Myocardial perfusion in patients with permanent ventricular pacing and normal coronary arteries.
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OBJECTIVES: The purposes of this study were to test the specificity of dipyridamole myocardial perfusion scintigraphy in patients with permanent ventricular pacing (PVP) and to evaluate coronary blood flow and reserve in these patients. BACKGROUND: Permanent ventricular pacing is associated with exercise perfusion defects on myocardial scintigraphy in the absence of coronary artery disease (CAD). On the basis of studies in patients with left bundle brunch block, coronary vasodilation with dipyridamole has been proposed as an alternative to exercise testing for detecting CAD in paced patients, but this approach has never been tested. METHODS: Fourteen patients with a PVP and normal coronary arteries underwent stress thallium-201 scintigraphy and cardiac catheterization. In these patients and in eight control subjects, coronary flow velocities were measured in the left anterior descending coronary artery (LAD) and in the dominant coronary artery before and after adenosine administration. RESULTS: In the paced patients, coronary flow velocities in the LAD and in the dominant coronary artery were significantly lower than those in the control subjects. In addition, seven patients showed perfusion defects on dipyridamole thallium-201 single-photon emission computed tomography, with a specificity of 50% for this test. The defect-related artery in these patients had lower coronary flow reserve (2.6 +/- 0.5) as compared with those without perfusion defects (3.9 +/- 1.0, p < 0.05) or the control group (3.5 +/- 0.5, p < 0.05). CONCLUSIONS: Permanent ventricular pacing is associated with alterations in regional myocardial perfusion. Furthermore, abnormalities of microvascular flow, as indicated by reduced coronary flow reserve in the defect-related artery, are at least partially responsible for the uncertain specificity of dipyridamole myocardial perfusion scintigraphy. (+info)
Diagnosis and long-term follow-up of the Brugada syndrome in patients with idiopathic ventricular fibrillation.
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AIMS: Some patients with idiopathic ventricular fibrillation may suffer from the Brugada syndrome. The diagnostic criteria for the Brugada syndrome are uncertain and arbitrarily set. Therefore, we studied the prevalence of the Brugada syndrome using various diagnostic criteria and long-term follow-up in 37 idiopathic ventricular fibrillation patients. METHODS AND RESULTS: Idiopathic ventricular fibrillation was diagnosed after thorough clinical evaluation in 37 survivors of an out-of-hospital cardiac arrest referred to our institute (UMC Utrecht). Retrospectively, nine patients (24%, group I) were classified as potentially having the Brugada syndrome based on the presence of (in)complete right bundle branch block and ST-segment elevation in leads V(1)-V(3)of > or =1 mm. Only three patients (8%, group II) showed (in)complete right bundle branch block and > or =2 mm ST-segment elevation. With the intermittent presence of these ECG features and/or their (re)appearance with class I antiarrhythmic drugs included as criteria, the percentage of the Brugada syndrome was attenuated in group I (2/37; 5%) and group II (1/37; 3%). Sixteen (43%) of all idiopathic ventricular fibrillation patients (mean follow-up 77+/-41 months) had a recurrent episode of syncope, ventricular tachyarrhythmias or sudden death. Recurrence rate was 3/9 (33%) in Brugada patients group I, 2/3 (66%) in group II and 13/28 (46%) in patients without the Brugada syndrome (P=ns). CONCLUSIONS: Depending on the diagnostic criteria used, the Brugada syndrome was observed in 3% to 24% of patients with idiopathic ventricular fibrillation, underlining the importance of defining the precise diagnostic criteria in these patients. For all idiopathic ventricular fibrillation patients, the ventricular tachyarrhythmia recurrence rate was substantial during an average follow-up of more than 6 years. (+info)
Bundle-branch reentry and the postpacing interval after entrainment by right ventricular apex stimulation: a new approach to elucidate the mechanism of wide-QRS-complex tachycardia with atrioventricular dissociation.
