Ventricular tachycardia originating from the right ventricular free wall in a patient with an old myocardial infarction

A 64-year-old woman with right ventricular infarction had ventricular tachycardia (VT) with left bundle-branch block morphology. Pace-mapping during sinus rhythm and the earliest ventricular potential during VT suggested that the VT originated in the inflow-inferior site of the right ventricular free wall.     

Importance of left anterior hemiblock development in inferior wall acute myocardial infarction.

The aim of this study was to investigate the clinical and angiographic importance of left anterior hemiblock (LAHB) during acute inferior myocardial infarction (AIMI) by comparing patient groups with and without LAHB after AIMI. One hundred seventy-two patients (141 men and 31 women) between 28 and 84 years of age (mean 55 +/-10 years) with AIMI were included in the study. Patients were divided into 2 groups according to electrocardiogram (ECG) criteria: group I comprised 25 patients in whom ECG pattern characteristic of LAHB developed, group II comprised 147 patients without this pattern. According to the electrocardiogram, patients were placed in group I if the mean QRS axis was deviated to the left < 30 degrees in the frontal plane with the following pattern: increased S-wave voltage and decreased R-wave voltage in leads II, the appearance of a deep S-wave in lead II, and a terminal positive R-wave in lead aVR. Coronary angiography was performed within 2 weeks. A coronary stenosis was considered if the vessel diameter was narrowed by > 50%. The dominant coronary artery was classified as right or left or balanced. The left ventricular ejection fraction (LVEF) was calculated from left ventriculography. The mean age of the patients in group I was significantly higher (58 vs 54 years, p = 0.007), while the risk factors were similar in both groups. Left anterior descending (LAD) and multi-vessel coronary artery disease (CAD) were found to be significantly higher in group I compared with group 11 (80% vs 38%, p=0.0001; 84% vs 52%, p=0.001, respectively). The mean LVEF was found to be lower in group I (51% vs 56%, p=0.04). Peak creatine phosphokinase MB (CKMB) values were not different (216 vs 162 IU/L, p = 0.09). The frequency of left dominant or balanced coronary artery was determined to be higher in group I (44% vs 17%, p = 0.018). LAHB development during AIMI can be an indicator of LAD lesions, multivessel coronary artery disease, and impaired left ventricular systolic function.     

起源于左心室游离壁的单形室性心动过速和早搏的射频导管消融

目的 起源于左心室游离壁的室性心动过速(ventricular tachycardia, VT)及早搏(premature ventricular contraction, PVC)是较少见的心律失常,本文报道对其进行标测及射频导管消融的初步经验。方法 11例患者(男性9例,女性2例),平均年龄(37.3±17.2)岁。其中7例有持续性VT,4例为短阵非持续性单形VT和/或频发PVC,体表心电图均为右束支阻滞(RBBB)和心电轴右偏。3例患者伴明显的左心室扩大及充血性心力衰竭。对全部患者进行了左心室电生理标测,其中6例采用了心内非接触式标测。在标测到的最早激动部位进行温度控制下的射频导管消融。结果 11例患者均标测到自发的单形VT或PVC。其室性心律的平均周长(443.3±76.6)ms。全部室性心律均起源于左心室游离壁,其中2例位于偏前的高位近二尖瓣环处,2例位于后外侧游离壁中、高位,6例源于游离壁中高位,1例位于游离壁中下部。VT或PVC最早电位平;啕领先体表心电图(31.8±11.8)ms。全部患者的消融均获得即时成功,且不再服用抗心律失常药物,平均随访(11.8±8.0)个月,仅1例VT患者有单形PVC(<1000次/24h),3例左心室增大者均有明显缩小,其中1例基本恢复正常。结论 单形VT或PVC可发生于无缺血性心脏病的患者,表现为右束支阻滞和心电轴右偏,其频率较慢,可被射频导管消融消除。     

Acute inferior wall myocardial infarction associated with complete atrioventricular block and left posterior hemiblock.

Three cases of acute inferior wall myocardial infarction associated with complete atrioventricular block and junctional escape rhythm showing left posterior hemiblock are presented. The triad appears to consitiute a distinct syndrome. It is postuated that the subsidiary pacemaker is situated either in the bundle of His or the proximal part of the anterior division of the left bundle-branch.     

Acute inferior wall myocardial infarction associated with complete atrioventricular block and left posterior hemiblock.

Three cases of acute inferior wall myocardial infarction associated with complete atrioventricular block and junctional escape rhythm showing left posterior hemiblock are presented. The triad appears to consitiute a distinct syndrome. It is postuated that the subsidiary pacemaker is situated either in the bundle of His or the proximal part of the anterior division of the left bundle-branch.     

Assessment of left ventricular wall thickness in healed myocardial infarction by magnetic resonance imaging

The ability of magnetic resonance imaging (MRI) to detect and localize healed myocardial infarction (MI) was assessed. Seventeen consecutive patients with healed MI assessed by biplane contrast ventriculography underwent MRI using oblique imaging planes. Seven normal subjects underwent MRI as controls. In each patient, ventriculography identified regional wall motion abnormalities. MRI, performed with a 0.15-Tesla resistive magnet and oblique imaging planes relating to the left ventricle, detected zones of regional wall thinning conforming to the wall motion abnormalities localized by ventriculography in 16 patients. In these patients, adjacent areas of intact myocardium were identified in areas shown by ventriculography to be normal. The left ventricular wall thickness at the site of MI was significantly less than adjacent noninfarcted myocardium (p less than 0.001) and normal hearts (p less than 10(-6)). The ratio of the thickness of the infarct to adjacent normal wall averaged 0.40 (range 0.22 to 0.62). MRI could differentiate healed MI from adjacent noninfarcted myocardium and normal hearts.     

