Obstructive Coronary Disease Research Articles

Coronary artery disease in women.

Cardiovascular disease is the leading global cause of death in women but remains underdiagnosed and undertreated. Health professionals play an important role in improving the heart health of Australian women. Routine heart health checks should be offered to all women 45 years of age and older and to all Aboriginal and Torres Strait Islander women 30 years of age and older. Cardiovascular risk assessment in women must include traditional and sex-specific risk factors, including their pregnancy history and early-onset menopause. Women with pregnancy-related hypertensive and metabolic disorders have an increased long-term cardiovascular risk and require close monitoring. Women with acute coronary syndrome may not experience classical chest pain. More often, they experience cardiovascular events in the absence of obstructive coronary disease and have poorer cardiovascular outcomes. The recognition of sex-specific differences and more sex-specific trials are key to improving clinical outcomes.

Factors associated with nonadherence to surveillance for hepatocellular carcinoma among patients with hepatic C virus cirrhosis, 2000-2015.

Hepatocellular carcinoma (HCC) surveillance can detect the early stage of tumors and lead to improved survival. Adherence to guideline-concordant HCC surveillance is crucial in at-risk populations, including patients with hepatic C virus (HCV) cirrhosis. This study was conducted to identify patient and provider factors associated with nonadherence to HCC surveillance in patients with HCV cirrhosis. Data were primarily obtained from the Taiwan National Health Insurance Research Database for the 2000 to 2015 period. Adult patients newly diagnosed as having HCV cirrhosis between 2003 and 2012 were enrolled. Each patient was followed up for 3 years and until the end of 2015. Annual HCC surveillance was defined as the uptake of an abdominal ultrasound and alpha-fetoprotein (AFP) test annually during the 3-years follow-up. Nonannual surveillance was defined as the lack of an annual abdominal ultrasound and AFP test during the same 3-years period. Multinomial logistic regression models were applied to determine factors influencing adherence or nonadherence to annual HCC surveillance. We included a total of 4641 patients with HCV cirrhosis for analysis. Of these patients, only 14% adhered to annual HCC surveillance. HCC surveillance improved in later years, compared with the earlier phases of the study period. Patients with HCV cirrhosis comorbid with coronary artery disease (CAD) or chronic obstructive pulmonary disease (COPD) or those with a relatively high number of comorbidities had a significantly higher likelihood of nonadherence. Patients who primarily received care from internists were significantly less likely to exhibit nonadherence to annual HCC surveillance compared with patients receiving care from physicians of other specialties. Patients who primarily received care from physicians practicing in larger hospitals were significantly less likely to exhibit nonadherence. HCC surveillance rates remain unacceptably low among high-risk patients, and our findings may be helpful in the development of effective interventions to increase HCC surveillance. The effective incorporation of HCC surveillance into routine visits for other chronic comorbidities, particularly for CAD or COPD, may be crucial for increasing HCC surveillance.

Coronary microvascular dysfunction as assessed by angiography-derived index of microvascular resistance co-localizes with and may explain the presence of ischemia in stress-cardiac magnetic resonance imaging in the absence of coronary artery disease.

Ischemia with no obstructive coronary disease (INOCA) is a frequent phenomenon in the cath lab. A possible cause is coronary microvascular dysfunction (CMD), which may be assessed by invasive testing with possible complications; therefore, less invasive approaches have emerged, such as the angiography-derived index of microvascular resistance (aIMR). The aim of our study was to investigate the association of single-vessel aIMR as a measure of CMD with areas of INOCA in stress testing. We measured aIMR in 286 vessels from 102 patients undergoing both stress cMRI and coronary angiography. Groups were (a) INOCA group (93 vessels, 32 patients); (b) coronary artery disease (CAD) control group (116 vessels, 42 patients) with ischemia due to relevant stenosis; and (c) control group (77 vessels, 28 patients) without ischemia or relevant stenosis. INOCA patients presented higher mean aIMR (28.3 ± 5.7) compared to both CAD patients (17.4 ± 5.7, p < 0.001) and controls (22.1 ± 5.9, p < 0.001). Furthermore, in INOCA patients aIMR was significantly increased (33.0 ± 8.1 vs. 25.8 ± 6.3, p = 0.021) in vessels with vs. without ischemia. Single vessel aIMR presented a very good diagnostic efficiency in detecting INOCA [AUC 0.865 (0.804-0.925), optimal cut-off 27.1, p < 0.001]. CMD, as assessed by 3-vessel aIMR, co-localizes with and may explain the presence of ischemia in stress-cMRI in INOCA.

