Absence Of Myocardial Ischemia Research Articles

Abstract 16070: Prognostic Value of H2FPEF Score Among Symptomatic Patients Referred for Exercise Echocardiography

Introduction: The H2FPEF score is a recommended tool for estimating the likelihood of heart failure with preserved ejection fraction (HFpEF) in cases of unexplained dyspnea. Limited data is available regarding its prognostic ability. This restrospective study aimed to assess the prognostic value of the H2FPEF score for adverse cardiovascular outcomes. Methods: 532 patients [age 69±6 years, 57% female, and ejection fraction 61±5% (all >50%)] with suspected symptoms of heart failure (HF) referred for exercise echocardiography were included. H2FPEF score was calculated based on: BMI >30 kg/m2 (2 points), atrial fibrillation (3 points), age >60 years (1 point), use of ≥2 hypertension drugs (1 point), E/e’ ratio >9 (1 point), and pulmonary systolic pressure >35 mmHg (1 point). Comparisons were made for death and HF hospitalization. Results: During a median follow-up of 3.8 years, 13 patients died, 35 had HF hospitalizations, and 48 experienced the composite outcome. The score distribution was as follows: 0-1 in 69 (13%) patients, 2-5 in 430 (81%) patients, and ≥6 in 33 (6%) patients. The H2FPEF score averaged 3.2±1.5 and showed a progressive increase in the risk of adverse outcomes. A score of 0-1 was associated with the lowest risk, ≥6 with the highest risk, and 2-5 with an intermediate risk (Figure 1A-C). Compared to a score of 0-1, increased risk for combined outcomes occurred with a score of 2-5 (HR: 3.4, 95% CI: 1.5-8) and ≥6 (HR: 9.6, 95% CI: 3.6-26). Similar risk patterns were observed for death and HF hospitalization. Importantly, during exercise echocardiography, new wall motion abnormalities occurred in 105 (20%) patients and did not differ significantly among the different H2FPEF score groups (p=0.403). A H2FPEF score >1 was associated with an increased risk regardless of the presence or absence of myocardial ischemia (Figure 1D). Conclusions: H2FPEF score is a useful prognostic tool in suspected HFpEF, regardless of echocardiographic presence or absence of ischemia.

Post hoc labeling an acute ECG as ischemic or non-ischemic based on clinical data: A necessary challenge

The ECG is crucial in the prehospital (and early inhospital) phase of patients with symptoms suggestive of myocardial ischemia. Therefore, new algorithms for ECG-based myocardial ischemia detection are continuously being researched. Development and validation of these algorithms require a database of acute ECGs (from the prehospital or emergency department setting) including a representative mix of cases (ischemia present) and controls (no ischemia present). Therefore, for every patient in this mix, the “truth” regarding the actual presence or absence of myocardial ischemia during the recording of the acute ECG has to be determined to compare the newly developed algorithm against. This post hoc adjudication process of determining whether an acute (either prehospitally acquired or acquired in the emergency department) ECG was made under ischemic conditions should use all available clinical data (the clinical diagnosis, cardiac imaging data, and laboratory values) of the subsequent patient's admission.Even with all data at hand, post hoc labeling a patient and their acute ECG as a myocardial ischemia case or control cannot be forced into a binary division between definite cases and definite controls. More specifically, to be used for the development of a new algorithm, the patients' ECG has to be scored for the presence or absence of myocardial ischemia at the exact moment of its recording, which renders the classification even more difficult. For instance, even though it may be plausible that myocardial ischemia was present at a given moment during the patient's admission, this is not necessarily proof that the prehospital (or early inhospital) ECG was also made in ischemic conditions: ischemia can be a fluctuating process (as is, e.g., the case in unstable angina pectoris). Therefore, post hoc classification of an acute ECG in terms of the absence or presence of ischemia requires a multipoint scale ranging between definite ischemic to definite non-ischemic, for instance using a 5-point scale (presumed non-ischemic, probably non-ischemic, uncertain, probably ischemic, presumed ischemic).To summarize, the post hoc adjudication process of ECGs of ambulance (and emergency department) patients cannot result in a binary division into definite cases and controls (i.e., patients with or without myocardial ischemia during the recording of the acute ECG), as myocardial ischemia is often dynamic rather than constant. ECGs could be labeled on a multi-point scale, in which the label represents the probability of the actual presence (or absence) of myocardial ischemia at the exact moment of the recording of that ECG. Further development of algorithms for myocardial ischemia detection should consider this concept.

Clinical profile of patients and sensitivity of troponin I in patients with and without acute coronary syndrome: An observational study.

