P-wave indices in Japanese patients with ischemic stroke: Implication of atrial myopathy in subtype of ischemic stroke.

BACKGROUND: P-wave indices have been not fully studied in subtypes of ischemic stroke. We compared P-wave indices among embolic stroke, lacunar stroke and the control. METHODS: P-wave duration, advanced interatrial block (aIAB) defined as P-wave duration ≥120 ms and biphasic (positive negative) morphology in inferior leads, and P-terminal force in lead V1 (PTFV1) were measured at the time of the first episode of cardioembolic stroke in 81 patients with paroxysmal atrial fibrillation (PAF), and in 64 patients with lacunar stroke, and compared with 100 control subjects. The latter two groups had no episode of PAF. RESULTS: The age of participants was 76 ± 11 years. Age, sex distribution, body mass index and CHADS2 score were comparable among three groups. Maximum P-wave duration, the longest across 12 leads, was significantly prolonged in cardioembolic and lacuna stroke compared to the control; 118 ± 12 ms and 118 ± 11 ms vs. 110 ± 11 ms, respectively (P < 0.0001). P-wave duration ≥120 ms and aIAB were more prevalent in ischemic stroke groups than the control, and associated with a higher Odds ratio for stroke, more so in cardioembolic stroke. However, PTFV1 value and the prevalence of PTFV1 ≥ 4.0 ms·mV were significantly not different among the three groups. Abnormal P-wave duration and aIAB indicating the presence of atrial myopathy were present in cardioembolic and lacuna stroke. CONCLUSION: Atrial myopathy was present in cardioembolic and lacunar stroke, but it can't be the direct cause of small vessel occlusion in lacunar stroke. Roles of atrial myopathy in each subtype of ischemic stroke should be studied.

Asymptomatic Coronary Artery Disease in Japanese Patients With the Acute Ischemic Stroke.

OBJECTIVE: To investigate the prevalence and outcomes of asymptomatic coronary artery disease (CAD) in patients with the first episode of ischemic stroke. METHODS: Patients admitted to our hospital between November 2001 and January 2009 for the episode of an acute ischemic stroke/transient ischemic attack were included. Stress-Tl-201 scintigraphy was performed and followed by coronary angiography (CAG). The prevalence and risks for asymptomatic CAD, and long-term outcomes were studied. RESULTS: Of 1309 patients, only 15 (1.1%) patients presented with a history of CAD. Excluding 406 patients because of severity, systemic infection, early transfer to another hospital, or a refusal to participate, myocardial scintigraphy was performed in 903 patients (mean age, 72 ± 10 years, male 63.9%), and myocardial ischemia was diagnosed in 214 patients (23.7%). Of these patients, 76 patients underwent CAG, and showed significant stenosis (>75%) of a coronary artery in 61 (80.3%) patients. The risk factors for positive scintigraphy findings and CAG were high-grade premature complexes via Holter monitoring (P < .0001), enlarged left ventricle (P = .0051) and wall motion abnormalities (P = .0014) observed on echocardiography, and carotid artery stenosis observed in magnetic resonance angiography imaging (P < .0001). During the follow-up periods of 83 ± 47 months and of 91 ± 47 months, 17.2% of scintigraphy-positive and 2.8% of scintigraphy-negative patients developed episodes of myocardial ischemia, respectively (P < .001). CONCLUSIONS: Symptomatic CAD was rare in Japanese patients with the first episode of ischemic stroke, but asymptomatic CAD was identified by stress Tl-201 myocardial scintigraphy in one-quarter of the patients. Positive scintigraphy was associated with asymptomatic CAD and future cardiac events.

Successful Treatment of Acute Fulminant Eosinophilic Myocarditis in a Patient with Ulcerative Colitis Using Steroid Therapy and Percutaneous Cardiopulmonary Support.