Abstract 144: Impact Of Gender On Outcomes In The Extracorporeal Cardiopulmonary Resuscitation Population For Out-of-hospital Cardiac Arrest

Introduction: Extracorporeal Cardiopulmonary Resuscitation ( ECPR) is associated with improved neurologically favorable survival for refractory ventricular tachycardia/ventricular fibrillation (VT/VF) arrests. Women are known to have less coronary artery disease, and it is unknown if the lack of a reversible cause would be associated with worse outcomes after ECPR. Hypothesis: We hypothesize that female gender may be associated with worse outcomes after ECPR. Methods: Patients who presented for refractory VT/VF arrest between 2015 and 2021 were included. The primary outcomes included overall survival at 36 months and neurologically favorable survival on discharge (Cerebral Performance Categories scales of 1 or 2). Secondary outcomes included cardiopulmonary resuscitation (CPR) time, median lactate level on presentation, and bystander CPR. Results: Out of 357 patients who presented for out-of-hospital cardiac arrest, 68 patients (19%) were female. The median age for females was 57 years (IQR 57-52) and for males was 59 years (IQR 50-66). Women were more likely to receive ECPR and not to be excluded (5.9% of women were excluded vs. 14.9%, p=0.048) and were less likely to have obstructive coronary disease on coronary angiogram at presentation (39.5% vs. 62.9%, p=0.005). There was no difference in neurologically favorable survival based on gender (39.1% in women vs. 33.7%, p=0.42) nor 36 months survival (p= 0.58, figure). There was also no difference in median CPR time (62 minutes (IQR 51-76) in women vs. 59 minutes (IQR 45-70), p=0.16), median lactate levels (11.5 mmol/L (IQR 8-14.8) in women vs. 11.6 mmol/L (IQR 8.7-14.7), p=0.95), and in receiving bystander CPR (65.6% in women vs. 70.1%, p=0.49). Conclusion: There is no difference in neurologically favorable survival or overall survival based on gender in ECPR patients who had an out-of-hospital cardiac arrest, despite the difference in the prevalence of obstructive coronary artery disease on presentation.

Abstract 14648: Can GRACE Risk Score Predict Mortality in Pulmonary Embolism?

Introduction Risk stratifying of pulmonary embolism (PE) patients and treatment for normotensive patients is still challenging. We aimed to assess the utility of GRACE risk score for 30-day mortality. Methods All consecutive patients hospitalized with a diagnosis of PE between2016 -2021 were included in this retrospective study. GRACE and PESI scores were calculated online. Results A total of 197 patients were enrolled. Mean age was 63.98±15.51. 56 of patients died by the end of the 30-day. When patients divided into 2 groups according to 30-day mortality, both groups were similar in terms of gender, hypertension, diabetes mellitus, coronary artery disease, heart failure and chronic obstructive pulmonary disease. Troponin level (212.4± 24.6 vs. 850.8±231.1; p&lt;0.0001), PESI (122.3±27.2 vs. 170.1±49.1; p&lt;0.0001) and GRACE (127.1±28.8 vs. 182±21.3; p&lt;0.0001) were significantly higher in non-survivor group. The correlation analysis we observed strong positive correlation between PESİ and GRACE (r=0.732; p&lt;0.0001). Regression analysis revealed that only GRACE score [p=0.021, β: 1.146, OR (95% CI): 1.021-1.286] was an independent risk factor associated with 30-day mortality. ROC curve for accuracy of GRACE score for predicting 30-day mortality in PE patients is shown in figure 1. Area under curve (AUC) for GRACE score was 0.969 [%95 CI: 0.948-0.990]. A cut off value of 161.5 for GRACE score was associated with 90.0% sensitivity and 89.7% specificity in prediction of 30-day mortality. Conclusion In this study, the relation between GRACE score and the clinical course of PE patients evaluated and we found GRACE risk score as an independent risk factor associated with 30-day mortality and strong correlation between GRACE and PESİ risk scores. To predict the mortality of high-risk normotensive and hypotensive PE patients,GRACE risk score exhibited high specificity and positive probability.