Idiopathic ventricular tachycardia originating from the posteroseptal mitral annulus: a case report

We describe a 71-year-old man with a ventricular tachycardia (VT) originating from the mitral annulus. A sustained VT was induced by exercise or an isoproterenol administration, but not by pacing. Frequent premature ventricular contractions (PVCs) with the same QRS as the VT were transiently suppressed by an adenosine triphosphate injection, suggesting that it was due to cyclic-AMP mediated triggered activity. The PVCs and VT were all abolished by radiofrequency catheter ablation guided by the earliest activation and a perfect pace map, which was located at the posteroseptal mitral annulus. The patient has been free from any symptoms for 2 years.     

Incidence and significance of left anterior hemiblock complicating acute inferior wall myocardial infarction.

The hospital course and serial vectorcardiograms of 56 consecutive patients with acute inferior wall myocardial infarction were reviewed. Left anterior hemiblock (LAH) complicating inferior wall myocardial infarction was diagnosed by vectorcardiographic criteria. Seven patients (12.5%) developed LAH between the first and third hospital day, while 49 patients did not. There was no significant difference between these two groups when compared for age, sex, incidence of congestive heart failure, atrial and ventricular arrhythmias, atrioventricular (A-V) block, hospital mortality, and previous hypertension, diabetes mellitus, and myocardial infarction. We conclude that LAH is a relatively common complication of acute inferior wall myocardial infarction, with no apparent effect on the clinical course.     

Importance of accounting for the variability of electrocardiographic data among diagnostically similar patients with inferior wall healed myocardial infarction

The authors describe a method to account for patient-to-patient variability in electrocardiographic data. The method yielded criteria for healed inferior myocardial infarction with diagnostic performances better than those of traditional electrocardiographic parameters.     

Fistula from coronary arteries to left ventricle after myocardial infarction.

Coronary arteriography and left ventriculography, performed in a 42-year old patient with unstable angina seven months after a myocardial infarct showed communications from both the left anterior descending and right coronary arteries to the left ventricular chamber. The area of communication corresponded to the site of infarction as established by electrocardiogram and left ventriculogram. Whether this is a congenital or acquired lesion is unclear.     

Early diagnosis of right ventricular or posterior infarction associated with inferior wall left ventricular acute myocardial infarction

Right ventricular (RV) or posterior infarction associated with inferior wall left ventricular acute myocardial infarction (AMI) has important therapeutic and prognostic implications. However, RV and posterior chest leads in addition to the 12-lead electrocardiogram are required for accurate detection. Body surface mapping (BSM) has greater spatial sampling and may further improve inferior wall AMI classification. Consecutive patients with chest pain lasting <12 hours were assessed to identify those with AMI and > or =0.1 mV ST elevation in > or =2 contiguous inferior leads of the 12-lead electrocardiogram (bundle branch block or left ventricular hypertrophy excluded). A 12-lead electrocardiogram, RV leads (V(2)R, V(4)R), posterior chest leads (V(7), V(9)), and a BSM were recorded. From each BSM, the 12 electrodes overlying the RV region (regional RV map) and 10 electrodes overlying the posterior wall (regional posterior map) were assessed for ST elevation. Infarct size was estimated by serial cardiac enzymes. AMI occurred in 173 of 479 patients. Of the 62 patients with inferior wall AMI, ST elevation > or =0.1 mV occurred in 26 patients (42 in V(2)R or V(4)R compared with 36 patients (58%) in > or =1 electrode on the regional RV map (p = 0.0019). ST elevation > or =0.1 mV occurred in 1 patient (2%) in V(7) or V(9) compared with 17 patients (27%) in > or =1 electrode on the regional posterior map (p = 0.00003). ST elevation > or =0.05 mV occurred in 6 patients (10%) in V(7) or V(9) compared with 22 patients (36%) in > or =1 electrode on the regional posterior map (p = 0.00003). Patients with ST elevation on regional RV and/or posterior maps had a trend toward larger infarct size (mean peak creatine kinase 1,789+/-226 vs. 1,546+/-392 mmol/L; p = NS). Thus, BSM, when compared with RV or posterior chest leads, provides improved classification of patients with inferior wall AMI and RV or posterior wall involvement.     

Pacemaker-induced ventricular tachycardia in patients with acute inferior myocardial infarction

We analysed a group of 35 consecutive patients with acute myocardial infarction—23 of the inferior, 12 of the anterior wall—who needed temporary pacing for bradycardiac arrhythmias. We observed in three patients ventricular tachycardias induced by pacemaker stimuli falling onto the vulnerable part of the cardiac cycle due to improper sensing. All three had an inferior myocardial infarction involving the right ventricle. Because the pacemaker electrode in this condition lies in the vicinity of the infarcted myocardium sensing problems occur more frequently and re-entry tachy-cardias can be triggered more easily. It represents a possible risk of pacemaker treatment in this group of patients who, on the other hand, often need cardiac pacing in the acute phase following the development of transient AV-block.