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Recent studies have reported on circadian variation in infarct size in ST-elevation myocardial infarction (STEMI) patients. Controversy remains as to whether this finding indicates circadian dependence of myocardial tolerance to ischemia/reperfusion injury or that it can simply be explained by confounding factors such as baseline profile and ischemic time. We assessed the clinical impact and independent association between symptom onset time and infarct size, accounting for possible subgroup differences. From a multicenter registry, 6799 consecutive STEMI patients undergoing primary percutaneous coronary intervention (PCI) between 2004 and 2010 were included. Infarct size was measured using peak creatine kinase (CK). Infarct size exhibited circadian variation with largest infarct size in patients with symptom onset around 03:00 at night (estimated peak CK 1322 U/l; 95% confidence interval (CI): 1217-1436) and smallest infarct size around 11:00 in the morning (estimated peak CK 1071 U/l; 95% CI: 1001-1146; relative reduction 19%; p = 0.001). Circadian variation in infarct size followed an inverse pattern in patients with prior myocardial infarction (p-interaction <0.001) and prior PCI (p-interaction = 0.006), although the later did not persist in multivariable analysis. Symptom onset time remained associated with infarct size after accounting for these interactions and adjusting for baseline characteristics and ischemic time. Symptom onset time did not predict one-year mortality ( p = 0.081). In conclusion, there is substantial circadian variation in infarct size, which cannot be fully explained by variations in baseline profile or ischemic time. Our results lend support to the hypothesis of circadian myocardial ischemic tolerance and suggest a different mechanism in patients with prior myocardial infarction. [ABSTRACT FROM AUTHOR]

The electrocardiogram is universally used to diagnose ST-segment elevation myocardial infarction and serves as guidance for the interventional cardiologist to identify the acute thrombotic lesion. However, this case illustrates that the electrocardiogram can also be deceiving., Competing Interests: The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2024 The Authors.)

Background: In order to facilitate fractional flow reserve (FFR)-guided lesion assessment, several 3-dimensional (3D)-angiography-based physiological indices have been recently validated. Thus far, limited data are available on the association of these indices with conventional forms of ischemia testing., Aim: The aim of the study was to determine the association between 3D-angiography-based vessel-FFR (vFFR) and myocardial ischemia as assessed by exercise electrocardiography (ECG) testing, dobutamine stress echocardiography, single photon emission computed tomography myocardial perfusion imaging (SPECTMPI), and stress cardiovascular magnetic resonance imaging (stress CMR)., Methods: FAST ISCHEMIA is a retrospective, single-center cohort study including patients who underwent non-invasive myocardial ischemia testing and subsequent coronary angiography (≤3 months). A total of 145 patients (340 vessels) were analyzed. The overall patient-based sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratio (LR+), and negative likelihood ratio (LR-) of vFFR ≤0.80 in any vessel for ischemia was 64% (95% confidence interval [CI], 53-74), 71% (95% CI, 54-84), 83% (95% CI, 72-91), 46% (95% CI, 33-60), 2.16 (95% CI, 1.25-3.74), and 0.52 (95% CI, 0.36-0.74), respectively. Multivariable logistic regression showed that vFFR ≤0.80 was significantly associated with ischemia on a patient level (odds ratio, 8.13; 95% CI, 2.51-30.06; P<.001) and on a vascular territory level (odds ratio, 2.75; 95% CI, 1.17-6.44; P<.01)., Conclusion: Our study suggests that vFFR ≤0.80 has a modest association with non-invasive myocardial ischemia testing using either exercise ECG or stress imaging modalities. After correcting for independent confounders, vFFR was independently associated with ischemia on a non-invasive myocardial ischemia detection test.