Abstract 11589: Total Artificial Heart Placement in a Case of Recurrent Ventricular Tachycardia Storm

Background: Electrical storm is defined as three or more episodes of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) within a 24-hour period requiring termination by cardioversion, anti-tachycardia pacing (ATP) or defibrillation. It can be a particularly challenging syndrome to treat when refractory to standard of care therapies, which include antiarrhythmics, sedation, and ablation. We present a case of refractory electrical storm requiring total artificial heart placement (TAH) as a bridge to transplant. Case: A 65-year-old male with a history of idiopathic non-ischemic cardiomyopathy presented with VF arrest. After return of spontaneous circulation, he was admitted to the cardiac intensive care unit. Implantable cardioverter defibrillator (ICD) interrogation showed 38 shocks delivered over the prior two-week period. Coronary angiography showed no obstructive coronary disease and an intraaortic balloon pump (IABP) was placed for cardiogenic shock. He was intubated and sedated on fentanyl and propofol. He continued to have episodes of VT despite treatment with lidocaine, procainamide, and amiodarone drips. Further trials of paralysis and left stellate ganglion nerve block did not suppress his VT. Since the patient was refractory to all prior interventions, was deemed too unstable for VT ablation, and had a prolonged anticipated wait time for heart transplant, he underwent TAH placement as a bridge to heart transplant. He recovered well and eventually underwent successful heart transplant. Discussion: Management of electrical storm requires a stepwise approach including administration of antiarrhythmics, sedation, mechanical hemodynamic support, and catheter ablation. Our patient had incessant VT despite exhaustive medical and supportive therapies, but was too unstable to undergo VT ablation. In cases of refractory VT storm, definitive treatment with heart transplantation must be considered, but bridging patients to transplant poses a challenge. Our patient underwent TAH placement and was successfully stabilized prior to transplant. In centers with this capability, TAH should be recognized as a legitimate option in the pathway for VT, particularly with a long anticipated wait time for heart transplant.

Abstract 15675: Mid-Ventricular Hypertrophic Cardiomyopathy Presenting With Minoca

Background: Mid-ventricular hypertrophic obstructive cardiomyopathy (HOCM) is an uncommon form of cardiomyopathy that is linked to an apical aneurysm, increasing the risk of sudden death. Cases: We described four patients who presented with chest pain or SOB. Troponin elevation, acute myocardial infarction on cardiac MRI and absence of obstructive coronary disease confirmed the diagnosis of MINOCA. Echo revealed a pressure gradient between the apical and basal chambers of the left ventricle. Cardiac MRI showed mid-ventricular HOCM and mid-cavity obliteration with akinetic apical chamber LGE revealed areas of sub-endocardial or transmural myocardial infarction at the level of obstruction and at the apical segments distal to the obstruction. The presence of myocardial edema on tissue mapping in the same area suggested acute myocardial injury (Figure). Discussion: The pathogenesis of development of apical myocardial scarring and aneurysm formation in mid-ventricular HOCM remains unknown. Other variant of hypertrophic cardiomyopathy shows mid-myocardial foci of scar inside the hypertrophied segments, indicating fibrosis. Whereas in our patients, the LGE revealed a sub-endocardial or transmural infarct (myocardial infarction pattern) - an uncommon pattern in other hypertrophic cardiomyopathy variants. This pattern and elevation of troponin during the acute phase of illness supports the hypothesis that apical aneurysm is due to apical myocardial ischemia in mid-ventricular HOCM. Tissue characterization and pattern of scar by cardiac MRI in these patients could be useful in understanding the pathophysiology of this type of HOCM.

Shark Fin Electrocardiogram in the Intensive Care Unit.

Shark Fin Electrocardiogram in the Intensive Care Unit.

Female sex and systolic blood pressure are independently associated with coronary microvascular dysfunction in asymptomatic adults with type 2 diabetes

Abstract Introduction Coronary microvascular dysfunction is frequently reported in people with type 2 diabetes (T2D), is associated with reduced exercise capacity, and is a prognostic marker. Identifying modifiable risk factors associated with microvascular dysfunction may facilitate early intervention to improve outcomes in these patients. Purpose To identify independent determinants of myocardial perfusion reserve (MPR) in asymptomatic adults with T2D and no prevalent cardiovascular disease. Methods Prospective cross-sectional study. People with and without T2D and no signs, symptoms or evidence of cardiovascular disease underwent comprehensive phenotyping with echocardiography, coronary artery calcium scoring, and multiparametric cardiac MRI including adenosine stress and rest perfusion with automated pixel-wise myocardial blood flow (MBF) mapping. Participants with regional perfusion defects indicating obstructive coronary disease or silent myocardial infarct on late-gadolinium enhancement were excluded from analysis. Univariable and multivariable linear regression was performed to identify independent determinants of MPR. Results Two-hundred people with T2D (diabetes duration 11±8 years) were compared with 39 sex- and ethnicity-matched non-diabetic controls (Table 1). People with T2D had higher body mass index (BMI) and ambulatory 24-hour systolic blood pressure (SBP). There was evidence of concentric left ventricular (LV) remodelling (higher LV mass/volume), extracellular matrix expansion (higher ECV fraction), and both systolic and diastolic dysfunction (lower global longitudinal systolic strain and E/A ratio, respectively) in those with T2D. Resting MBF was similar between groups, but stress MBF tended to be lower in T2D compared to controls with significantly reduced MPR in T2Ds (2.87±0.86 vs 3.18±0.82, p=0.043). In univariable analysis, MPR correlated with sex, 24-hour SBP, and E/e' ratio. In a multivariable model adjusting for clinical (age, sex, smoking status, BMI, ambulatory SBP, diabetes duration, HbA1c, low-density lipoprotein, albuminuria) and imaging variables (E/e' ratio, LV mass/volume, global longitudinal strain, myocardial ECV, coronary calcium score) known to affect coronary perfusion, female sex (β=−0.227, p=0.013) and 24-hour SBP (β=−0.275, p=0.001) were the only variables independently associated with MPR. Conclusion Female sex is associated with coronary microvascular dysfunction in asymptomatic people with T2D but not LV mass or myocardial extracellular volume. Systolic BP is the only modifiable independent determinant of MPR and may be an early target for intervention to prevent heart failure development in these patients. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): National Institute for Health Research (NIHR) United Kingdom through a Research Professorship award (RP-2017-08-ST2-007).British Heart Foundation through a Clinical Research Training Fellowship award (FS/16/47/32190).

