Coronary vessel diameters during and after primary percutaneous coronary artery intervention

Şahin, Müslüm; Demir, Serdar; Kocabay, Gönenç; Bulut, Mehmet; Alıcı, Gökhan; Özkan, Birol; Fedakar, Ali; Türkmen, Muhsin; Boztosun, Bilal

doi:10.1007/s00059-013-3865-4

Cited by 7 publications

(8 citation statements)

References 20 publications

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“…Infarct versus non-infarct setting was the only significant independent predictor of change in non-culprit stenosis. PDS was decreased significantly in our study consistent with the observations of Hanratty et al [8] and Sahin et al [19] MLD was increased and PDS was decreased significantly in our study on follow-up CAG. Hanratty et al [8] and Sahin et al [19] also reported similar significant changes in MLD and PDS.…”

Section: Discussionsupporting

confidence: 92%

“…They also found that there was no significant change in lesion length. RVD was increased significantly on follow-up CAG in our study similar to the reported by Sahin et al [19] However, Hanratty et al [8] and Cristea et al [20] found that there was no change in RVD. Hanratty et al [8] included 48 patients with 59 non-culprit lesions suitable for analysis in their study.…”

Section: Discussionsupporting

confidence: 90%

“…There was no significant change in lesion length in our study. In a study by Sahin et al [19] 58 patients with acute ST-seg ment elevation myocardial infarction (STEMI) were evaluated for changes in diameter of the infarct-related artery (IRA) during primary PCI and after an average of 3 days. CAG was performed on presentation and TIMI 3 flow was achieved either by simple balloon dilatation and/or thrombus aspiration.…”

Section: Discussionmentioning

confidence: 99%

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Primer perkütan koroner girişimlerde sorumlu olmayan lezyonların kontrol koroner anjiyografide değişimleri

Caner

Turen

Yildirim

2021

Journal of Contemporary Medicine

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Non-culprit lesion severity has often been exaggerated at the time of acute ST segment elevation myocardial infarction (STEMI). We aimed to determine changes in non-culprit lesions severity on follow-up coronary angiography (CAG) and independent predictors of these changes. Material and Method: We retrospectively evaluated the changes in non-culprit lesion stenosis on follow-up CAG which was done within 2 months after primary percutaneous coronary intervention (P-PCI) in patients presenting with STEMI. Results: 154 patients were included in this study and 207 nonculprit lesions (percentage diameter stenosis (PDS) ≥50%) were compared using quantitative coronary analyses (QCA). Minimal lumen diameter (1.30±0.38 mm vs. 1.54±0.46 mm, p<0.001) and reference vessel diameter (2.88±0.66 mm vs. 2.92±0.64 mm, p=0.001) were increased significantly and PDS (54.49±9.38 vs. 47.5±11.17, p<0.001) and percentage area stenosis (78.38±8.65 vs. 71.29±11.84, p= <0.001) were decreased significantly. There was no significant change in lesion length (13.52±5.59 mm vs. 13.25±5.31 mm, p= 0.078). 65 (31.4%) of these significant lesions (PDS ≥50% by QCA) were regressed (less than 50%) on follow-up CAG. In multivariable analyses; current smoking, clopidogrel use after the P-PCI and history of coronary artery disease were the independent predictors of decrease in PDS. Conclusion: Significant exaggeration of non-culprit lesion stenosis severity occurs at the time of acute STEMI.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Primer perkütan koroner girişimlerde sorumlu olmayan lezyonların kontrol koroner anjiyografide değişimleri

Caner

Turen

Yildirim

2021

Journal of Contemporary Medicine

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“…It is important to note that all patients responded well to PCI after the transient vasoconstriction incident. Moreover, multiple confounding factors may contribute to vasoconstriction during PCI, including the milieu of acute myocardial infarction itself 38 , 39 . In our experiments with long tone burst ultrasound (5,000 μs), we did observe a several minute delay in microvascular reperfusion following SRP therapy, which in the intact hindlimb was restored and returned to levels above baseline perfusion after 5 min.…”

