Ventricular tachycardic storm with a chronic total coronary artery occlusion treated with percutaneous coronary intervention Timothy A. Mixon, MD
A 66-year-old man with a history of coronary artery disease was evaluated due to ventricular tachycardic (VT) storm. The patient continued to have frequent recurrences of VT despite treatment with amiodarone and lidocaine. Since the ventricular arrhythmia could be related to myocardial ischemia related to a chronic total occlusion (CTO) of the right coronary artery, the patient underwent successful percutaneous coronary intervention of the CTO, followed by implantable cardioverter defibrillator implantation. He had no further episodes of VT during his hospital stay. After 9 months of follow-up, he had no further chest pain or clinically apparent recurrent ischemia. Interrogation of his defibrillator has shown brief nonsustained episodes of ventricular tachycardia, but the patient has not required delivery of a shock. The temporal association between treatment of the CTO and resolution of the VT, as well as the lack of recurrence of sustained VT, suggest a causative link between underlying ischemia produced by a chronically occluded coronary artery and provocation of VT and lend supportive evidence to this treatment approach.
P
atients with chronic total occlusions (CTOs) of the coronary arteries most commonly present with angina pectoris or exertional dyspnea. The role of a CTO in arrhythmogenesis is less clear. Advanced techniques now exist allowing percutaneous treatment of complex CTOs, which can not only improve patient symptoms but may also decrease arrhythmia. CASE DESCRIPTION A 66-year-old man with a history of coronary artery disease, for which he had undergone coronary artery bypass grafting 12 years previously, was transferred to our tertiary care facility due to ventricular tachycardic storm. He had been well until 4 days prior to admission, at which time he presented to an outside facility with syncope. He had spontaneous recovery of consciousness prior to the arrival of emergency medical services. Continuous telemetric monitoring showed no ventricular arrhythmia, an echocardiogram showed normal left ventricular size and normal systolic function, and a nuclear myocardial perfusion study showed a large perfusion defect involving the inferior and inferolateral walls, a mixture of infarction and ischemia. The etiology of syncope was unclear.
196
Two days after dismissal, he had acute onset of substernal chest discomfort that radiated toward his right shoulder and back. Emergency medical services was again summoned; en route to the hospital he was documented to have multiple episodes of ventricular tachycardia (VT) managed with direct current cardioversion and subsequent initiation of intravenous amiodarone. The patient continued to have frequent recurrences of VT (Figure 1a), which prompted the additional initiation of intravenous lidocaine (bolus and drip). Baseline laboratory results revealed normal serum potassium, magnesium, calcium, and phosphorus. Initial serum troponin levels were below assay limit but eventually climbed to a peak of 3.35 ng/mL (abnormal > 0.10 ng/mL). Baseline electrocardiogram (Figure 1b) showed sinus tachycardia, a right bundle branch block, and Q waves in leads II, III, and aVF, with mild diffuse ST segment depression. Cardiac catheterization revealed a patent left internal mammary artery to his left anterior descending artery and two occluded saphenous vein grafts, one previously anastomosed to the second obtuse marginal branch and one to the distal right coronary artery (RCA). The native mid left circumflex and proximal RCA were occluded. The occluded RCA was unchanged compared to the description of a prior angiogram done 5 years previously (Figures 2a, 2b). The decision was made that the ventricular arrhythmia could be related to myocardial ischemia related to the CTOs. Due to the findings of thinning and akinesis of the lateral wall, as well as the angiographic nature of the two CTOs, percutaneous coronary intervention (PCI) of the CTO of the RCA was planned, and the patient was transferred to our tertiary care center. The patient underwent successful PCI of the CTO. As all collaterals to the distal RCA were arising from the proximal RCA, a single 8F, AL1 guide was used to cannulate the RCA. The proximal “cap” was found to be hard, impenetrable to our workhorse wire, with no evidence of microchannels based on probing with a tapered-tip, polymer-coated wire (Fielder XT, Abbott Vascular, Temecula, CA). The proximal cap was able From the Department of Internal Medicine, Division of Cardiology, Texas A&M College of Medicine, Baylor Scott & White Health, Temple, Texas. Corresponding author: Timothy A. Mixon, MD, Division of Cardiology, Texas A&M College of Medicine, Baylor Scott & White Health, MS-33-ST156, 2401 S. 31st Street, Temple, TX 76508 (e-mail: [email protected]).