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BACKGROUND: Diagnosis of bundle-branch reentry ventricular tachycardia (BBR-VT) by the standard approach is challenging, and this may lead to nonrecognition of this tachycardia mechanism. Because the postpacing interval (PPI) after entrainment has been correlated with the distance from the pacing site to the reentrant circuit, BBR-VT entrainment by pacing from the right ventricular apex (RVA) should result in a PPI similar to the tachycardia cycle length (TCL). This factor may differentiate BBR-VT from other mechanisms of wide-QRS-complex tachycardia with AV dissociation, such as myocardial reentrant VT (MR-VT) or AV nodal reentrant tachycardia (AVNRT), in which the circuit is usually located away from the RVA. METHODS AND RESULTS: Transient entrainment by RVA pacing was attempted in 18 consecutive BBR-VTs and finally achieved in 13. Results were compared with those found in 59 consecutive MR-VTs and 50 consecutive AVNRTs. The mean PPI-TCL difference was significantly (P:<0.0001) shorter in the BBR-VT group (9+/-11 ms) than in the MR-VT (109+/-48 ms) and the AVNRT (150+/-29 ms) groups. No BBR-VT showed a PPI-TCL >30 ms (range -12 to 24 ms). Except for 2 MR-VTs, no MR-VT (range 21 to 211 ms) or AVNRT (range 100 to 215 ms) showed a PPI-TCL <30 ms. CONCLUSIONS: A PPI-TCL >30 ms, after entrainment by RVA stimulation, makes BBR-VT unlikely. Conversely, a PPI-TCL <30 ms is suggestive of BBR-VT but should lead to further investigation by use of conventional criteria. (+info)
The syndrome of right bundle branch block ST segment elevation in V1 to V3 and sudden death--the Brugada syndrome.
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In 1992 a new syndrome was described consisting of syncopal episodes and/or sudden death in patients with a structurally normal heart and an electrocardiogram (ECG) characteristic of right bundle branch block with ST segment elevation in leads V1 to V3. The disease is genetically determined, with an autosomal dominant pattern of transmission. Three different mutations that affect the structure and function of the cardiac sodium channel gene SCN5A have been identified. Two mutations result in total loss of function of the sodium channel. The other mutation results in acceleration of the recovery of the sodium channel from inactivation. The incidence of the disease is difficult to estimate, but it causes 4 to 10 sudden deaths per 10000 inhabitants per year in areas like Thailand and Laos. In these countries, the disease represents the most frequent cause of death in young adults. Up to 50% of the yearly sudden deaths in patients with a structurally normal heart are caused by this syndrome. The diagnosis is easily made by means of the ECG. The presence of concealed and intermittent forms, however, make the diagnosis difficult in some patients. The ECG can be modulated by changes in autonomic balance and the administration of antiarrhythmic drugs. Beta-adrenergic stimulation normalizes the ECG, while intravenous ajmaline, flecainide or procainamide accentuate ST segment elevation and are capable of unmasking concealed and intermittent forms of the disease. Recent data suggest that loss of the action potential dome in the right ventricular epicardium but not the endocardium underlies ST segment elevation seen in the Brugada syndrome. Also, electrical heterogeneity within the right ventricular epicardium leads to the development of closely coupled extrasystoles via a phase 2 reentrant mechanism, which then precipitates ventricular tachycardia-ventricular fibrillation. Right ventricular epicardium is preferentially affected because of the predominance of transient outward current in this tissue. Antiarrhythmic drugs like amiodarone and beta-blockers do not prevent sudden death in symptomatic or asymptomatic individuals. Gene therapy may offer a cure in future years. Implantation of an automatic cardioverter-defibrillator is the only currently proven effective therapy. (+info)
Comparison of scalar and vector electrocardiographic diagnosis and localization of myocardial infarction.
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A prospective study was made of 80 patients during typical clinical episodes of acute myocardial infarction with biochemical and scalar electrocardiographic confirmation. Nine patients had bundle-branch block and 12 had had previous episodes of myocardial infarction. Serial electrocardiograms and vectorcardiograms were recorded during the first week in hospital. The most striking finding was that in more than half the cases there was disagreement between the electrocardiogram and vectorcardiogram in the localizationof infarction. The earliest evidence of infarction in the electrocardiogram is often restricted to ST and T changes though in the corresponding vectorcardiograms evidence of infarction may be present in the QRS loop. In those cases in which both electrocardiogram and vectorcardiogram show QRS abnormalities these are frequently detected earlier in the vectorcardiogram, but the converse is rare. (+info)
Impaired conduction in the bundle branches of mouse hearts lacking the gap junction protein connexin40.