Background Various clinical conditions can cause troponin elevation in the absence of myocardial ischaemia. Elevated troponin represents the likely occurrence of myocardial necrosis and does not itself provide any indication of the aetiology. Identifying the cause for troponin elevation and its sensitivity and specificity in predicting acute coronary syndrome (ACS) and cardiac mortality is an important step in determining the optimal management for these patients. Methods We retrospectively collected data of inpatients who had troponin I (TnI) testing as part of their clinical assessment, either in the emergency department, medical wards, coronary care unit (CCU) or intensive care unit (ICU) with their final diagnosis. TnI was used as the index test of sensitivity to diagnose ACS and either echocardiography or coronary angiogram in those available as the reference gold standard. They were classified into two groups of normal and elevated TnI, and further divided into those with ACS and no ACS. Data on clinical parameters and aetiology of elevated TnI in patients without ACS were analysed. Results Of the 254 patients studied, 114 patients (45%) had normal TnI and 140 (55%) had elevated TnI. Seventy-eight patients had ACS, 66 (84.6%) of whom had elevated TnI and 12 (15.38%) had normal TnI. Seventy-four (52.85%) of 140 patients with elevated TnI had alternate causes of TnI elevation; the most common being sepsis, acute kidney injury (AKI) and heart failure without ACS. All-cause mortality was significantly higher in patients with elevated TnI with or without ACS. There was no cardiac mortality among patients with ACS with normal TnI. Sensitivity and specificity of TnI for predicting ACS was 84.6% (95% CI 74.7%-91.8%) and 58% (95% CI 50.3%-65.3%), respectively. Conclusion A variety of conditions apart from myocardial infarction can lead to elevated TnI. Hence, caution should be exercised while diagnosing a patient with ACS based on TnI value in the absence of other supporting evidence given its low specificity. Elevated TnI portends a worse prognosis regardless of the aetiology and has a role in predicting all-cause and cardiac mortality.

Cardiovascular events in patients with coronary artery disease with and without myocardial ischemia: Long-term follow-up

After the results of the ISCHEMIA Trial, the role of myocardial ischemia in the prognosis of coronary artery disease (CAD) was under debate. We sought to comparatively evaluate the long-term prognosis of patients with multivessel CAD with or without documented myocardial ischemia. This is a single-center, retrospective, observational cohort study that included patients with CAD obtained from the research protocols database of "The Medicine, Angioplasty or Surgery Study," the MASS Study Group. Patients were stratified according to the presence or absence of myocardial ischemia. Cardiovascular events (overall mortality and myocardial infarction) were tracked from the registry entry up to a median follow-up of 8.7 years. Myocardial ischemia was assessed at baseline by a functional test with or without imaging. From 1995 to 2018, 2015 patients with multivessel CAD were included. Of these, 1001 presented with conclusive tests at registry entry, 790 (79%) presenting with ischemia and 211 (21%) without ischemia. The median follow-up was 8.7 years (IQR 4.04 to 10.07). The primary outcome occurred in 228 (28.9%) patients with ischemia and in 64 (30.3%) patients without ischemia (plog-rank=0.60). No significant interaction was observed with the presence of myocardial ischemia and treatment strategies in the occurrence of the combined primary outcome (pinteration=0.14). In this sample, myocardial ischemia was not associated with a worse prognosis compared with no ischemia in patients with multivessel CAD. These results refer to debates about the role of myocardial ischemia in the occurrence of cardiovascular events.

Diastolic stress echocardiography in patients with normal resting diastolic function: prognostic utility in presence and absence of myocardial ischemia

Abstract Background Abnormal diastolic response to exercise is reportedly associated with worse cardiovascular events. However, this has not been well studied in patients with normal diastolic function at rest. Purpose We sought to study diastolic response to exercise in patients referred for exercise stress echocardiography (ExE) and to explore its association with adverse outcomes in the presence and absence of exercise-induced myocardial ischemia. Methods In a retrospective study, patients referred for ExE to assess myocardial ischemia between April 2017 and December 2018 were enrolled. Patients were included if they had guideline-defined normal diastolic function at rest and availability of a full set of post exercise diastolic variables (post exercise tissue Doppler derived septal mitral annular early diastolic velocity (e'), ratio of pulsed Doppler derived mitral forward flow early diastolic velocity (E) over e' (E/e') and continuous wave Doppler derived maximum tricuspid regurgitation velocity (TRV)). The patients were followed for a median of 3.4 years for the occurrence of composite death, acute coronary syndrome, cardiac hospitalization, and need of follow-up ischemia testing. Abnormal exercise diastolic variables were defined as e' <7 cm/s, E/e' >15, and TRV >2.8 m/s. Results We studied 492 patients [age: 55.7±12.9 year, 268 (54%) women, EF: 61±5.8%]. Mean achieved metabolic equivalents of tasks (METs) was 9.7±3.1, and a total of 49 (10%) patients had evidence of exercise-induced ischemia. At rest, mean left atrial volume index was 25.4±12 ml, e' was 8±2 cm/s, E/e' was 9.5±2.4, and TRV was 2.1±0.44 m/s. Post exercise e' was 10±3 cm/s [<7cm/s in 63 (13%)], E/e' was 11.1±3.9 [>15 in 95 (19%)], and TRV was 2.37±0.68 m/s [>2.8 m/s in 152 (31%)]. Ischemic ExE was found to be strongly associated with the outcome (HR: 4.46, 95% CI: 2.8 to 7.1, p<0.001). In addition, all diastolic variables predicted the outcome in isolation if they were abnormal (e': 2.28, 95% CI: 1.4 to 3.7, p=0.001, E/e': 1.81; 95% CI: 1.15 to 2.84, p=0.01; TRV: 1.58, 95% CI: 1.17 to 2.13, p=0.003). When combined, however, association with the outcome was seen only when 2 or 3 of these variables were abnormal simultaneously (Figure 1A). When patients were stratified by ischemia and abnormal diastolic variables (figure 1B), patients with 2 or 3 abnormal variables were more likely to experience the outcome compared to patients with 0 or 1 abnormal variables in both absence of ischemia (p<0.001) and presence of ischemia (p=0.016). The stratified groups were different in their clinical and exercise profiles, with worse profiles in patients with both ischemia and 2 or 3 abnormal variables, and best profiles in patients with no ischemia and 0 or 1 abnormal variables. Conclusions In patients referred for ExE to assess ischemia with normal baseline diastolic function, exercise can unmask abnormal diastolic properties and stratify patients' risk regardless of the overt myocardial ischemia. Funding Acknowledgement Type of funding sources: None.