Proc (Bayl Univ Med Cent) 2015;28(2):196–199
a
b
Figure 1. Twelve-lead electrocardiograms (a) showing ventricular tachycardia and (b) after resolution of ventricular tachycardia, showing sinus rhythm, right bundle branch block, and evidence of prior inferior wall myocardial infarction.
to be penetrated using a Confianza Pro 12 (Abbott Vascular, Temecula, CA) with support of a FineCross (Terumo Medical Somerset, NJ) microcatheter. Once engaged in the occlusion, the Confianza Pro 12 was exchanged for a Pilot 200 (Abbott Vascular, Temecula, CA), which was able to be advanced into a medium-sized right ventricular marginal branch beyond the occlusion (Figure 2c). A small channel was made in the occlusion with an Apex 1.5 mm balloon (Boston Scientific, Natick, MA), after which the pilot wire was able to be moved into the main RCA channel. Angiography confirmed intraluminal placement (Figures 2d, 2e). The pilot wire was exchanged for a standard workhorse wire (Luge, Boston Scientific, Natick, MA), and further angioplasty was performed culminating in placement of a single 2.75 × 28 Promus element drug-eluting stent (Boston Scientific, Natick, MA), which was postdilated with a April 2015
3.0 mm noncompliant balloon (NC Apex, Boston Scientific, Natick, MA). Subsequent images revealed excellent results, with Thrombolysis in Myocardial Infarction grade 3 flow (Figure 2f ). The patient received intravenous unfractionated heparin during the case, with a target activated clotting time of 250 to 300 seconds. He had been loaded with clopidogrel 600 mg a few hours prior to the procedure. Subsequently, he had no further episodes of VT during his hospital stay. His intravenous amiodarone and lidocaine were discontinued approximately 12 hours after the procedure. Serial troponin I peaked at 3.35 ng/mL. An implantable cardioverter defibrillator (ICD) was placed the following day without complication. He was observed another 24 hours in the hospital, during which no further ventricular arrhythmia was seen, and no complications from either the PCI or ICD implantation
Ventricular tachycardic storm with a chronic total coronary artery occlusion treated with percutaneous coronary intervention
197
a
b
c
d
e
f
Figure 2. (a) Angiogram of the right coronary artery (RCA) in the left anterior oblique projection (LAO) showing a moderate length occlusion (arrow) with bridging collaterals. (b) Baseline image in the right anterior oblique (RAO) projection (arrow). (c) Angiogram after the wire was successfully passed through the occlusion, but terminating in a right ventricular marginal branch (arrow). (d) An RAO projection reveals successful wire placement into the distal RCA (arrow). (e) An LAO projection shows successful wire placement into the distal RCA (arrow). (f) Final angiogram after placement of a single drug-eluting stent (arrow).
