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Anatomic Distribution of the Culprit Lesion in Patients With Non–ST-Segment Elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention
Journal of the American College of Cardiology © 2008 by the American College of Cardiology Foundation Published by Elsevier Inc.
Vol. 52, No. 16, 2008 ISSN 0735-1097/08/$34.00
CORRESPONDENCE
Research Correspondence
Anatomic Distribution of the Culprit Lesion in Patients With Non–ST-Segment Elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention Findings From the National Cardiovascular Data Registry Clinical Outcomes by Culprit Lesion Patency
To the Editor: Studies of ST-segment elevation myocardial infarction (STEMI) have described unequal distribution of culprit lesions, with the majority occurring in the left anterior descending artery (LAD) and right coronary artery (RCA) (1,2). However, among patients with non–ST-segment elevation myocardial infarction (NSTEMI), there appears to be more uniform distribution (3,4). One potential explanation is that occluded vessels that perfuse the anterior or inferior walls are more likely to be diagnosed as STEMI on the standard 12-lead electrocardiogram than those vessels that perfuse the posterolateral wall (5). We analyzed the American College of Cardiology National Cardiovascular Data Registry (ACC-NCDR) database, a national registry of diagnostic cardiac catheterization and percutaneous coronary intervention (PCI) procedures: 1) to describe the anatomic distribution and patency of culprit lesions; and 2) to evaluate clinical outcomes in a large cohort of patients with NSTEMI undergoing PCI. From January 2004 to March 2006, data from 47,454 consecutive patients undergoing PCI for the indication of NSTEMI were entered into the ACC-NCDR database. A total of 16,301 patients with a prior history of coronary artery bypass grafting or myocardial infarction were excluded. The first lesion attempted during multivessel PCI was assumed to be the culprit. Patients with missing lesion information (n ⫽ 767) were excluded. The final study population consisted of 30,386 patients. Clinical outcomes within the ACC-NCDR registry were limited to recorded inhospital events without central adjudication. Details of the definitions are available online (6). Among the 30,386 NSTEMI patients evaluated, the culprit lesion was located in the LAD in 11,609 (38%), RCA in 10,418 (34%), and left circumflex (LCX) in 8,359 (28%). A total of 7,199 patients (24%) had an occluded infarct artery at the time of angiography. Although patients with an occluded infarct artery were younger than patients with a nonoccluded artery (58 years vs. 73 years), with a lower prevalence of comorbidities such as diabetes (22% vs. 28%), hypertension (60% vs. 69%), prior stroke (6% vs. 10%), and peripheral vascular disease (6% vs. 9%, p ⬍ 0.0001 for all), the rates of mortality, post-procedural cardiogenic shock, and heart failure for the occluded group were higher (Table 1). Overall procedural success rates for occluded culprit lesions were lower (p ⬍ 0.0001) with more frequent procedural complications (p ⬍ 0.0001). There were no significant differences in post-procedural renal failure or vascular or bleeding complications.
Table 1
Clinical Outcomes by Culprit Lesion Patency
Mortality (%) Cardiogenic shock (%) Congestive heart failure (%) Stroke (%) Renal failure (%)* Vascular complications (%)† Bleeding complications (%)‡
Occluded Culprit (n ⴝ 7,199)
Nonoccluded Culprit (n ⴝ 23,187)
p Value
2.5 1.6 1.8
1.4 1.0 1.3
⬍0.0001 ⬍0.0001 0.0002
0.7 1.0 1.1
0.6 0.9 1.4
0.14 0.25 0.24
3.4
3.7
0.23
The p values are based on Pearson chi-square tests for all categorical row variables and Wilcoxon rank sum and signed rank tests for all continuous/ordinal row variables. *Renal failure is defined as serum creatinine increase to ⬎2.0 mg/dl and ⬎2 times the baseline creatinine level or a new requirement for dialysis. †Vascular complications are defined as any bleeding complication, access site occlusion, peripheral embolization, dissection, pseudoaneurysm, or arteriovenous fistula. ‡Bleeding complications are defined as any percutaneous access site, retroperitoneal, gastrointestinal, genitourinary, or other bleeding.