Absolute coronary flow and microvascular resistances in severe aortic stenosis: invasively quantification

Abstract Background Chest pain in aortic stenosis (AS) has been attributed to the loss of coronary flow reserve however; this has not been directly quantified to date. Purpose To determine whether there is a decrease in coronary flow as a cause of chest pain or dyspnea in patients with severe AS Methods Patients with AS and normal left ventricular ejection fraction (LVEF) underwent coronariography previous to valve replacement. In those patients without obstructive coronary disease, an invasive physiological evaluation was performed to measure absolute coronary flow (Q) and microvascular resistances (R). Left anterior descending artery (LAD) was explored in all cases and, in a subgroup of patients, we also studied the circumflex (CX). Results 51 patients were included. 86% presenting with dyspnea, 26% also reported chest pain, and 11.8% syncope. No patient was admitted due to heart failure. Mean pressure gradient for AS was 52.44±15.41 mmHg with a mean aortic valve area of 0.76±0.17 cm2. Mean LVEF was 63±8.35%. The physiological study of LAD was successfully completed in all patients. 68.6% presented a normal / increased LAD-Q with a mean quantified flow of 262.118±161.99 mL/min. LAD-R proved normal in 56.9% of the cases and low in 13.7%. The quantified mean LAD-R was 400.78±195.89 UW. The physiological study of the CX was carried out in 34 patients. 82.3% presented normal / increased CX-Q, with a mean value of 201.82±117.91 mL/min. CX-R proved normal in 76.5% of the cases and low in 17.6%, with a mean value of 604.147±367.23 UW. Conclusion Invasive intracoronary measurements demonstrated most of patients with severe AS maintain normal values of Q and R Funding Acknowledgement Type of funding sources: None.

Diagnostic value of computed tomography myocardial perfusion to detect coexisting microvascular dysfunction in patients with obstructive epicardial coronary disease

Abstract Background The usefulness of computed tomography myocardial perfusion (CTP) to assess hemodynamically significant epicardial coronary artery lesions has been previously reported. However, the diagnostic value of quantitative evaluation of absolute coronary flow by CTP to detect microvascular dysfunction remains unknown. Purpose The aim of study is to assess the diagnostic value of CTP to evaluate coronary microvascular dysfunction (CMD) in patients with significant epicardial coronary stenosis, and to analyze the predicting factors for lesions with CMD. Methods Sixty-eight chronic coronary syndrome patients with de novo single functionally significant stenosis (Fractional flow reserve [FFR] &amp;lt;0.80) were investigated. CMD was defined by the index of microcirculatory resistance (IMR) ≥25. Clinical characteristics and CTP findings were compared between the two groups with and without CMD (CMD, n=29, non-CMD, n=39, respectively). The computed tomography angiography (CCTA) assessment included CTP findings and quantitative and qualitative assessment of plaques. Results In wire-based analysis, FFR, coronary flow reserve (CFRwire) and IMR were 0.68 (0.59–0.74), 1.71 (1.24–2.88), and 22.6 (15.1–34.5), respectively. In CTP analysis, culprit territory regional absolute myocardial blood flow (MBF) at rest (rest-MBF) and hyperemia (hyperemic-MBF) were evaluated semi-automatically. CTP-derived CFR (CFRCTP) was calculated as hyperemic-MBF divided by rest-MBF. Rest and hyperemic-MBF and CFRCTP were 0.83 (0.64–1.03) ml/min/g, 2.14 (1.30–2.92) ml/min/g, and 2.19 (1.44–3.37). In the lesions with CMD, hyperemic-MBF was significantly lower than those without CMD (1.68 [0.84–2.44] vs 2.31 [1.67–3.34] ml/min/g, p=0.015) and the prevalence of CFRCTP&amp;lt;2.0 was higher in the lesions with CMD than those without CMD (62.1% vs 28.2%, p=0.007). CCTA analysis showed that fibrofatty and necrotic core component (FFNC) volume was greater in the lesions with CMD than in the lesions without CMD (31.8 [19.0–48.9] vs 25.1 [17.2–32.1] mm3, p=0.045). The multivariable logistic regression analysis, hyperemic-MBF and FFNC volume were independent predictors for lesions with CMD (Odds ratio [OR] 0.583 [0.355–0.958], p=0.033 and OR 1.040 [1.010–1.070], p=0.018). Conclusion Quantitative assessment of absolute coronary flow by CTP and comprehensive plaque analysis by CCTA may help detect coexisting subtended microvascular dysfunction in patients with functionally significant epicardial coronary lesions. Further studies are needed to elucidate the clinical significance of coexisting CMD in CCS patients. Funding Acknowledgement Type of funding sources: None.