were present. He was initially discharged on oral amiodarone, but this was stopped shortly after discharge due to concern for potential side effects. At 9-month follow-up, the patient had no further chest pain or clinically apparent recurrent ischemia. ICD interrogation has shown brief nonsustained episodes of VT, but he has not required delivery of a shock. DISCUSSION CTOs can lead to a number of clinical sequelae. The most common scenario that prompts revascularization is the presence of stable, exertional angina pectoris. Many present with dyspnea and decreased exercise tolerance (often attributed to other causes including aging), and reports have documented a higher incidence of left ventricular dysfunction, ventricular arrhythmia, and cardiac death among patients with a CTO. Additionally, retrospective studies of treatment of CTOs have suggested improvements not just in anginal class, but in ventricular performance (1, 2), exercise tolerance (3), tolerance of future ischemic events (4), and even mortality (5–8). While the retrospective nature of these trials limits the conclusions, they nonetheless suggest that treatment of CTOs may benefit the patient beyond simply a reduction in angina. 198
Elegant studies have shown that virtually all CTOs are ischemic when tested by fractional flow reserve, regardless of the maturity of collateral channels (9, 10). Most are ischemic at rest, even in the absence of vasodilators and hyperemia. Furthermore, there is supportive evidence that a CTO not only produces ischemia in the zone supplied by the CTO, but may also provoke ischemia in the territory of donor collateral vessels (11). Animal studies have shown that hibernating myocardium can be a focus of ventricular arrhythmia and sudden cardiac death, even in the absence of acute or prior myocardial infarction. Furthermore, even though adaptations may have occurred that allow for normal myocardial functioning, the potential for life-threatening arrhythmia still exists (12). Prior studies have explored the link between CTOs and ventricular arrhythmia. Nombela-Franco et al studied 162 patients who had received an ICD to prevent sudden cardiac death (13). Among that group, 44% had at least one CTO. Over a 26-month period, appropriate device therapy was delivered to 18% of the patients. The presence of a CTO was found to be associated with higher rates of ventricular arrhythmia and death and was independently associated with appropriate ICD therapy (hazard ratio 3.5).
Baylor University Medical Center Proceedings
Volume 28, Number 2
In conclusion, percutaneous treatment of CTOs may lead not only to relief of angina and dyspnea, but also to resolution of ventricular arrhythmia by minimizing underlying ischemia. 1.
2.
3.
4.
5.
6.
Baks T, van Geuns RJ, Duncker DJ, Cademartiri F, Mollet NR, Krestin GP, Serruys PW, de Feyter PJ. Prediction of left ventricular function after drug-eluting stent implantation for chronic total coronary occlusions. J Am Coll Cardiol 2006;47(4):721–725. Sirnes PA, Myreng Y, Mølstad P, Bonarjee V, Golf S. Improvement in left ventricular ejection fraction and wall motion after successful recanalization of chronic coronary occlusions. Eur Heart J 1998;19(2):273–281. Finci L, Meier B, Favre J, Righetti A, Rutishauser W. Long-term results of successful and failed angioplasty for chronic total coronary arterial occlusion. Am J Cardiol 1990;66(7):660–662. Claessen BE, van der Schaaf RJ, Verouden NJ, Stegenga NK, Engstrom AE, Sjauw KD, Kikkert WJ, Vis MM, Baan J Jr, Koch KT, de Winter RJ, Tijssen JG, Piek JJ, Henriques JP. Evaluation of the effect of a concurrent chronic total occlusion on long-term mortality and left ventricular function in patients after primary percutaneous coronary intervention. JACC Cardiovasc Interv 2009;2(11):1128–1134. Suero JA, Marso SP, Jones PG, Laster SB, Huber KC, Giorgi LV, Johnson WL, Rutherford BD. Procedural outcomes and long-term survival among patients undergoing percutaneous coronary intervention of a chronic total occlusion in native coronary arteries: a 20-year experience. J Am Coll Cardiol 2001;38(2):409–414. Olivari Z, Rubartelli P, Piscione F, Ettori F, Fontanelli A, Salemme L, Giachero C, Di Mario C, Gabrielli G, Spedicato L, Bedogni F; TOASTGISE Investigators. Immediate results and one-year clinical outcome after
April 2015
7.
8.
9.
10.
11.
12.