Section: Discussionmentioning

confidence: 99%

The Role of Nitric Oxide during Sonoreperfusion of Microvascular Obstruction

Chen

Straub

et al. 2017

Theranostics

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Rationale: Microembolization during PCI for acute myocardial infarction can cause microvascular obstruction (MVO). MVO severely limits the success of reperfusion therapies, is associated with additional myonecrosis, and is linked to worse prognosis, including death. We have shown, both in in vitro and in vivo models, that ultrasound (US) and microbubble (MB) therapy (termed “sonoreperfusion” or “SRP”) is a theranostic approach that relieves MVO and restores perfusion, but the underlying mechanisms remain to be established.Objective: In this study, we investigated the role of nitric oxide (NO) during SRP.Methods and results: We first demonstrated in plated cells that US-stimulated MB oscillations induced a 6-fold increase in endothelial nitric oxide synthase (eNOS) phosphorylation in vitro. We then monitored the kinetics of intramuscular NO and perfusion flow rate responses following 2-min of SRP therapy in the rat hindlimb muscle, with and without blockade of eNOS with LNAME. Following SRP, we found that starting at 6 minutes, intramuscular NO increased significantly over 30 min and was higher than baseline after 13 min. Concomitant contrast enhanced burst reperfusion imaging confirmed that there was a marked increase in perfusion flow rate at 6 and 10 min post SRP compared to baseline (>2.5 fold). The increases in intramuscular NO and perfusion rate were blunted with LNAME. Finally, we tested the hypothesis that NO plays a role in SRP by assessing reperfusion efficacy in a previously described rat hindlimb model of MVO during blockade of eNOS. After US treatment 1, microvascular blood volume was restored to baseline in the MB+US group, but remained low in the LNAME group. Perfusion rates increased in the MB+US group after US treatment 2 but not in the MB+US+LNAME group.Conclusions: These data strongly support that MB oscillations can activate the eNOS pathway leading to increased blood perfusion and that NO plays a significant role in SRP efficacy.

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“…25 Myocardial ischaemia is known to stimulate catecholamine release and the renin-angiotensin system, resulting in systemic vasoconstriction proportional to the degree of ischaemia. 26 Mirroring this is the vasoconstriction seen in the coronary vessels during infarction, 27 and so systemic hypertension represents greater ischaemia and increased vasoconstriction, resulting in higher levels of ischaemic and perfusion injury contributing to NR.…”

Section: Risk Scorementioning

confidence: 99%

No-reflow phenomenon and comparison to the normal-flow population postprimary percutaneous coronary intervention for ST elevation myocardial infarction: case–control study (NORM PPCI)

et al. 2020

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IntroductionNo-reflow (NR) phenomenon is characterised by the failure of myocardial reperfusion despite the absence of mechanical coronary obstruction. NR negatively affects patient outcomes, emphasising the importance of prediction and management. The objective was to evaluate the incidence and independent predictors of NR in patients presenting with ST-elevation myocardial infarction (STEMI).MethodsThis was a single-centre prospective case–control study. Cases were subjects who suffered NR, and the control comparators were those who did not. Clinical outcomes were documented. Salient variables relating to the patients and their presentation, history and angiographical findings were compared using one-way analysis of variance or χ2 test. Multiple regression determined the independent predictors, and a risk score was established based on the β coefficient.ResultsOf 173 consecutive patients, 24 (13.9%) suffered from NR, with 46% occurring post stent implantation. Patients with NR had increased risk of in-hospital death (OR 7.0, 95% CI 1.3 to 36.7, p=0.022). From baseline variables available prior to percutaneous coronary intervention, the independent predictors of NR were increased lesion complexity, admission systolic hypertension, weight of <78 kg and history of hypertension. Continuous data were transformed into best-fit binary variables, and a risk score was defined. Significant difference was demonstrated between the risk score of patients with NR (4.1±1) compared with controls (2.6±1) (p<0.001), and the risk score was considered a good test (area under the curve=0.823). A score of ≥4 had 75% sensitivity and 76.5% specificity.ConclusionPatients with NR have a higher rate of mortality following STEMI. Predictors of NR include lesion complexity, systolic hypertension and low weight. Further validation of this risk model is required.

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Coronary vessel diameters during and after primary percutaneous coronary artery intervention

Cited by 7 publications

References 20 publications

Primer perkütan koroner girişimlerde sorumlu olmayan lezyonların kontrol koroner anjiyografide değişimleri

Primer perkütan koroner girişimlerde sorumlu olmayan lezyonların kontrol koroner anjiyografide değişimleri

The Role of Nitric Oxide during Sonoreperfusion of Microvascular Obstruction

No-reflow phenomenon and comparison to the normal-flow population postprimary percutaneous coronary intervention for ST elevation myocardial infarction: case–control study (NORM PPCI)

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