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Biomedical subjects

M C Fishbein

Publications and source records attributed to M C Fishbein.

At least 55 records · Page 3Linked to original sources
PubMed2000

Chronic right-sided myocarditis mimicking arrhythmogenic right ventricular dysplasia.

Arrhythmogenic right ventricular dysplasia (ARVD) is a cause of right ventricular heart failure and has been implicated in some cases of sudden death in young adults. It is well known that a large majority of patients with ARVD have histological evidence suggestive of inflammation. Here we report a unique case of chronic myocarditis limited to the right ventricle and right side of the interventricular septum which presented clinically as ARVD. The fact that right sided myocarditis can clinically mimic the genetic disease of classic arrhythmogenic right ventricular dysplasia has therapeutic implications for the patient and relatives.

Adult↗
PubMed2000

Nicotine increases ventricular vulnerability to fibrillation in hearts with healed myocardial infarction.

The vulnerability of the infarcted hearts to ventricular fibrillation (VF) was tested in in situ canine hearts during nicotine infusion. The activation pattern was mapped with 477 bipolar electrodes in open-chest anesthetized dogs (n = 8) 5-6 wk after permanent occlusion of the left anterior descending coronary artery. Nicotine (129 +/- 76 ng/ml) lengthened (P < 0.01) the pacing cycle length at which VF was induced from 171 +/- 8.9 to 210 +/- 14. 7 ms. Nicotine selectively amplified the magnitude of conduction time and monophasic action potential (MAP) amplitude and duration (MAPA and MAPD, respectively) alternans in the epicardial border zone (EBZ) but not in the normal zone. With critical reduction of the MAPA and MAPD in the EBZ, conduction block occurred across the long axis of the EBZ cells. Block led immediately to reentry formation in the EBZ with a mean period of 105 +/- 10 ms, which, after one to two rotations, degenerated to VF. Nicotine widened the range of diastolic intervals over which the dynamic MAPD restitution curve had a slope >1. We conclude that nicotine facilitates conduction block, reentry, and VF in hearts with healed myocardial infarction by increasing the magnitude of depolarization and repolarization alternans consistent with the restitution hypothesis of vulnerability to VF.

Action Potentials↗
PubMed1999

Echocardiographic and pathologic features of explanted Hancock and Carpentier-Edwards bioprosthetic valves in the mitral position.

Modes of failure of Hancock and Carpentier-Edwards (C-E) porcine bioprosthetic valves placed in the mitral position are not completely understood. We reviewed transesophageal echocardiographic (n = 19) and pathologic features of failed Hancock (n = 22) and C-E (n = 8) porcine mitral valves in 30 patients (mean age 70 +/- 13 years). Age at implantation (59 +/- 14 vs 58 +/-14 years, p = 0.9), time to implanted valve degeneration (13 +/- 5 vs 11 +/- 2 years, p = 0.3), and size of bioprosthesis (30 +/- 2 vs 31 +/- 2 mm, p = 0.14) of the implanted Hancock and C-E valves were similar. Anterior leaflet was flail in 15 versus flail posterior leaflet in 5 patients (p = 0.0004). Eccentric posterior mitral regurgitation jet was present in 12, eccentric anterior jet in 2, central jet in 2, and paravalvular jet in 3 patients. Stenosis of bioprosthesis was present in 1 1 Hancock versus 1 C-E valve (p = 0.06). Stent creep at any stent post was present in 14 Hancock versus no C-E valve (p = 0.0013). Large commissural dehiscence was present in 5 C-E versus 1 Hancock valve (p = 0.0006). Ring margin perforation was the most common perforation in Hancock valves (p <0.05, analysis of variance versus all other Hancock perforations). Dehiscence at the stent posts was the most common perforation in C-E valves (p <0.05 vs other C-E perforations, analysis of variance and p <0.001 versus Hancock valves). Thus, Hancock valves showed greater stenosis and stent creep, whereas C-E valves showed large dehiscences at the stent posts on explantation. The anterior leaflet degenerated most frequently in both valves. These findings suggest that the valve design may influence the mechanisms of porcine valve degeneration.

Adult↗
PubMed1999

Role of papillary muscle in the generation and maintenance of reentry during ventricular tachycardia and fibrillation in isolated swine right ventricle.

