iFR uncovers profound but mostly reversible ischemia in CTOs and helps to optimize PCI results

2020 ◽  
Author(s):  
Peter Kayaert ◽  
Mathieu Coeman ◽  
Benny Drieghe ◽  
Johan Bennett ◽  
Keir McCutcheon ◽  
...  
Keyword(s):  
Reversible Ischemia

Beta-Blockade in Intraseptal Anomalous Coronary Artery With Reversible Myocardial Ischemia

2021 ◽  
Vol 12 (1) ◽  
pp. 145-148
Author(s):  
Tam T. Doan ◽  
Athar M. Qureshi ◽  
Shagun Sachdeva ◽  
Cory V. Noel ◽  
Dana Reaves-O’Neal ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischemia ◽  
Dobutamine Stress ◽  
Medical Intervention ◽  
Beta Blockade ◽  
Fractional Flow ◽  
Flow Reserve ◽  
Reversible Ischemia ◽  
Improve Patient

Anomalous aortic origin of a left coronary artery (L-AAOCA) with an intraseptal course is a rare anomaly and can be associated with myocardial ischemia and sudden cardiac death. No surgical or medical intervention is known to improve patient outcomes. A 7-year-old boy with intraseptal L-AAOCA presented with nonexertional chest pain, syncope, and had reversible myocardial ischemia on provocative testing. The patient was started on β-blockade, following which his symptoms improved and resolved over a period of six years. A follow-up dobutamine stress magnetic resonance imaging no longer showed reversible ischemia, and cardiac catheterization with fractional flow reserve did not show coronary flow compromise.

Abstract 13980: Cardiac Magnetic Resonance Imaging Quantification of Myocardial Ischemia and Necrosis Using a Novel Risk Prediction Model Allows for Better Risk Stratification in Coronary Artery Disease

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Dominik Buckert ◽  
Nils Dyckmanns ◽  
Volker Rasche ◽  
Wolfgang Rottbauer ◽  
Peter Bernhardt
Keyword(s):  
Magnetic Resonance Imaging ◽  
Coronary Artery Disease ◽  
Cardiac Magnetic Resonance ◽  
Myocardial Ischemia ◽  
Risk Stratification ◽  
Myocardial Necrosis ◽  
Hazard Ratio ◽  
Resonance Imaging ◽  
Reversible Ischemia ◽  
Artery Disease

Background: Cardiac magnetic resonance imaging (CMR) provides information about inducible myocardial ischemia and necrosis in one single examination in coronary artery disease (CAD) patients. Both variables have been shown to correlate with prognosis. However, there is no consensus on how to assess and quantify these two variables. Hypothesis: Objective of the present prospective study in consecutive patients was to provide a simple algorithm for quantification of ischemia and necrosis and to test for risk stratification models. Methods: Patients with known or suspected CAD referred for adenosine-stress CMR were consecutively enrolled from 2003 to 2007. Examination was conducted on a 1.5-T whole-body scanner. Reversible ischemia was diagnosed by adenosine stress first pass perfusion imaging. Myocardial necrosis was assessed by late gadolinium enhancement (LGE). In a semiautomatic approach, extent of reversible ischemia and scar was quantified and reported as percentage of the left ventricle. Primary endpoint was defined as cardiac death, non-fatal myocardial infarction and stroke. Results: The study cohort consisted of 845 patients. Median age was 64 years, 271 patients were women. During a median follow-up period of 3.8 years 61 primary endpoints occurred. Statistical analysis yielded a ≥6% optimal threshold for reversible ischemia to predict a primary endpoint (univariate hazard ratio 4.91, p<.0001). Similarly, thresholds for extent of myocardial necrosis were defined (LGE >15% and ≤33%: univariate hazard ratio 2.75, p<.0001; LGE >33%: univariate hazard ratio 16.27, p<.0001). The risk prediction model containing both, quantified ischemia and necrosis, proved to be superior in comparison to the dichotomous model (ischemia present: yes/no; necrosis present: yes/no) on multivariate testing (increase in χ 2 -values: 45.004 to 61.545; increase in integrated discrimination improvement: .02269 to .03187; net reclassification index for optimal model: .25593, p=.001). Conclusion: CMR cut-off values for quantification of myocardial ischemia (≥6%) and necrosis (>15% and >33%) have been found which allow for better risk stratification in CAD patients. The combination of both has been shown to yield the superior risk stratification model.