Intracellular Toxic Advanced Glycation End-Products May Induce Cell Death and Suppress Cardiac Fibroblasts.

Cardiovascular disease (CVD) is a lifestyle-related disease (LSRD) induced by the dysfunction and cell death of cardiomyocytes. Cardiac fibroblasts are activated and differentiate in response to specific signals, such as transforming growth factor-β released from injured cardiomyocytes, and are crucial for the protection of cardiomyocytes, cardiac tissue repair, and remodeling. In contrast, cardiac fibroblasts have been shown to induce injury or death of cardiomyocytes and are implicated in the pathogenesis of diseases such as cardiac hypertrophy. We designated glyceraldehyde-derived advanced glycation end-products (AGEs) as toxic AGEs (TAGE) due to their cytotoxicity and association with LSRD. Intracellular TAGE in cardiomyocytes decreased their beating rate and induced cell death in the absence of myocardial ischemia. The TAGE levels in blood were elevated in patients with CVD and were associated with myocardial ischemia along with increased risk of atherosclerosis in vascular endothelial cells in vitro. The relationships between the dysfunction or cell death of cardiac fibroblasts and intracellular and extracellular TAGE, which are secreted from certain organs, remain unclear. We examined the cytotoxicity of intracellular TAGE by a slot blot analysis, and TAGE-modified bovine serum albumin (TAGE-BSA), a model of extracellular TAGE, in normal human cardiac fibroblasts (HCF). Intracellular TAGE induced cell death in normal HCF, whereas TAGE-BSA did not, even at aberrantly high non-physiological levels. Therefore, only intracellular TAGE induced cell death in HCF under physiological conditions, possibly inhibiting the role of HCF.

Long-term prognostic implications of PCI in ACS patients without ischemia on the basis of computational pressure-flow dynamics derived fractional flow reserve

Abstract Background A substantial proportion of patients with acute coronary syndrome (ACS) may have intermediate lesion that are non-ischemic during emergency coronary angiography. The prognosis of such patients, compared to those with stable ischemic heart disease (SIHD) without ischemic lesion is however uncertain. Recently, a novel index, computational pressure-flow dynamics derived fractional flow reserve (caFFR), has been developed to assess myocardial ischemia, without the need of invasive pressure wire and hyperaemic stimulus as required in conventional fractional flow reserve (FFR). By utilizing caFFR to assess for ischaemic status during coronary angiography, the aim of our study is first to assess the prognostic difference between ACS and SIHD with non-ischaemia intermediate lesions. Second, we ascertain whether PCI in patients with ACS with non-ischaemia intermediate lesions provides survival benefit in addition to medical therapy. Methods We retrospectively recruited 551 patients (mean age 64.4 years; male 59.9%) with absence of myocardial ischaemia, defined as caFFR ≥0.80 in all vessels, from our Hospital. Patients were stratified into those with index presentation of ACS (n=132) and those with SIHD (n=491). Among the ACS cohort, patients were further divided into those with PCI (n=83) and with medical therapy alone (n=49). The SIHD cohort (n=491), all of whom were treated with medical therapy alone, was considered as referent group. The primary end point was major adverse cardiovascular events (MACE) at 3 years, which was defined as a composite of all-cause mortality, non-fatal myocardial infarction (MI), and any unplanned revascularization. Results During a median follow-up of 36 months, 54 composite events occurred, including 38 all-cause mortality, 5 MI, and 14 unplanned revascularization. Compared to those with SIHD, patients with ACS was independently associated with MACE even in the absence of myocardial ischaemia (adjusted Hazard Ratios=2.531; 95% confidence interval=1.397–4.586; P=0.002). The 3-year incidence rate of MACE was the highest in ACS patients with medical therapy alone, followed by ACS patients with immediate PCI; the SIHD cohort had the lowest incidence rates (30.6% vs 12.0% vs 5.9%, P<0.001). This was mainly driven by the rate of all-cause death (26.5% vs 12.0% vs 3.1%; P<0.001). Similar findings were observed for hospitalisation due to heart failure (14.3% vs 6.0% vs 3.1%, P=0.031) and cardiac death (8.2% vs 4.8% vs 0.4%, P<0.001) at 3 years. Conclusion In patients with intermediate lesion without myocardial ischaemia (defined as caFFR ≥0.8), those presented with ACS had a higher risk of MACE at 3 years compared to SIHD. Among ACS patients with intermediate lesion without myocardial ischaemia, PCI significantly reduces the rate of MACE. In patients with ACS, our finding suggests that PCI should be advocated to intermediate lesion even without myocardial ischaemia. Funding Acknowledgement Type of funding sources: None. Kaplan-Meier curve for MACECumulative Events at 3 Years

Exploration of the efficacy of radiomics applied to left ventricular tomograms obtained from D-SPECT MPI for the auxiliary diagnosis of myocardial ischemia in CAD.