The culprit lesion was identified more frequently in the posterolateral territory among patients with an occluded infarct artery (Coronary Artery Surgery Study segment numbers 3 to 8 and 18 to 27) compared with patients with a nonoccluded artery (40% vs. 32%, p ⬍ 0.0001). Clinical outcomes were similar between posterolateral and nonposterolateral culprit groups in both occluded and nonoccluded vessels, with a few exceptions (Table 2). Bleeding rates were mildly, but significantly, lower in patients with posterolateral culprits in both occluded and nonoccluded groups. A nonoccluded posterolateral culprit was associated with the lowest mortality. In this study, patients with NSTEMI undergoing PCI were least likely to present with a LCX culprit lesion, confirming what has been described in studies of STEMI. This implies that plaque rupture and thrombosis resulting in myocardial necrosis occur less often in the LCX compared with the LAD and RCA. Why plaque rupture would be less likely in the circumflex distribution is not clear. Studies of coronary calcification have not shown differential sparing of the LCX (7). One potential explanation is that the geometry of the LCX and its branches results in differences in wall shear stress compared with the LAD and RCA (8,9). Alternatively, depending on anatomic variations in vessel size and surface area, as well as total amount of left ventricular mass perfused by the LCX, simple probability may be a determining factor in the incidence of plaque rupture and thrombosis.
1348
Correspondence
JACC Vol. 52, No. 16, 2008 October 14, 2008:1347–51
Clinical Outcomes by Culprit Lesion Location Table 2
Clinical Outcomes by Culprit Lesion Location Occluded Culprit
Mortality (%) Cardiogenic shock (%) Congestive heart failure (%) Stroke (%) Renal failure (%)* Vascular complications (%)† Bleeding complications (%)‡
Nonoccluded Culprit
Posterolateral (n ⴝ 2,856)
Nonposterolateral (n ⴝ 4,343)
p Value
Posterolateral (n ⴝ 7,293)
Nonposterolateral (n ⴝ 15,894)
p Value
2.3 1.3 1.9 0.8 1.0 1.0 2.7
2.7 1.8 1.7 0.6 1.0 1.1 3.8
0.42 0.14 0.76 0.19 0.94 0.75 0.02
1.0 1.0 1.4 0.6 0.7 1.4 3.3
1.6 1.1 1.3 0.7 0.9 1.4 4.0
0.0004 0.169 0.76 0.01 0.09 0.35 0.005
The p values are based on Pearson chi-square tests for all categorical row variables and Wilcoxon tests for all continuous/ordinal row variables. *Renal failure is defined as serum creatinine increase to ⬎2.0 mg/dl and ⬎2 times the baseline creatinine level or a new requirement for dialysis. †Vascular complications are defined as any bleeding complication, access site occlusion, peripheral embolization, dissection, pseudoaneurysm, or arteriovenous fistula. ‡Bleeding complications are defined as any percutaneous access site, retroperitoneal, gastrointestinal, genitourinary, or other bleeding.
Approximately one-quarter of patients with NSTEMI had an occluded culprit vessel at the time of angiography. Of these, 66% occurred in the posterolateral distribution, demonstrating the limitations of the current diagnostic approach to acute coronary syndromes, which relies heavily on STEMI/NSTEMI dichotomization for early treatment decisions. Because patients who were found to have an occluded infarct artery suffered worse outcomes, the need for additional methods to rapidly identify patients with occluded arteries despite the absence of ST-segment elevation is highlighted. Currently, the use of posterior electrocardiographic leads (V7 to V9) is a Class IIa recommendation in patients presenting with ischemic chest discomfort (10). Other potential diagnostic modalities include emergent transthoracic echocardiography, immediate nuclear myocardial perfusion imaging, computed tomographic coronary angiography, or traditional invasive coronary angiography on a time scale usually reserved for STEMI patients. These approaches, alone or in combination, deserve further investigation. *William C. Dixon, IV, MD *Cardiology Service Dwight D. Eisenhower Army Medical Center 300 Hospital Road Fort Gordon, Georgia 30905 E-mail: [email protected] Tracy Y. Wang, MD, MS David Dai, MS Kendrick A. Shunk, MD, PhD Eric D. Peterson, MD, MPH Matthew T. Roe, MD, MHS on behalf of the National Cardiovascular Data Registry doi:10.1016/j.jacc.2008.07.029 Please note: Dr. Wang has received research grants to institution from Bristol-Myers Squibb, Sanofi-Aventis, Schering-Plough, The Medicines Co., Heartscape Inc., and Stacks Inc. Dr. Peterson has received research grants to institution from Bristol-
Myers Squibb, Sanofi-Aventis/Bristol-Myers Squibb Partnership, Bristol-Myers Squibb/Merck Partnership, and Schering-Plough. Dr. Roe has received research grants to institution from Bristol-Myers Squibb, Sanofi-Aventis, Schering-Plough, KAI Pharmaceuticals, Portola Pharmaceuticals, Lilly, and Daiichi-Sankyo.