A 47-year-old man with ulcerative colitis was transferred to our hospital due to progressive dyspnea. Electrocardiography on admission showed ST elevation in leads II, III, aVF, and V5-V6. Coronary angiography revealed no remarkable coronary stenosis, and left ventriculography showed a depressed left ventricular ejection fraction (EF) of 23%. Although the patient received percutaneous cardiopulmonary support, his EF progressively decreased (7-15%), and both ventricular tachycardia (VT) and high-degree atrial-ventricular block occurred. An endomyocardial biopsy showed eosinophilic infiltration in the myocardium. Steroid therapy improved the patient's EF. However, his severe inferior wall hypokinesis and non-sustained VT remained after the abovementioned treatment.

Secondly ECG recordings in the emergency room revealed Garenoxacin-induced abnormal QT interval prolongation in a patient with multiple syncopal attacks.

A 73-year-old woman first visited our emergency room with multiple syncopal attacks. Before admission, she had received an antibiotic (Garenoxacin) for 3 days from a local clinic. First electrocardiogram (ECG) showed no ST-segment deviation but mild QT interval prolongation with a positive U wave. Second ECG recording 3 h later showed slightly slower heart rate and revealed marked QTU interval prolongation suggesting the cause of her syncopal attacks. After cessation of Garenoxacin, the QTU interval prolongation shortened. However, both epinephrine infusion and treadmill exercise test reproduced similar QTU interval prolongation and T wave deformities. Later, genetic analysis demonstrated that this patient had a mutation in KCNH2 gene, and she was diagnosed as a type-2 long-QT syndrome which was accentuated by use of garenoxacin. At the emergency out-patient clinic, repetitive ECG recordings can be useful and should be considered in order to identify the cause of syncopal attacks in patients who were prescribed antibiotics and had mild QT interval abnormalities.

Ventricular Rhythm and Hypotension in a Patient with Pheochromocytoma-induced Myocardial Damage and Reverse Takotsubo Cardiomyopathy.

A 33-year-old woman experienced near-syncope at a hospital. Electrocardiography revealed an intermittent ventricular rhythm. The echocardiogram at admission indicated mild hypokinesis and severe diffuse hypokinesis with reverse takotsubo cardiomyopathy on the following day. The patient experienced abdominal pain on the admission day, and computed tomography identified a large left adrenal mass. Her catecholamine levels increased remarkably on the third day. The wall motion improved on the twelfth day. The tumor was successfully resected and the patient was diagnosed with an ectopic pheochromocytoma. The ventricular rhythm with myocardial damage and hypotension induced by the reverse takotsubo cardiomyopathy masked the characteristic symptoms of pheochromocytoma.

Characteristics of electrocardiographic repolarization in acute myocardial infarction complicated by ventricular fibrillation.

BACKGROUND AND PURPOSE: Some de- and re-polarization patterns can reflect an increased risk of ventricular tachyarrhythmias. We studied whether some electrocardiographic (ECG) patterns are able to predict the development of ventricular fibrillation (VF) during acute myocardial infarction (MI). METHODS: We compared the patterns of ST-T segment of 78 patients who developed VF during acute MI (patient with VF) vs 170 comparable patients with acute MI but with no VF complications. RESULTS: Of the VF group, 47 developed out-of-hospital VF and 31 developed VF after their admission to the hospital. A steep downsloping ST segment toward a negative T wave with or without a short, flat, or rising portion at the initial portion was observed in 69.2% of the 78 patients: 61.3% in patients with pre-VF and 74.5% in patients with post-VF, vs 9.4% of patients who did not develop VF (P < .0001). In 90.6% of the latter, a typical upward-concave or convex "ischemic" pattern of the ST segment was observed. Thus, the characteristic ST-T patterns were highly associated with VF with a specificity greater than 90%. CONCLUSIONS: A steep downsloping ST segment may characterize the ECGs of patients who develop VF during acute MI.

Recurrence of ventricular fibrillation in a patient with non-type 1 Brugada electrocardiographic morphology.

A healthy 25-year-old man suffered from loss of consciousness due to ventricular fibrillation (VF). Emergency services required multiple cardioversion to restore sinus rhythm. Repeated electrocardiographic (ECG) recordings after admission showed non-type 1 Brugada ST-segment elevation in V1 and V2. Intravenous pilsicainide infusion augmented the ST-segment elevation but its morphology did not represent type-1 ECG. Intravenous administration of isoproterenol normalized the ST-segment elevation, and programmed electrical stimulation induced VF. Spontaneous VF recurred 1 year after introduction of implantable cardioverter defibrillator. Non-type 1 ST-segment elevation, to which pharmacological responses are similar to Brugada syndrome, may be used as a hallmark of ventricular tachyarrhythmia.

