Multiple spontaneous coronary thrombosis causing ST-elevation myocardial infarction in a patient with COVID-19.

ST-Segment Elevation in Patients with COVID-19: A Late Complication

BackgroundIn-hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is higher in those with COVID-19 than in those without COVID-19. The factors that predispose to this mortality rate and their relative contribution are poorly understood. This study developed a risk score inclusive of clinical variables to predict in-hospital mortality in patients with COVID-19 and STEMI.MethodsBaseline demographic, clinical, and procedural data from patients in the North American COVID-19 Myocardial Infarction registry were extracted. Univariable logistic regression was performed using candidate predictor variables, and multivariable logistic regression was performed using backward stepwise selection to identify independent predictors of in-hospital mortality. Independent predictors were assigned a weighted integer, with the sum of the integers yielding the total risk score for each patient.ResultsIn-hospital mortality occurred in 118 of 425 (28%) patients. Eight variables present at the time of STEMI diagnosis (respiratory rate of >35 breaths/min, cardiogenic shock, oxygen saturation of <93%, age of >55 ​years, infiltrates on chest x-ray, kidney disease, diabetes, and dyspnea) were assigned a weighted integer. In-hospital mortality increased exponentially with increasing integer risk score (Cochran-Armitage χ2, P ​< ​.001), and the model demonstrated good discriminative power (c-statistic ​= ​0.81) and calibration (Hosmer-Lemeshow, P ​= ​.40). The increasing risk score was strongly associated with in-hospital mortality (3.6%-60% mortality for low-risk and very high–risk score categories, respectively).ConclusionsThe risk of in-hospital mortality in patients with COVID-19 and STEMI can be accurately predicted and discriminated using readily available clinical information.

Fibrinolytic therapy (FT) and primary percutaneous coronary intervention (PCI) are both well-accepted reperfusion therapies in ST-segment elevation myocardial infarction (STEMI). The evidence of randomized clinical trials indicates a relatively modest difference in 30-day mortality (≈1%) in favor of primary PCI over fibrin-specific FT and was based on very timely primary PCI (ie, a primary PCI–related delay of 40 minutes [door-to-balloon less door-to-needle time]).1 Longer delays to primary PCI, which are far more frequent in clinical practice,2 are associated with attenuated benefit or no benefit at all, particularly when compared with fibrin-specific FT.3,4 The benefit of timely primary PCI over FT is likely to especially apply to higher-risk patients.5,6 Irrespective of the method of reperfusion, the potential for myocardial salvage and better clinical outcome is inversely proportional to ischemic time or its only available clinical surrogate, symptom duration.7–12 These considerations underpin the notion expressed in the American College of Cardiology/American Heart Association (ACC/AHA) guidelines on the treatment of STEMI that timely reperfusion therapy is likely more important in determining outcome than whether FT or primary PCI is the chosen reperfusion method.13 Response by Armstrong et al p 1310 The ACC/AHA STEMI guidelines highlight the time point of 3 hours of symptom duration in guiding the choice of reperfusion therapy. They state that if symptom duration is <3 hours, no preference exists between FT and primary PCI provided that treatment is timely (for FT, door-to-needle time <30 minutes; for primary PCI, door-to-balloon time <90 minutes and ≤60 minutes between estimated needle time and estimated balloon time). However, if symptom duration exceeds 3 hours, these guidelines favor primary PCI over FT, again provided that primary PCI can be performed in a timely fashion.13 This article reexamines the evidence that may or may not be the basis …

57-Year-Old Man With Atypical Chest Pain

A major goal of any antithrombotic regimen administered during percutaneous coronary intervention (PCI) is the preservation of coronary microvascular perfusion, which is critical for myocardial survival. In addition to macrovascular thrombosis, microembolization into the downstream coronary artery bed that occurs during spontaneous plaque rupture and PCI plays a prominent role in the development of microvascular dysfunction that leads to myocardial infarction. In addition to physical obstruction of the lumen by the embolus, vasoconstriction and edema due to inflammation also impair microvascular flow.1 These events likely occur more frequently during PCI performed in the setting of unstable coronary syndromes.2 With Doppler guidewire technology, it was estimated that an average of 25 embolic events occurred during primary PCI for ST-segment elevation myocardial infarction.3 Article see p 784 Platelet aggregates are important components of coronary microemboli, along with leukocytes, erythrocytes, platelet-leukocyte aggregates, cholesterol crystals, and hyalin. Platelets and leukocytes within microemboli play a particularly important role in the pathophysiological changes of blood flow by promoting in situ microvascular thrombosis, vasoconstriction, and inflammation. Interestingly, the composition of the embolized material is similar in the settings of spontaneous and catheter-induced plaque rupture.1 In animal models, distal microembolization of inert microspheres is associated with an immediate reduction in flow due to vessel occlusion, followed by enhanced blood flow due to the effects of adenosine released from the embolized myocardium into the adjacent noninvolved myocardium.4 Microembolization results in overall reduced flow reserve and the progressive loss of contractile function, which often reverses within weeks. The degree of myocardial contractile dysfunction is disproportionate to the degree of infarction and is the result of inflammation.5 However, in the clinical condition, a more complex pathophysiology exists due to the influence of multiple components of the emboli. Platelets aggregate when fibrinogen binds to the active …

