Intraoperative electrophysiologic mapping of the ventricles during sinus rhythm in patients with a previous myocardial infarction. Identification of the electrophysiologic substrate of ventricular arrhythmias.

Klein, Helmut U.; Karp, Robert B.; Kouchoukos, N. T.; Zorn, Gerlinde; James, Thomas N.; Waldo, Albert L.

doi:10.1161/01.cir.66.4.847

Cited by 148 publications

(46 citation statements)

References 39 publications

(6 reference statements)

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“…16 It is known that ventricular tachycardia occurring after the acute stage of myocardial infarction is most likely caused by reentry4 and that arrhythmias are more common in those patients with poor cardiac function.3 This finding implicates infarct size as a contributing factor for ventricular tachycardia,`7 since cardiac function is inversely related to infarct size. '0 Our findings substantiate the presence of large infarct size in patients with ventricular tachycardia.…”

Section: Discussionmentioning

confidence: 99%

Quantitative analysis of myocardial infarct structure in patients with ventricular tachycardia.

Bolick¹,

Hackel²,

Reimer³

et al. 1986

Circulation

106

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To study whether myocardial infarction differs in patients with and without ventricular tachycardia, the hearts of 22 deceased patients with ventricular tachycardia and 21 deceased control patients were analyzed quantitatively. The hearts from the ventricular tachycardia group were heavier and more dilated than those from the control group. Histologic analysis of a representative cross section from each heart showed that the ventricular tachycardia group had larger, more solid infarcts than did the control group. The ventricular tachycardia group also had a greater area of spared subendocardium, more hydropic change of the spared subendocardium, and more "ribbon type" spared subendocardium, which was defined as spared subendocardium of uniform contour 1 mm thick or less. The ventricular tachycardia group was divided into a subacute subgroup (n = 14, dying c 10 weeks after infarction) and a chronic subgroup (n = 8, dying > 10 weeks after infarction). The infarcts of the subacute ventricular tachycardia group were more solid and had a greater amount of ribbon type spared subendocardium than those of the chronic ventricular tachycardia group. This information can serve as a baseline for the evaluation of animal preparations of tachycardia and, when combined with knowledge of the location of the arrhythmogenic region furnished by intraoperative mapping, should lead to better understanding of the anatomic substrate for ventricular tachycardia. Circulation 74, No. 6, 1266No. 6, -1279No. 6, , 1986 VENTRICULAR TACHYCARDIA is a common complication of myocardial infarction and is associated with increased morbidity and mortality. 1 Although the size of infarcts in patients with ventricular tachycardia has not previously been quantified morphometrically, arrhythmias have been reported to be associated with large creatine kinase infarct size index2 and with poor cardiac function,3 thus implicating large infarct size as a contributing factor for ventricular tachycardia. Although the mechanism by which a large infarct can lead to an arrhythmia is not definitely known, ventricular tachycardia occurring after the acute stage of an infarct is thought to be caused by reentry within the structurally altered tissue in or adjacent to the infarct. Laboratory between January 1975 and March 1985 were entered into the study if they (1) had a myocardial infarction, (2) had survived 10 days or longer after infarction, and (3) met the following criteria for either the ventricular tachycardia or the control group.The patients in the control group (group A) must have had no history of ventricular fibrillation or ventricular tachycardia lasting 10 beats or more after the first 48 hr after infarction and no history of ventricular tachycardia lasting 3 beats or more or coupled premature ventricular contractions after the first 4 days after infarction. The patients must have been hospitalized through at least day 10 after infarction and must have undergone some form of electrocardiographic monitoring such as routine heart monitoring i...

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Section: Discussionmentioning

confidence: 99%

Quantitative analysis of myocardial infarct structure in patients with ventricular tachycardia.

Bolick¹,

Hackel²,

Reimer³

et al. 1986

Circulation

106

View full text Add to dashboard Cite

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“…Inverse ECG mapping technology is able to identify fibrotic tissue due to the abnormal electrical properties exhibited by scarred myocardium, specifically low-amplitude electrical potentials with broad fractionated electrograms typically in areas exhibiting delayed or slow activation [77–79]. A degree of discrepancy between CMR and EAM is expected as CMR can struggle to detect areas of homogenous microscopic diffuse fibrosis due to the low resolution of the image, while inverse ECG EAM can be more sensitive at detecting zones of epicardial and transmural fibrosis but may miss sub-endocardial scar.…”

Section: Tissue Characterizationmentioning

confidence: 99%

Optimal site selection and image fusion guidance technology to facilitate cardiac resynchronization therapy

Sieniewicz

Gould

Porter

et al. 2018

Expert Review of Medical Devices

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Introduction: Cardiac resynchronization therapy (CRT) has emerged as one of the few effective treatments for heart failure. However, up to 50% of patients derive no benefit. Suboptimal left ventricle (LV) lead position is a potential cause of poor outcomes while targeted lead deployment has been associated with enhanced response rates. Image-fusion guidance systems represent a novel approach to CRT delivery, allowing physicians to both accurately track and target a specific location during LV lead deployment.Areas covered: This review will provide a comprehensive evaluation of how to define the optimal pacing site. We will evaluate the evidence for delivering targeted LV stimulation at sites displaying favorable viability or advantageous mechanical or electrical properties. Finally, we will evaluate several emerging image-fusion guidance systems which aim to facilitate optimal site selection during CRT.Expert commentary: Targeted LV lead deployment is associated with reductions in morbidity and mortality. Assessment of tissue characterization and electrical latency are critical and can be achieved in a number of ways. Ultimately, the constraints of coronary sinus anatomy have forced the exploration of novel means of delivering CRT including endocardial pacing which hold promise for the future of CRT delivery.

