Prognostic clinical and angiographic characteristics for the development of a new significant lesion in remote segments after successful percutaneous coronary intervention

Tsiamis, Eleftherios; Toutouzas, Konstantinos; Synetos, Αndreas; Karambelas, John; Καρανάσος, Αντώνιος; Demponeras, Christos; Drakopoulou, Maria; Stefanadi, Elli; Tsioufis, Costas; Tousoulis, Dimitrios; Stefanadis, Christodoulos

doi:10.1016/j.ijcard.2009.01.026

Cited by 13 publications

(8 citation statements)

References 39 publications

(33 reference statements)

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“…Hanratty et al 9 demonstrated exaggeration of non-culprit lesions during acute myocardial infarction and indicated that inflammatory and spastic mechanisms may be involved in non-culprit lesion progression. On follow-up angiography of 117 patients with acute coronary syndrome, Tsiamis et al 10 found that non-culprit lesions may progress and that acute myocardial infarction may be an independent predictive factor for this progression. Our previous study 11 suggested that non-culprit lesion progression may be the most important prognostic factor in patients with STEMI after successful PPCI.…”

Section: Discussionmentioning

confidence: 99%

Effect of Ischemic Postconditioning on Cell Apoptosis and Expression of Relevant Genes in Non-Culprit Coronary Arteries

Wang

2020

Journal of Investigative Medicine

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This study was performed to determine the effect of ischemic postconditioning on cell apoptosis and angiotensin II receptor type 1 (AT1), connexin 43 (Cx43), and β-tubulin mRNA expression in non-culprit arteries. Non-culprit arterial tissues were isolated from a rabbit myocardial ischemia-reperfusion model and randomly divided into sham, ischemia-reperfusion, and ischemic postconditioning groups. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Expression of angiotensin II, AT1, Cx43, and β-tubulin mRNA was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). TUNEL analysis indicated significantly higher ratios of apoptotic cells in the ischemia-reperfusion group than in the sham group. However, significantly fewer apoptotic cells were observed in the ischemic postconditioning group than in the ischemia-reperfusion group. The qRT-PCR results indicated significantly higher expression of AT1, Cx43, and β-tubulin mRNA in the ischemia-reperfusion group than in the sham group. However, expression of AT1, Cx43, and β-tubulin was lower in the ischemic postconditioning group than in the ischemia-reperfusion group. The ratios of apoptotic cells and mRNA expression of AT1, Cx43, and β-tubulin in non-culprit arteries were increased after ischemia-reperfusion. Ischemic postconditioning may decrease these features and inhibit the progression of non-culprit arteries.

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Section: Discussionmentioning

confidence: 99%

Effect of Ischemic Postconditioning on Cell Apoptosis and Expression of Relevant Genes in Non-Culprit Coronary Arteries

Wang

2020

Journal of Investigative Medicine

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“…However, almost 40%~65% of patients with STEMI have presented with 3 vessel lesions, 3,4) and a clinical follow-up study of patients with 3 vessel lesions after successful PCI suggested that nonculprit lesions may be progression, and patients with AMI and complex morphology of a nonculprit artery lesion are at increased risk for a new intervention after successful PCI. 5) Hanratty, et al demonstrated exaggeration of nonculprit lesions during acute myocardial infarction, and indicated that infl ammation and spasm mechanism may be involved in nonculprit lesion progression. 6) In the present study, we investigated clinical and angiographic factors that may predict the progression of nonculprit lesions.…”

Section: Discussionmentioning

confidence: 99%

Nonculprit Lesion Progression in Patients With ST Elevation Myocardial Infarction After Primary Percutaneous Coronary Intervention