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BACKGROUND: Connexin (Cx)40 and Cx45 are the major protein subunits of gap junction channels in the conduction system of mammals. To determine the role of Cx40, we correlated cardiac activation with Connexin distribution in normal and Cx40-deficient mice hearts. METHODS AND RESULTS: Epicardial and septal activation was recorded in Langendorff-perfused adult mice hearts with a 247-point compound electrode (interelectrode distance, 0.3 mm). After electrophysiological measurements, hearts were prepared for immunohistochemistry and histology to determine Connexin distribution and fibrosis. In both wild-type and Cx40-deficient animals, epicardial activation patterns were similar. The right and left ventricular septum was invariably activated from base to apex. Histology revealed a continuity of myocytes from the common bundle to the septal myocardium. Within this continuity, colocalization was found of Cx43 and Cx45 but not of Cx40 and Cx43. Both animals showed similar His-bundle activation. In Cx40-deficient mice, the proximal bundle branches expressed Cx45 only. The absence of Cx40 in the proximal bundles correlated with right bundle-branch block. Conduction in the left bundle branch was impaired as compared with wild-type animals. CONCLUSIONS: Our data show that (1) in mice, a continuity exists between the common bundle and the septum, and (2) Cx40 deficiency results in right bundle-branch block and impaired left bundle-branch conduction. (+info)
Adverse events with transvenous left ventricular pacing in patients with severe heart failure: early experience from a single centre.
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AIMS: Assessment of complications following implantation of transvenous ventricular electrodes to pace the left ventricle. METHODS AND RESULTS: Twenty-eight patients with severe cardiac failure and left bundle branch block were prospectively followed for adverse effects of implantation of a left ventricular transvenous pacing system. Immediate follow-up was associated with loss of left ventricular pacing in nine patients (32%). This was due to lead dislodgement in four cases (corrected by re-operation in three of these cases), and due to increased threshold in five cases (corrected by programming a higher pacing amplitude in all five cases, but with intermittent diaphragmatic contraction in one case). After 1 month, one patient died, one patient with severe coronary heart disease suffered a myocardial infarction, and left ventricular pacing was lost in two patients. Pericardial effusion, new significant ventricular arrhythmias or other adverse effects were not observed. After a mean follow-up of 16 +/- 9.2 months, pacing leads remained stable and no late complications related to the transvenous left ventricular epicardial pacing were observed. CONCLUSION: Placement of a permanent lead in a tributary of the coronary sinus is feasible without serious adverse effects during the first month. The only frequent adverse event was lead dislodgement; a finding which emphasizes the need for development of specially designed leads for this application. (+info)
Ventricular tachycardias arising from the aortic sinus of valsalva: an under-recognized variant of left outflow tract ventricular tachycardia.
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OBJECTIVES: To describe a normal heart left bundle branch block, inferior axis ventricular tachycardia (VT), that could not be ablated from the right or left ventricular outflow tracts. BACKGROUND: Whether these VTs are epicardial and can be identified by a specific electrocardiographic pattern is unclear. METHODS: Twelve patients with normal heart left bundle branch block, inferior axis VT and previously failed ablation were included in this study. Together with mapping in the right and left ventricular outflow tracts, we obtained percutaneous epicardial mapping in the first five patients and performed aortic sinus of Valsalva mapping in all patients. RESULTS: No adequate pace mapping was observed in the right and left ventricular outflow tracts. Earliest ventricular activation was noted in the epicardium and the aortic cusps. All patients were successfully ablated from the aortic sinuses of Valsalva (95% CI 0% to 18%). The electrocardiographic pattern associated with this VT was left bundle branch block, inferior axis and early precordial transition with Rs or R in V2 or V3. Ventricular tachycardia from the left sinus had rS pattern in lead I, and VT from the noncoronary sinus had a notched R wave in lead I. None of the patients had complications and all remained arrhythmia-free at a mean follow-up of 8 +/- 2.6 months. CONCLUSIONS: Normal heart VT with left bundle branch block, inferior axis and early precordial transition can be ablated in the majority of patients from either the left or the noncoronary aortic sinus of Valsalva. (+info)