REFERENCES
1. Wang JC, Normand ST, Mauri L, et al. Coronary artery spatial distribution of acute myocardial infarction occlusions. Circulation 2004;110:278 – 84. 2. Schmitt C, Gunter L, Schmeider S, et al. Diagnosis of acute myocardial infarction in angiographically documented occluded infarct vessel. Chest 2001;120:1540 – 6. 3. Abbas A, Boura J, Brewington S, et al. Acute angiographic analysis of non-ST-segment elevation myocardial infarction. Am J Cardiol 2004; 94:907–9. 4. Jacobs A, French J, Col J, et al. Cardiogenic shock with non-STsegment elevation myocardial infarction: a report from the SHOCK Trial Registry. J Am Coll Cardiol 2000;36:1091– 6. 5. Matetzky S, Freimark D, Feinberg MS, et al. Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7–9. J Am Coll Cardiol 1999;34:748 –53. 6. American College of Cardiology. ACC National Cardiac Catheterization Module 3.04. July 30, 2004. Available at: http://www.accncdr.com/ WebNCDR/NCDRDocuments/datadictdefsonlyv30.pdf. Accessed December 11, 2006. 7. Kajinami K, Seki H, Takekoshi N, et al. Coronary calcification and coronary atherosclerosis: site by site comparative morphologic study of electron beam computed tomography and coronary angiography. J Am Coll Cardiol 1997;29:1549 –56. 8. Soulis JV, Farmakis TM, Giannoglou GD, et al. Wall shear stress in normal left coronary tree. J Biomech 2006;39:742–9. 9. Wahle A, Lopez JJ, Olszewski ME, et al. Plaque development, vessel curvature, and wall shear stress in coronary arteries assessed by x-ray, angiography, and intravascular ultrasound. Med Image Anal 2006;10: 615–31. 10. Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non– ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction). J Am Coll Cardiol 2007;50:e1–157.
Vol. 52, No. 16, 2008 ISSN 0735-1097/08/$34.00
CORRESPONDENCE
Research Correspondence
Anatomic Distribution of the Culprit Lesion in Patients With Non–ST-Segment Elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention Findings From the National Cardiovascular Data Registry Clinical Outcomes by Culprit Lesion Patency
To the Editor: Studies of ST-segment elevation myocardial infarction (STEMI) have described unequal distribution of culprit lesions, with the majority occurring in the left anterior descending artery (LAD) and right coronary artery (RCA) (1,2). However, among patients with non–ST-segment elevation myocardial infarction (NSTEMI), there appears to be more uniform distribution (3,4). One potential explanation is that occluded vessels that perfuse the anterior or inferior walls are more likely to be diagnosed as STEMI on the standard 12-lead electrocardiogram than those vessels that perfuse the posterolateral wall (5). We analyzed the American College of Cardiology National Cardiovascular Data Registry (ACC-NCDR) database, a national registry of diagnostic cardiac catheterization and percutaneous coronary intervention (PCI) procedures: 1) to describe the anatomic distribution and patency of culprit lesions; and 2) to evaluate clinical outcomes in a large cohort of patients with NSTEMI undergoing PCI. From January 2004 to March 2006, data from 47,454 consecutive patients undergoing PCI for the indication of NSTEMI were entered into the ACC-NCDR database. A total of 16,301 patients with a prior history of coronary artery bypass grafting or myocardial infarction were excluded. The first lesion attempted during multivessel PCI was assumed to be the culprit. Patients with missing lesion information (n ⫽ 767) were excluded. The final study population consisted of 30,386 patients. Clinical outcomes within the ACC-NCDR registry were limited to recorded inhospital events without central adjudication. Details of the definitions are available online (6). Among the 30,386 NSTEMI patients evaluated, the culprit lesion was located in the LAD in 11,609 (38%), RCA in 10,418 (34%), and left circumflex (LCX) in 8,359 (28%). A total of 7,199 patients (24%) had an occluded infarct artery at the time of angiography. Although patients with an occluded infarct artery were younger than patients with a nonoccluded artery (58 years vs. 73 years), with a lower prevalence of comorbidities such as diabetes (22% vs. 28%), hypertension (60% vs. 69%), prior stroke (6% vs. 10%), and peripheral vascular disease (6% vs. 9%, p ⬍ 0.0001 for all), the rates of mortality, post-procedural cardiogenic shock, and heart failure for the occluded group were higher (Table 1). Overall procedural success rates for occluded culprit lesions were lower (p ⬍ 0.0001) with more frequent procedural complications (p ⬍ 0.0001). There were no significant differences in post-procedural renal failure or vascular or bleeding complications.
