The evaluation and management of pericardial disease.
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Cardiac Tamponade↗
Biomedical subjects
M M LeWinter
Publications and source records attributed to M M LeWinter.
Decreased contractile efficiency and increased nonmechanical energy cost in hyperthyroid rabbit heart. Relation between O2 consumption and systolic pressure-volume area or force-time integral.
Both systolic pressure-volume area (PVA) and force-time integral (FTI) have been used as measures of oxygen consumption per beat (VO2) in the isolated left ventricle. The reciprocal of the slope of the VO2-PVA relation has been considered to reflect the chemomechanical energy transduction efficiency of the contractile machinery (contractile efficiency), whereas its VO2 intercept consists of energy cost of excitation-contraction coupling and basal metabolism. To examine whether the increase in myosin isoform V1/V3 ratio in hyperthyroid rabbits decreases contractile efficiency and to determine overall mechanisms of higher oxygen consumption in hyperthyroid hearts, the VO2-PVA and VO2-FTI relations as well as the end-systolic pressure-volume relation were assessed in cross-circulated, isovolumically beating hearts isolated from normal, hyperthyroid, and hypothyroid rabbits. Normalized initial slopes of the rising limb of the curvilinearly fitted end-systolic pressure-volume relation (E'max, ventricular contractility index) were similar for normal and hyperthyroid groups. However, the slopes and VO2 intercepts of the VO2-PVA and VO2-FTI relations were greater in hyperthyroid hearts than in normal hearts. Accordingly, in the hyperthyroid hearts, the contractile efficiency (27 +/- 6%) was lower and left ventricular VO2 for excitation-contraction coupling (0.028 +/- 0.004 ml O2/beat/100 g) was higher than in normal hearts (40 +/- 4% and 0.021 +/- 0.005 ml O2/beat/100 g, respectively). This decreased contractile efficiency in the hyperthyroid hearts was attributable to myosin isoform alteration rather than to increased beta-adrenoceptors because isoproterenol did not affect the slope of the VO2-PVA relation in all groups. In contrast, the slope of the VO2-FTI relation was significantly increased by isoproterenol in all groups. Neither the VO2-PVA nor the VO2-FTI relations in hypothyroid hearts were different from those in normal hearts except for significantly lower VO2 for basal metabolism. We conclude that in hyperthyroid rabbits, the left ventricle has decreased contractile efficiency and increased energy cost of excitation-contraction coupling and that the decreased contractile efficiency in hyperthyroid hearts is probably due to the increased V1/V3 ratio of the myosin isoform component. In addition, this study demonstrates that the VO2-PVA and VO2-FTI relations dissociate depending on the intervention, even in the same isovolumic contraction mode.
Animals↗
Nonuniform regional deformation of the pericardium during the cardiac cycle in dogs.
We hypothesized that local contact forces between the pericardium and the heart cause regional variation in pericardial deformation during the cardiac cycle, reflecting volume changes of the underlying cardiac chambers. To test this, we measured regional pericardial area over the right atrium (RA) and right ventricle (RV) with orthogonal pairs of sonomicrometers in six open-chest dogs. At a left ventricular end-diastolic pressure of 5 mm Hg, RV pericardial area paralleled RV volume, that is, shrinkage during ejection by 10 +/- 8% and expansion during filling. RA pericardial area was reciprocally related to RV pericardial area, with average expansion during ventricular ejection of 2 +/- 2%, thus paralleling RA volume during RV ejection. With volume loading, RV pericardial shrinkage during ejection increased to 14 +/- 6%, but the RA pericardial area change was no longer reciprocal (0 +/- 3% change during RV ejection). Elimination of contact forces by cardiac tamponade resulted in both marked attenuation of RV pericardial area changes and synchronization of the RV and RA pericardial area pattern; that is, both shrank during RV ejection. In two additional dogs, measurement of pericardial area over left ventricle and atrium showed similar results. We conclude that dynamic pericardial contact forces cause regional variation in pericardial deformation, which reflects volume changes of the underlying chambers. These findings imply that the influence of the pericardium on filling and ejection may be more complex than previously recognized, varying both by chamber and dynamically over the course of the cardiac cycle.
Animals↗
Direct diastolic ventricular interaction gain measured with sudden hemodynamic transients.