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“…[22][23][24][25][26][27][28][29][30] In brief, the magnetic mapping system includes a magnetic sensor in the catheter tip that can be localized in 3D space with the ultralow magnetic field generators placed under the fluoroscopic table. A 7F Navi-Star catheter, which consisted of a 4-mm distal tip electrode and a 2-mm ring electrode with an interelectrode distance of 1 mm, was introduced into the RV under fluoroscopic guidance and used as the mapping catheter.…”

Section: Electroanatomic Voltage Mappingmentioning

confidence: 99%

“…Therefore, in this study the reference value for electrogram amplitude used to define normal RV endocardium was set at 1.5 mV, which was the value above which 95% of all bipolar signal voltages from the endocardium of normal RVs were included. According to previous experiences on intraoperative 30 and catheter mapping, 24,25,28 -31 "electroanatomic scar" area was defined as an area Ն1 cm 2 including at least 3 adjacent points with bipolar signal amplitude Ͻ0.5 mV. The color display for depicting normal and abnormal voltage myocardium ranged from red, representing electroanatomic scar tissue (amplitude Ͻ0.5 mV), to purple, representing electroanatomic normal tissue (amplitude Ն1.5 mV).…”

Section: Electroanatomic Voltage Mappingmentioning

confidence: 99%

Three-Dimensional Electroanatomic Voltage Mapping Increases Accuracy of Diagnosing Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia

et al. 2005

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Background— Three-dimensional electroanatomic voltage mapping offers the potential to identify low-voltage areas that correspond to regions of right ventricular (RV) myocardial loss and fibrofatty replacement in patients with arrhythmogenic RV cardiomyopathy/dysplasia (ARVC/D). Methods and Results— Thirty-one consecutive patients (22 men and 9 women; mean age, 30.8±7 years) who fulfilled the criteria of the Task Force of the European Society of Cardiology and International Society and Federation of Cardiology (ESC/ISFC) for ARVC/D diagnosis after noninvasive clinical evaluation underwent further invasive study including RV electroanatomic voltage mapping and endomyocardial biopsy (EMB) to validate the diagnosis. Multiple RV endocardial, bipolar electrograms (175±23) were sampled during sinus rhythm. Twenty patients (group A; 65%) had an abnormal RV electroanatomic voltage mapping showing ≥1 area (mean 2.25±0.7) with low-voltage values (bipolar electrogram amplitude <0.5 mV), surrounded by a border zone (0.5 to 1.5 mV) that transitioned into normal myocardium (>1.5 mV). Low-voltage electrograms appeared fractionated with significantly prolonged duration and delayed activation. In 11 patients (group B; 35%), electroanatomic voltage mapping was normal, with preserved electrogram voltage (4.4±0.7 mV) and duration (37.2±0.9 ms) throughout the RV. Low-voltage areas in patients from group A corresponded to echocardiographic/angiographic RV wall motion abnormalities and were significantly associated with myocyte loss and fibrofatty replacement at EMB ( P <0.0001) and familial ARVC/D ( P <0.0001). Patients from group B had sporadic disease and histopathological evidence of inflammatory cardiomyopathy ( P <0.0001). During the time interval from onset of symptoms to the invasive study, 11 patients (55%) with electroanatomic low-voltage regions received an implantable cardioverter/defibrillator because of life-threatening ventricular arrhythmias, whereas all but 1 patient with a normal voltage map remained stable on antiarrhythmic drug therapy ( P =0.02). Conclusions— Three-dimensional electroanatomic voltage mapping enhanced accuracy for diagnosing ARVC/D (1) by demonstrating low-voltage areas that were associated with fibrofatty myocardial replacement and (2) by identifying a subset of patients who fulfilled ESC/ISFC Task Force diagnostic criteria but showed a preserved electrogram voltage, an inflammatory cardiomyopathy mimicking ARVC/D, and a better arrhythmic outcome.

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Intraoperative electrophysiologic mapping of the ventricles during sinus rhythm in patients with a previous myocardial infarction. Identification of the electrophysiologic substrate of ventricular arrhythmias.

Cited by 148 publications

References 39 publications

Quantitative analysis of myocardial infarct structure in patients with ventricular tachycardia.

Quantitative analysis of myocardial infarct structure in patients with ventricular tachycardia.

Optimal site selection and image fusion guidance technology to facilitate cardiac resynchronization therapy

Three-Dimensional Electroanatomic Voltage Mapping Increases Accuracy of Diagnosing Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia

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