Pilsicainide-induced ST segment elevation and ST segment depression in two patients with variant forms of Brugada-type electrocardiographic abnormalities.

In two patients with variant forms of Brugada electrocardiographic abnormalities, ST segment elevation, and reciprocal ST segment depression developed during intravenous administration of pilsicainide. In one patient, pilsicainide accentuated the ST segment elevation in leads I, aV(L), and V(1)-V(3) and caused ST segment depression in leads II, III, and aV(F). Coronary angiograms at the time of ST segment elevation were normal. In the other patient, pilsicainide accentuated the coved-type ST segment elevation in leads II, III, and aV(F) and caused ST segment depression in leads I, aV(L), and V(2)-V(5). Frequent premature ventricular complexes (PVCs) with two different left bundle branch block patterns developed during ST segment elevation. Intravenous isoproterenol returned the ST segment to baseline in both patients and suppressed the PVCs in the second patient. We hypothesize that a wide area of epicardial myocardium with large I(to) current might explain the reciprocal ST segment depression observed at the time of accentuated ST segment elevation.

Effects of verapamil on anterior ST segment and ventricular fibrillation cycle length in patients with Brugada syndrome.

PURPOSE: This study examined the effects of verapamil (5-10 mg intravenous) on the cardiac electrical activity of 10 Brugada syndrome (BS) patients having vasospastic angina, atrial fibrillation, and/or hypertension. RESULTS: Verapamil showed no significant change in the ST-segment elevation. Likewise, there was no significant change in the lengths of QRS complex, HV and corrected QT intervals, or effective refractory period at the right ventricle. The conduction time between right ventricular apex and outflow tract, measured at 400-millisecond pacing, was mildly prolonged by verapamil. At baseline, induced ventricular fibrillation (VF) was terminated by a 200-J shock in all patients. After verapamil, VF was reinduced in 7, was noninducible in 2, and self-terminated in 1 patient. Mean F-F interval was shorter after than before verapamil, and a 360-J shock was required in 2 of the 7 patients. CONCLUSION: In some BS patients, calcium channel blockade may modify the electrical characteristics of VF.

Evaluating patients with acute ischemic stroke with special reference to newly developed atrial fibrillation in cerebral embolism.

BACKGROUND: Cardioembolic strokes are extensive and have a poor prognosis. To identify the cardiovascular risk factors of cardioembolic stroke, we evaluated the cardiovascular status with special reference to persistent atrial fibrillation (AF) and paroxysmal atrial fibrillation (PAF) combined with the type of acute ischemic stroke. METHODS: We divided 315 consecutive patients admitted to our Department of Neurosurgery with an acute ischemic stroke into four types of brain infarction using clinical history, onset pattern of stroke, and brain imaging: cardioembolic (group E, n = 105), lacunar (group L, n = 92), atherothrombotic (group T, n = 111), and unclassified (n = 7). All patients underwent standard electrocardiography (ECG), a 24-hour ECG recording (Holter ECG) and transthoracic echocardiography (UCG). RESULTS: Persistent AF or PAF was detected in 97 patients (31.5%) using Holter ECG: more frequently in group E (67.6%) than in groups L (15.2%) or T (9.2%). Persistent AF or PAF was first diagnosed on admission using a standard ECG in 16 patients (5.2%) with no previous history and 14 of these patients belonged to group E (13.3%). PAF was newly detected on Holter ECG in another 26 patients (8.4%) and 13 of these patients (12.4%) belonged to group E. Concerning UCG, left atrial enlargement and mitral regurgitation were more frequent in group E than in group L or T. CONCLUSION: Holter ECG in addition to ECG on admission is important for detecting persistent AF or PAF in patients with ischemic stroke, especially with cardioembolism as diagnosed by neuroimaging.