Reversible ischemia increases levels of Alzheimer amyloid protein precursor without increasing levels of mRNA in the rabbit spinal cord

1997 ◽  
Vol 49 (1-2) ◽  
pp. 103-112 ◽  
Author(s):  
Naoka Komori ◽  
Agnes Kittel ◽  
David Kang ◽  
Deborah Shackelford ◽  
Eliezer Masliah ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Amyloid Protein ◽  
Protein Precursor ◽  
Amyloid Protein Precursor ◽  
Reversible Ischemia

Radionuclide evidence for reversible ischemia after percutaneous treatment of anomalous right coronary artery with dynamic compression by great vessels

2008 ◽  
Vol 9 (11) ◽  
pp. 1134-1137 ◽  
Author(s):  
Morocutti Giorgio ◽  
Pecoraro Rosa ◽  
Zanuttini Davide ◽  
Spedicato Leonardo ◽  
Slavich Gianaugusto ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Right Coronary Artery ◽  
Dynamic Compression ◽  
Percutaneous Treatment ◽  
Great Vessels ◽  
Reversible Ischemia

scholarly journals Transplantation-Induced Ischemia-Reperfusion Injury Modulates Antigen Presentation by Donor Renal CD11c+F4/80+ Macrophages through IL-1R8 Regulation

2020 ◽  
Vol 31 (3) ◽  
pp. 517-531 ◽  
Author(s):  
Sistiana Aiello ◽  
Manuel Alfredo Podestà ◽  
Pamela Y. Rodriguez-Ordonez ◽  
Francesca Pezzuto ◽  
Nadia Azzollini ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Antigen Presentation ◽  
Kidney Transplant ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cold Ischemia ◽  
Reversible Ischemia ◽  
Antigen Presenting

BackgroundIn donor kidneys subjected to ischemia-reperfusion injury during kidney transplant, phagocytes coexpressing the F4/80 and CD11c molecules mediate proinflammatory responses and trigger adaptive immunity in transplantation through antigen presentation. After injury, however, resident renal macrophages coexpressing these surface markers acquire a proreparative phenotype, which is pivotal in controlling inflammation and fibrosis. No data are currently available regarding the effects of transplant-induced ischemia-reperfusion injury on the ability of donor-derived resident renal macrophages to act as professional antigen-presenting cells.MethodsWe evaluated the phenotype and function of intragraft CD11c+F4/80+ renal macrophages after cold ischemia. We also assessed the modifications of donor renal macrophages after reversible ischemia-reperfusion injury in a mouse model of congeneic renal transplantation. To investigate the role played by IL-1R8, we conducted in vitro and in vivo studies comparing cells and grafts from wild-type and IL-R8–deficient donors.ResultsCold ischemia and reversible ischemia-reperfusion injury dampened antigen presentation by renal macrophages, skewed their polarization toward the M2 phenotype, and increased surface expression of IL-1R8, diminishing activation mediated by toll-like receptor 4. Ischemic IL-1R8–deficient donor renal macrophages acquired an M1 phenotype, effectively induced IFNγ and IL-17 responses, and failed to orchestrate tissue repair, resulting in severe graft fibrosis and aberrant humoral immune responses.ConclusionsIL-1R8 is a key regulator of donor renal macrophage functions after ischemia-reperfusion injury, crucial to guiding the phenotype and antigen-presenting role of these cells. It may therefore represent an intriguing pathway to explore with respect to modulating responses against autoantigens and alloantigens after kidney transplant.

scholarly journals Сравнительный анализ данных перфузионной сцинтиграфии миокарда у пациентов с поражением коронарных артерий различной степени выраженности

2019 ◽  
Author(s):  
E DENISENKO-KANKIYA ◽  
F.N. CHANAKHCHIAN ◽  
E.I. VASILENKO ◽  
M.N. VAKHROMEEVA
Keyword(s):  
Myocardial Perfusion ◽  
Single Photon ◽  
Photon Emission ◽  
Emission Computed Tomography ◽  
Vulnerable Atherosclerotic Plaque ◽  
Gated Perfusion Spect ◽  
Perfusion Spect ◽  
Perfusion Defects ◽  
Reversible Ischemia ◽  
Myocardial Perfusion Defects