Background: Identification of people with hypertrophic cardiomyopathy (HCM) who are at risk of sudden cardiac death (SCD) and require a prophylactic implantable cardioverter defibrillator is challenging. In 2014, the European Society of Cardiology proposed a new risk stratification method based on a risk prediction model (HCM Risk-SCD) that estimates the 5-year risk of SCD. The aim was to externally validate the 2014 European Society of Cardiology recommendations in a geographically diverse cohort of patients recruited from the United States, Europe, the Middle East, and Asia., Methods: This was an observational, retrospective, longitudinal cohort study., Results: The cohort consisted of 3703 patients. Seventy three (2%) patients reached the SCD end point within 5 years of follow-up (5-year incidence, 2.4% [95% confidence interval {CI}, 1.9-3.0]). The validation study revealed a calibration slope of 1.02 (95% CI, 0.93-1.12), C-index of 0.70 (95% CI, 0.68-0.72), and D-statistic of 1.17 (95% CI, 1.05-1.29). In a complete case analysis (n= 2147; 44 SCD end points at 5 years), patients with a predicted 5-year risk of <4% (n=1524; 71%) had an observed 5-year SCD incidence of 1.4% (95% CI, 0.8-2.2); patients with a predicted risk of ≥6% (n=297; 14%) had an observed SCD incidence of 8.9% (95% CI, 5.96-13.1) at 5 years. For every 13 (297/23) implantable cardioverter defibrillator implantations in patients with an estimated 5-year SCD risk ≥6%, 1 patient can potentially be saved from SCD., Conclusions: This study confirms that the HCM Risk-SCD model provides accurate prognostic information that can be used to target implantable cardioverter defibrillator therapy in patients at the highest risk of SCD., (© 2017 American Heart Association, Inc.)

Background: A subgroup of patients presenting with suspected ST-elevation myocardial infarction (STEMI) have no culprit lesion during coronary angiography (false-positive STEMI). Little is known about patient- and system-related factors that are associated with false-positive STEMI. We evaluated the incidence, correlates, delay, final diagnosis, and outcome of patients with false-positive STEMI., Methods: We studied 827 consecutive patients presenting with suspected STEMI between January 2011-September 2012., Results: A false positive STEMI activation was identified in 68 patients (8.2%). Patients with false-positive STEMI were younger (57 vs 63 year; p=0.020), less often had hypercholesterolemia (19 vs 43%; p=0.001), and had a higher heart rate (82 vs 75 bpm; p=0.014). The association between these factors and false-positive STEMI activation persisted in multivariate analysis. The duration of symptoms to call was longer in false-positive STEMI patients (128 vs 83 min; p=0.030), although this did not reach statistical significance in multivariate analysis. Final diagnosis in patients with false-positive STEMI activation was particularly from unknown origin (41%). There were no significant differences in mortality at 30 days and one year between patients with STEMI and false-positive STEMI., Conclusion: The incidence of false-positive STEMI was 8.2% in patients suspected of STEMI. Patients with false-positive STEMI differ from STEMI patients in certain baseline characteristics and in patient delay. Interestingly, absence of coronary disease did not translate into better clinical outcome., (© The European Society of Cardiology 2015.)

Objectives: The aim of this study was to perform an individual patient-level pooled analysis of randomised trials, comparing intracoronary versus intravenous abciximab bolus use in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI)., Background: Abciximab represents a cornerstone in the treatment of STEMI patients undergoing primary PCI. Intracoronary abciximab bolus administration has been proposed as an alternative strategy to the standard intravenous route. However, whether intracoronary abciximab effectively improves clinical outcomes compared with standard route remains unknown., Methods: Individual data of 1198 patients enrolled in five trials were entered into the pooled analysis. The primary endpoint of the study was the occurrence of all-cause death and reinfarction at 30-day follow-up. Secondary endpoints were all-cause death, reinfarction and target-vessel revascularisation (TVR)., Results: No significant heterogeneity was found across trials. Compared with the intravenous route, intracoronary abciximab administration significantly reduced the risk of the composite of death and reinfarction (HR 0.52, 95% CI 0.29 to 0.94; p=0.03), death (HR 0.44, 95% CI 0.20 to 0.95; p=0.04) and TVR (HR 0.53, 95% CI 0.29 to 0.99; p=0.045), without a significant impact on the risk of reinfarction (HR 0.54, 95% CI 0.24 to 1.21; p=0.13). However, after correction for baseline differences, only the composite of death/reinfarction and death remained significant., Conclusions: In STEMI patients undergoing primary PCI, intracoronary abciximab administration, when compared with the intravenous standard route, can improve short-term clinical outcomes mainly by reducing the risk of death.