BACKGROUND: The role of papillary muscle (PM) in the generation and maintenance of reentry is unclear. METHODS AND RESULTS: Computerized mapping (477 bipolar electrodes, 1.6-mm resolution) was performed in fibrillating right ventricles (RVs) of swine in vitro. During ventricular fibrillation (VF), reentrant wave fronts often transiently anchored to the PM. Tissue mass reduction was then performed in 10 RVs until VF converted to ventricular tachycardia (VT). In an additional 6 RVs, procainamide infusion converted VF to VT. Maps showed that 77% (34 of 44) of all VT episodes were associated with a single reentrant wave front anchored to the PM. Purkinje fiber potentials preceded the local myocardial activation, and these potentials were recorded mostly around the PM. When PM was trimmed to the level of endocardium (n = 4), sustained VT was no longer inducible. Transmembrane potential recordings (n = 5) at the PM revealed full action potential during pacing, without evidence of ischemia. Computer simulation studies confirmed the role of PM as a spiral wave anchoring site that stabilized wave conduction. CONCLUSIONS: We conclude that PM is important in the generation and maintenance of reentry during VT and VF.

Animals↗
PubMed1999

Relation between ligament of Marshall and adrenergic atrial tachyarrhythmia.

BACKGROUND: The mechanism of the adrenergic atrial tachyarrhythmia is unclear. We hypothesize that the ligament of Marshall (LOM) is sensitive to adrenergic stimulation and may serve as a source of the adrenergic atrial tachyarrhythmia. METHODS AND RESULTS: We performed computerized mapping studies in isolated-perfused canine left atrial tissues from normal dogs (n=9) and from dogs with chronic atrial fibrillation (AF) induced by 10 to 41 weeks of rapid pacing (n=3). Before isoproterenol, spontaneous activity occurred in only one normal tissue (cycle length, CL >1300 ms). During isoproterenol infusion, automatic rhythm was induced in both normal tissues (CL=578+/-172 ms) and AF tissues (CL=255+/-29 ms, P<0.05). The origin of spontaneous activity was mapped to the LOM. In the AF tissues, but not the normal tissues, we observed the transition from rapid automatic activity to multiple wavelet AF. Ablation of the LOM terminated the spontaneous activity and prevented AF. Immunocytochemical studies of the LOM revealed muscle tracts surrounded by tyrosine hydroxylase-positive (sympathetic) nerves. CONCLUSIONS: We conclude that the LOM is richly innervated by sympathetic nerves and serves as a source of isoproterenol-sensitive focal automatic activity in normal canine atrium. The sensitivity to isoproterenol is upregulated after long-term rapid pacing and may contribute to the development of AF in this model.

Animals↗
PubMed1999

Membrane type 1 matrix metalloproteinase expression in human atherosclerotic plaques: evidence for activation by proinflammatory mediators.

BACKGROUND: Matrix metalloproteinases (MMPs) are expressed in atherosclerotic plaques, where in their active form, they may contribute to vascular remodeling and plaque disruption. In this study, we tested the hypothesis that membrane type 1 MMP (MT1-MMP), a novel transmembrane MMP that activates pro-MMP-2 (gelatinase A), is expressed in human atherosclerotic plaques and that its expression is regulated by proinflammatory molecules. METHODS AND RESULTS: MT1-MMP expression was examined in normal and atherosclerotic human arteries by immunocytochemistry with specific antibodies. MT1-MMP expression in human saphenous vein-derived smooth muscle cells (SMCs) maintained in tissue culture was determined under basal conditions and in response to proinflammatory molecules (interleukin [IL]-1alpha, tumor necrosis factor [TNF]-alpha, and oxidized LDL [ox-LDL]) by use of Northern blot and ribonuclease protection assays for mRNA, Western blot and immunoprecipitation for protein, and gelatin zymography for catalytic activity. Medial SMCs of normal vessel wall expressed MT1-MMP. In atherosclerotic arteries, MT1-MMP expression was noted within the complex atheroma colocalizing with SMCs and macrophages (Mphi). Cultured SMCs constitutively expressed MT1-MMP mRNA and protein, which increased 2- to 4-fold over control in a time-dependent manner within 4 to 8 hours of exposure to IL-1alpha, TNF-alpha, and ox-LDL (thiobarbituric acid-reactive substances, 13.4 nmol/mg LDL protein), whereas native LDL had no effect. Flow cytometry revealed MT1-MMP expression by human monocyte-derived Mphi, which increased 3.8-fold over baseline within 6 hours after exposure to 10 ng/mL TNF-alpha. CONCLUSIONS: This study demonstrates that MT1-MMP, an activator of pro-MMP-2, is expressed by SMCs and Mphi in human atherosclerotic plaques. Furthermore, proinflammatory molecules upregulate MT1-MMP expression in vascular SMCs and Mphi. Thus, activation of SMCs and Mphi by proinflammatory molecules may influence extracellular matrix remodeling in atherosclerosis by regulating MT1-MMP expression.