Atherosclerotic Coronary Plaque features in patients with Acute Coronary Syndrome and Chronic Obstructive Pulmonary Disease

Abstract Background Chronic obstructive pulmonary disease (COPD) is a common respiratory disorder characterized by airflow limitation, persistent respiratory symptoms and chronic lung inflammation. Previous studies reported a robust relationship between COPD and coronary artery disease (CAD). Local and systemic inflammation, known to play a role in atherosclerosis development, has been reported in patients with COPD, and has been proposed as one of the possible pathogenetic factors linking COPD and CAD. However, data on atherosclerotic coronary pattern and coronary inflammation in COPD patients are lacking. Purpose To study the characteristics of atherosclerotic coronary plaques and local inflammation by using optical coherence tomography (OCT) in COPD patients presenting with acute coronary syndromes (ACS). Methods ACS patients undergoing intracoronary OCT imaging of the culprit vessel were retrospectively identified. Coronary plaque characteristics and OCT-defined macrophage infiltration (MØI) were assessed by OCT. ACS patients were divided into 2 groups according to the presence or the absence of an established diagnosis of COPD, and coronary plaque features and MØI both at the culprit plaque site and along the culprit vessel were compared between the two groups. Results Among 146 ACS patients (mean age, 66,1±12,7 years, 109 males), 47 (32,2%) had COPD. Patients with COPD were older, were more frequently on therapy with an angiotensin receptor blocker, had lower hemoglobin, total cholesterol and triglycerides levels, and had higher serum creatinine levels. The prevalence of different mechanisms of ACS were similar between COPD and noCOPD patients (plaque rupture: 57,4% vs. 45,4%, plaque erosion: 23,4% vs. 32,3%, calcified plaque: 19,1% vs. 22,2%, respectively, overall p=0,381). OCT analysis of plaque microstructures showed that COPD patients had significantly higher prevalence of MØI (78,7% vs. 54,4%, p=0,005), thin cap fibroatheroma (TCFA) (48,9% vs. 22,2%, p=0,001), spotty calcium (68,1% vs. 26,3%, p&amp;lt;0,001) and calcifications (83,0% vs. 66,7%, p=0,040) at the culprit site than noCOPD patients. In the multivariate logistic regression analysis performed to adjust for clinical features, COPD was independently associated with MØI both at the culprit site (OR: 4,726, CI: 1,599; 13,971, p=0,005) and along the culprit vessel (OR: 2,193, CI: 1,110; 4,332, p=0,024). Similarly, COPD was independently associated with the presence of TCFA both at the culprit site (OR: 5,737, CI: 1,877; 17,540, p=0,002) and along the culprit vessel (OR: 2,796, CI: 1,408; 5,553, p=0,003). Conclusions In ACS patients undergoing OCT imaging of the culprit vessel, COPD was an independent predictor of local plaque inflammation and plaque vulnerability both at the culprit site and along the culprit vessel. Our results may suggest that a higher inflammatory milieu in COPD patients might enhance local coronary inflammation, promoting CAD development and plaque vulnerability. Funding Acknowledgement Type of funding sources: None.