Changes in right ventricular volume affect left ventricular function via direct ventricular interaction mediated by the septum, common myocardial fibers in the free wall, and the pericardium, and also via series interaction mediated by changes in right ventricular output reaching the left ventricle through the pulmonary circulation. To study direct interaction, series interaction must be held constant or removed from the experimental preparation. Because there has been no way to directly measure direct ventricular interaction in the intact circulation, we developed a new method to experimentally separate these two components of ventricular interaction by combining abrupt occlusion of both venae cavae and quick withdrawal of 10-15 ml of blood from the right ventricle. This procedure decreased right ventricular end-diastolic pressure (RVEDP) on the next beat without changing pulmonary venous flow, left ventricular end-diastolic segment lengths, or left ventricular systolic function. The direct interaction gains, quantified as delta LVEDP/delta RVEDP, where LVEDP is left ventricular end-diastolic pressure, and delta refers to the change between the beats before and after reducing right ventricular volume, were (means +/- SD) 0.32 +/- 0.32 at steady-state LVEDP = 5 mmHg, 0.38 +/- 0.23 at LVEDP = 10 mmHg, and 0.28 +/- 0.32 at LVEDP = 15 mmHg. These gains were not significantly different (P greater than 0.50). Therefore, we calculated an overall average gain by pooling data from the three base-line LVEDP conditions. This value is 0.33 with 95% confidence interval 0.16-0.51. This 95% confidence interval indicates our data are consistent with many previous reports of diastolic direct interaction.
Animals↗
Nonhomogeneous left ventricular regional shortening during acute right ventricular pressure overload.
Acute right ventricular pressure overload shifts the interventricular septum leftward and decreases systolic shortening of the left ventricular (LV) septal-lateral diameter. These changes should alter regional shortening in the LV minor axis. To test this hypothesis, LV minor axis circumferential segment lengths of the septum and anterior, lateral, and posterior walls were measured during pulmonary artery or venae caval constriction in seven open-chest dogs with intact pericardia. Starting at an end-diastolic pressure of 10 mm Hg, venae caval constriction decreased LV end-systolic pressure by 19 +/- 6% and stroke volume by 40 +/- 15% and produced uniform decreases in systolic shortening and end-diastolic length around the minor axis. However, during pulmonary artery constriction resulting in similar decreases in end-systolic pressure (22 +/- 7%) and stroke volume (39 +/- 11%), decreases in systolic shortening were significantly larger in the anterior (-34 +/- 10%) and posterior (-33 +/- 21%) walls than in the septum (-10 +/- 9%) or lateral wall (-8 +/- 13%). The mechanisms of these large anterior and posterior shortening decreases differed: anterior end-diastolic length decreased more than posterior and lateral end-diastolic lengths, while posterior end-systolic length decreased less than anterior and lateral end-systolic lengths. Similar changes were seen at starting end-diastolic pressures of 5 and 15 mm Hg. Propranolol did not alter this nonuniform response, while pericardiectomy attenuated the regional variations. Thus, changes in LV geometry during acute right ventricular pressure overload are associated with nonuniform regional changes in systolic shortening in the LV minor axis that are enhanced by the pericardium.
Animals↗
Systolic direct ventricular interaction affects left ventricular contraction and relaxation in the intact dog circulation.
Changes in right ventricular systolic function directly influence left ventricular systolic function. Most of our knowledge of this systolic direct ventricular interaction comes from studies of isolated hearts, which suggest that changes in right ventricular size only affect left ventricular systolic function at low pressures and volumes. However, almost nothing is known about systolic direct ventricular interaction in a heart functioning in situ as a part of the intact circulation. We used sudden constriction of the pulmonary artery to assess the immediate effect of a change in right ventricular pressure and contraction pattern on left ventricular contraction and relaxation on the beat following the pulmonary artery constriction in anesthetized open-chest dogs. By focusing on this first beat, we were able to avoid the confounding effect of series ventricular interaction, which changes left ventricular filling and, thus, indirectly influences left ventricular function. At baseline left ventricular end-diastolic pressure of 9.6 +/- 2.1 mm Hg (mean +/- SD), sudden pulmonary artery constriction increased left ventricular peak systolic pressure by 3 +/- 2 mm Hg (2% change), left ventricular stroke volume by 2 +/- 2 ml (8% change), and monoexponential time constant of left ventricular pressure fall during relaxation by 9 +/- 6 msec (22% change). This increased left ventricular relaxation time constant was associated with altered regional segment length changes in the posterior and anterior left ventricular free walls during relaxation. We conclude that systolic direct ventricular interaction affects left ventricular systolic function and relaxation under normal conditions in the intact circulation.
