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Treatment of Multifocal Atrial Tachycardia by Treatment of Pulmonary Insufficiency

2000; Elsevier BV; Volume: 117; Issue: 1 Linguagem: Inglês

10.1378/chest.117.1.7

1931-3543

Toby Engel, Selvaratnam Radhagopalan,

Cardiac pacing and defibrillation studies

“He is the best physician who knows the worthlessness of the most medicines.”Benjamin Franklin, Poor Richard's AlmanacIn this issue of CHEST, Ueng et al (see page 52) use radiofrequency energy to modify or control the ventricular response to multifocal atrial tachycardia (MAT) in the setting of COPD, for the most part avoiding drugs that might exacerbate lung or heart failure. Their 13 patients did not receive mechanical ventilation, they were not given very high doses of theophyline, and they did not have uncorrected blood gas disturbances. Ventricular rate was immediately reduced from an average of 145 beats/min to 89 beats/min (one patient later required a pacemaker; one required a second procedure). Symptoms and quality of life improved at 6-month follow-up, as did left ventricular ejection fraction. Serum theophyline levels, FEV1, and FVC were unchanged, and do not explain the better quality of life or that most patients did not have recurrence of MAT, even transiently when searched for on a Holter monitor.MAT presumably results from right atrial hypertension and distension, in turn resulting from pulmonary hypertension. At first glance, the latter is simply the result of the pulmonary disease. However, in the obstructive pulmonary disease population there is often concomitant left ventricular disease, whether from coronary artery disease, systemic hypertension, or aortic stenosis. Indeed, left ventricular failure frequently accompanies the MAT,1Scher DL Arsura EL Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment.Am Heart J. 1989; 118: 574-580Abstract Full Text PDF PubMed Scopus (49) Google Scholar, 2Kastor JA Multifocal atrial tachycardia.N Engl J Med. 1990; 322: 1713-1718Crossref PubMed Scopus (87) Google Scholar, 3McCord J Borzak S Multifocal atrial tachycardia.Chest. 1998; 113: 203-209Abstract Full Text Full Text PDF PubMed Scopus (76) Google Scholar although hemodynamic and other functional data are largely lacking. Hazard and Burnett,4Hazard PB Burnett CR Verapamil in multifocal atrial tachycardia: hemodynamic and respiratory changes.Chest. 1987; 91: 68-70Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar half of whose patients had clinical evidence of congestive heart failure, found the average pulmonary capillary wedge pressure to be elevated (15.5 + 2.1 mm Hg). Further, there is abnormal left ventricular filling in cor pulmonale.5Tutar E Kaya A Gulec S et al.Echocardiographic evaluation of left ventricular diastolic function in chronic cor pulmonale.Am J Cardiol. 1999; 83: 1414-1416Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar Thus, elevated left ventricular diastolic and pulmonary capillary pressure can contribute to the pulmonary hypertension, ultimately expressed as MAT.Moreover, there are two ways that MAT can contribute to elevation of left ventricular diastolic pressure and thereby to pulmonary hypertension (thereby facilitating MAT, a vicious cycle). First, tachycardia limits the portion of time spent in diastolic filling, especially elevating left atrial and pulmonary capillary pressure when filling is limited by left ventricular disease. Second, prolonged bouts of tachycardia can cause cardiomyopathy. In animals, sustained rapid pacing causes deterioration of ventricular function within a day, with end-stage heart failure within 3 to 5 weeks, largely reversible; in humans, reversal of cardiomyopathy with rate or rhythm control of chronic supraventricular tachycardia is not uncommon.6Shinbane JS Wood MA Jensen DN et al.Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies.J Am Coll Cardiol. 1997; 29: 709-715Abstract Full Text Full Text PDF PubMed Scopus (660) Google ScholarIf MAT indeed contributes to pulmonary dysfunction by these mechanisms, then control of the ventricular response to MAT should not only improve pulmonary symptoms, it should make paroxysms of the arrhythmia less frequent or sustained (interruption of the vicious cycle). Perhaps that is why Ueng et al saw few and transient episodes of MAT after radiofrequency modification of AV conduction. The trick is to control ventricular rate without hampering left ventricular or pulmonary function, which can be problematic with both beta- and calcium blockers; antiarrhythmic drugs notoriously worsen left ventricular function; amiodarone causes pulmonary fibrosis; and digitalis is insufficient when there is sympathetic stimulation.However, returning to the rapid ventricular response to MAT, we postulate that MAT is facilitated by pulmonary dysfunction in turn exacerbated by the fast ventricular rate in MAT and by the drugs used for its control. Ueng et al describe a treatment that interrupts this