Antibodies, Monoclonal↗
PubMed1999

Tenascin-C is expressed in macrophage-rich human coronary atherosclerotic plaque.

BACKGROUND: Tenascin is a large extracellular matrix glycoprotein generally found in adult tissues undergoing active remodeling such as healing wounds and tumors. To determine the potential role of tenascin-C (TN-C) in the pathophysiology of atherosclerosis, we investigated the pattern of expression of TN-C in human coronary atherosclerotic plaques. METHODS AND RESULTS: Immunohistochemical staining and in situ hybridization demonstrated minimal and random expression of TN-C in fibrotic but lipid-poor atherosclerotic plaques. In contrast, all plaques with an organized lipid core or ruptured intimal surface strongly expressed TN-C, which was preferentially concentrated around the lipid core, shoulder regions, and ruptured area of the plaques but not in the fibrous cap. TN-C was not detected in normal arterial tissue. To identify the cellular source of TN-C, the plaques were stained with smooth muscle cell- and macrophage-specific antibodies. TN-C expression correlated with the infiltration of macrophages. Northern blot and immunoprecipitation analysis showed that macrophages expressed 7. 0-kb TN-C mRNA and 220-kDa protein. Reverse transcription-polymerase chain reaction of total RNA derived from macrophages showed that they express the small isoform of TN-C. Zymogram analysis revealed that macrophages markedly increased MMP-9 expression. CONCLUSIONS: This study demonstrates that the level of TN-C expression correlates with the degree of inflammation present, not with plaque size. In addition, cultured macrophages have the capacity to express the TN-C gene. These findings suggest the significance of macrophages in the remodeling of atherosclerotic plaque matrix composition.

Adult↗
PubMed1999

Mechanism of acceleration of functional reentry in the ventricle: effects of ATP-sensitive potassium channel opener.

BACKGROUND: The effect of effective refractory period (ERP) shortening on the vulnerability and characteristics of induced functional reentry in the ventricle remain poorly defined. We hypothesized that ERP shortening increases ventricular vulnerability to reentry and accelerates its rate, as is the case in the atrium. METHODS AND RESULTS: The epicardial surfaces of 19 isolated and superfused canine right ventricular slices (4x4 cm and <2 mm thick) were mapped with 480 bipolar electrodes 1.6 mm apart. Vulnerability was tested during pacing at a cycle length (CL) of 600 ms and with a single premature stimulus of 5-ms duration at increasing current strength of 1 to 100 mA. Cromakalim (10 micromol/L), an ATP-sensitive potassium channel opener, caused a significant (P<0. 001) shortening of the ERP but had no effect on conduction velocity. Cromakalim increased (P<0.01) the vulnerability (product of current and the stimulus coupling interval) for reentry induction. Reentry had a significantly shorter CL and lasted for a longer duration (P<0. 001). The central core around which the wave front rotated became smaller, which caused shortening of the CL of reentry. A significant (P<0.001) linear correlation was found between core size and reentry CL. These effects of cromakalim were reversible. Two-dimensional simulation studies using the modified Luo-Rudy I model of cardiac action potential, in which the refractory period was variably shortened by a progressive increase of the time-independent potassium conductance, reproduced the experimental findings. CONCLUSIONS: ERP shortening by an ATP-sensitive potassium channel opener increases ventricular vulnerability to reentry and accelerates its rate by decreasing the core size around which the wave front rotates.

Action Potentials↗
PubMed1999

Arterialization of human vein grafts is associated with tenascin-C expression.

