Culprit Lesions (culprit + lesion)

Distribution by Scientific Domains


Selected Abstracts


Utility of Lead aVR for Identifying the Culprit Lesion in Acute Myocardial Infarction

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2009
B.Sc., Jørgen Tobias Kühl M.A.
Background: Lead aVR is a neglected, however, potentially useful tool in electrocardiography. Our aim was to evaluate its value in clinical practice, by reviewing existing literature regarding its utility for identifying the culprit lesion in acute myocardial infarction (AMI). Methods: Based on a systematic search strategy, 16 studies were assessed with the intent to pool data; diagnostic test rates were calculated as key results. Results: Five studies investigated if ST-segment elevation (STE) in aVR is valuable for the diagnosis of left main stem stenosis (LMS) in non,ST-segment AMI (NSTEMI). The studies were too heterogeneous to pool, but the individual studies all showed that STE in aVR has a high negative predictive value (NPV) for LMS. Six studies evaluated if STE in aVR is valuable for distinguishing proximal from distal lesions in the left anterior descending artery (LAD) in anterior ST-segment elevation AMI (STEMI). Pooled data showed a sensitivity of 47%, a specificity of 96%, a positive predicative value (PPV) of 91% and a NPV of 69%. Five studies examined if ST-segment depression (STD) in lead aVR is valuable for discerning lesions in the circumflex artery from those in the right coronary artery in inferior STEMI. Pooled data showed a sensitivity of 37%, a specificity of 86%, a PPV of 42%, and an NPV of 83%. Conclusion: The absence of aVR STE appears to exclude LMS as the underlying cause in NSTEMI; in the context of anterior STEMI, its presence indicates a culprit lesion in the proximal segment of LAD. [source]


Increased serum anandamide level at ruptured plaque site in patients with acute myocardial infarction

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2009
Naotaka Maeda
Abstract Inflammation caused by activated macrophages and T lymphocytes may trigger plaque rapture in acute coronary syndrome (ACS). Anandamide and 2-arachidonylglycerol (2-AG) are macrophage-derived signal lipids and may be involved in the pathogenesis of ACS, but no clinical relevant data have been reported. In 43 acute myocardial infarction (AMI) patients (66 ± 2 years), blood samples were obtained from the aortic root and the infarct-related coronary artery (IRA) using a PercuSurge system during primary percutaneous coronary intervention (PCI). In six patients with stable effort angina (SEA) (56 ± 6 years), blood samples were obtained from the site of stenosis during elective PCI. In 25 of the 43 AMI patients, anandamide was detected in the serum. Serum anandamide level was 35 ± 20 pmol/mL in the aorta and was significantly increased to 401 ± 134 pmol/mL in the IRA (P < 0.01). 2-AG was undetectable in most of the patients. In patients with SEA, neither anandamide nor 2-AG was detected in the serum at the plaque site. In AMI patients with anandamide detected, left ventricular ejection fraction at 2 weeks after PCI was increased by 3.7 ± 2.1% compared with that at the acute phase, while it was decreased by 3.0 ± 1.8% in those without anandamide detected (P < 0.05). The serum anandamide level at the culprit lesion was elevated compared with the systemic level in a significant number of AMI patients, indicating the synthesis of anandamide at the IRA. Anandamide was suggested to be derived from ruptured plaque and may exert beneficial effects in humans. [source]


"Backdoor" Alternative Approach to Stenting of a Post-Anastomotic Coronary Artery Lesion via a Chronically Obstructed Right Coronary Artery after Failure to Stent through a Tortuous Free Internal Mammary Graft

JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2007
RICHARD Y.J. CHAN M.B.Ch.B.
We describe the case of a patient who previously had coronary artery bypass grafting including a free right internal mammary artery graft anastomosed to a chronic totally occluded right coronary artery (RCA) proximally and distally and who presented with a high-risk acute coronary syndrome. Coronary angiography revealed the graft to be patent with a distal post-anastomotic culprit lesion within the posterolateral branch of the native RCA. Because of technical challenges, PCI could not be performed through the graft and the lesion was stented via the chronically occluded RCA instead, in a "backdoor" approach with a good final result. [source]


Does Proximal Location of Culprit Lesion Confer Worse Prognosis in Patients Undergoing Primary Percutaneous Coronary Intervention for ST Elevation Myocardial Infarction?

JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2006
KISHORE J. HARJAI M.D.
ST segment elevation myocardial infarction (STEMI) from proximally located culprit lesion is associated with greater myocardium at jeopardy. In STEMI patients treated with thrombolytics, proximal culprit lesions are known to have worse prognosis. This relation has not been studied in patients undergoing primary percutaneous coronary intervention (PCI). In 3,535 STEMI patients with native coronary artery occlusion pooled from the primary angioplasty in myocardial infarction database, we compared in-hospital and 1-year outcomes between those with proximal (n = 1,606) versus nonproximal (n = 1,929) culprit lesions. Patients with proximal culprits were more likely to die and suffer major adverse cardiovascular events (MACE) during the index hospital stay (3.8% vs 2.2%, P = 0.006; 8.2% vs 5.8%, P = 0.0066, respectively) as well as during 1-year follow-up (6.9% vs 4.5%, P = 0.0013; 22% vs 17%, P = 0.003, respectively) compared to those with nonproximal culprits. After adjustment for baseline differences, proximal culprit was independently predictive of in-hospital death (adjusted odds ratio% 1.58, 95% confidence intervals, CI 1.05,2.40) and MACE (OR 1.41, CI 1.06,1.86), but not 1-year death or MACE. In addition, proximal culprit was independently associated with higher incidence of ventricular arrhythmias and sustained hypotension during the index hospitalization. The univariate impact of proximal culprit lesion on in-hospital death and MACE was comparable to other adverse angiographic characteristics, such as multivessel disease and poor initial thrombolysis in myocardial infarction flow, and greater than that of anterior wall STEMI. In conclusion, proximal location of the culprit lesion is a strong independent predictor of worse in-hospital outcomes in patients with STEMI undergoing primary PCI. [source]


Utility of Lead aVR for Identifying the Culprit Lesion in Acute Myocardial Infarction

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2009
B.Sc., Jørgen Tobias Kühl M.A.
Background: Lead aVR is a neglected, however, potentially useful tool in electrocardiography. Our aim was to evaluate its value in clinical practice, by reviewing existing literature regarding its utility for identifying the culprit lesion in acute myocardial infarction (AMI). Methods: Based on a systematic search strategy, 16 studies were assessed with the intent to pool data; diagnostic test rates were calculated as key results. Results: Five studies investigated if ST-segment elevation (STE) in aVR is valuable for the diagnosis of left main stem stenosis (LMS) in non,ST-segment AMI (NSTEMI). The studies were too heterogeneous to pool, but the individual studies all showed that STE in aVR has a high negative predictive value (NPV) for LMS. Six studies evaluated if STE in aVR is valuable for distinguishing proximal from distal lesions in the left anterior descending artery (LAD) in anterior ST-segment elevation AMI (STEMI). Pooled data showed a sensitivity of 47%, a specificity of 96%, a positive predicative value (PPV) of 91% and a NPV of 69%. Five studies examined if ST-segment depression (STD) in lead aVR is valuable for discerning lesions in the circumflex artery from those in the right coronary artery in inferior STEMI. Pooled data showed a sensitivity of 37%, a specificity of 86%, a PPV of 42%, and an NPV of 83%. Conclusion: The absence of aVR STE appears to exclude LMS as the underlying cause in NSTEMI; in the context of anterior STEMI, its presence indicates a culprit lesion in the proximal segment of LAD. [source]


Acute Myocardial Infarction Without Disrupted Yellow Plaque in Young Patients Below 50 Years Old

JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 3 2007
F.A.C.C., F.E.S.C., F.J.C.C., Ph.D., YASUNORI UEDA M.D.
Objective: Thrombosis caused by disrupted yellow plaque is regarded as a cause of acute myocardial infarction (MI). However, it has not been clarified if young patients have the same pathophysiology as older ones. Therefore, we elucidated clinical and angioscopic characteristics of young patients. Methods: Among a series of patients (n = 893) who received catheterization for acute MI, clinical characteristics were compared between patients <50 years (n = 66) and the rest of patients. Angioscopic appearance of culprit lesions was evaluated in 20 young patients in whom angioscopic examination was successfully performed. It was determined if culprit lesions had disrupted yellow plaque with thrombus (DYP&T). Results: Patients <50 years had higher prevalence of smoking (68% vs. 48%, P = 0.001), obesity (42% vs. 15%, P < 0.0001), and hypercholesterolemia (56% vs. 35%, P = 0.0005) than those ,50 years. DYP&T was detected at culprit lesions in 14 (70%) patients. Prevalence of DYP&T was lower in patients <40 years (44% vs. 91%, P = 0.02) than those between 40 and 50 years. Patients <40 years had a trend for higher prevalence of smoking (88% vs. 62%, P = 0.05) than those between 40 and 50 years. Conclusions: Patients with acute MI < 50 years, especially <40 years, had lower prevalence of DYP&T but higher prevalence of smoking, obesity, and hypercholesterolemia. Smoking may play an important role for thrombotic occlusion at lesions with relatively low thrombogenic potential. [source]


Does Proximal Location of Culprit Lesion Confer Worse Prognosis in Patients Undergoing Primary Percutaneous Coronary Intervention for ST Elevation Myocardial Infarction?

JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2006
KISHORE J. HARJAI M.D.
ST segment elevation myocardial infarction (STEMI) from proximally located culprit lesion is associated with greater myocardium at jeopardy. In STEMI patients treated with thrombolytics, proximal culprit lesions are known to have worse prognosis. This relation has not been studied in patients undergoing primary percutaneous coronary intervention (PCI). In 3,535 STEMI patients with native coronary artery occlusion pooled from the primary angioplasty in myocardial infarction database, we compared in-hospital and 1-year outcomes between those with proximal (n = 1,606) versus nonproximal (n = 1,929) culprit lesions. Patients with proximal culprits were more likely to die and suffer major adverse cardiovascular events (MACE) during the index hospital stay (3.8% vs 2.2%, P = 0.006; 8.2% vs 5.8%, P = 0.0066, respectively) as well as during 1-year follow-up (6.9% vs 4.5%, P = 0.0013; 22% vs 17%, P = 0.003, respectively) compared to those with nonproximal culprits. After adjustment for baseline differences, proximal culprit was independently predictive of in-hospital death (adjusted odds ratio% 1.58, 95% confidence intervals, CI 1.05,2.40) and MACE (OR 1.41, CI 1.06,1.86), but not 1-year death or MACE. In addition, proximal culprit was independently associated with higher incidence of ventricular arrhythmias and sustained hypotension during the index hospitalization. The univariate impact of proximal culprit lesion on in-hospital death and MACE was comparable to other adverse angiographic characteristics, such as multivessel disease and poor initial thrombolysis in myocardial infarction flow, and greater than that of anterior wall STEMI. In conclusion, proximal location of the culprit lesion is a strong independent predictor of worse in-hospital outcomes in patients with STEMI undergoing primary PCI. [source]


Safety, Efficacy, and Cost Advantages of Combined Coronary Angiography and Angioplasty

JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 3 2003
CLAUDE LE FEUVRE M.D., F.E.S.C.
Aim: The safety and efficacy of ad hoc PTCA has been previously reported and this approach is performed in many angioplasty centers as a routine procedure. The aim of this study is to examine whether this approach reduces the length, and cost of hospital stay. Methods and results: To determine the hospital costs we studied 2,440 PTCAs over 11 years in our institution (1990,2000). Urgent PTCA for acute coronary syndromes refractory to medical treatment were excluded. In 1809 patients (74%) angioplasty was performed immediately after coronary angiography, while separate procedures were performed in 631 patients. Indication for PTCA was unstable angina in 1342 patients (55%). In the ad hoc PTCA group, 92% of the culprit lesions were successfully treated; complications included myocardial infarction (2%), urgent bypass surgery (0.6%) and death (0.9%). The rate of combined procedure progressively increased from 54% in 1990 to 88% in 2000, with a significant decrease in the rate of complications. After adjusting for clinical and angiographic differences between combined and separate procedures, angiographic success and complication rates were not statistically different in the two groups. Mean length of hospital stay decreased all along the years, and was 45% less in the ad hoc PTCA group (11.4 ± 6.9vs18.2 ± 7.7in 1990,5.4 ± 4.3vs10.8 ± 5.7in 2000,P < 0.0001). The cost was 40% lower in the ad hoc PTCA group. For patients with stable angina, the savings were 49%, and for those with unstable angina, they were 29%. Conclusion: In the era of coronary stenting, ad hoc PTCA can be performed in most of the patients as safely and successfully as a separate procedure. It reduces the length, and the cost of hospital stay in patients with stable or unstable angina. (J Interven Cardiol 2003;16:195,199) [source]


Predictors of Cardiac Arrest Occurring in the Context of Acute Myocardial Infarction

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2007
HAITHAM HREYBE M.D.
Background:Cardiac arrest (CA) concurrent with acute myocardial infarction (AMI) claims the life of many patients with coronary artery disease (CAD). In this study, we investigated the predictors of CA during AMI. Method:Patients admitted with CA concurrent with AMI (n = 31) were matched by age, gender, race, and left ventricular ejection fraction (LVEF) to patients with AMI but no CA (n = 70). All patients underwent coronary angiography. Binary logistic regression was used to identify independent predictors of CA during AMI. Results:A total of 101 patients (age = 61 ± 13 years, men 76%, Caucasians 98%, LVEF 33 ± 12%) admitted to the University of Pittsburgh Medical Center with AMI were included in this analysis. Patients with CA concurrent with the AMI were more likely to have proximal rather than distal coronary artery culprit lesions (odds ratio (OR) = 7.2, P = 0.019). Other predictors of CA in the context of AMI included negative family history of CAD (OR = 8.0, P = 0.026) and absence of sinus rhythm upon hospital admission (OR = 5.1, P = 0.030). Conclusion:Proximity of culprit coronary lesion and presence of rhythm other than sinus rhythm at hospital admission are two strong predictors of CA in the context of AMI. The implication is that the mechanism of CA is primarily that of a large area of myocardial ischemia leading to lethal ventricular arrhythmia. Other predispositions such as genetic make-up cannot be ruled out. [source]


Percutaneous coronary intervention or bypass surgery in multivessel disease?

CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 2 2004
A tailored approach based on coronary pressure measurement
Abstract The optimal revascularization strategy, percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG), for patients with multivessel coronary artery disease (MVD) remains controversial. The aim of the present study was to compare the long-term outcomes after selective PCI of only hemodynamically significant lesions (fractional flow reserve, or FFR < 0.75) to CABG of all stenoses in patients with MVD. In 150 patients with MVD referred for CABG, FFR was determined in 381 coronary arteries considered for bypass grafting. If the FFR was less than 0.75 in three vessels or in two vessels including the proximal left anterior descending (LAD) artery, CABG was performed (CABG group). If only one or two vessels were physiologically significant (not including the proximal LAD), PCI of those lesions was performed (PCI group). Of the 150 patients, 87 fulfilled the criteria for CABG and 63 for PCI. There were no significant differences in the angiographic or other baseline characteristics between the two groups. At 2-year follow-up, no differences were seen in adverse events, including repeat revascularization (event-free survival 74% in the CABG group and 72% in the PCI group). A similar number of patients were free from angina (84% in the CABG group and 82% in the PCI group). Importantly, the results in both groups were as good as the surgical groups in previous studies comparing PCI and CABG in MVD. In patients with multivessel disease, PCI in those with one or two hemodynamically significant lesions as identified by an FFR < 0.75 yields a similar favorable outcome as CABG in those with three or more culprit lesions despite a similar angiographic extent of disease. Catheter Cardiovasc Interv 2004;63:184,191. © 2004 Wiley-Liss, Inc. [source]