Известно, что дестабилизация атеросклеротической бляшки коронарных артерий (КА) играет ключевую роль в развитии осложнений хронической ишемической болезни сердца (ИБС). Ранняя диагностика ишемии миокарда и определение субклинического стеноза КА с помощью неинвазивного метода визуализации сердца может стать важным методом в предотвращении развития сердечно-сосудистых осложнений у данной популяции больных. Цель исследования. Определить выраженность преходящих нарушений перфузии миокарда, выявленных при однофотонной эмиссионной компьютерной томографии (ОЭКТ) миокарда у пациентов со стенозами КА различной степени тяжести. Материал и методы. В исследование включен 231 пациент (средний возраст 6210лет). Проанализированы факторы кардиального риска. Всем пациентам проводили ОЭКТ миокарда по стандартному протоколу. Региональную перфузию миокарда оценивали с использованием стандартизированной 20-сегментной модели, на которой оценивали: SSS общий счет снижения перфузии миокарда при нагрузке SDS общую разницу счета, соответствующую степени выраженности преходящей ишемии левого желудочка (ЛЖ). На основании полученных данных обследуемых пациентов классифицировали на группы: с нормальной перфузией (SSS4), незначительной (SSS4-6), умеренной и выраженной степенью снижения (SSS712 и SSS13 соответственно) перфузии миокарда ЛЖ. Результаты SDS классифицировали как: отсутствие ишемии (SDS2), умеренная преходящая ишемия (SDS2-6) и выраженная преходящая ишемия (SDS7). Количественные показатели перфузии миокарда сравнивали с результатами инвазивной коронароангиографии (КАГ). Результаты. Из 231 пациента у 69 (29,9) по данным КАГ были выявлены стенозы до 20, у 126 (54,5) стенозы 2049, у 36 (15,6) стенозы 50 и более. Сравнительный анализ количественных показателей перфузии миокарда (SSS и SDS) и результатов КАГ показал, что достоверные дефекты перфузии после нагрузки и преходящая ишемия ЛЖ определены в основном у пациентов со стенозами КА50 (47,2 и 63,9 соответственно, р0,01). В группе пациентов с стенозами КА 2049 у 42,1 показатели SSS соответствовали незначительной (25,4) и умеренной (16,7) степени снижения перфузии после нагрузки (р0,01). При сопоставлении данных перфузионной сцинтиграфии миокарда выявлена связь между показателем SSS, наличием факторов риска и наличием сопутствующих заболеваний у пациентов с ИБС (р0,05). Заключение. Перфузионная ОЭКТ миокарда может использоваться в качестве метода выявления преходящей ишемии миокарда у пациентов со стенозами КА различной тяжести. Ключевые слова: ишемическая болезнь сердца, однофотонная эмиссионная компьютерная томография, перфузия миокарда, сцинтиграфия миокарда, необструктивное поражение, обструктивное поражение, коронароангиография.Vulnerable atherosclerotic plaque in coronary arteries (CA) is the primary mechanism responsible for complications of CAD even in the terms of non-obstructive CAD. Early determination of myocardial ischemia and CA stenosis with non-invasive imaging technique could predict the development of major cardiac events in patients with CAD. Aim: evaluation the severity of myocardial perfusion defects with single photon emission computed tomography (SPECT) in patients with obstructive or non-obstructive CAD. Material and methods: Overall 231patients (average age of 6210) were analyzed. All patients underwent 1-day gated perfusion SPECT protocol before coronary angiography (CAG). SPECT images were quantified by SSS and SDS using Cedars-Sinai QPS. Normal myocardial perfusion was considered if SSS4 mildly abnormal: SSS4-7 moderate and significantly abnormal: SSS8-12 and SSS13, respectively. Reversible ischemia was defined as SDS2. Degree of ischemia was assessed to moderate (SDS2-7) and severe (SDS7). Obstructive CAD was defined as 50 stenosis in 1 vessel on CAG. Results: From 231 patients 69 (29,9) have non-significant CA stenosis (20), 126 (54,5) have non-obstructive CAD (20-49) and 36 (15,6) - obstructive CAD (50). There were significant differences between CA stenosis severity via CAG and SSS via SPECT. In obstructive CAD significant myocardial perfusion defect at stress (SSS) and reversible ischemia (SDS) were observed in 47,2 and 63,9 patients, respectively (p0,01). In patients with non-obstructive CAD although the majority has normal myocardial perfusion in stress (SSS4 55,6), 42,1 has both mild (25,4) and moderate (16,7) myocardial perfusion defects in stress (p0,001). In this subgroup 45,2 of patients have moderate and 18,3 - severe reversible ischemia according to SDS (p0,001). Abnormal perfusion in stress was associated with hazards of cardiac risk factors or associated diseases (p0,05). Conclusion: Perfusion SPECT has a prognostic value over invasive CAG. The addition SPECT quantitative analysis to CAG allows improved risk stratification of patients with non-obstructive CAD.

