Percutaneous Endocardial Ablation of Scar-Related Ventricular Tachycardia
Reporter: Aviva Lev-Ari, PhD, RN
UPDATED on 11/15/2013
Atrial Fibrillation Catheter Ablation Versus Surgical Ablation Treatment (FAST)
A 2-Center Randomized Clinical Trial
- Lucas V.A. Boersma, MD, PhD, FESC;
- Manuel Castella, MD, PhD;
- WimJan van Boven, MD;
- Antonio Berruezo, MD;
- Alaaddin Yilmaz, MD;
- Mercedes Nadal, MD;
- Elena Sandoval, MD;
- Naiara Calvo, MD;
- Josep Brugada, MD, PhD, FESC;
- Johannes Kelder, MD;
- Maurits Wijffels, MD, PhD;
- Lluís Mont, MD, PhD, FESC
+Author Affiliations
From the Departments of Cardiology (L.V.A.B., J.K., M.W.) and Cardiothoracic Surgery (W.J.v.B., A.Y.), St. Antonius Hospital, Nieuwegein, the Netherlands, and Thorax Institute, Hospital Clinic, University of Barcelona, Barcelona, Catalonia, Spain (M.C., A.B., M.N., E.S., N.C., J.B., L.M.).
- Correspondence to Lucas V.A. Boersma, MD, PhD, FESC, Cardiology Department, St. Antonius Hospital, PO 2500, Nieuwegein, Netherlands. E-maill.boersma@antoniusziekenhuis.nl
Abstract
Background—Catheter ablation (CA) and minimally invasive surgical ablation (SA) have become accepted therapy for antiarrhythmic drug–refractory atrial fibrillation. This study describes the first randomized clinical trial comparing their efficacy and safety during a 12-month follow-up.
Methods and Results—One hundred twenty-four patients with antiarrhythmic drug–refractory atrial fibrillation with left atrial dilatation and hypertension (42 patients, 33%) or failed prior CA (82 patients, 67%) were randomized to CA (63 patients) or SA (61 patients). CA consisted of linear antral pulmonary vein isolation and optional additional lines. SA consisted of bipolar radiofrequency isolation of the bilateral pulmonary vein, ganglionated plexi ablation, and left atrial appendage excision with optional additional lines. Follow-up at 6 and 12 months was performed by ECG and 7-day Holter recording. The primary end point, freedom from left atrial arrhythmia >30 seconds without antiarrhythmic drugs after 12 months, was 36.5% for CA and 65.6% for SA (P=0.0022). There was no difference in effect for subgroups, which was consistent at both sites. The primary safety end point of significant adverse events during the 12-month follow-up was significantly higher for SA than for CA (n=21 [34.4%] versus n=10 [15.9%]; P=0.027), driven mainly by procedural complications such as pneumothorax, major bleeding, and the need for pacemaker. In the CA group, 1 patient died at 1 month of subarachnoid hemorrhage.
Conclusion—In atrial fibrillation patients with dilated left atrium and hypertension or failed prior atrial fibrillation CA, SA is superior to CA in achieving freedom from left atrial arrhythmias after 12 months of follow-up, although the procedural adverse event rate is significantly higher for SA than for CA.
Clinical Trial Registration—URL: http://clinicaltrials.gov. Unique identifier:NCT00662701.
Key Words:
SOURCE
http://circ.ahajournals.org/content/125/1/23.short
A single-center experience of clinical and electrophysiologic outcomes of patients undergoing percutaneous endocardial ablation of scar-related Ventricular Tachycardia (VT) is reported in
IMAJ Isr Med Assoc J 2010; 12: 667-670.
http://www.ima.org.il/imaj/ar10nov-04.pdf
Catheter ablation can control or prevent recurrent ischemic VT and reduce incidence of implantable cardioverter defibrillator (ICD) therapy. The ablation can be done during VT in patients with stable VTs or during sinus rhythm in patients with unstable unmappable VTs by targeting the scar border using electroanatomic substrate mapping. VT ablation should be offered to ischemic patients with recurrent uncontrolled VT. Radiofrequency ablation of VT in patients with ischemic cardiomyopathy was proposed to treat and control recurrent VT
J Cardiovasc Electrophys 2005; 16(Suppl 1): S59-70.
Curr Opin Cardiol 2005; 20: 42-7.
An experience with VT ablation in patients with ischemic cardiomyopathy using the electroanatomic mapping system (CARTO) was presented in
There are several reasons for the limited success of ischemic VT ablation. Ventricular scars are not electrically homogenous. They are composed of variable regions of dense fibrosis that create conduction block and surviving myocyte bundles with interstitial fibrosis and diminished coupling, which produce circuitous slow conduction paths that promote reentry
Repeated programmed stimulation typically induces more than one monomorphic VT. Multiple VTs can be due to different circuits in widely disparate areas of scar, different axis from the same region of the scar, or changes in activation remote from the circuit due to functional regions of block
Circulation 2007; 115: 2750-60.
Catheter ablation using conventional techniques are suitable for stable VT. VT reentry circuit can be defined using electroanatomic mapping (CARTO) only during stable and tolerable tachycardia. However, many patients with reduced ejection fraction secondary to coronary heart disease have unstable VTs. These patients do not tolerate sustained VT or rapid pacing. Thus, electric or pace mapping is not available in most cases (unmappable VT with catheter technique). In these cases, scar mapping and ablation can be done only during sinus rhythm using the CARTO system
IMAJ Isr Med Assoc J 2007; 9: 260-4.