13.
percutaneous coronary interventions in chronic total occlusions: data from a multicenter, prospective, observational study (TOAST-GISE). J Am Coll Cardiol 2003;41(10):1672–1678. Jones DA, Weerackody R, Rathod K, Behar J, Gallagher S, Knight CJ, Kapur A, Jain AK, Rothman MT, Thompson CA, Mathur A, Wragg A, Smith EJ. Successful recanalization of chronic total occlusions is associated with improved long-term survival. JACC Cardiovasc Interv 2012;5(4):380–388. Moses JW, Karmpaliotis D. Percutaneous revascularization of chronic total coronary occlusions: are the benefits underappreciated? JACC Cardiovasc Interv 2012;5(4):389–392. Werner GS, Surber R, Ferrari M, Fritzenwanger M, Figulla HR. The functional reserve of collaterals supplying long-term chronic total coronary occlusions in patients without prior myocardial infarction. Eur Heart J 2006;27(20):2406–2412. Sachdeva R, Agrawal M, Flynn SE, Werner GS, Uretsky BF. The myocardium supplied by a chronic total occlusion is a persistently ischemic zone. Catheter Cardiovasc Interv 2014;83(1):9–16. Sachdeva R, Agrawal M, Flynn SE, Werner GS, Uretsky BF. Reversal of ischemia of donor artery myocardium after recanalization of a chronic total occlusion. Catheter Cardiovasc Interv 2013;82(4):E453–E458. Canty JM Jr, Suzuki G, Banas MD, Verheyen F, Borgers M, Fallavollita JA. Hibernating myocardium: chronically adapted to ischemia but vulnerable to sudden death. Circ Res 2004;94(8):1142–1149. Nombela-Franco L, Mitroi CD, Fernández-Lozano I, García-Touchard A, Toquero J, Castro-Urda V, Fernández-Diaz JA, Perez-Pereira E, BeltránCorreas P, Segovia J, Werner GS, Javier G, Luis AP. Ventricular arrhythmias among implantable cardioverter-defibrillator recipients for primary prevention: impact of chronic total coronary occlusion (VACTO Primary Study). Circ Arrhythm Electrophysiol 2012;5(1):147–154.
Ventricular tachycardic storm with a chronic total coronary artery occlusion treated with percutaneous coronary intervention
199
A 66-year-old man with a history of coronary artery disease was evaluated due to ventricular tachycardic (VT) storm. The patient continued to have frequent recurrences of VT despite treatment with amiodarone and lidocaine. Since the ventricular arrhythmia could be related to myocardial ischemia related to a chronic total occlusion (CTO) of the right coronary artery, the patient underwent successful percutaneous coronary intervention of the CTO, followed by implantable cardioverter defibrillator implantation. He had no further episodes of VT during his hospital stay. After 9 months of follow-up, he had no further chest pain or clinically apparent recurrent ischemia. Interrogation of his defibrillator has shown brief nonsustained episodes of ventricular tachycardia, but the patient has not required delivery of a shock. The temporal association between treatment of the CTO and resolution of the VT, as well as the lack of recurrence of sustained VT, suggest a causative link between underlying ischemia produced by a chronically occluded coronary artery and provocation of VT and lend supportive evidence to this treatment approach.
P
atients with chronic total occlusions (CTOs) of the coronary arteries most commonly present with angina pectoris or exertional dyspnea. The role of a CTO in arrhythmogenesis is less clear. Advanced techniques now exist allowing percutaneous treatment of complex CTOs, which can not only improve patient symptoms but may also decrease arrhythmia. CASE DESCRIPTION A 66-year-old man with a history of coronary artery disease, for which he had undergone coronary artery bypass grafting 12 years previously, was transferred to our tertiary care facility due to ventricular tachycardic storm. He had been well until 4 days prior to admission, at which time he presented to an outside facility with syncope. He had spontaneous recovery of consciousness prior to the arrival of emergency medical services. Continuous telemetric monitoring showed no ventricular arrhythmia, an echocardiogram showed normal left ventricular size and normal systolic function, and a nuclear myocardial perfusion study showed a large perfusion defect involving the inferior and inferolateral walls, a mixture of infarction and ischemia. The etiology of syncope was unclear.