A 52-year-old obese male without a prior history of diabetes mellitus (DM) presented with angina and an anterior ST-segment–elevation myocardial infarction (STEMI). Physical examination and chest x-ray were consistent with congestive heart failure. Admission glucose was 230 mg/dL. Coronary angiography revealed an occluded left anterior descending coronary artery, and stenting reestablished TIMI grade 2 flow in that artery within 90 minutes of symptom onset. Left ventricular ejection fraction was 35% with severe anterior hypokinesis. Peak creatine kinase was 600 IU. The next day, fasting glucose was 180 mg/dL. An echocardiogram performed 6 weeks after discharge revealed an ejection fraction of 35% without change in the anterior wall motion. Fasting glucose as an outpatient was 156 mg/dL. The scenario described above is commonly encountered and illustrates how hyperglycemia can affect the outcome of patients with STEMI. Hyperglycemia could have affected the following features of this case: (1) Congestive heart failure was present despite only modest myocardial injury by creatine kinase level; (2) despite successful percutaneous coronary intervention, subnormal coronary perfusion was observed; and (3) left ventricular recovery after STEMI did not occur. Cardiologists need to be cognizant of the hazards associated with hyperglycemia in this setting because these patients will be encountered more frequently as a result of the increasing prevalence of insulin resistance syndromes. Acute hyperglycemia is common in patients with STEMI even in the absence of a history of type 2 DM. Hyperglycemia is encountered in up to 50% of all STEMI patients, whereas previously diagnosed DM is present in only 20% to 25% of STEMI patients.1 The prevalence of type 2 DM or impaired glucose tolerance may be as high as 65% in MI patients without prior DM when oral glucose tolerance testing is performed.2 Elevated …

To facilitate interpretation of this algorithm and a more detailed discussion in the text, each box is assigned a letter code that reflects its level in the algorithm and a number that is allocated from left to right across the diagram on a given level. ACC/AHA American College of Cardiology/American Heart Association; ACS acute coronary syndrome; ECG electrocardiogram; LV left ventricular. Anderson et al ACC/AHA UA/NSTEMI Guideline Revision e159 Downloaded from http://ahajournals.org by on August 29, 2023 a 12-lead ECG and biomarker determination (e.g., an ED or other acute care facility). (Level of Evidence: C) 2. Patients with symptoms of ACS (chest discomfort with or without radiation to the arm[s], back, neck, jaw or epigastrium; shortness of breath; weakness; diaphoresis; nausea; lightheadedness) should be instructed to call 9-1-1 and should be transported to the hospital by ambulance rather than by friends or relatives. (Level of Evidence: B) 3. Health care providers should actively address the following issues regarding ACS with patients with or at risk for CHD and their families or other responsible caregivers: a. The patient's heart attack risk; (Level of Evidence: C) b. How to recognize symptoms of ACS; (Level of Evidence: C) c. The advisability of calling 9-1-1 if symptoms are unimproved or worsening after 5 min, despite feelings of uncertainty about the symptoms and fear of potential embarrassment; (Level of Evidence: C) d. A plan for appropriate recognition and response to a potential acute cardiac event, including the phone number to access EMS, generally 9-1-1 (74). (Level of Evidence: C) 4. Prehospital EMS providers should administer 162 to 325 mg of ASA (chewed) to chest pain patients suspected of having ACS unless contraindicated or already taken by the patient. Although some trials have used enteric-coated ASA for initial dosing, more rapid buccal absorption occurs with non-enteric-coated formulations. (Level of Evidence: C) 5. Health care providers should instruct patients with suspected ACS for whom nitroglycerin [NTG] has been prescribed previously to take not more than 1 dose of NTG sublingually in response to chest discomfort/pain. If chest discomfort/pain is unimproved or is worsening 5 min after 1 NTG dose has been taken, it is recommended that the patient or family member/friend/caregiver call 9-1-1 immediately to access EMS before taking additional NTG. In patients with chronic stable angina, if symptoms are significantly improved by 1 dose of NTG, it is appropriate to instruct the patient or family member/friend/caregiver to repeat NTG every 5 min for a maximum of 3 doses and call 9-1-1 if symptoms have not resolved completely. (Level of Evidence: C) 6. Patients with a suspected ACS with chest discomfort or other ischemic symptoms at rest for greater than 20 min, hemodynamic instability, or recent syncope or presyncope should be referred immediately to an ED. Other patients with suspected ACS who are experiencing less severe symptoms and who have none of the above high-risk features, including those who respond to an NTG dose, may be seen initially in an ED or an outpatient facility able to provide an acute evaluation. (Level of Evidence: C) CLASS IIa 1. It is reasonable for health care providers and 9-1-1 dispatchers to advise patients without a history of ASA allergy who have symptoms of ACS to chew ASA (162 to 325 mg) while awaiting arrival of prehospital EMS providers. Although some trials have used entericcoated ASA for initial dosing, more rapid buccal absorption occurs with non-enteric-coated formulations. (Level of Evidence: B) 2. It is reasonable for health care providers and 9-1-1 dispatchers to advise patients who tolerate NTG to repeat NTG every 5 min for a maximum of 3 doses while awaiting ambulance arrival. (Level of Evidence: C) 3. It is reasonable that all prehospital EMS providers perform and evaluate 12-lead ECGs in the field (if available) on chest pain patients suspected of ACS to assist in triage decisions. Electrocar-diographs with validated computer-generated interpretation algorithms are recommended for this purpose. (Level of Evidence: B) 4. If the 12-lead ECG shows evidence of acute injury or ischemia, it is reasonable that prehospital ACLS providers relay the ECG to a predetermined medical control facility and/or receiving hospital. (Level of Evidence: B) Downloaded from http://ahajournals.org