To explore the feasibility and efficacy of radiomics with left ventricular tomograms obtained from D-SPECT myocardial perfusion imaging (MPI) for auxiliary diagnosis of myocardial ischemia in coronary artery disease (CAD). The images of 103 patients with CAD myocardial ischemia between September 2020 and April 2021 were retrospectively selected. After information desensitization processing, format conversion, annotation using the Labelme tool on an open-source platform, lesion classification, and establishment of a database, the images were cropped for analysis. The ResNet18 model was used to automate two steps (classification and segmentation) with five randomization, training and validation steps. The sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, positive predictive value, negative predictive value, Youden's index, agreement rate, and kappa value were calculated as evaluation indexes of the classification results for each training-validation step; then, receiver operating characteristics (ROC) curves were drawn, and the areas under the curve (AUCs) were calculated. The Dice coefficient, intersection over union, and Hausdorff distance were calculated as evaluation indexes of the segmentation results for each training-validation step; then, the predicted images were exported. Under the existing conditions, the radiomics model used in this study had an AUC above 0.95 in identifying the presence or absence of myocardial ischemia; in the prediction of the extent of myocardial ischemia, its evaluation index distribution is also close to that of the gold standard. Radiomics can be feasibly applied to left ventricular tomograms obtained from D-SPECT MPI for auxiliary diagnosis. With more in-depth research and the development of technology, adding this method to the existing auxiliary diagnosis will likely further improve the diagnostic accuracy and efficiency, and patients will therefore benefit.

Total coronary atherosclerotic plaque burden is associated with myocardial ischemia in non-obstructive coronary artery disease.

AimWhether the total coronary atherosclerotic plaque burden is independently associated with myocardial ischemia in non-obstructive coronary artery disease (CAD) is not well established. We aimed to test the association of total plaque burden quantified by coronary computed tomography angiography (CCTA) with myocardial ischemia in patients with chronic coronary syndrome and non-obstructive CAD.MethodsWe included 125 patients (age 62 ± 9 years, 58% women) with chronic coronary syndrome and non-obstructive CAD (stenosis < 50%) by CCTA, who were grouped according to presence or absence of myocardial ischemia by myocardial contrast stress echocardiography. Total plaque burden was quantified by CCTA as the total plaque volume in the main coronary arteries, and positive remodelling was defined as remodelling index > 1.10.ResultsPatients with myocardial ischemia (n = 66) had higher total plaque burden (847 ± 245 mm3 vs. 758 ± 251 mm3, p = 0.049) and higher left ventricular (LV) mass index (42.1 ± 9.9 g/m2.7 vs. 37.3 ± 8.0 g/m2.7, p = 0.004), while age, sex, prevalence of hypertension, diabetes, calcium score and positive remodelling did not differ between the groups (all p > 0.05). In multivariable regression analysis, total plaque burden remained associated with presence of myocardial ischemia (OR 1.02, 95% CI 1.00–1.04, p = 0.045) independent of age, sex, hypertension, diabetes, LV mass index, coronary calcium score and positive remodelling.ConclusionTotal coronary artery plaque burden by CCTA was independently associated with myocardial ischemia in patients with non-obstructive CAD. Whether plaque quantification is useful for clinical management of patients with non-obstructive CAD should be tested in prospective studies.ClinicalTrials.gov: Identifier NCT01853527.

Polymorphic ventricular tachycardia, ischaemic ventricular fibrillation, and torsade de pointes: importance of the QT and the coupling interval in the differential diagnosis.

Distinctive types of polymorphic ventricular tachycardia (VT) respond differently to different forms of therapy. We therefore performed the present study to define the electrocardiographic characteristics of different forms of polymorphic VT. We studied 190 patients for whom the onset of 305 polymorphic VT events was available. The study group included 87 patients with coronary artery disease who had spontaneous polymorphic VT triggered by short-coupled extrasystoles in the absence of myocardial ischaemia. This group included 32 patients who had a long QT interval but nevertheless had their polymorphic VT triggered by ectopic beats with short coupling interval, a subcategory termed 'pseudo-torsade de pointes] (TdP). For comparison, we included 50 patients who had ventricular fibrillation (VF) during acute myocardial infarction ('ischaemic VF' group) and 53 patients with drug-induced TdP ('true TdP' group). The QT of patients with pseudo-TdP was (by definition) longer than that of patients with polymorphic VT and normal QT (QTc 491.4 ± 25.2 ms vs. 447.3 ± 55.6 ms, P < 0.001). However, their QT was significantly shorter than that of patients with true TdP (QTc 564.6 ± 75.6 ms, P < 0.001). Importantly, the coupling interval of the ectopic beat triggering the arrhythmia was just as short during pseudo-TdP as during polymorphic VT with normal QT (359.1 ± 38.1 ms vs. 356.6 ± 39.4 ms, P = 0.467) but was much shorter than during true TdP (581.2 ± 95.3 ms, P < 0.001). The coupling interval helps discriminate between polymorphic VT that occurs despite a long QT interval (pseudo-TdP) and polymorphic arrhythmias striking because of a long QT (true TdP).

Myocardial ischemia by radionuclide imaging and long-term outcomes after kidney transplantation.