Transient left ventricular apical ballooning developing after the Central Niigata Prefecture Earthquake: two case reports.

Two patients presented with transient left ventricular apical ballooning (takotsubo cardiomyopathy) induced by emotional stress caused by the Central Niigata Prefecture Earthquake in 2004. These patients complained of chest pain immediately after the earthquake. In patient 1, electrocardiography (ECG) showed slight ST elevation in leads V5 to V6 and 1 mm ST depression in lead III. Serial ECG revealed inverted giant T waves in leads V3 to V6 and inverted T waves in leads I, II, aVL and aVF 13 days after the earthquake occurred. Patient 2 also complained of chest pain right after the earthquake, but consulted a doctor 15 days after the earthquake occurred. ECG showed inverted giant T wave in leads V1 to V6 and inverted T waves in leads I, II and aVL. Transthoracic echocardiography showed hypokinesis of the apical area of the left ventricle with normokinesis in the basal area in both patients. Coronary angiography showed no stenotic segments and coronary spasms were not induced by provocative testing. Serial cardiac radionuclide single photon emission computed tomography of myocardial functional sympathetic innervation using iodine-123-metaiodobenzyl-guanidine (MIBG) and thiallium-201 (201Tl) showed an MIBG uptake defect and increased wash-out in the apical area, but only mild decrease of apical 201Tl uptake. Due to strong emotional stress, earthquakes may induce transient left ventricular apical ballooning (takotsubo cardiomyopathy).

Shortening of the ventricular fibrillatory intervals after administration of verapamil in a patient with Brugada syndrome and vasospastic angina.

A 43-year-old man presented with electrocardiographic findings consistent with Brugada syndrome. Though the baseline coronary angiogram was normal, intracoronary infusion of ergonovine maleate caused complete occlusion of the left anterior descending and a 99% occlusion of the proximal right coronary artery, each relieved by intracoronary isosorbide dinitrate. Double extrastimuli delivered at the right ventricular outflow tract induced ventricular fibrillation terminated by a 200-J shock. Verapamil, 10 mg IV, increased ST-segment elevation and programmed stimulation repeated after the drug induced ventricular fibrillation with shorter F-F intervals and lower amplitude signals, which was not terminated by 200 J and required an additional 360-J shock. Ca2+ antagonism may have been adverse in this patient with Brugada syndrome because the drug has the potential to increase the voltage gradient through the right ventricle and to slow intraventricular conduction at very fast heart rates.

Effects of intravenous magnesium in a prolonged QT interval model of polymorphic ventricular tachycardia focus on transmural ventricular repolarization.

BACKGROUND: This study was performed to clarify the antiarrhythmic effects of magnesium sulfate (Mg(++)) in a prolonged QT interval canine model of polymorphic ventricular tachyarrhythmia (VTA). METHODS: In six experiments in a canine model of prolonged QT by anthopleurin-A, Mg(++) was administered in boluses of 0.2 mL/kg during repetitive episodes of self-terminating polymorphic VTA or frequent premature ventricular complexes (PVCs). The distribution of ventricular repolarization across the left ventricular(LV) wall and dispersion of transmural repolarization were analyzed before, and 30 and 120 seconds after Mg(++) administration, during ventricular pacing at 100 bpm. Transmural unipolar electrograms were recorded from multipolar needle electrodes, and local activation-recovery intervals (ARI) were measured. RESULTS: Mg(++) rapidly eliminated self-terminating polymorphic VTA and all isolated PVCs. During ventricular pacing at 100 bpm, Mg(++) caused modest shortening of ARI at all recording sites. Since the magnitude of ARI shortening was greater at mid-myocardial sites than at other ventricular sites, mean transmural ARI dispersion decreased from 80 +/- 22 to 45 +/- 18 ms within 30 seconds after Mg(++) injection. However, this effect was transient, and, at 120 seconds after Mg(++) administration, ARI had increased all sites and transmural ARI dispersion lengthened to 65 +/- 18 ms. Besides suppression of triggered premature activity, homogenization of transmural ventricular repolarization was associated with the antiarrhythmic effects of intravenous Mg(++) in this model. CONCLUSION: Since these effects were transient, a continuous intravenous infusion of Mg(++) is preferred to prevent recurrences of VTA.

