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CULPRIT LESION SEVERITY IN ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
October 2007, Vol 132, No. 4_MeetingAbstracts Abstract: Poster Presentations | October 2007
CULPRIT LESION SEVERITY IN STSEGMENT ELEVATION MYOCARDIAL INFARCTION Cinzia Razzini, MD; Kunal Sarkar, MD*; Fransesco Romeo, MD; Rajesh Sachdeva, MD; Jawahar L. Mehta, MD University of Arkansas for Medical Sciences, Little Rock, AR Chest. 2007;132(4_MeetingAbstracts):544. doi:10.1378/chest.132.4_MeetingAbstracts.544
Abstract PURPOSE: To identify the culprit lesion severity in STEMI patients. METHODS: Patients who received thrombolytic therapy for STEMI in the emergency department (ER) between October 2005 and June 2006 and had clinical and electrocardiographic criteria of reperfusion (resolution of chest pain, >70% resolution of ST-segments and presence of reperfusion arrhythmias) were included in the study. Patients who subsequently underwent rescue PCI or had a history of prior PCI or CABG were excluded. Cardiac risk factors and demographic data were collected. Coronary angiography was performed at a mean of 48 hrs from presentation to ER. Quantitative coronary analysis (QCA) was performed offline. The severity of culprit lesion was assessed in two nearly orthogonal views in all patients. Patients were divided into four groups based on stenosis severity. Group1: 0–49%; Group 2: 50–69%; Group 3: 70–89% and Group 4: > 90%. RESULTS: Study cohort was formed by 119 patients. Mean age was 63 ± 12 years and 86% were males. Forty-nine percent were active smokers, 23% were diabetics, 48% had hypercholesterolemia, 54% had hypertension and 26% had family history of coronary artery disease. Culprit vessel distribution was as follows: Left anterior descending 42% (n=49), left circumflex 13% (n=15) and right coronary artery 45% (n=55). The degree of culprit lesion stenosis varied from 35–95%, mean 80 ± 13%. The distribution of culprit lesion severity was as follows: Group 1: 3 % (n= 4); Group 2: 4% (n=5); Group 3: 56% (n=66); and Group 4: 37% (n=44).
CONCLUSION: Culprit lesion severity greater than 70% accounted for majority of STEMI. Moderately stenotic lesions account for only a small number of STEMI. CLINICAL IMPLICATIONS: This study provides new data on the severity of culprit lesion stenosis in Acute ST elevation MI. The prevailing paradigm that rupture or erosion in non occlusive plaques is the precipitating event in the genesis of acute coronary syndromes may be too simplistic and insufficient to explain these events in a large majority of patients. DISCLOSURE: Kunal Sarkar, No Financial Disclosure Information; No Product/Research Disclosure Information
Wednesday, October 24, 2007 12:30 PM - 2:00 PM
CULPRIT LESION SEVERITY IN STSEGMENT ELEVATION MYOCARDIAL INFARCTION Cinzia Razzini, MD; Kunal Sarkar, MD*; Fransesco Romeo, MD; Rajesh Sachdeva, MD; Jawahar L. Mehta, MD University of Arkansas for Medical Sciences, Little Rock, AR Chest. 2007;132(4_MeetingAbstracts):544. doi:10.1378/chest.132.4_MeetingAbstracts.544
Abstract PURPOSE: To identify the culprit lesion severity in STEMI patients. METHODS: Patients who received thrombolytic therapy for STEMI in the emergency department (ER) between October 2005 and June 2006 and had clinical and electrocardiographic criteria of reperfusion (resolution of chest pain, >70% resolution of ST-segments and presence of reperfusion arrhythmias) were included in the study. Patients who subsequently underwent rescue PCI or had a history of prior PCI or CABG were excluded. Cardiac risk factors and demographic data were collected. Coronary angiography was performed at a mean of 48 hrs from presentation to ER. Quantitative coronary analysis (QCA) was performed offline. The severity of culprit lesion was assessed in two nearly orthogonal views in all patients. Patients were divided into four groups based on stenosis severity. Group1: 0–49%; Group 2: 50–69%; Group 3: 70–89% and Group 4: > 90%. RESULTS: Study cohort was formed by 119 patients. Mean age was 63 ± 12 years and 86% were males. Forty-nine percent were active smokers, 23% were diabetics, 48% had hypercholesterolemia, 54% had hypertension and 26% had family history of coronary artery disease. Culprit vessel distribution was as follows: Left anterior descending 42% (n=49), left circumflex 13% (n=15) and right coronary artery 45% (n=55). The degree of culprit lesion stenosis varied from 35–95%, mean 80 ± 13%. The distribution of culprit lesion severity was as follows: Group 1: 3 % (n= 4); Group 2: 4% (n=5); Group 3: 56% (n=66); and Group 4: 37% (n=44).
CONCLUSION: Culprit lesion severity greater than 70% accounted for majority of STEMI. Moderately stenotic lesions account for only a small number of STEMI. CLINICAL IMPLICATIONS: This study provides new data on the severity of culprit lesion stenosis in Acute ST elevation MI. The prevailing paradigm that rupture or erosion in non occlusive plaques is the precipitating event in the genesis of acute coronary syndromes may be too simplistic and insufficient to explain these events in a large majority of patients. DISCLOSURE: Kunal Sarkar, No Financial Disclosure Information; No Product/Research Disclosure Information
Wednesday, October 24, 2007 12:30 PM - 2:00 PM