We examined the incidence of myocardial ischemia (MI) in kidney transplant recipients (KTR) using myocardial perfusion imaging (MPI), and its association with long-term outcomes after transplantation. A retrospective observational study was conducted of asymptomatic KTRs who underwent post-transplant MPI screening for MI, as defined by moderate to severe myocardial perfusion defects, post-stress myocardial stunning or balanced ischemia. A composite outcome of all-cause mortality, graft loss, and major adverse cardiovascular events (MACE) was examined over minimum 5years. We studied 135 KTRs who underwent 226 MPIs, with follow-up duration of 10 (7-13) years. 110 (81%) patients had normal MPIs, 11 (8%) had mild perfusion defects, and 14 (10%) had MI. Correspondingly, composite outcome developed in 6%, 27%, and 43% (p = 0.04), and MACE occurred in 7%, 0%, and 21% (p = 0.11), of the respective subgroups. Twenty-six patients developed the composite outcome after 5 (3-7) years post-transplantation, including 11 patients with MACE. On multivariate analysis, MI, higher low-density lipoprotein levels, and proteinuria > 0.3g/day independently predicted the composite outcome; only MI predicted MACE (all p < 0.05). Ninety-one patients had two serial MPIs, which increased the positive predictive value for MACE from 17 to 25%. Absence of MI had negative predictive value of 83% for MACE and 93% for the composite outcome. MI that is detected early post-kidney transplantation predicts long-term mortality, graft loss, and MACE in KTRs, with excellent negative but poor positive predictive values.

Local peribulbar anesthesia before glaucoma filtering surgery in a patient with Brugada syndrome

We report anesthetic management in a patient with Brugada syndrome, an inherited syndrome characterized by normal QT interval, typical ST-segment-elevation in the right precordial leads, and increased risk of sudden cardiac death in the absence of myocardial ischemia or structural heart disease. A 69-year-old man scheduled for glaucoma filtering surgery underwent local peribulbar anesthesia using 5 mL of lidocaine 20 mg/mL solution that was slowly injected into two different sites approximately 10 min prior to the surgical procedure. The surgery proceeded uneventful and data of patient's blood pressure, heart rate, oxygen saturation were collected. Continuous electrocardiography monitoring before, during, and up to 6 h after surgery did not reveal any arrhythmia or tachycardia. A certain number of drugs should be avoided in patients with Brugada syndrome because of their potential risk to trigger an arrhythmia. Among them there are some anesthetics and in particular those that are sodium channel blockers. Ropivacaine and bupivacaine, commonly used for peribulbar block, have been associated with onset of severe arrhythmias. Contrarily, the use of class IB drugs mexiletine and lidocaine is generally considered safe. Local anesthetic agent should be carefully chosen, and anesthesia should be obtained using the minimal necessary drug dose.

P642 Coronary arteriovenous fistulas

Abstract Clinical case A 53 years woman in good health and un uneventful clinical history except for a mild hypercholesteremia was evaluated for palpitations. At the clinical examination she had a systolic murmur 3/6 Levine, with no signs of heart failure. The ECG showed normal sinus rhythm with a normal heart rate (62bpm), normal atrio-ventricular and intraventricular conduction and normal repolarisation, one supraventricular premature beat. The echocardiography showed normal biventricular dimension and function, no valvular heart diseases, no septal defects, regular aortic dimensions. A giant right coronary was evidenced (Figure, panel a) with an arteriovenous fistula originating from the right coronary artery and draining through the coronary sinus into the right atrium (Figure, panel b). The CT coronary angiogram evidenced an dilated right coronary artery communicating with the coronary sinus (arteriovenous fistula) draining into the right atrium. A smaller arteriovenous fistula was evidenced between the circumflex artery (slightly dilated) and the great cardiac vein. (Figure, panel c-e) The Treadmill test didn’t evidence an induced ischemia; however the patient didn’t perform a maximal exercise (double product 20400mmHb*bpm). Moreover, during the first steps of recovery frequent supraventricular premature beats were registered with phases of bigeminies followed by a junctional rhythm phase. Thus, a Gated myocardial Perfusion SPECT was performed evidenced a mild stress induced ischemia of the inferolateral and apical left ventricle wall with normal rest perfusion and normal left ventricle volumes (125ml during exercise and 134ml at rest) with a normal ejection fraction ( &amp;gt; 65%). (Figure, panel f)An elective coronarography was planned. The patient is on therapy with beta-blockers and aspirin. The patient is asymptomatic for angina. Antibiotic prophylaxis was recommended for dental, gastrointestinal, or urologic procedures. Discussion: Coronary arteriovenous fistula (CAVF), first described in 1865 by Krausein (1), are a rare congenital heart disease representing less than 0.5% of all congenital heart diseases with an extremely rare prevalence 0.002% in the general population (2). Moreover, therapy of CAVF is still controversial with previous data showing a relatively high rate of myocardial infarction after surgical repair (3). The recent AHA/ACC guideline for the management of adults with Congenital heart disease recommend a review by a knowledgeable team that may include congenital or noncongenital cardiologists and surgeons to determine the role of medical therapy and/or percutaneous or surgical closure (4) Conclusion: CAVF is a very rare congenital heart defect and might be asymptomatic and evidenced by hazard in adults patients. Therapy strategy demands a multidisciplinary team evaluation and should be be individualized according to the clinic presentation, the presence or absence of myocardial ischemia or ventricular dysfunction. Abstract P642 Figure.