Lower stress perfusion in patients with myocardial infarction with non-obstructive coronary arteries compared to controls in long-term follow-up with quantitative perfusion mapping

Abstract Introduction Myocardial infarction with non-obstructive coronary arteries (MINOCA) constitutes a heterogenous condition with different coronary, cardiac and non-cardiac etiologies. Cardiovascular magnetic resonance imaging (CMR) has emerged as an important diagnostic tool in recent years and is now recommended in patients with MINOCA as a working diagnosis. However, despite early CMR following admission for MINOCA, no cause can be found in around 25% of all patients. A pathophysiological mechanism may be diffuse global coronary microvascular dysfunction (CMD) which has emerged as an important cause of myocardial ischemia. Quantitative adenosine stress CMR perfusion mapping allows for absolute quantification of myocardial perfusion, reflecting CMD in the absence of obstructive coronary disease in MINOCA patients. Purpose To study the presence of CMD in MINOCA patients with an initial normal CMR scan compared to healthy controls. Methods Patients from the multicenter myocardial infarction in our city with normal Coronaries 2 (SMINC-2) study, with a normal CMR scan 2–4 days after hospitalization, and healthy age- and sex-matched controls underwent stress perfusion at 1.5T (MAGNETOM Aera). Native rest T1 and T2 short-axis maps were acquired. Quantitative perfusion maps were acquired during adenosine stress (140 micrograms/kg/min) and at rest following an intravenous contrast bolus (0.05 mmol/kg of gadoteric acid, Gd-DOTA). Post contrast T1 maps were acquired after intravenous contrast (total dose 0.2 mmol/kg) rendering extracellular volume (ECV) maps. Global native T1, T2, ECV and rest and stress perfusion values were acquired by averaging segmental values per patient. Myocardial perfusion reserve (MPR) was calculated as perfusion in stress divided by rest. Values were presented as mean±standard deviation and compared with the independent t-test in normally distributed data, and with the Mann-Whitney U test in non-normally distributed data. Clinical data regarding cardiovascular risk factors, smoking and medications were presented as numbers (percentages) and compared with Fisher's exact test. Rate pressure product (RPP) was calculated as systolic blood pressure multiplied by heart rate in rest and stress. Results In total, 15 patients (59±16 years old, 60% female), and 15 healthy age- and sex-matched controls, were included. There was a trend towards higher incidence of hypertension in patients compared to controls, however no difference in other risk factors (Table 1). Compared to controls, MINOCA patients had lower perfusion in stress (Figure 1). There was no difference in global native T1, T2, ECV, rest perfusion, MPR or hemodynamic parameters between the MINOCA patients and the controls (p&amp;gt;0.05 for all, Table 1). Conclusions Myocardial stress perfusion is lower in MINOCA patients with a normal initial CMR scan compared to age- and sex-matched controls suggesting CMD as a possible pathophysiological mechanism in MINOCA. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Swedish Heart and Lung Foundation

COVID-19 associated Brugada pattern electrocardiogram: systematic review of case reports

Abstract Objective To summarize published case reports of patients diagnosed with COVID-19 infection and Brugada pattern electrocardiogram (ECG). Background Fever is a common clinical manifestation of COVID-19 infection. Fever has also been associated with unmasking Brugada pattern ECG in patients and may result in life-threatening arrhythmia. Little is known regarding COVID-19 associated Brugada pattern ECG. There is paucity of data and guidance in how to manage these patients. Methods To identify all published case reports, the latest Preferred Reporting Items for Systematic Reviews and Meta-Analyses checklist was followed. A literature search was conducted using PubMed, EMBASE, and Scopus through September 2021. A systematic review was performed to identify the incidence, clinical characteristics, and management outcomes of COVID-19 patients with a Brugada pattern ECG. Results A total of 18 cases were collected. The mean age was 47.1 years and 11.1% were women. No patient had prior confirmed diagnosis of Brugada syndrome. The most common presenting clinical symptoms were fever (83.3%), chest pain (38.8%), shortness of breath (38.8%), and syncope (16.6%). All 18 patients presented with type 1 Brugada pattern ECG. Four patients (22.2%) underwent left heart catheterization, and none demonstrated the presence of obstructive coronary disease. The most common reported therapies included antipyretics (55.5%), hydroxychloroquine (27.7%), and antibiotics (16.6%). One patient (5.5%) died during hospitalization. Three patients (16.6%) who presented with syncope received either an implantable cardioverter defibrillator or wearable cardioverter defibrillator at discharge. At follow up, thirteen patients (72.2%) had resolution of type 1 Brugada pattern ECG. Conclusion COVID-19 associated Brugada pattern ECG is rare. Most patients may see resolution of the ECG pattern once their symptoms have improved. Increased awareness and timely use of antipyretics is warranted in this population. Funding Acknowledgement Type of funding sources: None.