OBJECTIVES: This study was performed to test the hypothesis that tenascin-C (TN-C), an extracellular matrix (ECM) protein with counteradhesive chemotactic and vascular growth-promoting effects, is expressed in "arterialized" human saphenous vein grafts (SVGs). BACKGROUND: Tenascin-C is expressed in the vessel wall after vascular injury in the experimental model, where it has been implicated in the formation of neointima. Overexpression of TN-C has also been implicated in the development and progression of pulmonary hypertension. Saphenous vein grafts are exposed to hemodynamic stress when interposed in the arterial circulation and mechanical stress upregulates expression of TN-C, whereas stress-relaxation suppresses its synthesis. We hypothesized that the hemodynamic stress of increased arterial pressure could also induce TN-C expression in SVG. METHODS: We examined the expression of TN-C protein and mRNA in normal vein and "arterialized" human SVG using immunohistochemistry and in situ hybridization, respectively. RESULTS: TN-C protein was not detected in control human saphenous veins; however, it was uniformly and strongly expressed in the adventitia and media of patent human vein grafts, with minimal or no expression in the neointima (n = 27, 100%). In situ hybridization showed that TN-C mRNA was not detected in the neointima, but was strongly upregulated in the adventitia and media, corroborating immunostaining data (n = 10, 100%). Unlike patent SVG, TN-C was not expressed in the adventitia of occluded grafts, except for a low level of expression around the newly formed vessels in neointima (n = 5, 100%). Smooth muscle cell-specific staining demonstrated that the lack of expression of TN-C in occluded vein grafts is not due to the lack of presence of smooth muscle cells in the graft. CONCLUSIONS: These findings suggest that placement of a venous graft in the arterial system leads to expression of TN-C, which may in turn facilitate graft remodeling. Conversely, loss of flow and intravascular pressure, associated with vein graft occlusion, is accompanied by disappearance of TN-C expression.

Arteries↗
PubMed1999

Relation between cellular repolarization characteristics and critical mass for human ventricular fibrillation.

INTRODUCTION: The critical mass for human ventricular fibrillation (VF) and its electrical determinants are unclear. The goal of this study was to evaluate the relationship between repolarization characteristics and critical mass for VF in diseased human cardiac tissues. METHODS AND RESULTS: Eight native hearts from transplant recipients were studied. The right ventricle was immediately excised, then perfused (n = 6) or superfused (n = 2) with Tyrode's solution at 36 degrees C. The action potential duration (APD) restitution curve was determined by an S1-S2 method. Programmed stimulation and burst pacing were used to induce VF. In 3 of 8 tissues, 10 microM cromakalim, an ATP-sensitive potassium channel opener, was added to the perfusate and the stimulation protocol repeated. Results show that, at baseline, VF did not occur either spontaneously or during rewarming, and it could not be induced by aggressive electrical stimulation in any tissue. The mean APD at 90% depolarization (APD90) at a cycle length of 600 msec was 227+/-49 msec, and the mean slope of the APD restitution curve was 0.22+/-0.08. Among the six tissues perfused, five were not treated with any antiarrhythmic agent. The weight of these five heart samples averaged 111+/-23 g (range 85 to 138). However, after cromakalim infusion, sustained VF (> 30 min in duration) was consistently induced. As compared with baseline in the same tissues, cromakalim shortened the APD90 from 243+/-32 msec to 55+/-18 msec (P < 0.001) and increased the maximum slope of the APD restitution curve from 0.24+/-0.11 to 1.43+/-0.10 (P < 0.01). CONCLUSION: At baseline, the critical mass for VF in diseased human hearts in vitro is > 111 g. However, the critical mass for VF can vary, as it can be reduced by shortening APD and increasing the slope of the APD restitution curve.

Action Potentials↗
PubMed1998

Assessment of myocardial viability by dobutamine echocardiography, positron emission tomography and thallium-201 SPECT: correlation with histopathology in explanted hearts.