196
Two days after dismissal, he had acute onset of substernal chest discomfort that radiated toward his right shoulder and back. Emergency medical services was again summoned; en route to the hospital he was documented to have multiple episodes of ventricular tachycardia (VT) managed with direct current cardioversion and subsequent initiation of intravenous amiodarone. The patient continued to have frequent recurrences of VT (Figure 1a), which prompted the additional initiation of intravenous lidocaine (bolus and drip). Baseline laboratory results revealed normal serum potassium, magnesium, calcium, and phosphorus. Initial serum troponin levels were below assay limit but eventually climbed to a peak of 3.35 ng/mL (abnormal > 0.10 ng/mL). Baseline electrocardiogram (Figure 1b) showed sinus tachycardia, a right bundle branch block, and Q waves in leads II, III, and aVF, with mild diffuse ST segment depression. Cardiac catheterization revealed a patent left internal mammary artery to his left anterior descending artery and two occluded saphenous vein grafts, one previously anastomosed to the second obtuse marginal branch and one to the distal right coronary artery (RCA). The native mid left circumflex and proximal RCA were occluded. The occluded RCA was unchanged compared to the description of a prior angiogram done 5 years previously (Figures 2a, 2b). The decision was made that the ventricular arrhythmia could be related to myocardial ischemia related to the CTOs. Due to the findings of thinning and akinesis of the lateral wall, as well as the angiographic nature of the two CTOs, percutaneous coronary intervention (PCI) of the CTO of the RCA was planned, and the patient was transferred to our tertiary care center. The patient underwent successful PCI of the CTO. As all collaterals to the distal RCA were arising from the proximal RCA, a single 8F, AL1 guide was used to cannulate the RCA. The proximal “cap” was found to be hard, impenetrable to our workhorse wire, with no evidence of microchannels based on probing with a tapered-tip, polymer-coated wire (Fielder XT, Abbott Vascular, Temecula, CA). The proximal cap was able From the Department of Internal Medicine, Division of Cardiology, Texas A&M College of Medicine, Baylor Scott & White Health, Temple, Texas. Corresponding author: Timothy A. Mixon, MD, Division of Cardiology, Texas A&M College of Medicine, Baylor Scott & White Health, MS-33-ST156, 2401 S. 31st Street, Temple, TX 76508 (e-mail: [email protected]).
Proc (Bayl Univ Med Cent) 2015;28(2):196–199
a
b
Figure 1. Twelve-lead electrocardiograms (a) showing ventricular tachycardia and (b) after resolution of ventricular tachycardia, showing sinus rhythm, right bundle branch block, and evidence of prior inferior wall myocardial infarction.
to be penetrated using a Confianza Pro 12 (Abbott Vascular, Temecula, CA) with support of a FineCross (Terumo Medical Somerset, NJ) microcatheter. Once engaged in the occlusion, the Confianza Pro 12 was exchanged for a Pilot 200 (Abbott Vascular, Temecula, CA), which was able to be advanced into a medium-sized right ventricular marginal branch beyond the occlusion (Figure 2c). A small channel was made in the occlusion with an Apex 1.5 mm balloon (Boston Scientific, Natick, MA), after which the pilot wire was able to be moved into the main RCA channel. Angiography confirmed intraluminal placement (Figures 2d, 2e). The pilot wire was exchanged for a standard workhorse wire (Luge, Boston Scientific, Natick, MA), and further angioplasty was performed culminating in placement of a single 2.75 × 28 Promus element drug-eluting stent (Boston Scientific, Natick, MA), which was postdilated with a April 2015
