Is There Space for Surgery in the Treatment of Tachyarrhythmias?

Curative treatment of both supraventricular and ventricular tachyarrhythmias started with the introduction of surgical therapy. Surgical treatment modalities were often very successful and associated with low mortality and morbidity, especially in patients with various supraventricular tachyarrhythmias. However, results were acceptable in patients with ventricular tachyarrhythmias, with often a very complex and extended arrhythmogenic area associated with structural heart disease. Because of the development and proven effectiveness of catheter ablation and defibrillator implantation, the role of surgical therapy became limited. In the treatment of supraventricular arrhythmias, surgical therapy is an option after failure of catheter ablation. Since His-bundle catheter ablation is only a palliative treatment for atrial fibrillation, the potentially curative Maze operation may be an acceptable alternative. However, its potential against formation of intracavitary thrombi has not yet been proven. In the treatment of ventricular tachyarrhythmias, ischemia related polymorphic ventricular tachycardia and ventricular fibrillation can be treated very effectively by revascularization. Map-guided surgery is an appropriate treatment modality for patients with monomorphic ventricular tachycardia and an extended arrhythmogenic area. However, patients with very poor left ventricular function may have an unacceptable perioperative risk. In patients with congenital long QT syndrome who are refractory to beta blocking agents, left-sided sympathectomy is the most appropriate choice.     

Recanalization of Chronically Occluded Coronary Arteries: Single-Center Experience in 400 Cases, Including Long-Term Angiographic Follow-Up

The study presented comprises the initial and angiographic long-term results of a consecutive series of recanaliza-tion procedures in a single center. Between 1988 and 1992, a total of 400 patients underwent transluminal recanalization for total coronary occlusions. In 82% of successfully attempted patients, the occlusion could be passed by a standard guidewire. The overall initial success rate was 75% (298 of 400). The highest success rates could be achieved in the left circumflex artery (84%) and left anterior descending coronary artery (77%). Complications were uncomplicated myocardial infarction in ten patients (2.5%) and death in two patients (0.5%). Angiographic follow-up 3–6 months after recanalization could be achieved in 263 (88%) of 298 patients. Significant restenosis (≥ 50% minimum lumen diameter) was found in 57 (22%) of 263, and reocclusion was present in 38 (14%) of 263 patients, resulting in a total recurrence rate of 36%. In conclusion, recanalization can be performed with an initial success rate of 75% using bare-wire technique under the prerequisite operator experience. If a nearly complete angiographic follow-up is performed, the overall recurrence rate is 36%, which seems to be very acceptable in comparison with PTC A results for incomplete obstructions published so far . (J Interven Cardiol 1996;9:73–79)     

Absence of effects of prolonged simvastatin therapy on nocturnal sleep in a large randomized placebo-controlled study

1It has been suggested that lipophilic HMG CoA reductase inhibitors, like lovastatin and simvastatin, may cause sleep disturbance. 2Six hundred and twenty-one patients at increased risk of coronary heart disease were randomized in a single centre to receive 40 mg daily simvastatin, 20 mg daily simvastatin or matching placebo. To assess the effects of prolonged use of simvastatin on nocturnal sleep quality and duration, a sleep questionnaire was administered to 567 patients (95% of 595 survivors) at an average of 88 weeks (range: 44–129 weeks) after randomization. 3The main outcome measures were sleep-related problems and use of sleep-enhancing medications reported during routine study follow-up visits, and responses to the sleep questionnaire about changes in sleep duration and about various sleep events during the preceding month. 4No differences were observed between the treatment groups in the frequency of sleep-related problems reported, in the proportion of follow-up visits at which such problems were reported, or in the use of sleep-enhancing medications. The numbers who stopped study treatment were similar in the different treatment groups, and no patient stopped principally because of insomnia. In response to the sleep questionnaire, there were no significant differences between the treatment groups in reports of various sleep events during the preceding month, except that slightly fewer patients allocated simvastatin reported waking often. No differences in sleep duration were observed. 5This placebo-controlled trial does not indicate any adverse effects of prolonged treatment with simvastatin on systematically sought measures of sleep disturbance.     

Abnormal Automaticity as Mechanism of Atrial Tachycardia in the Human Heart—Electrophysiologic and Histologic Correlation:

Abnormal Automaticity in Human Atrium, introduction: A 32-year-old woman was operated upon because of drug refractory atrial tachycardia.
Methods and Results: Electrophysiologic study was performed prior to operation. During surgery, epicardial mapping of the electrical activity of the left atrium was performed. The left atrial appendage was resected and studied in a tissue bath. Thereafter, histologic examination was performed. Polarity of the P wave in the surface ECG suggested that the tachycardia originated high in the left atrium. Epicardial mapping disclosed earliest activation in the apex of the left atrial appendage. Intracellular recordings from surgical specimen made at the site of origin, which was marked during surgery, revealed cells with phase 4 depolarization at cycle lengths ranging from 360 to 540 msec. Exit block prevented spread of activation from the spontaneously firing cells to surrounding tissue. Histology showed that spontaneous activity arose in an area with abnormal cells-characterized by an amorphous, pale eosinophilic staining cytoplasm and absence of nuclei-surrounded by normal myocytes.
Conclusion: The observations indicate that the mechanism of the atrial tachycardia was based on abnormal automaticity in an area consisting of a conglomeration of normal and abnormal myocytes.     