vicious cycle. Radiofrequency modification of AV conduction during an episode of MAT improved quality of life in their patients disabled from obstructive pulmonary disease. In a sense, these were not paired long-term observations on AV modification and each patient did not serve as his or her own control in terms of the ventricular response; rather, the arrhythmia went away. One could argue therefore that AV modification of the ventricular response to MAT could not explain patient improvement if in fact the MAT was no longer problematic. On the other hand, one can argue that modification of the ventricular response to the MAT actually eliminated the arrhythmia; otherwise, the rapid ventricular rates in response to MAT would have caused the arrhythmia to be sustained or recurrent because of exacerbated pulmonary hypertension secondary to tachycardia-induced left ventricular dysfunction. A simpler explanation for patient improvement would be the avoidance of drugs that are deleterious to pulmonary or ventricular function. Both explanations are simultaneously attractive, because radiofrequency modification of AV conduction both eliminates the need for drug control and is quite effective.There are problems with accepting the results of Ueng et al, even if our explanation for the amelioration of MAT is held tenable. Their patients did not serve as their own controls in terms of MAT frequency, in that we do not know the arrhythmia frequency in the 6 months prior to the study. There were no controls denied AV modification, and perhaps better treatment of obstructive lung disease (study patients do tend to receive more attention) explains both improved symptoms and less MAT. But even so, the nagging question remains as to whether better pulmonary function resulted from elimination of MAT, and not vice versa.The role of radiofrequency modification of AV conduction in refractory MAT therefore requires more controlled study for confirmation. For example, a control group would have antiarrhythmic or AV blocking drugs continued after the procedure in a double-blinded fashion. Comparison of pulmonary function, blood gases, potassium, and magnesium needs to be done in a structured design. Objective measures of function could include exercise performance, as a 6-min walk test. Perhaps the procedure should be extended to other obstructive pulmonary disease patients: those with MAT not refractory to potentially deleterious drugs, those with atrial fibrillation or flutter, or even those merely at risk for MAT. In summary, we need to study whether obstructive pulmonary disease responds to arrhythmia treatment, and not vice versa. “He is the best physician who knows the worthlessness of the most medicines.” Benjamin Franklin, Poor Richard's Almanac In this issue of CHEST, Ueng et al (see page 52) use radiofrequency energy to modify or control the ventricular response to multifocal atrial tachycardia (MAT) in the setting of COPD, for the most part avoiding drugs that might exacerbate lung or heart failure. Their 13 patients did not receive mechanical ventilation, they were not given very high doses of theophyline, and they did not have uncorrected blood gas disturbances. Ventricular rate was immediately reduced from an average of 145 beats/min to 89 beats/min (one patient later required a pacemaker; one required a second procedure). Symptoms and quality of life improved at 6-month follow-up, as did left ventricular ejection fraction. Serum theophyline levels, FEV1, and FVC were unchanged, and do not explain the better quality of life or that most patients did not have recurrence of MAT, even transiently when searched for on a Holter monitor. MAT presumably results from right atrial hypertension and distension, in turn resulting from pulmonary hypertension. At first glance, the latter is simply the result of the pulmonary disease. However, in the obstructive pulmonary disease population there is often concomitant left ventricular disease, whether from coronary artery disease, systemic hypertension, or aortic stenosis. Indeed, left ventricular failure frequently accompanies the MAT,1Scher DL Arsura EL Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment.Am Heart J. 1989; 118: 574-580Abstract Full Text PDF PubMed Scopus (49) Google Scholar, 2Kastor JA Multifocal atrial tachycardia.N Engl J Med. 1990; 322: 1713-1718Crossref PubMed Scopus (87) Google Scholar, 3McCord J Borzak S Multifocal atrial tachycardia.Chest. 1998; 113: 203-209Abstract Full Text Full Text PDF PubMed Scopus (76) Google Scholar although hemodynamic and other functional data are largely lacking. Hazard and Burnett,4Hazard PB Burnett CR Verapamil in multifocal atrial tachycardia: hemodynamic and respiratory changes.Chest. 1987; 91: 68-70Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar half of whose patients had clinical evidence of congestive heart failure, found the average pulmonary capillary wedge pressure to be elevated (15.5 + 2.1 mm Hg). Further, there is abnormal left ventricular filling in cor pulmonale.5Tutar E Kaya A Gulec S et al.Echocardiographic evaluation of left ventricular diastolic function in chronic cor pulmonale.Am J Cardiol. 