Diagnostic evaluation of CT-based non-invasive fractional flow reserve in coronary artery lesions with calcification

Objective To analyze the correlation between calcification factors and fractional flow reserve derived from CT (CT-FFR). And to evaluate the diagnostic efficacy of CT-FFR in coronary artery lesions with calcification compared with that of invasive FFR. Methods Sixty-five patients (74 coronary artery vessels) who were admitted to Beijing Anzhen Hospital from July 2014 to December 2016 were included in this study retrospectively. All patients had completed CCTA (coronary CT angiography), coronary angiography and invasive FFR measurements, and had coronary lesions contain calcifications. The evaluation of CCTA data included quantitative analyses of plaque components, coronary artery stenosis, and CT-FFR measurements. The patients′ basic data were grouped and compared according to the FFR values. The measurement data was tested by independent-samples t tests, and the categorical data were analyzed by χ2 tests. Quantitative measurements of plaques were compared between groups using independent-sample t tests or rank sum tests based on FFR and CT-FFR values. The reproducibility of CT-FFR measurement software was evaluated by inter-class correlation coefficient (ICC) and the Youden index was calculated to determine the threshold for CT-FFR diagnosis of ischemia. Pearson or Spearman correlation analyses were used to assess the correlations between CT plaque quantitative indicators, CT-FFR and invasive FFR. Multivariate logistic regression analysis was used to analyze the predictors of ischemia by FFR and CT-FFR. In contrast to invasive FFR results, the sensitivity, specificity, negative predictive value, positive predictive value (PPV) of CT-FFR in the diagnosis of coronary ischemic lesions were evaluated, and the diagnostic consistency was evaluated by the Bland-Altman method. Results Compared with invasive FFR, CT-FFR had a more significant correlation with calcification volume and ratio of calcification in plaques (r=-0.519 and -0.547, respectively, both P=0.001). Multivariate logistic regression analysis showed that plaque length was a predictor of invasive FFR in the diagnosis of pathological ischemia (OR=1.13, 95%CI: 1.05—1.23, P=0.002), and was associated with CT-FFR to determine pathological ischemia. In addition to plaque length (OR=1.10, 95%CI: 1.02—1.18, P=0.010), the predictor also included ratio of calcification in plaque (OR=1.09, 95%CI: 1.03—1.15, P=0.003). Compared with invasive FFR results, the diagnostic sensitivity of CT-FFR was 79.1%, the specificity was 80.6%, the PPV was 85.0%, and the area under the ROC curve was 0.78. The result for the diagnosis of ischemia lesion by using CT-FFR had significant statistical differences with the results by according coronary artery stenosis (χ2=10.05, P=0.002; χ2=34.71, P=0.001; χ2=7.65, P=0.006; Z=2.10, P=0.029). The Bland-Altman analysis showed a mean difference of -0.01 (-0.26—0.25) between the CT-FFR and the invasive FFR. Conclusions There is no significant correlation between the proportion of calcification components of coronary plaque and the presence or absence of myocardial ischemia, but the proportion of calcification in plaque will affect the result that is evaluated by CT-FFR. However, compared with CT-based stenosis evaluation, CT-FFR can still significantly improve the ability of CCTA to diagnose ischemia lesion with calcification. Key words: Tomography, X-ray computed; Coronary vessels; Calcification, physiologic; Fractional flow reserve, myocardial

Myocardial Injury in the Era of High-Sensitivity Cardiac Troponin Assays

ImportanceTraditionally, elevated troponin concentrations were synonymous with myocardial infarction. But with improvements in troponin assays, elevated concentrations without overt myocardial ischemia are now more common; this is referred to as myocardial injury. Physicians may be falsely reassured by the absence of myocardial ischemia; however, recent evidence suggests that myocardial injury is associated with even more detrimental outcomes. Accordingly, this article reviews the definition, epidemiology, differential diagnosis, diagnostic evaluation, and management of myocardial injury.ObservationsCurrent epidemiological evidence suggests that myocardial injury without overt ischemia represents about 60% of cases of abnormal troponin concentrations when obtained for clinical indications, and 1 in 8 patients presenting to the hospital will have evidence of myocardial injury. Myocardial injury is a concerning prognosis; the 5-year mortality rate is approximately 70%, with a major adverse cardiovascular event rate of 30% in the same period. The differential diagnosis is broad and can be divided into acute and chronic precipitants. The initial workup involves an assessment for myocardial ischemia. If infarction is ruled out, further evaluation includes a detailed history, physical examination, laboratory testing, a 12-lead electrocardiogram, and (if there is no known history of structural or valvular heart disease) an echocardiogram. Unfortunately, no consensus exists on routine management of patients with myocardial injury. Identifying and treating the underlying precipitant is the most practical approach.Conclusion and RelevanceMyocardial injury is the most common cause of abnormal troponin results, and its incidence will likely increase with an aging population, increasing prevalence of cardiovascular comorbidities, and greater sensitivity of troponin assays. Myocardial injury represents a challenge to clinicians; however, given its serious prognosis, it warrants a thorough evaluation of its underlying precipitant. Future strategies to prevent and/or manage myocardial injury are needed.

