Incidence Coronary
and Presumed Angioplasty
Etiology
of Ventricular
Fibrillation
During
Edmund Brennan, MD, Peter R. Mahrer, MD, and Vicken J. Aharonian, MD entricular fibrillation (VF) is not an infrequent complication of percutaneoustransluminal coronary anV gioplasty (PTCA). 1,2Similar to diagnostic coronary angiography, it is readily treated by defibrillation and death rarely results.3 There appears to be no relation to the severity of coronary artery disease,and the causeis probably partially related to the use of contrast agents.4We analyzed in detail every case of VF occurring in 922 consecutivePTCA procedures. The patient population comprised members of the Kaiser Permanente Health Plan in Southern California referred to the Regional Cardiac Catheterization Laboratory. For a PTCA to be considered, the following criteria were required: (I) angina that continued with adequate medical therapy, or &hernia demonstrated during exercise or thallium stress testing; and (2) diameter stenosis of >60% as measured by calipers in 2 orthogonal views. Single-vessel, multivessel and graft stenoses were treated. The patients’ electrocardiograms were continually monitored. In patients with right coronary artery or dominant circumflex stenosis, a balloon-tipped pacemaker was advanced to the junction of the inferior vena cava and right atrium. The guiding catheter was used to perform angiography with 2 or 3 injections, which optimally demonstrated the lesion. Arterial pressure was continuously monitoredfrom the tip of the guiding catheter, and if it differed from the previously recorded aortic pressure, the guide position was adjusted, or the guide was replaced by a different type, or one with side holes was used until an undamped pressure tracing was available. Immediately after the appropriate frames were selected, the balloon wire assembly was advanced through the guide and the wire manipulated across the lesion. Most of the time the guide remained in the vessel orifice during balloon and wire introduction. The duration of balloon inflation and the pressure was determined to attain an optimal angiographic appearance. Seventysix percent of Hypaqub (diatrizoate sodium meglumine) was routinely used. Nonionic contrast was used only rarely in patients with ventricular impairment or ventricular irritability. VF occurred in 19 patients. The incidence of this arrhythmia was significantly higher (p = 0.00017) during PTCA of the right coronary artery (n = 14,4%) than during PTCA of the left coronary artery (n = 5, 0.65%). In only 2 patients was the arrhythmia related to hemodynamic instability or prolonged ischemia. In most events VF took place before the balloon was inflated. There was no difference in severity of stenoFrom the Regional Cardiac Catheterization Laboratory, Southern California Permanente Medical Group, 1526 North Edgemont Avenue, Los Angeles, California 90027. Manuscript received September 24, 1990; revised manuscript received December 10, 1990, and accepted December 12.
sis between left and right coronary arteries. Ejection fraction was satisfactory in most patients. One patient died in whom PTCA was attempted as a salvage procedure in the presence of cardiogenic shock where VF was a terminal rhythm. Another patient had vessel occlusion and subsequently myocardial infarction. In the remaining patients the procedure was completed without further ventricular arrhythmia.