Non-Invasive Imaging in Coronary Syndromes: Recommendations of The European Association of Cardiovascular Imaging and the American Society of Echocardiography, in Collaboration with The American Society of Nuclear Cardiology, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance

<i>Circulation: Cardiovascular Interventions</i> Editors’ Picks

Cardiac biomarkers of necrosis provide clinicians with important “messages” from the heart. They are released into the interstitium of the myocardium after loss of the integrity of cardiac myocyte membranes. The pattern of the rise and fall of an individual biomarker (ie, its release kinetics) depends on its intracellular location in the myocyte, molecular weight, and clearance from the interstitium of the myocardium and ultimately the circulation.1 Cardiac biomarkers play an integral role in the clinical diagnosis of myocardial infarction (MI). Referring to the spontaneous occurrence of MI in patients, the World Health Organization required that at least 2 of the following be present to fulfill the criteria for MI: a history of ischemia-type chest discomfort, evolutionary changes on serially obtained ECG tracings, and a rise and fall in serum cardiac markers.2 Article see p 10 See Editorial Circulation . 2008;118:609–611 See Article Circulation . 2008;118:632–638 Several dramatic advances have occurred in the biomarker component of the diagnosis of MI. Analytes with greater specificity for the myocardium were introduced into clinical medicine, with creatine kinase-MB replacing total creatine kinase and subsequently cardiac-specific troponins replacing creatine kinase-MB as the biomarker of choice for diagnosing MI.3 Assay technology improved as clinical chemists moved from enzymatic activity assays for CK to highly specific immunoassays that can detect progressively smaller concentrations of cardiac troponins in the peripheral circulation.4 Although ST-elevation MI (STEMI) is easily identified on the 12-lead ECG, we now recognize that many patients previously diagnosed with unstable angina are more properly diagnosed as having non–ST-elevation MI (NSTEMI) on the basis of the detection of elevated levels of cardiac troponins in their blood.5 Cardiac biomarkers are used as a rough guide to the extent of myocardial necrosis. The higher the peak biomarker level after STEMI, the larger the …