3.0 mm noncompliant balloon (NC Apex, Boston Scientific, Natick, MA). Subsequent images revealed excellent results, with Thrombolysis in Myocardial Infarction grade 3 flow (Figure 2f ). The patient received intravenous unfractionated heparin during the case, with a target activated clotting time of 250 to 300 seconds. He had been loaded with clopidogrel 600 mg a few hours prior to the procedure. Subsequently, he had no further episodes of VT during his hospital stay. His intravenous amiodarone and lidocaine were discontinued approximately 12 hours after the procedure. Serial troponin I peaked at 3.35 ng/mL. An implantable cardioverter defibrillator (ICD) was placed the following day without complication. He was observed another 24 hours in the hospital, during which no further ventricular arrhythmia was seen, and no complications from either the PCI or ICD implantation
Ventricular tachycardic storm with a chronic total coronary artery occlusion treated with percutaneous coronary intervention
197
a
b
c
d
e
f
Figure 2. (a) Angiogram of the right coronary artery (RCA) in the left anterior oblique projection (LAO) showing a moderate length occlusion (arrow) with bridging collaterals. (b) Baseline image in the right anterior oblique (RAO) projection (arrow). (c) Angiogram after the wire was successfully passed through the occlusion, but terminating in a right ventricular marginal branch (arrow). (d) An RAO projection reveals successful wire placement into the distal RCA (arrow). (e) An LAO projection shows successful wire placement into the distal RCA (arrow). (f) Final angiogram after placement of a single drug-eluting stent (arrow).
were present. He was initially discharged on oral amiodarone, but this was stopped shortly after discharge due to concern for potential side effects. At 9-month follow-up, the patient had no further chest pain or clinically apparent recurrent ischemia. ICD interrogation has shown brief nonsustained episodes of VT, but he has not required delivery of a shock. DISCUSSION CTOs can lead to a number of clinical sequelae. The most common scenario that prompts revascularization is the presence of stable, exertional angina pectoris. Many present with dyspnea and decreased exercise tolerance (often attributed to other causes including aging), and reports have documented a higher incidence of left ventricular dysfunction, ventricular arrhythmia, and cardiac death among patients with a CTO. Additionally, retrospective studies of treatment of CTOs have suggested improvements not just in anginal class, but in ventricular performance (1, 2), exercise tolerance (3), tolerance of future ischemic events (4), and even mortality (5–8). While the retrospective nature of these trials limits the conclusions, they nonetheless suggest that treatment of CTOs may benefit the patient beyond simply a reduction in angina. 198
Elegant studies have shown that virtually all CTOs are ischemic when tested by fractional flow reserve, regardless of the maturity of collateral channels (9, 10). Most are ischemic at rest, even in the absence of vasodilators and hyperemia. Furthermore, there is supportive evidence that a CTO not only produces ischemia in the zone supplied by the CTO, but may also provoke ischemia in the territory of donor collateral vessels (11). Animal studies have shown that hibernating myocardium can be a focus of ventricular arrhythmia and sudden cardiac death, even in the absence of acute or prior myocardial infarction. Furthermore, even though adaptations may have occurred that allow for normal myocardial functioning, the potential for life-threatening arrhythmia still exists (12). Prior studies have explored the link between CTOs and ventricular arrhythmia. Nombela-Franco et al studied 162 patients who had received an ICD to prevent sudden cardiac death (13). Among that group, 44% had at least one CTO. Over a 26-month period, appropriate device therapy was delivered to 18% of the patients. The presence of a CTO was found to be associated with higher rates of ventricular arrhythmia and death and was independently associated with appropriate ICD therapy (hazard ratio 3.5).
Baylor University Medical Center Proceedings
Volume 28, Number 2
In conclusion, percutaneous treatment of CTOs may lead not only to relief of angina and dyspnea, but also to resolution of ventricular arrhythmia by minimizing underlying ischemia. 1.
2.
3.
4.
5.
6.