VF is not an uncommon complication of coronary angioplasty.The incidenceof VF was noted by Dorros et al1 to be 1.6%in the report of the National Heart, Lung, and Blood Institute Registry seriesof 1,500casesof coronary angioplasty. Bredlow et al2 reported on the Emory experiencein 3,500 patients in which 1.5%neededdirectcurrent shockfor ventricular arrhythmia. Ventricular arrhythmia occurred more often during PTCA of the right coronary artery. In Dorros’ series, 33% of the patients with VF had a major complication (coronary artery bypassgrafting, myocardial infarction or death), but in the Emory seriesonly a small proportion required an intervention other than defibrillation. In our series,only 10% of the arrhythmias were due to occlusion of the vessel, whether by balloon or disruption, or to hemodynamic instability. Impaired left ventricular function was conlined to that same group becausein most patients the ejection fraction was normal. Thus, the usual cause of VF, as seenduring acute coronary artery occlusion,plays only a minor part in the developmentof VF during angioplasty. In seekingthe mechanismof VF in most patients, one must examine the incidence of this arrhythmia during diagnostic angiography.5Several large retrospective serieshaveexaminedthe incidenceof VF during diagnostic studies. Nishimura et al4 reported a 0.5% incidence, 62% of which occurred during right coronary artery injections. They concludedthat although VF can be caused by ischemiaor mechanicalcomplications,almost all VFs have been associatedwith contrast toxicity. Davis et al6 reported an incidenceof 0.6%,and Johnsonet al7 reported an incidenceof 0.56%of significant arrhythmia during coronary arteriography. Contrast material decreasesthe threshold for VF.8,gIschemia, slow prolonged injection, and injection through impacted catheters was noted to lower VF threshold disproportionately. The use of nonionic contrast agents,agentswith supplementalcalcium added,and agentswithout calcium ion-sequesteringstabilizing agentshavebeenassociatedwith a decreasedrisk of VF during coronary angiography.‘O-l4Murdock et all5 demonstratedin canine experiments that repolarization changesreliably precededthe occurrenceof VF, changes that were all but eliminated by modification of the contrast agent. The role of contrast agents in the genesisof VF is thus well established;however,2 questionsremain to be answered.First, why is the incidence of VF higher THE AMERICAN JOURNAL OF CARDIOLOGY APRIL 1. 1991
769
during PTCA than during diagnostic angiography, even when the obviouscausesof vesselobstruction or ventiicular dysfunction are removed? Second,,why is there a marked discrepancy in the incidence of right and left coronary.artery injections? Occlusion by the guide or contrast injection into the sinus node artery plays only a small part-in our series only one casewas associatedwith significant bradycardia. Answers to both questionsare likely related to impairment of flow and stagnation of contrast in the vascular bed. The guiding catheters are larger than the standard 7Fr size used in diagnostic studies, Although we meticulously monitored pressures,this does not assure that adequateflow was present, particularly in casesin which side holes in the guide were necessaryto attain a good pressure contour. Damping of pressuresand the needfor side holesis much lessfrequent during cannulation of the left main coronary artery. We believe that stagnation of contrast material in the vascular bed supplied by the right coronary artery is the major and largely avoidable causeof VF during angioplasty. The preventive proceduresin avoiding this troublesome complication are obvious, and we are currently gathering data to confirm the efficacy of reducing the rate of VF by removing the right guiding cathetersfrom the orifice during wire and balloon introduction, by flushing the orifice with saline solution if the ostium is difficult to ~nnulate, or by using nonionic contrast during PTCA of the right coronary artery. 1. Dorros G, Cowley MJ, Simpson.I, Bentivoglio LG, Block PC, BourassaM, Detre K, Goss&n AJ, Gruentzig AR, K&y SF, Kent KM, Mock MB, Mullin
770
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 67
SM. Myler RK, PassamaniER, Stertzer SH, Williams DO. Percutaneoustransluminal coronary angioplasty:report of complicationsfrom the National Heart, Lung, and Blood Institute.PTCA registry. Circulation 1983;67:723-730. 2. Bredlau CE, Roubin GS, Leimgruber PP. Douglas JS, King SB, Gruentzig AR. In hospital morbidity and mortality in patientsundergoingelectivecoronary angioplasty. Circulation 1985;72:1044-1052. 3. MacAlpin RN, Weidner WA, Katfus AA, Hanfee WN. Electrocardiographic changes during selective coronary cineangiography. Circulation 1966;34: 627-637. 4. Nishimura RA, HolmesDR, McFarland TM, Smith HC, BoveAA. Ventricular arrhythmias during coronary angiographyin patientswith angina pectorisor chest pain syndromes.Am J Cmdiol 1984,53:1496-1499. 