Budesonid as a means of intraoperative lung protection during coronary bypassing in patients with concomitant chronic obstructive pulmonary disease and coronary heart disease: a pilot study

Lung protection during surgeries with artificial circulation (AC) is a vital task in clinical medicine.The aim. Evaluation of the effectiveness of intraoperative administration of nebulized budesonide for correcting the volume status of the lungs and oxygen transport in patients with concomitant coronary heart disease (CHD) and chronic obstructive pulmonary disease (COPD) during coronary artery bypass grafting (CABG) with artificial circulation (AC).Methods. The pilot clinical study included 40 patients with concomitant CHD and COPD who were admitted for scheduled CABG with AC. The first groups consisted of 20 patients who underwent low-volume artificial lung ventilation (AVL) with inhalation of nebulized budesonide in the process of AC; the second group consisted of 20 patients who underwent AC according to a routine technique with AVL off. Lung volemic status parameters were recorded by transpulmonary thermodilution using the Pulsion PiCCO in three stages: before the onset of AC, after its completion and one day after AC.Results. It was established that after withdrawal from AC, indices of extravascular water in the lungs (IEWL) decreased by 23% in the first group and increased by 24% in the second group. After the completion of AC and a day after it, IEWL significantly decreased in patients receiving budesonide and increased with a maximum rise at the second stage of the study in the second group. The index of oxygen delivery and utilization over time was within the reference range in all patients. The index of oxygen consumption did not reach the physiologically normal lower limit. The maximum level of pulmonary bypass blood fraction (16 and 12%, respectively) and a significant decrease in oxygenation index (240 – 290 c. u.) were recorded in this cohort of patients at the 2nd and 3rd stages of the study. The duration of postoperative ventilation was significantly longer in the second group, while the duration of in-hospital treatment did not differ significantly before the groups.Conclusion. The protective effects of the combination of aerosol therapy with budesonide and low-volume AVL were manifested by a decrease in the permeability of the pulmonary capillaries, the volume of IEWL, an improvement in the oxygenating function of the lungs, a decrease in the number of respiratory complications and the postoperative duration of AVL.

EP02.01-001 Plasma Cell-Free DNA as a Point-of-Care Wellbeing Biomarker for Early-Stage Non-Small Cell Lung Cancer Patients

Lung cancer is the worldwide leading cause of cancer-related death. Thoracic Surgical lung cancer patients often possess smoking associated comorbidities including coronary artery disease (CAD) and chronic obstructive pulmonary disease (COPD). The Charlson Comorbidity Index (CCI) is currently used to quantify wellbeing and risk of postoperative complications. An objective biomarker surrogate for wellbeing such as circulating cell-free DNA (cfDNA) could aide in perioperative risk estimation and monitoring.

Predicting Patients With Troponin Positive Chest Pain and Unobstructed Coronary Arteries With Electrocardiogram, Troponin Kinetics and GRACE Score.

Troponin positive chest-pain with unobstructed coronary arteries (TPCP-UCA), occurs in 6% of cases of patients presenting with acute coronary syndrome (ACS). Whilst TPCP-UCA patients are known to be younger with less cardiovascular risk factors when compared to obstructive coronary disease (MICAD), no validated methods exist to reliably delineate these two conditions prior to coronary angiography. We analysed 142 patients with MICAD and 127 patients with TPCP-UCA from 2015 to 2019. Several key predetermined clinical, biochemical and electrocardiograph (ECG) parameters, as well as Global Registry of Acute Coronary Events (GRACE) score, were collected for all patients. All TPCP-UCA patients underwent cardiac magnetic resonance imaging (cMRI). Patients with TPCP-UCA were younger than MICAD (44 vs 68 yrs, p<0.01), and with less cardiac risk factors of hypertension (31% vs 68%, p<0.01), hypercholesterolaemia (23% vs 56%, p<0.01), diabetes (11% vs 45%, p<0.01), prior ischaemic heart disease (8% vs 42%, p<0.01) and smoking history (29% vs 50%, p<0.01). Peak troponin (MICAD 2,084.5 ng/L vs TPCP-UCA 847.0 ng/L, p=0.02), serial-to-initial troponin ratio (MICAD 13.5 vs TPCP-UCA 5.1, p<0.01), and peak-to-initial troponin ratio (MICAD 69.6 vs TPCP-UCA 14.0, p<0.01) were all higher in the MICAD group. GRACE scores were significantly different across the two cohorts (TPCP UCA 74 vs MICAD 106, p<0.01), with a receiver operator characteristic (ROC) curve statistic of 0.794 (95% CI 0.739-0.850). On ECG analysis, MICAD had greater prevalence and sum of ST depression (40% vs 19% p<0.01; 1.6 mm vs 0.44 mm, p<0.01) and T wave inversion (37% vs 17%, p<0.01), whilst TPCP-UCA had greater presence of PR depression (20% vs 3% p<0.01), and longer repolarisation (T wave peak to end 89 ms vs 83 ms, p=0.04; T wave peak to end/corrected QT 0.208 ms vs 0.193 ms, p=0.03). All TPCP-UCA patients underwent cMRI. Aetiology was found in 82% of cases, with the leading diagnosis being myocarditis (58%), followed by infarction (8%), whilst 18% had a normal cMRI. TPCP-UCA is an important differential for patients presenting with ACS, and has several key demographic, biochemical and electrocardiographic differences. The present findings are hypothesis generating, thus prospective studies are required to determine and validate potential clinical utility.