Table 1
Clinical Outcomes by Culprit Lesion Patency
Mortality (%) Cardiogenic shock (%) Congestive heart failure (%) Stroke (%) Renal failure (%)* Vascular complications (%)† Bleeding complications (%)‡
Occluded Culprit (n ⴝ 7,199)
Nonoccluded Culprit (n ⴝ 23,187)
p Value
2.5 1.6 1.8
1.4 1.0 1.3
⬍0.0001 ⬍0.0001 0.0002
0.7 1.0 1.1
0.6 0.9 1.4
0.14 0.25 0.24
3.4
3.7
0.23
The p values are based on Pearson chi-square tests for all categorical row variables and Wilcoxon rank sum and signed rank tests for all continuous/ordinal row variables. *Renal failure is defined as serum creatinine increase to ⬎2.0 mg/dl and ⬎2 times the baseline creatinine level or a new requirement for dialysis. †Vascular complications are defined as any bleeding complication, access site occlusion, peripheral embolization, dissection, pseudoaneurysm, or arteriovenous fistula. ‡Bleeding complications are defined as any percutaneous access site, retroperitoneal, gastrointestinal, genitourinary, or other bleeding.
The culprit lesion was identified more frequently in the posterolateral territory among patients with an occluded infarct artery (Coronary Artery Surgery Study segment numbers 3 to 8 and 18 to 27) compared with patients with a nonoccluded artery (40% vs. 32%, p ⬍ 0.0001). Clinical outcomes were similar between posterolateral and nonposterolateral culprit groups in both occluded and nonoccluded vessels, with a few exceptions (Table 2). Bleeding rates were mildly, but significantly, lower in patients with posterolateral culprits in both occluded and nonoccluded groups. A nonoccluded posterolateral culprit was associated with the lowest mortality. In this study, patients with NSTEMI undergoing PCI were least likely to present with a LCX culprit lesion, confirming what has been described in studies of STEMI. This implies that plaque rupture and thrombosis resulting in myocardial necrosis occur less often in the LCX compared with the LAD and RCA. Why plaque rupture would be less likely in the circumflex distribution is not clear. Studies of coronary calcification have not shown differential sparing of the LCX (7). One potential explanation is that the geometry of the LCX and its branches results in differences in wall shear stress compared with the LAD and RCA (8,9). Alternatively, depending on anatomic variations in vessel size and surface area, as well as total amount of left ventricular mass perfused by the LCX, simple probability may be a determining factor in the incidence of plaque rupture and thrombosis.
1348
Correspondence
JACC Vol. 52, No. 16, 2008 October 14, 2008:1347–51
Clinical Outcomes by Culprit Lesion Location Table 2
Clinical Outcomes by Culprit Lesion Location Occluded Culprit
Mortality (%) Cardiogenic shock (%) Congestive heart failure (%) Stroke (%) Renal failure (%)* Vascular complications (%)† Bleeding complications (%)‡
Nonoccluded Culprit
Posterolateral (n ⴝ 2,856)
Nonposterolateral (n ⴝ 4,343)
p Value
Posterolateral (n ⴝ 7,293)
Nonposterolateral (n ⴝ 15,894)
p Value
2.3 1.3 1.9 0.8 1.0 1.0 2.7
2.7 1.8 1.7 0.6 1.0 1.1 3.8
0.42 0.14 0.76 0.19 0.94 0.75 0.02
1.0 1.0 1.4 0.6 0.7 1.4 3.3
1.6 1.1 1.3 0.7 0.9 1.4 4.0
0.0004 0.169 0.76 0.01 0.09 0.35 0.005
The p values are based on Pearson chi-square tests for all categorical row variables and Wilcoxon tests for all continuous/ordinal row variables. *Renal failure is defined as serum creatinine increase to ⬎2.0 mg/dl and ⬎2 times the baseline creatinine level or a new requirement for dialysis. †Vascular complications are defined as any bleeding complication, access site occlusion, peripheral embolization, dissection, pseudoaneurysm, or arteriovenous fistula. ‡Bleeding complications are defined as any percutaneous access site, retroperitoneal, gastrointestinal, genitourinary, or other bleeding.
