probability during nonblank sweeps (associated with increased open time constant and/or promotion of mode 2 gating) were observed in patches were the increased nonblank rate was already established in the control state. In contrast with the report by D. T. Yue, S. Herzig, and E. Marban (Proc. Natl. Acad. Sci. USA 87: 753-757, 1990), graded changes in the open time constant could take place independently from the potentiation of mode 2 gating behavior. Our results suggest that the enhancement of cardiac L-type Ca channels during beta-stimulation involves multiple functional modulatory sites, which might be phosphorylated independently.

Arrhythmogenic effects of isoproterenol-activated Cl- current in guinea-pig ventricular myocytes.

Possible arrhythmogenic effects of the isoproterenol-activated Cl- current were examined in isolated guinea-pig ventricular myocytes under various intra- and extracellular Cl- concentrations. Experiments were carried out with external K+ concentration ([K+]o) decreased to 2 or 3 mM. Under symmetrical concentrations of Cl- in intra- and extra-cellular solutions (ECl = 0 mV), 1 microM isoproterenol (ISP) depolarized resting membrane potential (RMP) by 6.2 +/- 1.1 mV and slowed repolarization with induction of early afterdepolarizations (EADs) in 9 out of 9 cells. EADs appeared at voltages positive to -40 mV, where L-type Ca2+ current is assumed to be activated. When Cl- concentrations were settled near physiological conditions (ECl = -40 - -50 mV), ISP depolarized RMP by 2.8 +/- 0.4 mV and elicited abnormal repolarization with occasional EADs in 6 out of 19 cells. When ECl was set to -80 mV, however, ISP depolarized RMP by only 0.5 +/- 0.5 mV without induction of abnormal activities. Thus, depolarizing effects of ISP and incidence of repolarization abnormalities including EADs were increased as ECl shifted to more positive potential levels. At [K+]o = 4 mM, no abnormal activities were observed when ECl was around -50 mV (0/8), and 6 out of 6 cells showed abnormal activities when ECl was set to 0 mV. ISP-elicited abnormal activities were abolished by 1 mM DNDS (4,4'-dinitrostilbene-2,2'-disulphonic acid), a blocker for Cl- channels.(ABSTRACT TRUNCATED AT 250 WORDS)