Pathophysiology of Coronary Microvascular Dysfunction.

Ischemic heart disease (IHD) is commonly recognized as the consequence of coronary atherosclerosis and obstructive coronary artery disease (CAD). However, a significant number of patients may present angina or myocardial infarction even in the absence of any significant coronary artery stenosis and impairment of the coronary microcirculation has been increasingly implicated as a relevant cause of IHD. The term "coronary microvascular dysfunction" (CMD) encompasses several pathogenic mechanisms resulting in functional and/or structural changes in the coronary microcirculation and determining angina and myocardial ischemia in patients with angina without obstructive CAD ("primary" microvascular angina), as well as in several other conditions, including obstructive CAD, cardiomyopathies, Takotsubo syndrome and heart failure, especially the phenotype with preserved ejection fraction. The pathogenesis of CMD is complex and involves the combination of functional and structural alterations leading to impaired coronary blood flow and resulting in myocardial ischemia. In the absence of therapies specifically targeting CMD, attention has been focused on the role of modifiable risk factors. Here, we provide updated evidence regarding the pathophysiological mechanisms underlying CMD, with a particular focus on the role of cardiovascular risk factors and comorbidities. Moreover, we discuss the specific pathogenic mechanisms of CMD across the different cardiovascular diseases, aiming to pave the way for further research and the development of novel strategies for a precision medicine approach.

Impact of Gd-153 scanning line source attenuation correction on downstream invasive testing

BackgroundAttenuation correction (AC) using hardware and software solutions has been shown to increase the specificity of SPECT MPI by decreasing false positive results and improving prognostic ability. Theoretically this should reduce downstream testing and unnecessary costs. We sought to assess the consequences of the use of Gd-153 scanning line source attenuation correction during SPECT myocardial perfusion imaging (MPI) on downstream invasive testing. MethodsAll patients who underwent a clinically indicated Tc-99m stress SPECT MPI study from 2013 to 2015 at five hospitals (2 with AC and 3 without) were retrospectively reviewed. Patient demographics, results of testing, subsequent coronary angiography within 3 months, and revascularization were recorded. The results of the MPI studies, downstream angiogram utilization, and results of angiography were compared and a propensity matched subgroup analysis was performed. ResultsA total of 9968 patients underwent SPECT MPI during the study time period (6106 performed with AC and 3862 without). Out of 3928 patients included in the propensity matched cohort, there was no difference in the proportion of abnormal MPI results between the two groups (31.5% vs 30.4%, P = 0.47), however, more patients underwent coronary angiography within 90 days in the AC group (10.6% vs 8.7%, P = 0.05). There was no significant difference in the proportion of patients with angiographically significant obstructive disease (53.4% vs 56.1%, P = 0.19), however, fewer patients in the AC group with obstructive coronary disease were revascularized (36.1% vs 46.8%, P = 0.04). The findings remained consistent after sub-group analysis in patients without known coronary disease. ConclusionThe use of scanning line source AC did not meaningfully influence the rate of abnormal MPI results or downstream invasive testing in this cohort. The clinical utility of scanning line source AC may be limited to facilitating stress-first imaging protocols.

Spasm, inflammation, coronary microcirculation and metabolism: how big is the iceberg under the stenosis

Ischemic heart disease (IHD) is a leading global cause of death and coronary artery disease has long been considered the main determinant of inducible ischemia and symptoms. However, after the performance of hundreds of thousands of percutaneous coronary revascularizations (PCI) worldwide, outcome analysis suggests that the direct relationship between chronic obstructive coronary atherosclerosis and ischemic heart disease (IHD) may represent a too simplified view of IHD; growing evidence has demonstrated the importance of a number of other underlying mechanisms. The purpose of this review is to highlight the multiple mechanisms responsible of myocardial ischemia.