Left ventricular hypertrophy contributes to Myocardial Ischemia in Non-obstructive Coronary Artery Disease (the MicroCAD study)

BackgroundThe underlying mechanisms causing myocardial ischemia in non-obstructive coronary artery disease (CAD) are still unclear. We explored whether left ventricular hypertrophy (LVH) was associated with myocardial ischemia in patients with stable angina and non-obstructive CAD. Methods132 patients (mean age 63 ± 8 years, 56% women) with stable angina and non-obstructive CAD diagnosed as <50% stenosis by coronary computed tomography angiography (CCTA) underwent myocardial contrast stress echocardiography. Left ventricular (LV) hypertrophy (LVH) was identified by LV mass index >46.7 g/m2.7 in women and >49.2 g/m2.7 in men. Patients were grouped according to presence or absence of myocardial ischemia by myocardial contrast stress echocardiography. The number of LV segments with ischemia at peak stress was taken as a measure of the extent of myocardial ischemia. ResultsMyocardial ischemia was found in 52% of patients, with on average 5 ± 3 ischemic LV segments per patient. The group with myocardial ischemia had higher prevalence of LVH (23 vs. 10%, p = 0.035), while age, sex and prevalence of hypertension did not differ between groups (all p > 0.05). In multivariable regression analyses, LVH was associated with presence of myocardial ischemia (odds ratio 3.27, 95% confidence interval [1.11–9.60], p = 0.031), and larger extent of myocardial ischemia (β = 0.22, p = 0.012), independent of confounders including age, hypertension, obesity, hypercholesterolemia, calcium score and segment involvement score by CCTA. ConclusionsLVH was independently associated with both presence and extent of myocardial ischemia in patients with stable angina and non-obstructive CAD by CCTA. These results suggest LVH as an independent contributor to myocardial ischemia in non-obstructive CAD.Clinical trial registration number: ClinicalTrials.gov, identifier NCT018535271.

Coronary Physiology in the Cardiac Catheterization Laboratory

Coronary angiography has been the principle modality for assessing the severity of atherosclerotic coronary artery disease for several decades. However, there is a complex relationship between angiographic coronary stenosis and the presence or absence of myocardial ischemia. Recent technological advances now allow for the assessment of coronary physiology in the catheterization laboratory at the time of diagnostic coronary angiography. Early studies focused on coronary flow reserve (CFR) but more recent work has demonstrated the physiologic accuracy and prognostic value of the fractional flow reserve (FFR) and instantaneous wave free ratio (iFR) for the assessment of coronary artery disease. These measurements have been validated in large multi-center clinical trials and have become indispensable tools for guiding revascularization in the cardiac catheterization laboratory. The physiological assessment of chest pain in the absence of epicardial coronary artery disease involves coronary thermodilution to obtain the index of microcirculatory resistance (IMR) or Doppler velocity measurement to determine the coronary flow velocity reserve (CFVR). Physiology-based coronary artery assessment brings “personalized medicine” to the catheterization laboratory and allows cardiologists and referring providers to make decisions based on objective findings and evidence-based treatment algorithms. The purpose of this review is to describe the theory, technical aspects, and relevant clinical trials related to coronary physiology assessment for an intended audience of general medical practitioners.

Is coronary calcium scoring too late? Total body arterial calcium burden in patients without known CAD and normal MPI

BackgroundPatients with normal myocardial perfusion imaging (MPI) have a good prognosis. However, pre-clinical coronary and extracoronary atherosclerosis may exist in the absence of myocardial ischemia. Methods154 Egyptian patients (mean age 53 years) underwent whole-body non-contrast CT following normal MPI. ResultsAtherosclerosis in the form of calcification was observed in ≥1 vascular bed in 115 of 154 (75%) patients. This included the iliofemoral (62%), abdominal aorta (53%), thoracic aorta (47%), coronary (47%), and carotid (25%) vascular beds. Mean total body calcium score was 3172 ± 530 AU. Extracoronary atherosclerosis in patients with a zero coronary artery calcium (CAC) score was common, occurring in the above-listed beds 42%, 36%, 29%, and 7% of the time, respectively. CAC was rarely present without iliofemoral or abdominal aortic calcification. ConclusionQuantitative assessment of calcification in different vascular beds demonstrates that extracoronary atherosclerosis is common in patients who have normal MPI. Atherosclerotic calcifications are most common in the iliofemoral arteries and abdominal aorta, which typically predate coronary calcifications. An imaging strategy to detect extracoronary atherosclerosis could lead to greater understanding of the natural history of atherosclerosis in its long pre-clinical phase and possibly to earlier preventive strategies.