Animals↗
Hypertension, exercise, and beta-adrenergic blockade.
STUDY OBJECTIVE: To determine whether beta-adrenergic blocking agents affect exercise tolerance, exercise conditioning response, and blood pressure response to conditioning in hypertensive patients. DESIGN: Randomized, double-blinded, placebo-controlled trial with a 10-week exercise period. SETTING: Outpatient, monitored exercise program at a community-based, university-sponsored cardiac rehabilitation facility. PATIENTS: Thirty adults with mean resting blood pressure of 145 mm Hg or greater (systolic), 95 mm Hg or greater (diastolic), or a combined systolic and diastolic pressure of 140/90 mm Hg or greater. Mean systolic pressure of 170 mm Hg or more or mean diastolic pressure of 105 mm Hg or more was exclusionary. Mean blood pressure was 145/95 mm Hg; mean age was 46.5 years. INTERVENTION: The beta-1-nonselective blocker was propranolol, 80 mg twice daily. The beta-1-selective blocker was metoprolol, 100 mg twice daily, compared with placebo. All patients did exercise conditioning consisting of 40 sessions of aerobic exercise with heart rate monitoring. MEASUREMENTS AND MAIN RESULTS: Resting systolic blood pressure measured without drug therapy was lowered markedly after exercise conditioning on placebo (146 to 135 mm Hg) and on metoprolol (144 to 133 mm Hg) (P less than 0.05), but not on propranolol (no change). Acutely, propranolol decreased both maximal oxygen consumption (VO2max) and exercise duration compared with metoprolol and placebo. Chronically, VO2max increased 24% (95% CI, 8 to 40) in response to training on placebo and 8% on metoprolol (95% CI, 3 to 14); it did not increase on propranolol (95% CI, -10 to 15). CONCLUSIONS: If an exercise program is to be recommended as an adjunct to pharmacologic beta-blockade for hypertension, blood-pressure-lowering effects are preserved and exercise capacity is less affected with a beta-1-selective agent than with a beta-1-nonselective agent. Antihypertensive medications may be avoided altogether for selected patients who sustain an aerobic exercise program.
Adrenergic beta-Antagonists↗
Similar normalized Emax and O2 consumption-pressure-volume area relation in rabbit and dog.
The end-systolic pressure-volume relation (ESPVR), a measure of ventricular contractile state, and systolic pressure-volume area (PVA), a primary determinant of cardiac oxygen consumption per beat (VO2), have been derived from the pressure-volume diagram of the cross-circulated dog left ventricle. The slope of the PVA-VO2 relation represents the efficiency of chemomechanical energy transduction of the contractile machinery. To see whether these relationships were similar in other animals, we studied the isovolumic ESPVR and the VO2-PVA relation in nine excised, cross-circulated rabbit left ventricles. The base-line ESPVR was linear (r = 0.94-0.99) with the slope (Emax) and volume-axis intercept (V0) equal to 83.4 +/- 18.3 mmHg/ml and 0.43 +/- 0.17 ml, respectively. When normalized for left ventricular weight, Emax (4.1 +/- 1.1 mmHg.ml-1.100 g) and V0 (8.9 +/- 3.7 ml/100 g) were similar to values reported for the dog left ventricle. The correlation between PVA and VO2 was linear (r = 0.93-1.00), and the slope (1.90 X 10(-5) +/- 0.44 X 10(-5) ml O2.mmHg-1.ml-1) and VO2-axis intercept (0.040 +/- 0.009 ml O2.beat-1.100 g-1) were similar to values found in the dog left ventricle. Hence, despite the greatly different heart size, the base-line contractile state and chemomechanical energy conversion efficiency of the excised, cross-circulated rabbit left ventricle are similar to those of the dog left ventricle.
Animals↗
Accuracy of volume measurement of rabbit left ventricle by balloon method.
