Concomitant coronary microvascular dysfunction and spontaneous coronary artery dissection resulting in ST-segment elevation myocardial infarction.
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SUBMITTER: Matthia E
PROVIDER: S-EPMC8766347 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background Invasive measures of microvascular resistance in the culprit coronary artery have potential for risk stratification in acute ST-segment-elevation myocardial infarction. We aimed to investigate the pathological and prognostic significance of coronary thermodilution waveforms using a diagnostic guidewire. Methods and Results Coronary thermodilution was measured at the end of percutaneous coronary intervention, (PCI) and contrast-enhanced cardiac magnetic resonance imaging (MRI) was intended on day 2 and 6 months later to assess left ventricular (LV) function and pathology. All-cause death or first heart failure hospitalization was a pre-specified outcome (median follow-up duration 1469 days). Thermodilution recordings underwent core laboratory assessment. A total of 278 patients with acute ST-segment elevation myocardial infarction EMI (72% male, 59±11 years) had coronary thermodilution measurements classified as narrow unimodal (n=143 [51%]), wide unimodal (n=100 [36%]), or bimodal (n=35 [13%]). Microvascular obstruction and myocardial hemorrhage were associated with the thermodilution waveform pattern ( P=0.007 and 0.011, respectively), and both pathologies were more prevalent in patients with a bimodal morphology. On multivariate analysis with baseline characteristics, thermodilution waveform status was a multivariable associate of microvascular obstruction (odds ratio [95% confidence interval]=5.29 [1.73, 16.22];, P=0.004) and myocardial hemorrhage (3.45 [1.16, 10.26]; P=0.026), but the relationship was not significant when index of microvascular resistance (IMR) >40 or change in index of microvascular resistance (5 per unit) was included. However, a bimodal thermodilution waveform was independently associated with all-cause death and hospitalization for heart failure (odds ratio [95% confidence interval]=2.70 [1.10, 6.63]; P=0.031), independent of index of microvascular resistance>40, ST-segment resolution, and TIMI (Thrombolysis in Myocardial Infarction) Myocardial Perfusion Grade. Conclusions The thermodilution waveform in the culprit coronary artery is a biomarker of prognosis and may be useful for risk stratification immediately after reperfusion therapy.
| S-EPMC6201480 | biostudies-literature
Project description:Primary PCI of infarct-related arteries is the preferred reperfusion strategy in patients presenting with ST-segment elevation myocardial infarction (STEMI). Up to 40 % of such patients demonstrate evidence of multivessel, non-infarct-related artery coronary disease. Previous non-randomised observational studies and their associated meta-analyses have suggested that in such cases only the culprit infarct-related artery (IRA) lesion should be treated. However, recent randomised controlled trials have demonstrated improved clinical outcomes with lower major adverse cardiovascular events (MACE) rates when complete revascularisation is undertaken either at index primary percutaneous coronary intervention (PPCI) or during index admission. These trials suggest that current guidelines pertaining to treatment of non-infarct-related artery (N-IRA) lesions in STEMI patients with multivessel disease may need to be reconsidered depending on future trials. However, issues remain around timing of N-IRA intervention, the use of fractional flow reserve (FFR) or intravascular imaging to guide intervention in N-IRA lesions and the need to demonstrate reductions in hard clinical endpoints (death and MI) after complete revascularisation; these issues will need to be addressed through future trials. Clinicians must judge on the currently available data, whether it is still safer to leave important stenosis in N-IRA untreated.
| S-EPMC4523695 | biostudies-literature
Project description:Early mechanical reperfusion of the epicardial coronary artery by primary percutaneous coronary intervention (PCI) is the guideline-recommended treatment for ST-elevation myocardial infarction (STEMI). Successful restoration of epicardial coronary blood flow can be achieved in over 95% of PCI procedures. However, despite angiographically complete epicardial coronary artery patency, in about half of the patients perfusion to the distal coronary microvasculature is not fully restored, which is associated with increased morbidity and mortality. The exact pathophysiological mechanism of post-ischaemic coronary microvascular dysfunction (CMD) is still debated. Therefore, the current review discusses invasive and non-invasive techniques for the diagnosis and quantification of CMD in STEMI in the clinical setting as well as results from experimental in vitro and in vivo models focusing on ischaemic-, reperfusion-, and inflammatory damage to the coronary microvascular endothelial cells. Finally, we discuss future opportunities to prevent or treat CMD in STEMI patients.
| S-EPMC7061278 | biostudies-literature
Project description:As a result of increased life expectancy, octogenarians constitute an increasing proportion of patients admitted to hospital for ST-segment elevation myocardial infarction (STEMI). Primary percutaneous coronary intervention is currently the treatment of choice for octogenarians presenting with STEMI. The recent literature on this topic has yielded controversial results, even though advances in drug-eluting stents and new types of antithrombotic agents are improving the management of STEMI and postoperative care. In this paper, we review the current status of percutaneous coronary intervention in the elderly with STEMI, including the reasons for their high mortality and morbidity, predictors of mortality, and strategies to improve outcomes.