High Rate of Late Dislodgements of an Active Fixation Atrial Lead

Between May 1985 and May 1991 we implanted 115 DFH-leads as unipolar atrial leads. The active fixation mechanism of this electrode consists of two sickle-shaped anchoring hooks which are placed at a distance of 0.9 mm parallel to the distal flat end of the electrode. All leads were affixed to the free wall of the right atrium. One hundred eight leads (93.9%) were implanted for dual chamber pacing and seven leads (6.1%) for single chamber atrial pacing. Parameters measured at implantation were (mean values): stimulation threshold 1.06 ± 0.42 V at 0.5 msec pulse width, P wave amplitude 5.12 ± 2.04 mV, and lead impedance 560 ± 76.1 Ohms. Within the first week after implantation, three early dislodgements occurred (2.6%). The follow-up period averaged 30.4 ± 16.2 months (range 2–76 months). During this time, 14 late macrodislodgements (12.2%) occurred after a mean period of 18.4 months (range 2–59 months). All of them required reoperation. The active fixation mechanism of the DEH-lead appears to be unreliable, if implanted in the free wall of the right atrium for dual chamber pacing.     

Coarctation of the Aorta: Quantitative Analysis by Transesophageal Echocardiography

Transesophageal echocardiography and standard two-dimensional echocardiography were performed in 15 patients with suspected coarctation of the aorta. Aortic diameters and crosssectional areas were determined by means of TEE and compared with clinical findings and catheterization data. The isthmus of the aorta could be imaged in all patients using TEE, but in only seven patients using standard suprasternal echocardiography. Compared with controls, aortic diameters were narrowed in 9 of 15 patients, and cross-sectional areas were reduced in 13 of 15. There was a satisfactory correlation between TEE data and angiographic and hemodynamic data. TEE is a promising method of a diagnosing and quantifying coarctation of the aorta, and is more sensitive than conventional two-dimensional and Doppler echocardiography.     

In Vivo Ventricular Lesion Growth in Radiofrequency Catheter Ablation

While radiofrequency catheter ablation has proved highly effective in the treafment of various supravenfricular tQchyarrhythmias, resulls in the trentment of ventricular tachycardia invite improvement. Knowledge of lesion growth in vivo might improve understanding of this discrepancy. So far only information from in vitro and in vivo studies using a small 2 mm tip eiectrode is available. Growlh of ventricular radiofrequency lesions created with a 4 mm ahlalion electrode was studied in 11 closed-chest dogs. Endocardia] ablations were performed at 31 left and 35 right ventricuiar sites at a power setting of 25 Watts and 5, 10, 20, 30 or 60 seconds pulse duration. Macroscopic and histopathologic lesion examination were performed after one week survival. Mean lesion volume increased from 52 mm³ after 5 seconds pulse duration to a maximum 388 mm³ and approximately 7 mm depth after 30 seconds. Lesions were prolate spheroid in form, with a sparing of subendocardial myocardium and maximum lesion diameter at some millimeters depth. Results indicate that catheter positioning at no more tlian 7 mm from the target is required for successful ablation. Due to lesion geometry, subendocardial targets demand even more exact catheter positioning, while subepicardial substrates may not be ammenable to ablation if ventricular wall thickness exceeds 7 mm at the ablation site. Repeated pulses at adjacent sites may be required for ablation of extended arrhytbmogenic areas. Volume at 5 seconds was only approximately 15% of mature lesions. Therefore, the use of a short'test pulse after careful mapping may be useful to pinpoint the most appropriate site for ablation in discrete pathways.     

Atrial Natriuretic Peptide Levels Reflect Hemodynamic Changes Under Pacemaker Stimulation

Pacemaker stimulation influences plasma levels of atrial natriuretic peptide (ANP). This study evaluated in individuals without impaired myocardial function whether a consecutive increase of pacing rates results in reduced alteration of plasma ANP levels mirroring a putative decrease of atrial contribution to cardiac output. In nine resting patients with DDD pacemakers, absolute and relative ANP plasma levels were determined under DDD (175 msec AV delay) and VVI pacing at a pacing rate of 72, 82, 92, and 113 beats/min. When pacing rates were consecutively increased, higher plasma ANP concentrations were measured. However, the differences in relative ANP levels were nearly identical. Therefore, it seems likely that the atrial contribution to cardiac output at high pacing rates is less important than at lower frequencies, at least when the overall myocardial function is not impaired.     

Left Atrial Volume and Function Assessment by Magnetic Resonance Imaging

Left Atrial Volume and Function Assessment Introduction: In patients with atrial fibrillation undergoing catheter ablation, magnetic resonance imaging (MRI) can determine left atrial (LA) volume and function before and after ablation. The most accurate, but time consuming, method to determine LA volume is the multiple slice method (MSM), which involves manual tracing of LA area on each slice. The area length method (ALM) offers a simplified, but unvalidated, alternative for LA volume assessment by MRI. The aim of this study was to compare LA volume and function assessment by ALM with MSM. Methods and Results: MRI was performed before and after catheter ablation in 40 patients with atrial fibrillation (30 male, mean age 57 years). All patients had sinus rhythm during imaging. In total, 72 MRI scans were available. LA end‐diastolic and end‐systolic volumes (EDV, respectively ESV) were measured by both methods. LA function was determined by calculating LA ejection fraction (EF = (EDV‐ESV)/EDV). Measured by ALM, mean LA EDV and ESV were significantly lower than using MSM (102 mL and 49 mL vs 111 mL and 65 mL, respectively, P < 0.001) with a larger difference in mean ESV than EDV (16 mL vs 9 mL). This resulted in an overestimation of LA EF by ALM with a mean of 11% (54% by ALM and 42% by MSM, P < 0.001). ALM correlated well with MSM for LA EDV and ESV (r = 0.77, respectively 0.85), and showed no significant difference in intraobserver and interobserver variability. Conclusion: ALM significantly underestimates LA volumes and overestimates LA function, but correlates well with the more accurate MSM. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1247‐1250, November 2010)