et al. 2014

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SummaryThe majority of cardiovascular events in patients with ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary interventions (PPCI) arise from the progression of nonculprit lesions (NCL) during the long-term follow-up period. However, the clinical and angiographic factors related to the progression of nonculprit lesions are unknown.The purpose of the study was to investigate the clinical and angiographic factors related to the progression of nonculprit lesions of patients with STEMI undergoing PPCI.A total of 492 patients with STEMI who underwent PPCI from January 2006 to December 2009 were enrolled. All patients underwent PPCI as a treatment for the culprit lesion. The clinical and angiographic follow-up was performed at 12 months. Primary endpoint: Clinically driven nonculprit lesion PCI. The levels of serum catecholamines [epinephrine (E), norepinephrine (NE)] and C-reactive protein (CRP) were assayed, and the clinical and angiographic features were also analyzed.The clinical and angiographic follow-up was performed in 492 patients, and 45 patients underwent clinically driven nonculprit lesions PCI (study group). A total of 447 patients were free of additional PCI (control group). There were significant differences in the level of catecholamines (E (621.48 ± 79.31) pg/mL versus (268.14 ± 73.26) pg/mL, P < 0.0001), NE (6212.43 ± 822.41) pg/mL versus (3218.34 ± 614.16) pg/mL, P < 0.0001), CRP (3.29 ± 1.31) mg/dL versus (2.51 ± 1.14) mg/dL, P < 0.0001, cTnI peak value (27.27 ± 4.02) ng/mL versus (16.12 ± 3.23) ng/mL, P < 0.0001), thrombotic lesion rate ((62.22% versus 23.04%), P < 0.0001), ≥ 2 vessel lesions rate (80.00% versus 46.09%), P < 0.0001), culprit lesion length ((33.2 ± 2.9 versus 28.1 ± 3.1), P = 0.013), and complex lesion rate ((57.78% versus 36.02%), P = 0.006) between the two groups. Correlation analysis between nonculprit lesion stenosis degree and serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, and complex lesion rate showed that there were signifi cant correlations between serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, complex lesion rate, and nonculprit lesion stenosis degree. The correlation coeffi cients were 0.95, 0.97, 0.83, 0.90, 0.81, 0.84, 0.95, and 0.96, respectively, and P < 0.0001, P < 0.0001, P = 0.01, P = 0.01, P = 0.01, P = 0.01, P < 0.0001, and P < 0.0001, respectively.Recurrent PCI was mainly due to nonculprit lesion progression in patients with STEMI after primary PCI. Complex nonculprit lesions may be prone to for additional PCI. Chronic infl ammation and sustained stress may be involved in the progression of nonculprit lesions in patients with STEMI. (Int Heart J 2014; 55: 48-52) Key words: Recurrent percutaneous coronary intervention, Complex nonculprit lesion, Infl ammation, Stress A lthough primary PCI can salvage dying myocardium, reduce cardiovascular events, and improve prognosis in patients w...

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“…[52][53][54] Thus, non-culprit lesions of patients with MI have a more complex angiographic morphology and are associated with rapid lesion progression and increased event rates at follow-up. 55,56 In addition, patients with STEMI undergoing primary percutaneous coronary intervention of the culprit lesion with additional prophylactic revascularisation of non-culprit lesion with >50 % stenosis had fewer events than patients with culprit-only treatment. 57 Based on these observations, it has been hypothesised that non-culprit lesions of patients with ACS have more unstable plaque morphology than lesions of stable patients.…”

Section: Multiple Coronary Lesion Instability In Acute Coronary Syndrmentioning

confidence: 99%

Optical Coherence Tomography For the Detection of the Vulnerable Plaque

Toutouzas¹,

Καρανάσος²,

Tousoulis³

2016

European Cardiology Review

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Post-mortem OCT studies have defined the optical appearance and morphological characterisation of the plaque, 9-14 showing an overall good agreement with histology and high reproducibility (see Table 1). OCT can identify normal wall segments and early atherosclerotic lesions, 15,16 and also perform tissue characterisation in advanced atherosclerotic lesions (see Table 2). 5 The major plaque types identified by OCT are fibrous plaques, appearing as a signal-rich, homogeneous region with low signal attenuation; fibrocalcific plaques, appearing

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Prognostic clinical and angiographic characteristics for the development of a new significant lesion in remote segments after successful percutaneous coronary intervention

Cited by 13 publications

References 39 publications

Effect of Ischemic Postconditioning on Cell Apoptosis and Expression of Relevant Genes in Non-Culprit Coronary Arteries

Effect of Ischemic Postconditioning on Cell Apoptosis and Expression of Relevant Genes in Non-Culprit Coronary Arteries

Nonculprit Lesion Progression in Patients With ST Elevation Myocardial Infarction After Primary Percutaneous Coronary Intervention

Optical Coherence Tomography For the Detection of the Vulnerable Plaque

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