Radiofrequency catheter ablation as a cure for idiopathic tachycardia of both left and right ventricular origin.

OBJECTIVES: The purpose of this study was 1) to investigate the efficacy and safety of radiofrequency energy catheter ablation as curative treatment for idiopathic tachycardia of both left and right ventricular origin, and 2) to compare the usefulness of different methods used to map the site of origin of idiopathic ventricular tachycardia. BACKGROUND: Percutaneous radiofrequency catheter ablation has been used with dramatic success in the treatment of patients with Wolff-Parkinson-White syndrome, atrioventricular node reentrant tachycardia and bundle branch reentrant tachycardia. Limited data are available on the use of radiofrequency energy catheter ablation as curative treatment for idiopathic tachycardia of both left and right ventricular origin. METHODS: Twenty-eight consecutive patients (13 to 71 years old) presenting with idiopathic ventricular tachycardia were enrolled in the study. The site of origin of both left and right ventricular tachycardia was mapped using earliest endocardial activation times during tachycardia and by pace mapping. These mapping techniques were compared. RESULTS: Radiofrequency ablation was successful in all eight patients (100%) with left ventricular tachycardia. Tachycardia recurred in one patient. The ablation procedure was complicated by mild aortic insufficiency in one patient. Right ventricular outflow tract tachycardia was successfully ablated in 17 (85%) of 20 patients. The success rate at follow-up was 85%. In one patient, the ablation procedure was complicated by acute ventricular perforation and death. Pace maps from successful ablation sites were better than pace maps from unsuccessful sites (p < 0.004). Endocardial activation times at successful ablation sites were not different from unsuccessful sites (p < 0.13). CONCLUSIONS: Radiofrequency catheter ablation is an effective treatment for idiopathic ventricular tachycardia. The site of origin of tachycardia is best identified using pace mapping. Significant complications can occur and should be considered in the risk/benefit analysis for each patient.

Coronary air embolism complicating transseptal radiofrequency ablation of left free-wall accessory pathways.

Radiofrequency catheter ablation is an important new technique for curing patients with accessory pathway-mediated tachycardia. Ablation of left free-wall accessory pathways may be accomplished either by a retrograde, transarterial approach or via a transseptal approach using a long vascular sheath. We describe air embolization into the coronary artery as a complication of the transseptal approach, which was temporally associated with catheter exchange. While there were no permanent adverse sequelae, this report emphasizes the need for scrupulous attention to the possible insinuation of air during procedures involving long vascular sheaths across the atrial septum. To prevent air embolism, we recommend slow removal of the ablation catheter along with continuous flushing with heparinized saline during exchanges.

Does systolic subepicardial perfusion come from retrograde subendocardial flow?

To examine the influence of cardiac contraction on systolic coronary flow and transmural blood flow distribution, we measured phasic blood flow velocity in distal extramural coronary arteries by Doppler velocimeter and regional myocardial blood flow by radiolabeled microspheres while the heart was beating and during prolonged diastoles in 12 dogs. A servo-controlled coronary perfusion circuit allowed mean coronary pressure to be selected and maintained during beating and diastolic conditions. In epicardial arteries just proximal to their entrance into the myocardium, blood flow was either negligible or reverse in direction during systole. When the heart was beating, subepicardial blood flow was 24.2 +/- 12.3% higher than during asystole (5.05 +/- 0.91 and 4.11 +/- 0.79 ml.min-1.g-1 for beating and prolonged diastoles, respectively; P less than 0.01). In the subendocardium, flow was 49.8 +/- 14.7% lower in the beating condition than during prolonged diastoles (4.23 +/- 1.46 and 8.26 +/- 1.71 ml.min-1.g-1 for beating and asystole, respectively; P less than 0.01). When heart rate was increased stepwise from 60 to 150 beats/min, subendocardial flow fell approximately linearly; flow to the superficial layer was relatively unaffected. In beating hearts, lowering mean left main coronary artery (LMCA) pressure from 80 to 50 mmHg resulted in more systolic reverse flow and a fall in inner-to-outer flow ratio from 0.82 +/- 0.18 to 0.66 +/- 0.34 (P less than 0.05). Because mean LMCA pressure was held constant when the heart was stopped, differences in regional blood flow between beating and diastolic conditions were primarily due to cardiac contraction. Because little or no blood entered the myocardium from the extramural arteries during systole, we conclude that the decrease in subendocardial flow and the increase in subepicardial flow were caused by retrograde pumping of blood from the deep layer to the superficial layer of the left ventricle. Systolic retrograde flow to the subepicardium may help explain this layer's relative protection from ischemia.