Radiofrequency catheter ablation of ventricular tachycardia in the setting of ischemic cardiomyopathy has emerged recently as a useful adjunctive therapy to ICD. Scar related reentrant ventricular tachycardia is the most common underlying mechanism of sustained monomorphic VT in patients with ischemic heart disease.
Limitations of Alternative Treatment Methods:
1. Recurrent ICD shocks have had physiological and psychological side effects.
2. Antiarrythmic drugs are used to reduce incidence of ICD therapy, but their role in reducing mortality is not proven. In addition, these drugs have important side effects including pro-arrythmic effect and worsening of heart failure status.
Conclusions: Ablation of ischemic VT using electroanatomic scar mapping is feasible, has an acceptable success rate and should be offered for ischemic patients with recurrent uncontrolled VT.
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PUT IT IN CONTEXT OF CANCER CELL MOVEMENT
The contraction of skeletal muscle is triggered by nerve impulses, which stimulate the release of Ca2+ from the sarcoplasmic reticuluma specialized network of internal membranes, similar to the endoplasmic reticulum, that stores high concentrations of Ca2+ ions. The release of Ca2+ from the sarcoplasmic reticulum increases the concentration of Ca2+ in the cytosol from approximately 10-7 to 10-5 M. The increased Ca2+ concentration signals muscle contraction via the action of two accessory proteins bound to the actin filaments: tropomyosin and troponin (Figure 11.25). Tropomyosin is a fibrous protein that binds lengthwise along the groove of actin filaments. In striated muscle, each tropomyosin molecule is bound to troponin, which is a complex of three polypeptides: troponin C (Ca2+-binding), troponin I (inhibitory), and troponin T (tropomyosin-binding). When the concentration of Ca2+ is low, the complex of the troponins with tropomyosin blocks the interaction of actin and myosin, so the muscle does not contract. At high concentrations, Ca2+ binding to troponin C shifts the position of the complex, relieving this inhibition and allowing contraction to proceed.
Figure 11.25
Association of tropomyosin and troponins with actin filaments. (A) Tropomyosin binds lengthwise along actin filaments and, in striated muscle, is associated with a complex of three troponins: troponin I (TnI), troponin C (TnC), and troponin T (TnT). In (more ) Contractile Assemblies of Actin and Myosin in Nonmuscle Cells
Contractile assemblies of actin and myosin, resembling small-scale versions of muscle fibers, are present also in nonmuscle cells. As in muscle, the actin filaments in these contractile assemblies are interdigitated with bipolar filaments of myosin II, consisting of 15 to 20 myosin II molecules, which produce contraction by sliding the actin filaments relative to one another (Figure 11.26). The actin filaments in contractile bundles in nonmuscle cells are also associated with tropomyosin, which facilitates their interaction with myosin II, probably by competing with filamin for binding sites on actin.
Figure 11.26
Contractile assemblies in nonmuscle cells. Bipolar filaments of myosin II produce contraction by sliding actin filaments in opposite directions. Two examples of contractile assemblies in nonmuscle cells, stress fibers and adhesion belts, were discussed earlier with respect to attachment of the actin cytoskeleton to regions of cell-substrate and cell-cell contacts (see Figures 11.13 and 11.14). The contraction of stress fibers produces tension across the cell, allowing the cell to pull on a substrate (e.g., the extracellular matrix) to which it is anchored. The contraction of adhesion belts alters the shape of epithelial cell sheets: a process that is particularly important during embryonic development, when sheets of epithelial cells fold into structures such as tubes.
The most dramatic example of actin-myosin contraction in nonmuscle cells, however, is provided by cytokinesisthe division of a cell into two following mitosis (Figure 11.27). Toward the end of mitosis in animal cells, a contractile ring consisting of actin filaments and myosin II assembles just underneath the plasma membrane. Its contraction pulls the plasma membrane progressively inward, constricting the center of the cell and pinching it in two. Interestingly, the thickness of the contractile ring remains constant as it contracts, implying that actin filaments disassemble as contraction proceeds. The ring then disperses completely following cell division.
Figure 11.27
Cytokinesis. Following completion of mitosis (nuclear division), a contractile ring consisting of actin filaments and myosin II divides the cell in two.
http://www.ncbi.nlm.nih.gov/books/NBK9961/
This is good. I don’t recall seeing it in the original comment. I am very aware of the actin myosin troponin connection in heart and in skeletal muscle, and I did know about the nonmuscle work. I won’t deal with it now, and I have been working with Aviral now online for 2 hours.
I have had a considerable background from way back in atomic orbital theory, physical chemistry, organic chemistry, and the equilibrium necessary for cations and anions. Despite the calcium role in contraction, I would not discount hypomagnesemia in having a disease role because of the intracellular-extracellular connection. The description you pasted reminds me also of a lecture given a few years ago by the Nobel Laureate that year on the mechanism of cell division.
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Many thanks,Annette
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Open Journals vs. Subscription-based « Pharmaceutical Intelligenceâ, very compelling plus the blog post ended up being a good read.
Many thanks,Annette
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