5. Guidelines for coronary angiography. A report of the American College of Cardiology/American Heart Associationtask force on assessmentof diagnostic and therapeutic cardiovascularprocedures(subcommitteeon coronary angiography). J Am Co11 Cardioi 1987;10:935-950. 6. Davies K, Kennedy WJ, Harvey KG Jr, Judkins MP, GosselinAJ, Killip T. Complicationsof coronary arteriography from the collaborative study of coronary artery surgery (CASS). Circulafion 1979:59:1105-l112. 7. JohnsonLW, Lozner EC, JohnsonS, Krone R, Pichard AD, Vetrovec GW, Noto TJ. Coronary aiteriography 1984-87:a report of the registry of the Society for Cardiac Angiography and Interventions.I. Resultsand complications.Cathet Cardiouasc Diagn 1989;17:5-10. 8. FisherHW, ThomsonKR. Contrast mediain coronary arteriography: a review. Invest Radio1 1.978;13:450-459. 9. Wolf GL. The Iibrillatory properties of contrast agents. Imesf Radio1 1980:15:S208-S214. 10. Wolf GL, Hirshfeld JW. Changesin the QT interval inducedby Renografin 76 and Hypaque 76 during coronary arteriography. J Am Coil Cardiol 1983;1:1489-1492. 11. Zukerman LS, Friehling TD, Wolf NM, Meister SG, NahassG, Kowey PR. Effect of calcium-bindingadditives on ventricular fibrillation and repolarization changesduring coronary angiography.J Am Co11Cardiol 1987;10:1249-1253, 12. Murdock DK, JohnsonSA, Loeb HS, Scanlon PJ. Ventricular fibrillation during coronary angiography: reduced incidence in man with contrast media lacking calcium binding additives. Cafhef Cardiooasc Diagn 1985;11:153-159. 13. Wolf GL, Mulry CS, Kilzer K, Laski PA. New angiographicagentswith less iibrillatory propensity.Invest Radio1 1981;16:320-323. 14. Missri J, JeresatyRM. Ventricular fibrillation during coronary angiography. Reduced incidence with non-ionic contrast media. Cathet Cardiovasc Diagn 1990;19:4-7. 15. Murdock DK, Euler DE, Becker DM, Murdock JD, Scanlon PJ, Gunnar RM. Ventricular fibrillation during coronary angiography:an analysisof mechanisms.Am Heart J 1985;109:265-273.
and Presumed Angioplasty
Etiology
of Ventricular
Fibrillation
During
Edmund Brennan, MD, Peter R. Mahrer, MD, and Vicken J. Aharonian, MD entricular fibrillation (VF) is not an infrequent complication of percutaneoustransluminal coronary anV gioplasty (PTCA). 1,2Similar to diagnostic coronary angiography, it is readily treated by defibrillation and death rarely results.3 There appears to be no relation to the severity of coronary artery disease,and the causeis probably partially related to the use of contrast agents.4We analyzed in detail every case of VF occurring in 922 consecutivePTCA procedures. The patient population comprised members of the Kaiser Permanente Health Plan in Southern California referred to the Regional Cardiac Catheterization Laboratory. For a PTCA to be considered, the following criteria were required: (I) angina that continued with adequate medical therapy, or &hernia demonstrated during exercise or thallium stress testing; and (2) diameter stenosis of >60% as measured by calipers in 2 orthogonal views. Single-vessel, multivessel and graft stenoses were treated. The patients’ electrocardiograms were continually monitored. In patients with right coronary artery or dominant circumflex stenosis, a balloon-tipped pacemaker was advanced to the junction of the inferior vena cava and right atrium. The guiding catheter was used to perform angiography with 2 or 3 injections, which optimally demonstrated the lesion. Arterial pressure was continuously monitoredfrom the tip of the guiding catheter, and if it differed from the previously recorded aortic pressure, the guide position was adjusted, or the guide was replaced by a different type, or one with side holes was used until an undamped pressure tracing was available. Immediately after the appropriate frames were selected, the balloon wire assembly was advanced through the guide and the wire manipulated across the lesion. Most of the time the guide remained in the vessel orifice during balloon and wire introduction. The duration of balloon inflation and the pressure was determined to attain an optimal angiographic appearance. Seventysix percent of Hypaqub (diatrizoate sodium meglumine) was routinely used. Nonionic contrast was used only rarely in patients with ventricular impairment or ventricular irritability. VF occurred in 19 patients. The incidence of this arrhythmia was significantly higher (p = 0.00017) during PTCA of the right coronary artery (n = 14,4%) than during PTCA of the left coronary artery (n = 5, 0.65%). In only 2 patients was the arrhythmia related to hemodynamic instability or prolonged ischemia. In most events VF took place before the balloon was inflated. There was no difference in severity of stenoFrom the Regional Cardiac Catheterization Laboratory, Southern California Permanente Medical Group, 1526 North Edgemont Avenue, Los Angeles, California 90027. Manuscript received September 24, 1990; revised manuscript received December 10, 1990, and accepted December 12.