Although the intraventricular balloon method has been commonly used to measure left ventricular volume of the isolated heart preparation of various animals, the accuracy of the method has not been examined in the ventricle of small animals such as the rabbit. To assess the accuracy of the intraventricular balloon method in measuring left ventricular volume, we measured the space between the balloon inflated in the left ventricle and the endocardial surface in eight Formalin-fixed rabbit left ventricles. The space was only 0.05-0.12 ml (1.5-3.6% of total left ventricular volume) at intraballoon pressures of 40-160 mmHg. However, it increased to 0.37 ml (14.6% of total ventricular volume) with a decrease in pressure to 5 mmHg. We conclude that the intraventricular balloon method accurately measures left ventricular volume in the rabbit, especially in the high pressure range.
Animals↗
Biaxial mechanical properties of human pericardium and canine comparisons.
The two-dimensional mechanical properties of human pericardium from seven males undergoing coronary artery bypass surgery were studied. A 25-mm square piece of parietal pericardium overlying the right ventricle was excised. An approximately 8-mm square target was marked at the center, and its dimension was measured electrooptically. When immersed in physiological saline at 37 degrees C, the specimen was subjected to biaxial isotropic loading. Large deformations developed in the beginning of the loading; the pericardium became increasingly stiffer when load was increased, and then became almost inextensible. As in canine pericardium [Lee et al., Am. J. Physiol. 249 (Heart Circ. Physiol. 18): H222-H230, 1985], hysteresis was present and tension-stretch relationship was insensitive to loading frequency during cyclic loading, relaxation of tension was substantial, and creep was insignificant. Unlike canine specimens, however, human pericardium was nearly isotropic and almost three times as thick [mean 0.55 +/- 0.02 mm (SD)]. The human tension-area relation for isotropic loading could be described by an exponential function and was found to shift significantly to the left of the canine. Therefore, human pericardium is less extensible than canine.
Adult↗
Influence of the pericardium on right and left ventricular filling in the dog.
We compared the influence of the pericardium on left and right ventricular (LV, RV) filling by measuring LV and RV pressures and segment lengths (SL, LV free wall, and RV inflow and outflow tracts) in six open-chest, pentobarbital sodium-anesthetized dogs before and after pericardiectomy. End-diastolic pressure (EDP) was varied by partial caval occlusion and dextran infusion. At each site the ln EDP-SL relation was fitted by linear regression and characterized by its slope and 1-Torr EDP intercept. The slope and 1-Torr intercept of the LV ln EDP-SL relation changed variably after pericardiectomy, but in each dog a change occurred that shifted this relation downward. In contrast, the RV inflow tract slope invariably decreased significantly after pericardiectomy, whereas its intercept was unchanged in all but one dog. The RV outflow tract results were similar to the inflow tract but less consistent. By the use of the raw EDP-SL data points, we calculated that the absolute contribution of the pericardium to EDP (i.e., the effective pericardial surface pressure) was similar at the three sites. However, as EDP values increased the proportional contribution of the pericardium to right ventricular end-diastolic pressure (RVEDP) increased, whereas that to left ventricular end-diastolic pressure (LVEDP) remained relatively constant. As a result, at the higher EDP values tested, the pericardium was responsible for a larger proportion of RVEDP than LVEDP.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Right heart pressure does not equal pericardial pressure in the potassium chloride-arrested canine heart in situ.
Recently proposed concepts of pericardial surface pressure, as opposed to liquid pressure, have advanced our understanding of the relationship between pericardial and heart chamber pressures. However, the subsequent suggestion that right heart intracavitary pressure equals, or nearly equals, pericardial surface pressure is not strictly consistent with the physiology of pericardial constraint. If right heart pressure equals pericardial surface pressure, then transmural right heart pressure equals zero. Because of the difficulty in measuring pericardial pressure directly in the beating heart we designed an experiment in the recently arrested canine heart in situ to measure pericardial pressure indirectly and to test the hypothesis that right heart transmural pressure is zero under reasonably physiologic, static equilibrium conditions. According to a static equilibrium analysis of the pressures acting across the walls of the heart, at a given volume the change in right heart pressure caused by removing the pericardium is equal to the pericardial pressure when the pericardium is intact. We found that this drop in pressure caused by pericardiectomy did not equal right heart pressure and therefore that right heart transmural pressure does not equal zero.
Animals↗
Efficacy and safety of nicardipine for chronic, stable angina pectoris: a multicenter randomized trial.