Cardiac contraction affects deep myocardial vessels predominantly.

To evaluate the roles of intramyocardial forces and systolic ventricular pressure in myocardial flow in the different layers separately, we measured myocardial flow in rabbit hearts during stable systolic contracture with left ventricular pressures of 60 (n = 5) and 0 mmHg (n = 5) and during stable diastolic arrest (n = 5). We also measured the number and size of the intramyocardial vessels after perfusion fixation (systolic arrest, n = 5; diastolic arrest, n = 5). In 25 rabbits, hearts were excised and perfused from the aortic root. Systolic arrest was achieved by perfusion of a low-Ca2+ Tyrode solution containing 2.0 mM Ba2+. Diastolic arrest was achieved by intraventricular injection of 700-1,000 mg pentobarbital sodium and was maintained by perfusion with St. Thomas cardioplegic solution. At perfusion pressure of 100 mmHg, subendocardial flow was lower than subepicardial flow during systolic arrest regardless of left ventricular pressure, whereas during diastolic arrest, subendocardial flow was higher than subepicardial flow. Subendocardial-to-subepicardial flow ratios for a physiological range of perfusion pressures were lower during systolic arrest with low rather than with high left ventricular pressure. Small arteriolar and capillary densities showed no difference between subendocardium and subepicardium. During systolic arrest, diameters of subendocardial terminal arterioles (4.6 +/- 1.3 microns) and capillaries (4.0 +/- 1.3 microns) were smaller than those in the subepicardium (8.8 +/- 1.7 and 7.1 +/- 1.6 microns, respectively; P less than 0.0001), whereas during diastolic arrest, diameters of subendocardial terminal arterioles (10.1 +/- 2.0 microns) and capillaries (7.6 +/- 1.8 microns) were slightly larger than those in the subepicardium (9.5 +/- 1.5 and 6.7 +/- 1.0 microns, respectively; P less than 0.01). We conclude that cardiac contraction predominantly affects subendocardial vessels and impedes subendocardial flow more than subepicardial flow regardless of left ventricular pressure.

Nonuniform blood flow in the canine left ventricle.

In order to investigate the relationship between coronary perfusion pressure and blood flow distribution in the left ventricle (LV), we measured myocardial blood flow in small regions using radioactive microspheres in six anesthetized, open-chest dogs. Mean coronary perfusion pressure (CPP) was controlled with a femoral artery to left main coronary artery shunt which included a pressurized, servo-controlled blood reservoir. In each dog, we measured flow in 192 regions of the LV free wall (mean weight per region = 206 +/- 38 mg) at different perfusion pressures. At CPP = 80 mm Hg, blood flow to individual regions varied fourfold (0.30 to 1.18 ml/min/g; relative dispersion (RD) = 21.8 +/- 2.3%). At CPP = 50 mm Hg, flow varied over sevenfold (0.08 to 0.60 ml/min/g; RD = 42.8 +/- 10%; P less than 0.01 vs 80 mm Hg). This relationship between flow variability and CPP was present within individual LV layers as well between layers and is much higher than the error associated with the microsphere technique. We conclude that blood flow to small regions of the LV is markedly nonuniform. This heterogeneity becomes more profound at lower CPP. These findings suggest that (1) global measurements of coronary flow must be interpreted with caution, and (2) even in hearts with normal coronary arteries some regions of the LV are more susceptible to ischemia than others. In addition, these findings may help explain the patchy nature of myocardial damage that occurs following periods of low coronary pressure or inadequate myocardial protection during cardiopulmonary bypass.

Nonuniform loss of regional flow reserve during myocardial ischemia in dogs.