Ventricular tachyarrhythmias in a canine model of LQT3: arrhythmogenic effects of sympathetic activity and therapeutic effects of mexiletine.

The ventricular tachyarrhythmias associated with the LQT3 syndrome are typically bradycardia-dependent. However, some episodes can be associated with exercise or emotional stress, suggesting a different arrhythmogenic mechanism when sympathetic activity predominates. This study examined the potential arrhythmogenic mechanisms during periods of autonomically mediated transient heart rate acceleration in a canine anthopleurin-A model of LQT3 syndrome. Using plunge needle electrodes, transmural unipolar electrograms of the left ventricle were recorded from endocardial (Endo), mid-myocardial (Mid) and epicardial (Epi) sites. The activation-recovery interval (ARI) was measured to estimate local refractoriness. The cardiac cycle length was gradually shortened by cessation of vagal stimulation (vagal stimulation protocol (VSP)), and intramural electrograms and onset mode of ventricular tachyarrhythmias were analyzed in 7 experiments. The VSP was performed 8 times before and 5 times after administration of mexiletine in each experiment. Before mexiletine, vagal stimulation slowed the heart rate and created large transmural ARI dispersion because of a greater ARI prolongation at Mid rather than Epi/Endo sites. After cessation of vagal stimulation, unipolar electrograms started to show ARI alternans and ventricular premature beats developed sporadically. Sustained ventricular tachyarrhythmias were induced in 12 of the 56 trials of the VSP. Initiation of ventricular tachyarrhythmias was associated with delayed conduction at Mid/Endo sites. Mexiletine attenuated transmural ARI dispersion, and neither ARI alternans nor ventricular tachyarrhythmias was observed during all 35 trials of the VSP after mexiletine administration. Heart rate acceleration induced by an abrupt shift to a state of predominant sympathetic activity enhances arrhythmias in this LQT3 model. Mexiletine homogenizes ventricular repolarization, suppresses premature complexes and was antiarrhythmic during ventricular tachyarrhythmias induced by the VSP.

Triggers of ventricular tachyarrhythmias and therapeutic effects of nicorandil in canine models of LQT2 and LQT3 syndromes.

OBJECTIVES: We sought to identify the triggers of ventricular tachyarrhythmia (VTA) in experimental models of long QT type 2 (LQT2) and long QT type 3 (LQT3) syndromes. BACKGROUND: Most adverse cardiac events occurring in the long QT type 1 syndrome are related to sympathetic nerve activity. In contrast, various factors may trigger VTA in patients with LQT2 and LQT3. METHODS: The mode of onset of VTA and therapeutic effects of the potassium-adenosine triphosphate channel opener nicorandil were compared in canine models of LQT2 and LQT3, using three induction protocols: 1) bradycardia produced by atrioventricular block (BRADY); 2) programmed ventricular stimulation; and 3) electrical stimulation of the left stellate ganglion (left stellate stimulation [LSS]). Transmural unipolar electrograms were recorded, and the activation-recovery interval (ARI) was measured. RESULTS: Ventricular tachyarrhythmias developed during BRADY in all six experiments in the LQT3 model, but in none of the six experiments in LQT2. Programmed ventricular stimulation induced VTA in two experiments of the LQT2 model, but in none of the LQT3 experiments. Stimulation of the left stellate ganglion induced VTA in three experiments in LQT2 and in two experiments in LQT3. Nicorandil caused greater shortening of ARI and greater attenuation of transmural ARI dispersion in the LQT2 model than in the LQT3 model. After treatment with nicorandil, a single VTA was induced in the LQT2 model by LSS, whereas in the LQT3 model, VTA remained inducible by BRADY in four experiments and LSS in one experiment. CONCLUSIONS: An abrupt increase in sympathetic activity appeared arrhythmogenic in both models. Nicorandil attenuated the heterogeneity of ventricular repolarization and suppressed the induction of VTA in the LQT2 model, but had a limited therapeutic effect in the LQT3 model.