| S-EPMC4124048 | biostudies-literature
Project description:BACKGROUND:Failed myocardial reperfusion is common and prognostically important after acute ST-elevation myocardial infarction (STEMI). The purpose of this study was to investigate coronary flow reserve (CFR), a measure of vasodilator capacity, and the index of microvascular resistance (IMR; mmHg × s) in the culprit artery of STEMI survivors. METHODS:IMR (n = 288) and CFR (n = 283; mean age [SD], 60 [12] years) were measured acutely using guide wire-based thermodilution. Cardiac MRI disclosed left ventricular pathology, function, and volumes at 2 days (n = 281) and 6 months after STEMI (n = 264). All-cause death or first heart failure hospitalization was independently adjudicated (median follow-up 845 days). RESULTS:Myocardial hemorrhage and microvascular obstruction occurred in 89 (42%) and 114 (54%) patients with evaluable T2*-MRI maps. IMR and CFR were associated with microvascular pathology (none vs. microvascular obstruction only vs. microvascular obstruction and myocardial hemorrhage) (median [interquartile range], IMR: 17 [12.0-33.0] vs. 17 [13.0-39.0] vs. 37 [21.0-63.0], P < 0.001; CFR: 1.7 [1.4-2.5] vs. 1.5 [1.1-1.8] vs. 1.4 [1.0-1.8], P < 0.001), whereas thrombolysis in myocardial infarction blush grade was not. IMR was a multivariable associate of changes in left ventricular end-diastolic volume (regression coefficient [95% CI] 0.13 [0.01, 0.24]; P = 0.036), whereas CFR was not (P = 0.160). IMR (5 units) was a multivariable associate of all-cause death or heart failure hospitalization (n = 30 events; hazard ratio [95% CI], 1.09 [1.04, 1.14]; P < 0.001), whereas CFR (P = 0.124) and thrombolysis in myocardial infarction blush grade (P = 0.613) were not. IMR had similar prognostic value for these outcomes as <50% ST-segment resolution on the ECG. CONCLUSIONS:IMR is more closely associated with microvascular pathology, left ventricular remodeling, and health outcomes than the angiogram or CFR. TRIAL REGISTRATION:NCT02072850. FUNDING:A British Heart Foundation Project Grant (PG/11/2/28474), the National Health Service, the Chief Scientist Office, a Scottish Funding Council Senior Fellowship, a British Heart Foundation Intermediate Fellowship (FS/12/62/29889), and a nonfinancial research agreement with Siemens Healthcare.
| S-EPMC5033815 | biostudies-literature
Project description:The treatment of ST-segment elevation myocardial infarction (STEMI) has advanced dramatically over the past 30 years since the introduction of reperfusion therapies, such that mechanical reperfusion with primary percutaneous coronary intervention is now the standard of care. With STEMI, as with other forms of acute coronary syndrome, stent deployment in culprit lesions is the dominant form of reperfusion in the developed world and is supported by contemporary guidelines. However, the precise timing of stenting and the extent to which both culprit and non-culprit lesions should be treated continue to be active areas of study. In this review, we revisit key data that support the use of mechanical reperfusion therapy in STEMI patients and explore the optimal timing for and extent of stent implantation in this complex patient group. We also review data surrounding the deleterious effects of untreated residual myocardial ischemia, the importance of complete revascularization, and the recent data exploring culprit-only versus multivessel stenting in the STEMI setting.
| S-EPMC5880555 | biostudies-other
Project description:Percutaneous coronary intervention (PCI) is effective in opening the infarct related artery and restoring thrombolysis in myocardial infarction flow 3 (TIMI-flow 3) in large majority of ST-elevation myocardial infarction (STEMI). However there remain a small but significant proportion of patients, who continue to manifest diminished myocardial reperfusion despite successful opening of the obstructed epicardial artery. This phenomenon is called no-reflow. Clinically it manifests with recurrence of chest pain and dyspnea and may progress to cardiogenic shock, cardiac arrest, serious arrhythmias and acute heart failure. No reflow is regarded as independent predictor of death or recurrent myocardial infarction. No reflow is a multi-factorial phenomenon. However micro embolization of atherothrombotic debris during PCI remains the principal mechanism responsible for microvascular obstruction. This review summarizes the pathogenesis, diagnostic methods and the results of various recent randomized trials and studies on the prevention and management of no-reflow.