OBJECTIVES: We examined the relationship among viability assessment by dobutamine echocardiography (DE), positron emission tomography (PET) and thallium-201 single-photon emission computed tomography (TI-SPECT) to the degree of fibrosis. BACKGROUND: DE, PET and TI-SPECT have been shown to be sensitive in identifying viability of asynergic myocardium. However, PET and TI-SPECT indicated viability in a significant percentage of segments without dobutamine response or functional improvement after revascularization. METHODS: Twelve patients with coronary artery disease and severely reduced left ventricular function (EF 14.5+/-5.2%) were studied with DE prior to cardiac transplantation: 5 had additional PET and 7 had TI-SPECT studies. Results of the three techniques were compared to histologic findings of the explanted hearts. RESULTS: Segments with >75% viable myocytes by histology were determined to be viable in 78%, 89% and 87% by DE, PET and TI-SPECT; those with 50-75% viable myocytes in 71%, 50% and 87%, respectively. Segments with 25-50% viable myocytes showed response to dobutamine in only 15%, but were viable in 60% by PET and 82% by TI-SPECT. Segments with <25% viable myocytes responded to dobutamine in 19%; however, PET and TI-SPECT demonstrated viability in 33% and 38%, respectively. Discrepant segments without dobutamine response but viability by PET and SPECT had significantly more viable myocytes by pathology than did those classified in agreement to be nonviable but had significantly less viable myocytes than those classified in agreement to be viable (p < .001). CONCLUSIONS: These findings suggest that contractile reserve as evidenced by a positive dobutamine response requires at least 50% viable myocytes in a given segment whereas scintigraphic methods also identify segments with less viable myocytes. Thus, the methods may provide complementary information: Nuclear techniques appear to be highly sensitive for the detection of myocardial viability, and negative tests make it highly unlikely that a significant number of viable myocytes are present in a given segment. Conversely, dobutamine echo may be particularly useful for predicting recovery of systolic function after revascularization.

Aged↗
PubMed1998

Transmembrane potential properties at the core of functional reentrant wave fronts in isolated canine right atria.

BACKGROUND: The characteristics of transmembrane potential (TMP) at the core of functional reentry in the atrium are not well understood. METHODS AND RESULTS: In protocol 1 (11 dogs), isolated perfused canine right atria were mapped from the endocardial surface while simultaneous TMPs were recorded from the epicardial surface. Episodes of reentry (n=64) were induced in the presence of 1 to 5 micromol/L acetylcholine. Successful simultaneous TMP recordings and activation maps were made in 8 episodes. The TMP was "near the core" if it was within 3.2 mm of the core; otherwise, it was considered to be "in the periphery." The mean cycle length of reentry was 110+/-35 ms. The TMP amplitude, duration (90% repolarization), and (dV/dt)max near the core (n=106) were 58+/-22 mV, 46+/-14 ms, and 33+/-20 V/s, respectively, significantly less than those in the periphery (n=241): 70+/-8 mV, 94+/-32 ms, and 55+/-10 V/s (P<0.001 for all). In 2 episodes of reentry, the cell at the core remained unexcited at its resting membrane potential. In protocol 2 (2 dogs), we performed simultaneous high-density mapping in 4 episodes of reentry and showed synchronous activation patterns on both surfaces with similar locations of the core. CONCLUSIONS: During meandering functional reentry in isolated canine right atria, (1) TMPs of cells near the core have a reduced amplitude, duration, and (dV/dt)max, and (2) cells at the core may remain unexcited at their resting membrane potential. These findings are compatible with the spiral wave concept of functional reentry in the atrium.

Acetylcholine↗
PubMed1998

Posttransplant therapy using high-dose human immunoglobulin (intravenous gammaglobulin) to control acute humoral rejection in renal and cardiac allograft recipients and potential mechanism of action.

BACKGROUND: Intravenous gammaglobulin (i.v.IG) contains anti-idiotypic antibodies that are potent inhibitors of HLA-specific alloantibodies in vitro and in vivo. In addition, highly HLA-allosensitized patients awaiting transplantation can have HLA alloantibody levels reduced dramatically by i.v.IG infusions, and subsequent transplantation can be accomplished successfully with a crossmatch-negative, histoincompatible organ. METHODS: In this study, we investigated the possible use of i.v.IG to reduce donor-specific anti-HLA alloantibodies arising after transplantation and its efficacy in treating antibody-mediated allograft rejection (AR) episodes. We present data on 10 patients with severe allograft rejection, four of whom developed AR episodes associated with high levels of donor-specific anti-HLA alloantibodies. RESULTS: Most patients showed rapid improvements in AR episodes, with resolution noted within 2-5 days after i.v.IG infusions in all patients. i.v.IG treatment also rapidly reduced donor-specific anti-HLA alloantibody levels after i.v.IG infusion. All AR episodes were reversed. Freedom from recurrent rejection episodes was seen in 9 of 10 patients, some with up to 5 years of follow-up. Results of protein G column fractionation studies from two patients suggest that the potential mechanism by which i.v.IG induces in vivo suppression is a sequence of events leading from initial inhibition due to passive transfer of IgG to eventual active induction of an IgM or IgG blocking antibody in the recipient. CONCLUSION: I.v.IG appears to be an effective therapy to control posttransplant AR episodes in heart and kidney transplant recipients, including patients who have had no success with conventional therapies. Vascular rejection episodes associated with development of donor-specific cytotoxic antibodies appears to be particularly responsive to i.v.IG therapy.