BACKGROUND AND OBJECTIVESGender associations with acute coronary syndrome (ACS), remain inconsistent. Gender-specific data in the Saudi Project for Assessment of Coronary Events registry, launched in December 2005 and currently with 17 participating hospitals, were explored.DESIGN AND SETTINGSA prospective multicenter study of patient with ACS in secondary and tertiary care centers in Saudi Arabia were included in this analysis.PATIENTS AND METHODSPatients enrolled from December 2005 until December 2007 included those presented to participating hospitals or transferred from non-registry hospitals. Summarized data were analyzed.RESULTSOf 5061 patients, 1142 (23%) were women. Women were more frequently diagnosed with non ST-segment elevation myocardial infarction (NSTEMI [43%]) than unstable angina (UA [29%]) or ST-segment elevation myocardial infarction (STEMI [29%]). More men had STEMI (42%) than NSTEMI (37%) or UA (22%). Men were younger than women (57 vs 63 years) who had more diabetes, hypertension, and hyperlipidemia. More men had a history of coronary artery disease. More women received angiotensin receptor blockers (ARB) and fewer had percutaneous coronary intervention (PCI). Gender differences in the subset of STEMI patients were similar to those in the entire cohort. However, gender differences in the subset of STEMI showed fewer women given β-blockers, and an insignificant PCI difference between genders. Thrombolysis rates between genders were similar. Overall, in-hospital mortality was significantly worse for women and, by ACS type, was significantly greater in women for STEMI and NSTEMI. However, after age adjustment there was no difference in mortality between men and women in patients with NSTEMI. The multivariate-adjusted (age, risk factors, treatments, door-to-needle time) STEMI gender mortality difference was not significant (OR=2.0, CI: 0.7–5.5; P=.14).CONCLUSIONThese data are similar to other reported data. However, differences exist, and their explanation should be pursued to provide a valuable insight into understanding ACS and improving its management.

Reperfusion Strategies in ST-Elevation Myocardial Infarction

The randomized clinical trials leading to initial approval of drug-eluting stents (DES) by the United States Food and Drug Administration were conducted by design in a homogeneous group of lower risk patients with mostly noncomplex coronary lesions.1,2 These studies demonstrated a clear benefit in the reduction of restenosis without any evidence of a safety concern during 1 year follow-up. Shortly after approval of the sirolimus and paclitaxel-eluting stents, safety and effectiveness was reported from small nonrandomized studies in a variety of more complex patient and lesion subgroups and resulted in a large proportion of so-called off-label usage.3,4 Article see p 176 Increased concern over the safety of acute DES implantation during primary percutaneous coronary intervention for ST elevation myocardial infarction (MI) left this indication as one of the last to gain widespread usage in favor of bare-metal stents (BMS). A study from Rotterdam comparing 186 consecutive patients receiving a DES from April 2002 to January 2003 with 183 patients receiving a BMS during an immediately preceding time interval demonstrated no increase in subacute stent thrombosis (0% versus 1.6%, P =0.10) and a significantly lower risk for major adverse cardiac events at 300 days (9.4% versus 17.0%, P =0.02) due to a markedly lower risk for target lesion revascularization (TLR) (1.1% versus 8.2%, P 80% penetration of DES among all percutaneous coronary intervention procedures by early 2006.6 Two small randomized trials of DES versus BMS conducted in Europe and published in September 2006, also showed no increase in stent thrombosis for DES within 1 year.7,8 In the summer of 2006, there were new concerns regarding late safety of DES with …

"Goldilocks" Approach to Deferred Stenting in ST-Segment-Elevation Myocardial Infarction.

Advances in antithrombin and antiplatelet therapy have traditionally been associated with reductions in myocardial infarction and other thrombotic events in patients who have experienced an acute coronary syndrome (ACS), are undergoing a percutaneous coronary intervention (PCI), or are receiving long-term therapy for secondary prevention of stable vascular disease. Although individual trials of antithrombotic therapy have rarely been able to demonstrate that the reduction in ischemic events leads to a reduction in mortality (the most important end point), meta-analyses have often suggested that this is the case.1 And because myocardial infarction is an independent correlate of mortality, a link between a reduction in ischemic events and reduced mortality makes intuitive sense. Article p 2793 Unfortunately, more potent anticoagulants and antiplatelet agents are also associated with an increased risk of bleeding, especially when used in combination with one another, as is usually the case. Furthermore, there is a well-established body of evidence that indicates an association between bleeding and ischemic events.2,3 It has been unclear, however, whether the link between bleeding and thrombosis is the result of bleeding after the initial development of a thrombotic complication (and its treatment) or if bleeding precedes the development of an ischemic complication and actually leads to (actually causes) thrombosis. In support of the former possibility is that patients who, because of the presence of thrombus, undergo a longer or more complicated procedure, receive a higher dose or longer duration of antithrombotic medication, or require an intra-aortic balloon pump are surely more prone to bleed. However, the possibility that hemorrhage actually leads to thrombosis rather than results from it is supported by the observation that hemorrhage is a potent stimulus for thrombosis; all patients would surely die if bleeding did not trigger at least a local thrombotic reaction. Furthermore, as the Global Registry of …