Nicardipine, a new calcium channel blocking drug of the dihydropyridine family, was administered to 63 patients at a dose of 30 or 40 mg 3 times daily in a multicenter, randomized, double-blind, placebo-controlled, crossover trial. Nicardipine midly increased heart rate (HR) at rest and midly decreased the blood pressure (BP) at rest. When generally similar responses to the 30- and 40-mg doses were averaged, nicardipine produced a 7% increase in peak exercise HR, which was balanced by a 6% decrease in peak exercise BP. Thus, no change occurred in the exercise HR-BP product. With nicardipine, treadmill exercise duration increased 9%, time to angina increased 15%, time to 1-mm ST-segment depression increased 16%, and oxygen consumption at peak exercise increased 13%. Mean anginal frequency declined, as did mean weekly sublingual nitroglycerin consumption, but not significantly. There were more cardiovascular side effects with nicardipine than with placebo, with at least 3 patients having increased angina judged by investigators as probably related to the drug. Vasodilatory side effects were also more frequent with nicardipine, but were generally mild and well tolerated; the drug had to be discontinued in only 1 patient, because of vasodilatory effects. Nicardipine is effective and generally well tolerated in patients with chronic stable angina.
Adult↗
Hysteresis of left ventricular end ejection pressure-dimension relations after acute pressure loading in the intact canine heart.
The left ventricular end systolic pressure-volume relation of the isolated canine heart is linear and independent of the loading conditions. The effects of acute pressure loading on the left ventricular end ejection pressure-length relations were studied in the intact canine heart. The lengths of two wall segments of the left ventricle parallel to the minor axis were measured with pairs of miniature piezoelectric crystals. At two levels of filling pressure, with and without control of heart rate, acute increases in left ventricular afterload were produced for six successive beats by occluding the thoracic aorta. After abrupt release of this occlusion, at left ventricular end diastolic pressure less than 10 mmHg, end ejection lengths were longer than before the occlusion for both segments despite the same or lower end ejection pressures. When heart rate was not controlled the mean(SD) difference in end ejection length was 0.46(0.21) mm (n = 100). When heart rate was controlled by atrial pacing after autonomic blockade the difference was 0.37(0.11) mm (n = 80). In contrast, at left ventricular end diastolic pressure greater than 10 mmHg there was no significant difference between end ejection lengths before and after release of the aortic occlusion. Gradual release of the aortic occlusion over 4-5 beats produced clockwise hysteresis of the left ventricular end ejection pressure-length relation when left ventricular end diastolic pressure was less than 10 mmHg. No hysteresis occurred when left ventricular end diastolic pressure was greater than 10 mmHg. Hysteresis of the end systolic pressure-dimension relation was also seen when major and minor axis dimensions of the left ventricular were measured.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
In vivo mechanical behavior of canine pericardium.
We examined the in vivo mechanical behavior of the pericardium by measuring simultaneous atrial and intrapericardial pressures and mutually orthogonal, circumferential, and longitudinally oriented pericardial segment lengths (ultrasonic gauges) in 10 open-chest dogs. Venous return was varied by a combination of caval occlusion followed by volume loading. Up to a mean left atrial pressure of 25 mmHg, the pericardium lengthened virtually exclusively in the circumferential direction (n = 9). Thus, at an intrapericardial pressure of 6.0 +/- 1.0 (+/- SD) mmHg, circumferential strain (normalized to length at pericardial pressure 0 mmHg) was 0.30 +/- 0.28, whereas longitudinal strain was 0.02 +/- 0.06 (P less than 0.05). In five of these dogs, alteration of external pericardial loading by severing the pericardial diaphragmatic attachments did not change the difference between circumferential and longitudinal strain, and in two the same directional strain difference was observed during production of cardia tamponade. In three additional dogs the square of the circumferential segment length was closely correlated with the directly measured intrapericardial volume when saline was infused into the pericardial space in an in situ, arrested heart preparation. Our results indicate that there is marked directional variability in lengthening of the pericardium when the volume of its contents is altered in vivo. This phenomenon is probably the result of complex interactions between the properties of the pericardial tissue and the influence of its internal and external loads.
Animals↗
Determinants of intrapericardial pressure in dogs.