Baks T, van Geuns RJ, Duncker DJ, Cademartiri F, Mollet NR, Krestin GP, Serruys PW, de Feyter PJ. Prediction of left ventricular function after drug-eluting stent implantation for chronic total coronary occlusions. J Am Coll Cardiol 2006;47(4):721–725. Sirnes PA, Myreng Y, Mølstad P, Bonarjee V, Golf S. Improvement in left ventricular ejection fraction and wall motion after successful recanalization of chronic coronary occlusions. Eur Heart J 1998;19(2):273–281. Finci L, Meier B, Favre J, Righetti A, Rutishauser W. Long-term results of successful and failed angioplasty for chronic total coronary arterial occlusion. Am J Cardiol 1990;66(7):660–662. Claessen BE, van der Schaaf RJ, Verouden NJ, Stegenga NK, Engstrom AE, Sjauw KD, Kikkert WJ, Vis MM, Baan J Jr, Koch KT, de Winter RJ, Tijssen JG, Piek JJ, Henriques JP. Evaluation of the effect of a concurrent chronic total occlusion on long-term mortality and left ventricular function in patients after primary percutaneous coronary intervention. JACC Cardiovasc Interv 2009;2(11):1128–1134. Suero JA, Marso SP, Jones PG, Laster SB, Huber KC, Giorgi LV, Johnson WL, Rutherford BD. Procedural outcomes and long-term survival among patients undergoing percutaneous coronary intervention of a chronic total occlusion in native coronary arteries: a 20-year experience. J Am Coll Cardiol 2001;38(2):409–414. Olivari Z, Rubartelli P, Piscione F, Ettori F, Fontanelli A, Salemme L, Giachero C, Di Mario C, Gabrielli G, Spedicato L, Bedogni F; TOASTGISE Investigators. Immediate results and one-year clinical outcome after
April 2015
7.
8.
9.
10.
11.
12.
13.
percutaneous coronary interventions in chronic total occlusions: data from a multicenter, prospective, observational study (TOAST-GISE). J Am Coll Cardiol 2003;41(10):1672–1678. Jones DA, Weerackody R, Rathod K, Behar J, Gallagher S, Knight CJ, Kapur A, Jain AK, Rothman MT, Thompson CA, Mathur A, Wragg A, Smith EJ. Successful recanalization of chronic total occlusions is associated with improved long-term survival. JACC Cardiovasc Interv 2012;5(4):380–388. Moses JW, Karmpaliotis D. Percutaneous revascularization of chronic total coronary occlusions: are the benefits underappreciated? JACC Cardiovasc Interv 2012;5(4):389–392. Werner GS, Surber R, Ferrari M, Fritzenwanger M, Figulla HR. The functional reserve of collaterals supplying long-term chronic total coronary occlusions in patients without prior myocardial infarction. Eur Heart J 2006;27(20):2406–2412. Sachdeva R, Agrawal M, Flynn SE, Werner GS, Uretsky BF. The myocardium supplied by a chronic total occlusion is a persistently ischemic zone. Catheter Cardiovasc Interv 2014;83(1):9–16. Sachdeva R, Agrawal M, Flynn SE, Werner GS, Uretsky BF. Reversal of ischemia of donor artery myocardium after recanalization of a chronic total occlusion. Catheter Cardiovasc Interv 2013;82(4):E453–E458. Canty JM Jr, Suzuki G, Banas MD, Verheyen F, Borgers M, Fallavollita JA. Hibernating myocardium: chronically adapted to ischemia but vulnerable to sudden death. Circ Res 2004;94(8):1142–1149. Nombela-Franco L, Mitroi CD, Fernández-Lozano I, García-Touchard A, Toquero J, Castro-Urda V, Fernández-Diaz JA, Perez-Pereira E, BeltránCorreas P, Segovia J, Werner GS, Javier G, Luis AP. Ventricular arrhythmias among implantable cardioverter-defibrillator recipients for primary prevention: impact of chronic total coronary occlusion (VACTO Primary Study). Circ Arrhythm Electrophysiol 2012;5(1):147–154.
Ventricular tachycardic storm with a chronic total coronary artery occlusion treated with percutaneous coronary intervention
199