Approximately one-quarter of patients with NSTEMI had an occluded culprit vessel at the time of angiography. Of these, 66% occurred in the posterolateral distribution, demonstrating the limitations of the current diagnostic approach to acute coronary syndromes, which relies heavily on STEMI/NSTEMI dichotomization for early treatment decisions. Because patients who were found to have an occluded infarct artery suffered worse outcomes, the need for additional methods to rapidly identify patients with occluded arteries despite the absence of ST-segment elevation is highlighted. Currently, the use of posterior electrocardiographic leads (V7 to V9) is a Class IIa recommendation in patients presenting with ischemic chest discomfort (10). Other potential diagnostic modalities include emergent transthoracic echocardiography, immediate nuclear myocardial perfusion imaging, computed tomographic coronary angiography, or traditional invasive coronary angiography on a time scale usually reserved for STEMI patients. These approaches, alone or in combination, deserve further investigation. *William C. Dixon, IV, MD *Cardiology Service Dwight D. Eisenhower Army Medical Center 300 Hospital Road Fort Gordon, Georgia 30905 E-mail: [email protected] Tracy Y. Wang, MD, MS David Dai, MS Kendrick A. Shunk, MD, PhD Eric D. Peterson, MD, MPH Matthew T. Roe, MD, MHS on behalf of the National Cardiovascular Data Registry doi:10.1016/j.jacc.2008.07.029 Please note: Dr. Wang has received research grants to institution from Bristol-Myers Squibb, Sanofi-Aventis, Schering-Plough, The Medicines Co., Heartscape Inc., and Stacks Inc. Dr. Peterson has received research grants to institution from Bristol-
Myers Squibb, Sanofi-Aventis/Bristol-Myers Squibb Partnership, Bristol-Myers Squibb/Merck Partnership, and Schering-Plough. Dr. Roe has received research grants to institution from Bristol-Myers Squibb, Sanofi-Aventis, Schering-Plough, KAI Pharmaceuticals, Portola Pharmaceuticals, Lilly, and Daiichi-Sankyo.
REFERENCES
1. Wang JC, Normand ST, Mauri L, et al. Coronary artery spatial distribution of acute myocardial infarction occlusions. Circulation 2004;110:278 – 84. 2. Schmitt C, Gunter L, Schmeider S, et al. Diagnosis of acute myocardial infarction in angiographically documented occluded infarct vessel. Chest 2001;120:1540 – 6. 3. Abbas A, Boura J, Brewington S, et al. Acute angiographic analysis of non-ST-segment elevation myocardial infarction. Am J Cardiol 2004; 94:907–9. 4. Jacobs A, French J, Col J, et al. Cardiogenic shock with non-STsegment elevation myocardial infarction: a report from the SHOCK Trial Registry. J Am Coll Cardiol 2000;36:1091– 6. 5. Matetzky S, Freimark D, Feinberg MS, et al. Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7–9. J Am Coll Cardiol 1999;34:748 –53. 6. American College of Cardiology. ACC National Cardiac Catheterization Module 3.04. July 30, 2004. Available at: http://www.accncdr.com/ WebNCDR/NCDRDocuments/datadictdefsonlyv30.pdf. Accessed December 11, 2006. 7. Kajinami K, Seki H, Takekoshi N, et al. Coronary calcification and coronary atherosclerosis: site by site comparative morphologic study of electron beam computed tomography and coronary angiography. J Am Coll Cardiol 1997;29:1549 –56. 8. Soulis JV, Farmakis TM, Giannoglou GD, et al. Wall shear stress in normal left coronary tree. J Biomech 2006;39:742–9. 9. Wahle A, Lopez JJ, Olszewski ME, et al. Plaque development, vessel curvature, and wall shear stress in coronary arteries assessed by x-ray, angiography, and intravascular ultrasound. Med Image Anal 2006;10: 615–31. 10. Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non– ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction). J Am Coll Cardiol 2007;50:e1–157.