Abstract 16939: Reversible Myocardial Ischemia Sufficient to Produce Transient Stunning Leads to Delayed Cardiac Troponin I Release That Reflects Focal Myocyte Apoptosis in the Absence of Pathological Infarction

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Brian R Weil ◽  
Rebeccah F Young ◽  
Xiaomeng Shen ◽  
Gen Suzuki ◽  
Jun Qu ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Coronary Occlusion ◽  
Troponin I ◽  
Myocardial Necrosis ◽  
Heart Tissue ◽  
Cardiac Troponin I ◽  
Wall Thickening ◽  
Reversible Ischemia ◽  
Myocyte Apoptosis ◽  
Irreversible Injury

Introduction: The release of cardiac troponin I (cTnI) after reversible ischemia is controversial. It has been hypothesized that elevations in serum cTnI in this scenario reflect selective release from an exchangeable pool rather than cellular necrosis since irreversible injury with sarcolemmal membrane disruption does not begin until ischemia exceeds 15 minutes following a total coronary occlusion. Objective: To determine whether cTnI release occurs after a brief coronary occlusion when the duration of ischemia is insufficient to induce myocyte necrosis. Methods: Closed-chest propofol-anesthetized swine (n=10) were subjected to a 10 minute LAD occlusion. Blood sampling was performed to measure serum cTnI concentrations before, during and after ischemia. Myocardial tissue was collected either 1 hour (n=5) or 24 hours (n=5) after reperfusion for pathological assessment of infarction (TTC) and apoptosis (TUNEL). Results: Regional LAD wall thickening was 60 ± 4% at baseline and became dyskinetic during coronary occlusion (-4 ± 2%, p<0.05). One hour after reperfusion, wall thickening improved but remained depressed relative to baseline, indicative of myocardial stunning (37 ± 4%, p<0.05). It returned to normal after 24 hours (59 ± 2%). Serum cTnI was 0.01 ± 0.01 ng/mL at baseline and remained unchanged at the end of ischemia. A slight increase in cTnI was observed 1 hour after reperfusion (0.06 ± 0.02 ng/mL, p<0.05 vs. baseline), followed by a marked elevation at 24 hours (1.02 ± 0.57 ng/mL, p<0.05 vs. baseline). TTC staining demonstrated no evidence of infarction. Heart tissue collected 1 hour after reperfusion demonstrated a regional increase in apoptotic myocytes (LAD: 17.7 ± 3.7 myocytes/cm 2 vs. Remote: 3.1 ± 2.0 myocytes/cm 2 , p<0.05). Myocyte apoptosis normalized 24 hours after reperfusion (LAD: 5.2 ± 2.3 myocytes/cm 2 vs. Remote: 3.6 ± 1.5 myocytes/cm 2 ) when serum cTnI remained elevated. Conclusion: A duration of reversible ischemia compatible with angina can lead to cTnI release that is similar in magnitude to that occurring with myocardial infarction. Rather than infarction or release from an exchangeable cTnI pool, the rise in serum cTnI is delayed and appears to reflect focal programmed myocyte death from apoptosis rather than myocardial necrosis.

Influence of neutrophil depletion on myocardial function and flow after reversible ischemia

1989 ◽  
Vol 256 (2) ◽  
pp. H341-H351 ◽  
Author(s):  
P. G. O'Neill ◽  
M. L. Charlat ◽  
L. H. Michael ◽  
R. Roberts ◽  
R. Bolli
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Coronary Occlusion ◽  
Critical Factor ◽  
Wall Thickening ◽  
Collateral Flow ◽  
Vascular Abnormalities ◽  
Reversible Ischemia ◽  
Neutrophil Depletion ◽  
Mediate Cell

We explored the role of polymorphonuclear leukocytes (PMN) in the genesis of contractile dysfunction (myocardial "stunning") and of vascular abnormalities after reversible ischemia. Open-chest dogs underwent a 15-min coronary occlusion and 4 h of reperfusion (REP); treated animals (n = 16) received intravenous goat antiserum against canine PMN, whereas controls received nonimmune goat serum (n = 10) or saline (n = 15). In treated dogs, the average blood PMN levels were 10% of those in saline controls. During ischemia, collateral flow tended to be higher, and paradoxical systolic wall thinning tended to be less in neutropenic dogs, but despite this, recovery of wall thickening after REP was not enhanced in these animals. Similarly, arrhythmias during ischemia or REP did not differ among the three groups. Four hours after REP, both resting and minimal coronary resistance (the latter assessed by adenosine infusion) were higher in the stunned compared with the nonischemic myocardium; these vascular derangements, however, were similar in all three groups. Thus profound neutropenia failed to attenuate mechanical dysfunction, to reduce arrhythmias, and to prevent vascular abnormalities after a 15-min coronary occlusion. Although previous studies have suggested that neutrophils mediate cell death during prolonged ischemia, the present findings suggest that PMN do not contribute importantly to the damage associated with brief, reversible ischemia. The duration of flow reduction may be a critical factor determining whether PMN exacerbate ischemic injury.

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