sis between left and right coronary arteries. Ejection fraction was satisfactory in most patients. One patient died in whom PTCA was attempted as a salvage procedure in the presence of cardiogenic shock where VF was a terminal rhythm. Another patient had vessel occlusion and subsequently myocardial infarction. In the remaining patients the procedure was completed without further ventricular arrhythmia.
VF is not an uncommon complication of coronary angioplasty.The incidenceof VF was noted by Dorros et al1 to be 1.6%in the report of the National Heart, Lung, and Blood Institute Registry seriesof 1,500casesof coronary angioplasty. Bredlow et al2 reported on the Emory experiencein 3,500 patients in which 1.5%neededdirectcurrent shockfor ventricular arrhythmia. Ventricular arrhythmia occurred more often during PTCA of the right coronary artery. In Dorros’ series, 33% of the patients with VF had a major complication (coronary artery bypassgrafting, myocardial infarction or death), but in the Emory seriesonly a small proportion required an intervention other than defibrillation. In our series,only 10% of the arrhythmias were due to occlusion of the vessel, whether by balloon or disruption, or to hemodynamic instability. Impaired left ventricular function was conlined to that same group becausein most patients the ejection fraction was normal. Thus, the usual cause of VF, as seenduring acute coronary artery occlusion,plays only a minor part in the developmentof VF during angioplasty. In seekingthe mechanismof VF in most patients, one must examine the incidence of this arrhythmia during diagnostic angiography.5Several large retrospective serieshaveexaminedthe incidenceof VF during diagnostic studies. Nishimura et al4 reported a 0.5% incidence, 62% of which occurred during right coronary artery injections. They concludedthat although VF can be caused by ischemiaor mechanicalcomplications,almost all VFs have been associatedwith contrast toxicity. Davis et al6 reported an incidenceof 0.6%,and Johnsonet al7 reported an incidenceof 0.56%of significant arrhythmia during coronary arteriography. Contrast material decreasesthe threshold for VF.8,gIschemia, slow prolonged injection, and injection through impacted catheters was noted to lower VF threshold disproportionately. The use of nonionic contrast agents,agentswith supplementalcalcium added,and agentswithout calcium ion-sequesteringstabilizing agentshavebeenassociatedwith a decreasedrisk of VF during coronary angiography.‘O-l4Murdock et all5 demonstratedin canine experiments that repolarization changesreliably precededthe occurrenceof VF, changes that were all but eliminated by modification of the contrast agent. The role of contrast agents in the genesisof VF is thus well established;however,2 questionsremain to be answered.First, why is the incidence of VF higher THE AMERICAN JOURNAL OF CARDIOLOGY APRIL 1. 1991
769
during PTCA than during diagnostic angiography, even when the obviouscausesof vesselobstruction or ventiicular dysfunction are removed? Second,,why is there a marked discrepancy in the incidence of right and left coronary.artery injections? Occlusion by the guide or contrast injection into the sinus node artery plays only a small part-in our series only one casewas associatedwith significant bradycardia. Answers to both questionsare likely related to impairment of flow and stagnation of contrast in the vascular bed. The guiding catheters are larger than the standard 7Fr size used in diagnostic studies, Although we meticulously monitored pressures,this does not assure that adequateflow was present, particularly in casesin which side holes in the guide were necessaryto attain a good