| S-EPMC4990737 | biostudies-other
Project description:Abstract Background Microvascular dysfunction in the setting of ST-elevated myocardial infarction (STEMI) plays an important role in long-term poor clinical outcome. Coronary flow reserve (CFR) is a well-established physiological parameter to interrogate the coronary microcirculation. Together with hyperaemic average peak flow velocity, CFR constitutes the coronary flow capacity (CFC), a validated risk stratification tool in ischaemic heart disease with significant prognostic value. This mechanistic study aims to elucidate the time course of the microcirculation as reflected by alterations in microcirculatory physiological parameters in the acute phase and during follow-up in STEMI patients. Methods We assessed CFR and CFC in the culprit and non-culprit vessel in consecutive STEMI patients at baseline (n = 98) and after one-week (n = 64) and six-month follow-up (n = 65). Results A significant trend for culprit CFC in infarct size as determined by peak troponin T (p = 0.004), time to reperfusion (p = 0.038), the incidence of final Thrombolysis In Myocardial Infarction 3 flow (p = 0.019) and systolic retrograde flow (p = 0.043) was observed. Non-culprit CFC linear contrast analysis revealed a significant trend in C-reactive protein (p = 0.027), peak troponin T (p < 0.001) and heart rate (p = 0.049). CFC improved both in the culprit and the non-culprit vessel at one-week (both p < 0.001) and six-month follow-up (p = 0.0013 and p < 0.001) compared with baseline. Conclusion This study demonstrates the importance of microcirculatory disturbances in the setting of STEMI, which is relevant for the interpretation of intracoronary diagnostic techniques which are influenced by both culprit and non-culprit vascular territories. Assessment of non-culprit vessel CFC in the setting of STEMI might improve risk stratification of these patients following coronary reperfusion of the culprit vessel.
| S-EPMC8248849 | biostudies-literature
Project description:BackgroundCoronary artery embolism is an infrequent cause of type 2 myocardial infarction which can be due to arterial thromboembolism or septic embolism. While systemic embolization is one of the most acknowledged and threatened complications of infective endocarditis, coronary localization of the emboli causing acute myocardial infarction is exceedingly rare occurring in <1% of cases.Case summaryA 52-year-old man with a history of Bentall procedure and redo aortic valve replacement due to prosthetic degeneration (11 years prior to the current presentation) presented to the emergency department with high-grade fever and myalgias. Shortly after his arrival, he experienced typical chest pain and an electrocardiogram demonstrated signs of inferior ST-elevation myocardial infarction: coronary angiography showed a lesion of presumed embolic origin at the level of the mid-distal circumflex coronary artery which was treated with embolectomy. Transthoracic and transoesophageal echocardiography highlighted the presence of a periaortic abscess. The final diagnosis of infective endocarditis as the cause of septic coronary artery embolization was confirmed with a Positron Emission Tomography-Computed Tomography (PET-CT) exam and by the growth of Staphylococcus lugdunensis on repeated blood cultures. The patient underwent successful redo Bentall surgery the good outcome was confirmed at 1-month follow-up.DiscussionType 2 myocardial infarction caused by coronary embolism is a rare presentation of infective endocarditis and requires a high level of suspicion for its diagnosis. Prosthetic heart valves are a predisposing factor for infective endocarditis: aortic root abscess requires surgery as it rarely regresses with antibiotic therapy.
| S-EPMC8453402 | biostudies-literature
Project description:It is assumed that platelets in diseased conditions share similar properties to platelets in healthy conditions, although this has never been examined in detail for myocardial infarction (MI). We examined platelets from patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) compared with platelets from healthy volunteers to evaluate for differences in platelet phenotype and function. Platelet activation was examined and postreceptor signal transduction pathways were assessed. Platelet-derived plasma biomarkers were evaluated by receiver operator characteristic curve analysis. Maximum platelet activation through the thromboxane receptor was greater in STEMI than in NSTEMI but less through protease-activated receptor 1. Extracellular-signal related-kinase 5 activation, which can activate platelets, was increased in platelets from subjects with STEMI and especially in platelets from patients with NSTEMI. Matrix metalloproteinase 9 (MMP9) protein content and enzymatic activity were several-fold greater in platelets with MI than in control. Mean plasma MMP9 concentration in patients with MI distinguished between STEMI and NSTEMI (area under curve [AUC] 75% [confidence interval (CI) 60-91], P?=?0.006) which was superior to troponin T (AUC 66% [CI 48-85, P?=?0.08), predicting STEMI with 80% sensitivity (95% CI 56-94), 90% specificity (CI 68-99), 70% AUC (CI 54-86, P?<?0.0001), and NSTEMI with 50% sensitivity (CI 27-70), 90% specificity (CI 68-99), 70% AUC (CI 54-86, P?=?0.03). Platelets from patients with STEMI and NSTEMI show differences in platelet surface receptor activation and postreceptor signal transduction, suggesting the healthy platelet phenotype in which antiplatelet agents are often evaluated in preclinical studies is different from platelets in patients with MI.
| S-EPMC5898983 | biostudies-literature