1999; 83: 1414-1416Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar Thus, elevated left ventricular diastolic and pulmonary capillary pressure can contribute to the pulmonary hypertension, ultimately expressed as MAT. Moreover, there are two ways that MAT can contribute to elevation of left ventricular diastolic pressure and thereby to pulmonary hypertension (thereby facilitating MAT, a vicious cycle). First, tachycardia limits the portion of time spent in diastolic filling, especially elevating left atrial and pulmonary capillary pressure when filling is limited by left ventricular disease. Second, prolonged bouts of tachycardia can cause cardiomyopathy. In animals, sustained rapid pacing causes deterioration of ventricular function within a day, with end-stage heart failure within 3 to 5 weeks, largely reversible; in humans, reversal of cardiomyopathy with rate or rhythm control of chronic supraventricular tachycardia is not uncommon.6Shinbane JS Wood MA Jensen DN et al.Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies.J Am Coll Cardiol. 1997; 29: 709-715Abstract Full Text Full Text PDF PubMed Scopus (660) Google Scholar If MAT indeed contributes to pulmonary dysfunction by these mechanisms, then control of the ventricular response to MAT should not only improve pulmonary symptoms, it should make paroxysms of the arrhythmia less frequent or sustained (interruption of the vicious cycle). Perhaps that is why Ueng et al saw few and transient episodes of MAT after radiofrequency modification of AV conduction. The trick is to control ventricular rate without hampering left ventricular or pulmonary function, which can be problematic with both beta- and calcium blockers; antiarrhythmic drugs notoriously worsen left ventricular function; amiodarone causes pulmonary fibrosis; and digitalis is insufficient when there is sympathetic stimulation. However, returning to the rapid ventricular response to MAT, we postulate that MAT is facilitated by pulmonary dysfunction in turn exacerbated by the fast ventricular rate in MAT and by the drugs used for its control. Ueng et al describe a treatment that interrupts this vicious cycle. Radiofrequency modification of AV conduction during an episode of MAT improved quality of life in their patients disabled from obstructive pulmonary disease. In a sense, these were not paired long-term observations on AV modification and each patient did not serve as his or her own control in terms of the ventricular response; rather, the arrhythmia went away. One could argue therefore that AV modification of the ventricular response to MAT could not explain patient improvement if in fact the MAT was no longer problematic. On the other hand, one can argue that modification of the ventricular response to the MAT actually eliminated the arrhythmia; otherwise, the rapid ventricular rates in response to MAT would have caused the arrhythmia to be sustained or recurrent because of exacerbated pulmonary hypertension secondary to tachycardia-induced left ventricular dysfunction. A simpler explanation for patient improvement would be the avoidance of drugs that are deleterious to pulmonary or ventricular function. Both explanations are simultaneously attractive, because radiofrequency modification of AV conduction both eliminates the need for drug control and is quite effective. There are problems with accepting the results of Ueng et al, even if our explanation for the amelioration of MAT is held tenable. Their patients did not serve as their own controls in terms of MAT frequency, in that we do not know the arrhythmia frequency in the 6 months prior to the study. There were no controls denied AV modification, and perhaps better treatment of obstructive lung disease (study patients do tend to receive more attention) explains both improved symptoms and less MAT. But even so, the nagging question remains as to whether better pulmonary function resulted from elimination of MAT, and not vice versa. The role of radiofrequency modification of AV conduction in refractory MAT therefore requires more controlled study for confirmation. For example, a control group would have antiarrhythmic or AV blocking drugs continued after the procedure in a double-blinded fashion. Comparison of pulmonary function, blood gases, potassium, and magnesium needs to be done in a structured design. Objective measures of function could include exercise performance, as a 6-min walk test. Perhaps the procedure should be extended to other obstructive pulmonary disease patients: those with MAT not refractory to potentially deleterious drugs, those with atrial fibrillation or flutter, or even those merely at risk for MAT. In summary, we need to study whether obstructive pulmonary disease responds to arrhythmia treatment, and not vice versa.