PO616 Clinical Profile and Risk Factors of In-Hospital Mortality Among Filipino Patients With Infective Endocarditis

The underlying mechanisms causing myocardial ischemia in non-obstructive coronary artery disease (CAD) are still unclear. We explored whether left ventricular hypertrophy (LVH) was associated with myocardial ischemia in patients with stable angina and non-obstructive CAD.132 patients (mean age 63 ± 8 years, 56% women) with stable angina and non-obstructive CAD diagnosed as <50% stenosis by coronary computed tomography angiography (CCTA) underwent myocardial contrast stress echocardiography. Left ventricular (LV) hypertrophy (LVH) was identified by LV mass index >46.7 g/m2.7 in women and >49.2 g/m2.7 in men. Patients were grouped according to presence or absence of myocardial ischemia by myocardial contrast stress echocardiography. The number of LV segments with ischemia at peak stress was taken as a measure of the extent of myocardial ischemia.Myocardial ischemia was found in 52% of patients, with on average 5 ± 3 ischemic LV segments per patient. The group with myocardial ischemia had higher prevalence of LVH (23 vs. 10%, p = 0.035), while age, sex and prevalence of hypertension did not differ between groups (all p > 0.05). In multivariable regression analyses, LVH was associated with presence of myocardial ischemia (odds ratio 3.27, 95% confidence interval [1.11–9.60], p = 0.031), and larger extent of myocardial ischemia (β = 0.22, p = 0.012), independent of confounders including age, hypertension, obesity, hypercholesterolemia, calcium score and segment involvement score by CCTA.LVH was independently associated with both presence and extent of myocardial ischemia in patients with stable angina and non-obstructive CAD by CCTA. These results suggest LVH as an independent contributor to myocardial ischemia in non-obstructive CAD.Clinical trial registration number: ClinicalTrials.gov, identifier NCT018535271.

A CASE OF MASSIVE PULMONARY EMBOLISM CAUSING VENTRICULAR FIBRILLATION AND CARDIAC ARREST

SESSION TITLE: Critical Care 1 SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Massive Pulmonary Embolism (PE) is a known noncardiac cause of circulatory arrest, it is associated with very poor outcomes and high mortality. We herein report a unique case of cardiac arrest due to massive PE that presented with a dominant rhythm of Ventricular Fibrillation (VF). CASE PRESENTATION: A 42-year-old male with past medical history of morbid obesity and chronic back pain; presented to our hospital with acute on chronic low back pain and inability to ambulate. On admission, vital signs were normal. Physical examination showed signs of left lower extremity radiculopathy. Often times and because of the pain severity, patient used to refuse to participate in physical therapy and assisted ambulation. Given that, patient was on appropriate pharmacological deep venous thrombosis prophylaxis. During hospitalization, the patient was found unresponsive and pulseless, code blue was activated and cardiopulmonary resuscitation was started. Upon connecting it, the cardiac monitor showed VF rhythm (Image 1) for which a shock was delivered. After few minutes, return of spontaneous circulation achieved. A 12-lead electrocardiogram demonstrated sinus tachycardia and new right bundle branch block (Image 2) and that triggered the suspicion of PE. A stat bedside echocardiogram revealed dilatation of the right ventricle. Computed Tomography of chest with intravenous contrast (PE protocol) confirmed the diagnosis of PE in the left and right main pulmonary arteries(Image 3). As a result, systemic thrombolytic therapy was initiated. Few hours later, the patient went into three successive episodes of cardiac arrest in which VF was the recurrent rhythm and multiple shocks were delivered. DISCUSSION: PE is the third most common cause of hospital-related death[1]. The vast majority of VF cases are strongly linked to cardiac events; mainly coronary artery disease due to ischemia[2]. On the other hand, PE with circulatory arrest is highly associated with pulseless electric activity (PEA) followed by asystole[3]. For VF to be the dominant rhythm in the setting of cardiac arrest due to massive PE and without any evidence of myocardial ischemia is unreported. This case highlights the importance of considering PE in the differential diagnosis of cardiac arrest causes when the presenting and the dominant rhythm is VF particularly in the absence of myocardial ischemia. CONCLUSIONS: To our knowledge, this is the first case in the literature to provide a direct link between PE and VF in the context of circulatory arrest. It is crucial to recognize the initial rhythm that is associated with the cardiac arrest as it may guide toward the etiology of the arrest. While, PEA and asystole are by far the most common rhythms in massive PE with cardiac arrest, our case should encourage physicians to also consider PE as a possible cause of cardiac arrest when VF is the main rhythm and no signs of cardiac ischemia exist. Reference #1: Lindblad B, Eriksson A, Bergqvist D. Autopsy-verified pulmonary embolism in a surgical department: analysis of the period from 1951 to 1988. Br J Surg. 1991;78:849–852. [PubMed] Reference #2: Warnes CA, Roberts WC. Sudden coronary death: relation of amount and distribution of coronary narrowing at necropsy to previous symptoms of myocardial ischemia, left ventricular scarring and heart weight. Am J Cardiol. 1984 Jul 1. 54(1):65-73. Reference #3: Kürkciyan I, Meron G, Sterz F, Janata K, Domanovits H, Holzer M, Berzlanovich A, Bankl HC, Laggner AN. Pulmonary Embolism as Cause of Cardiac ArrestPresentation and Outcome. Arch Intern Med.2000;160(10):1529–1535. https://doi.org/10.1001/archinte.160.10.1529 DISCLOSURES: No relevant relationships by Michel Chalhoub, source=Web Response No relevant relationships by halim el hage, source=Web Response No relevant relationships by Cheikh Talal El Imad, source=Web Response No relevant relationships by Ahmad Itani, source=Web Response No relevant relationships by boutros karam, source=Web Response No relevant relationships by Ahmed Mahgoub, source=Web Response No relevant relationships by chadi salmane, source=Web Response No relevant relationships by Jay Solanki, source=Web Response