Adult↗
PubMed1998

Role of pectinate muscle bundles in the generation and maintenance of intra-atrial reentry: potential implications for the mechanism of conversion between atrial fibrillation and atrial flutter.

To determine the role of pectinate muscle (PM) bundles in the formation of intra-atrial reentry, 10 isolated canine right atrial tissues were perfused with Tyrode's solution containing 1 to 2.5 micromol/L acetylcholine (ACh). The endocardium was mapped using 477 bipolar electrodes with 1.6-mm resolution. Reentry was induced by a premature stimulus (S2). Computer simulation studies were used to investigate the importance of regional myocardial thickness in reentry formation. A total of 40 episodes of reentry were induced; 28 episodes were stationary, and the remaining 12 were nonstationary. The stationary reentry was induced either immediately after the S2 stimuli (n=9) or after an initial period of irregular activations that lasted 1460+/-1077 ms (n= 19). Of 28 episodes, 20 were initiated by conduction block along large PM ridges, leading to wave break and the initiation of reentry. The reentrant wave fronts remained stationary and rotated around these ridges as anchoring sites. During the transition from the initial irregular activations to stationary reentry, the electrogram morphology converted from "fibrillation-like" to "flutter-like" activity. In 8 episodes, initially stationary reentry converted to irregular activations because of interference with outside wave fronts (n=5) or spontaneous separation of waves from the ridges (n=3). Compared with stationary reentry, nonstationary reentry always occurred over an area without large PMs, and the mean life span was much shorter (102+/-151 versus 3.8+/-1.1 rotations, P<0.001). Computer simulation studies showed that a critical ridge thickness is needed for reentry to anchor, thereby converting fibrillation to flutter. We conclude that PM ridge forms an area where wave break occurs, allowing the initiation of reentry. It also provides a natural anchor to the reentrant wave front, lengthening the life span of reentry. The attachment and detachment of the reentrant wave front to and from the ridge determine "flutter-like" or "fibrillation-like" activity.

Animals↗
PubMed1998

Effects of procainamide on wave-front dynamics during ventricular fibrillation in open-chest dogs.

BACKGROUND: There is increasing evidence that both functional reentrant wave fronts and multiple wavelets are present during ventricular fibrillation (VF). However, the effects of procainamide on the characteristics of activation waves during VF are poorly understood. METHODS AND RESULTS: Seven dogs were studied; six underwent subendocardial chemical ablation procedures. A plaque with 317 to 480 bipolar electrodes was sutured to the right ventricular free wall, and the patterns of activation were registered with a computerized mapping system. VF was electrically induced, and the patterns of activation were registered at baseline and during procainamide infusion (serum concentration, 9.3+/-1.9 microg/mL). Among the six dogs that had their subendocardium ablated, reentrant wave fronts were present in 6 of the 108 runs of VF at baseline and in 6 of the 100 runs of VF during procainamide infusion. By analyzing the wave fronts, we found that the cycle length, refractory period, conduction velocity, and wavelength at baseline were 101+/-9 ms, 54+/-5 ms, 0.93+/-0.21 mm/ms, and 51+/-16 mm, respectively, and during procainamide infusion, values became 125+/-11 ms (P<.001), 119+/-7 ms (P<.001), 0.42+/-0.02 mm/ms (P<.001), and 50+/-4 mm (P=.8), respectively. The vast majority of the activation waves do not form organized reentry. These activation waves broke up more frequently at baseline than during procainamide administration. The number of activation waves was 7.25+/-1.39 s(-1) x cm(-2) at baseline and 4.45+/-1.80 s(-1) x cm(-2) during procainamide administration (P<.001). The dog without subendocardial ablation had similar results. CONCLUSIONS: Procainamide decreases the number of wavelets during VF by preventing spontaneous wave breaks. This represents a novel mechanism of antiarrhythmic drug action.

Animals↗