pressure contour. Damping of pressuresand the needfor side holesis much lessfrequent during cannulation of the left main coronary artery. We believe that stagnation of contrast material in the vascular bed supplied by the right coronary artery is the major and largely avoidable causeof VF during angioplasty. The preventive proceduresin avoiding this troublesome complication are obvious, and we are currently gathering data to confirm the efficacy of reducing the rate of VF by removing the right guiding cathetersfrom the orifice during wire and balloon introduction, by flushing the orifice with saline solution if the ostium is difficult to ~nnulate, or by using nonionic contrast during PTCA of the right coronary artery. 1. Dorros G, Cowley MJ, Simpson.I, Bentivoglio LG, Block PC, BourassaM, Detre K, Goss&n AJ, Gruentzig AR, K&y SF, Kent KM, Mock MB, Mullin
770
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 67
SM. Myler RK, PassamaniER, Stertzer SH, Williams DO. Percutaneoustransluminal coronary angioplasty:report of complicationsfrom the National Heart, Lung, and Blood Institute.PTCA registry. Circulation 1983;67:723-730. 2. Bredlau CE, Roubin GS, Leimgruber PP. Douglas JS, King SB, Gruentzig AR. In hospital morbidity and mortality in patientsundergoingelectivecoronary angioplasty. Circulation 1985;72:1044-1052. 3. MacAlpin RN, Weidner WA, Katfus AA, Hanfee WN. Electrocardiographic changes during selective coronary cineangiography. Circulation 1966;34: 627-637. 4. Nishimura RA, HolmesDR, McFarland TM, Smith HC, BoveAA. Ventricular arrhythmias during coronary angiographyin patientswith angina pectorisor chest pain syndromes.Am J Cmdiol 1984,53:1496-1499. 5. Guidelines for coronary angiography. A report of the American College of Cardiology/American Heart Associationtask force on assessmentof diagnostic and therapeutic cardiovascularprocedures(subcommitteeon coronary angiography). J Am Co11 Cardioi 1987;10:935-950. 6. Davies K, Kennedy WJ, Harvey KG Jr, Judkins MP, GosselinAJ, Killip T. Complicationsof coronary arteriography from the collaborative study of coronary artery surgery (CASS). Circulafion 1979:59:1105-l112. 7. JohnsonLW, Lozner EC, JohnsonS, Krone R, Pichard AD, Vetrovec GW, Noto TJ. Coronary aiteriography 1984-87:a report of the registry of the Society for Cardiac Angiography and Interventions.I. Resultsand complications.Cathet Cardiouasc Diagn 1989;17:5-10. 8. FisherHW, ThomsonKR. Contrast mediain coronary arteriography: a review. Invest Radio1 1.978;13:450-459. 9. Wolf GL. The Iibrillatory properties of contrast agents. Imesf Radio1 1980:15:S208-S214. 10. Wolf GL, Hirshfeld JW. Changesin the QT interval inducedby Renografin 76 and Hypaque 76 during coronary arteriography. J Am Coil Cardiol 1983;1:1489-1492. 11. Zukerman LS, Friehling TD, Wolf NM, Meister SG, NahassG, Kowey PR. Effect of calcium-bindingadditives on ventricular fibrillation and repolarization changesduring coronary angiography.J Am Co11Cardiol 1987;10:1249-1253, 12. Murdock DK, JohnsonSA, Loeb HS, Scanlon PJ. Ventricular fibrillation during coronary angiography: reduced incidence in man with contrast media lacking calcium binding additives. Cafhef Cardiooasc Diagn 1985;11:153-159. 13. Wolf GL, Mulry CS, Kilzer K, Laski PA. New angiographicagentswith less iibrillatory propensity.Invest Radio1 1981;16:320-323. 14. Missri J, JeresatyRM. Ventricular fibrillation during coronary angiography. Reduced incidence with non-ionic contrast media. Cathet Cardiovasc Diagn 1990;19:4-7. 15. Murdock DK, Euler DE, Becker DM, Murdock JD, Scanlon PJ, Gunnar RM. Ventricular fibrillation during coronary angiography:an analysisof mechanisms.Am Heart J 1985;109:265-273.