To determine whether coronary vasodilator reserve that persists during myocardial ischemia is present in all left ventricular regions, we measured regional blood flow in 192 left ventricular pieces (mean weight, 201 mg) in each of eight dogs by using radioactive microspheres while perfusing the left main coronary artery at 70, 50, 40, and 30 mm Hg. Flows were measured before and during adenosine infusion to determine flow reserve. Perfusion at 40 and 30 mm Hg produced ischemia in all dogs. At 70 mm Hg, 100% of left ventricular regions had significant flow reserve, compared with 92%, 55%, and 8% during perfusion at 50, 40, and 30 mm Hg, respectively. A greater amount of flow reserve and a greater number of regions responded to adenosine in the subepicardium than in the subendocardium at 50, 40, and 30 mm Hg. We conclude that coronary flow reserve persists in only a subset of left ventricular regions during ischemia and that the number of regions with persistent flow reserve decreases with perfusion pressure. These findings may best be explained by a model in which regional ischemia is a maximal coronary vasodilator and persistent pharmacological vasodilator reserve seen when global markers indicate ischemia simply reflects persistent endogenous flow reserve in myocardial regions not yet ischemic.

Profound spatial heterogeneity of coronary reserve. Discordance between patterns of resting and maximal myocardial blood flow.

We examined the ability of individual regions of the canine left ventricle to increase blood flow relative to baseline rates of perfusion. Regional coronary flow was measured by injecting radioactive microspheres over 90 seconds in seven anesthetized mongrel dogs. Preliminary experiments demonstrated a correlation between the regional distributions of blood flow during asphyxia and pharmacological vasodilatation with adenosine (mean r = 0.75; 192 regions in each of two dogs), both of which resulted in increased coronary flow. Subsequent experiments, during which coronary perfusion pressure was held constant at 80 mm Hg, examined the pattern of blood flow in 384 regions (mean weight, 106 mg) of the left ventricular free wall during resting flow and during maximal coronary flow effected by intracoronary adenosine infusion. We found that resting and maximal flow patterns were completely uncorrelated to each other in a given dog (mean r = 0.06, p = NS; n = 3 dogs). Furthermore, regional coronary reserve, defined as the ratio of maximal to resting flow, ranged from 1.75 (i.e., resting flow was 57% of maximum) to 21.9 (resting flow was 4.5% of maximum). Thus, coronary reserve is spatially heterogeneous and determined by two distinct perfusion patterns: the resting (control) pattern and the maximal perfusion pattern. Normal hearts, therefore, contain small regions that may be relatively more vulnerable to ischemia. This may explain the patchy nature of infarction with hypoxia and at reduced perfusion pressures as well as the difficulty of using global parameters to predict regional ischemia. Despite the wide dispersion of coronary reserve, we found, by autocorrelation analysis, that reserve in neighboring regions (even when separated by a distance of several tissue samples) was significantly correlated. This also applied to patterns of resting myocardial flow. Thus, both resting coronary blood flow and reserve appear to be locally continuous and may define functional zones of vascular control and vulnerability, respectively.

Heterogeneous delivery of cardioplegic solution in the absence of coronary artery disease.

The prevention of intraoperative myocardial damage with cardioplegic solution depends in large measure on the completeness of its delivery. We created a model to study the regional flow distribution of cardioplegic solutions in nondiseased, diastolically arrested, maximally vasodilated canine hearts. Global and regional myocardial flows were measured at different perfusion pressures in hearts perfused either with blood cardioplegic solution (n = 8) or oxygenated crystalloid cardioplegic solution (n = 2). As coronary perfusion decreased, flow in all layers fell significantly (p less than 0.001). This fall was most dramatic in the subendocardium (p less than 0.05). With both types of cardioplegic solutions, the relationship between pressure and flow was nonlinear: At low coronary perfusion pressures, a given change in pressure resulted in a smaller change in flow than at higher perfusion pressures. In addition, we found that in all dogs and at all pressures there was profound variability in the delivery of cardioplegic solution to different small regions of the left ventricular free wall. At a perfusion pressure of 40 mm Hg, the extremes of regional flow differed on average by 203%. This heterogeneity increased significantly with decreasing perfusion pressures. At the lowest perfusion pressure measured (20 mm Hg), the extremes of regional flow differed on average by 365%. These findings emphasize the importance of coronary pressure on the delivery of cardioplegic solution. At low perfusion pressures, not only is mean flow reduced, but a greater number of regions receive limited amounts of cardioplegic solution. These observations may explain the patchy nature of subendocardial damage seen with inadequate myocardial protection.