This study investigates factors that influence the pressure measured in the intrapericardial (IP) space. Seven dogs were studied after they were anesthetized with pentobarbital sodium. With the chest closed, intravascular volume expansion by dextran infusion from a mean left atrial (LA) transmural pressure of 8.4 +/- 1.2 (SD) to 15.5 +/- 1.6 Torr caused an increase in mean IP of from 2.6 +/- 1.2 to 3.9 +/- 1.7 Torr (P less than 0.01). This reflected a predominant increase in the influence of the cardiac fossa (CF), which accounted for 56% of the IP pressure after volume expansion. In the open-chest state an increase in mean LA transmural pressure from 9.5 +/- 2.5 to 16.4 +/- 0.6 Torr caused IP pressure to increase from 1.1 +/- 0.9 to 3.0 +/- 1.6 (P less than 0.005), representing the influence of the elastic pericardium alone. The use of positive end-expiratory pressure (PEEP) significantly increased the influence of the CF. Of note, the relation of LA to right atrial (RA) pressure was significantly different with and without the influence of the CF; the RA-to-LA ratio was higher with the chest open under each set of volume conditions with and without PEEP. In four dogs, acute transection of the pericardiodiaphragmatic ligaments led to a small (1-2 Torr) but distinct drop in IP pressure. Thus, IP pressure is affected by the intracardiac volume, the elastic pericardium, the CF, and the pericardiodiaphragmatic attachments, all of which must be considered in an analysis of diastolic properties of the heart in situ.
Animals↗
Regional comparison of midwall segment and area shortening in the canine left ventricle.
We used ultrasonic segment length gauges to examine the regional behavior of midwall fibers at different sites around the left ventricular minor axis in 12 anesthetized dogs. In six dogs (group I) with circumferentially oriented midwall gauges, significantly greater shortening of anterior than lateral or posterior wall segments was demonstrated over a range of left ventricular end-diastolic pressures from 2 to 18 mm Hg. Normalized end-diastolic segment lengths increased more in the anterior wall as end-diastolic pressure increased, suggesting that regional differences in diastolic distensibility may in part account for the observed shortening differences. To examine the extent to which shortening of longitudinally oriented fibers of the subendocardium and subepicardium might influence the behavior of the midwall circumferential fibers, we implanted mutually perpendicular midwall gauges circumferentially and longitudinally in the anterior and posterior walls in six dogs (group II). Longitudinal shortening of midwall fibers was negligible at low end-diastolic pressures, but increased significantly at higher end-diastolic pressures. In the anterior wall, there was greater circumferential than longitudinal shortening, whereas, in the posterior wall, shortening was similar in the two directions. Finally, we calculated the midwall area subtended by the mutually perpendicular gauges and found the systolic change in midwall area to be similar for the anterior and posterior walls at all end-diastolic pressures. We conclude that midwall fibers demonstrate considerable nonuniformity of contraction at different sites around the minor axis. This finding may be related in part to regional differences in diastolic distensibility or in functional interactions between fiber layers. Despite these complex regional, directional, and volume dependent differences in midwall segment function, the systolic changes in midwall area did not vary regionally. Thus, different midwall sites around the minor axis circumference appear to have similar overall contributions to the ejection of blood.
Animals↗
Absence of cardioversion-induced ventricular arrhythmias in patients with therapeutic digoxin levels.
To determine the incidence of cardioversion-induced ventricular arrhythmias in patients with therapeutic serum levels of digoxin, 19 patients (average age [+/- standard deviation] 61 +/- 12 years) undergoing elective direct current cardioversion for atrial fibrillation were studied. Only patients with therapeutic serum digoxin levels (range 0.5 to 1.9 ng/ml; mean 1.1 +/- 0.5) at the time of cardioversion were included. Patients with acute myocardial ischemia or unstable angina, serious electrolyte disturbance or those requiring class I antiarrhythmic agents for control of ventricular or supraventricular arrhythmias were excluded. Ambulatory electrocardiograms were recorded for 24 hours before and 6 hours after cardioversion. No patient developed malignant ventricular arrhythmias (ventricular triplets or tachycardia) in the immediate 3 hour period after cardioversion. Furthermore, there were no significant (p less than 0.05) differences in the frequency of ventricular premature beats or couplets before and after cardioversion. To determine whether the level of serum digoxin or the strength of the applied shock had a significant effect on the development of postcardioversion arrhythmias, the change in frequency of single premature ventricular beats after cardioversion was compared with the serum digoxin level (ng/ml) and the applied energy level (joules) by means of linear regression analysis. There was no significant (p less than 0.05) relation between these variables. These findings suggest that patients with therapeutic serum levels of digoxin may safely undergo cardioversion without the concomitant use of class I antiarrhythmic agents.
Adult↗