Quantitating error in blood flow measurements with radioactive microspheres.

Accurate determination of the reproducibility of measurements using the microsphere technique is important in assessing differences in blood flow to different organs or regions within organs, as well as changes in perfusion under various experimental conditions. The sources of error of the technique are briefly reviewed. In addition, we derived a method for combining quantifiable sources of error into a single estimate that was evaluated experimentally by simultaneously injecting eight or nine sets of microspheres (each with a different radionuclide label) into four anesthetized dogs. Each nuclide was used to calculate blood flow in 145-190 myocardial regions. We compared each flow determination (using a single nuclide label) with a weighted mean for the piece (based on the remaining nuclides). The difference was defined as "measured" error. In all, there were a total of 5,975 flow observations. We compared measured error with theoretical estimates based on the Poisson error of radioactive disintegration and microsphere entrapment, nuclide separation error, and reference flow error. We found that combined estimates based on these sources completely accounted for measured error in the relative distribution of microspheres. In addition, our estimates of the error in measuring absolute flows (which were established using microsphere reference samples) slightly, but significantly, underestimated measured error in absolute flow.

Hemodynamic recovery during simulated ventricular tachycardia: role of adrenergic receptor activation.

Ventricular tachycardia (VT) produces a wide variety of hemodynamic outcomes. Variations in autonomic nervous system response were studied in an animal model of VT. In 18 dogs anesthetized with chloralose VT was simulated by ventricular pacing (rate 240 bpm). Dynamic changes in left ventricular (LV) function were assessed during sinus rhythm and after VT was initiated, under variable autonomic conditions: ganglionic blockade with hexamethonium (n = 5), alpha-adrenergic blockade with terazosin (n = 7; 0.3 mg/kg), and beta-adrenergic blockade with propranolol (n = 6; 2 mg/kg). Micromanometers were used to measure LV pressure, and endocardial piezo crystals assessed changes in cavity size. Sinus interval, an index of autonomic tone, was determined immediately after tachycardia was terminated. Under control conditions the onset of simulated VT was accompanied by severe hypotension, with a decline in LV systolic pressure from 113 +/- 5 to 67 +/- 4 mm Hg within 10 seconds (p less than 0.05). Subsequently, during persistent tachycardia peak LV pressure recovered to sinus values, and maximum +dP/dt exceeded sinus values by 20 seconds (2604 +/- 413 vs 2112 +/- 184 mm Hg/sec; 20 seconds for VT vs sinus rhythm). Diastolic pressures were unchanged, and sinus rate accelerated. Ganglionic blockade with hexamethonium resulted in persistent hypotension, blunted +dP/dt, no change in diastolic pressures, and failure of the sinus rate to accelerate after the tachycardia. After beta blockade there was sustained hypotension (LV systolic pressure 78 +/- 4 vs 120 +/- 5 mm Hg; 20 seconds for VT vs sinus rhythm), maximum +dP/dt was blunted, and minimum diastolic ventricular pressure rose. This was due to an upward shift in the diastolic pressure-dimension relationship associated with prolongation of the time constant of LV relaxation. The sinus interval did not change. In contrast, tachycardia during alpha blockade produced a sustained fall in peak LV pressure; however, maximum +dP/dt recovered (2194 +/- 328 vs 2154 +/- 153 mm Hg/sec; 20 seconds for VT vs sinus rhythm), minimum diastolic LV pressure remained low, and sinus rate accelerated after ventricular tachycardia. Hemodynamic recovery during ventricular tachycardia is mediated by the response of the autonomic nervous system and requires both alpha-adrenergic vasoconstriction and beta-adrenergic augmentation of contraction and relaxation.