Evidence Of Coronary Artery Disease Research Articles

Evaluating the integration of CTCA as part of an accelerated diagnostic pathway for patients presenting to the Emergency Department with acute chest pain: a two-year review

Abstract Introduction Chest pain accounts for 8.8% of all presentations to an Hospital Emergency Department. In line with ESC guidelines (2019), an adapted HEART pathway, utilising CT Coronary Angiogram (CTCA) is delivered by our Emergency Cardiology Advanced Nurse Practitioners (ANP) and Clinical Nurse Specialists (CNS) as part of an ambulatory chest pain pathway. It is our first line diagnostic test for patients with a non-ischaemic 12-lead ECG and normal cardiac biomarkers, with a low-to-intermediate HEART score. Responsibility for the referral of patients onto the pathway is shared with the Cardiology Registrars. This is a collaborative interdisciplinary pathway between Emergency Medicine, Cardiology, and Radiology. Purpose To evaluate the effectiveness and safety of CTCA as part of an Accelerated Diagnostic Pathway (ADP), for evaluation of chest pain of possible cardiac origin in low-to-intermediate risk chest pain patients. Methods We examined the CTCA and safety outcomes of patients presenting between Jan 1st 2022 – Dec 31st 2023 who were risk stratified as low-to-intermediate risk for coronary artery disease, based on Heart score, 12-lead ECG and biomarker testing, using the electronic patient records. Institutional ethics was in place. Results Between January 1st and December 31st 2022, 290 patients were referred for CTCA, with a total of 268 CTCAs completed. The number of patients referred on the ADP increased by 53.4% in 2023 with 445 being referred for CTCA, 416 of which have been completed, with 12 pending completion. 38% of patients were found to have evidence of coronary artery disease (CAD). Coronary artery disease causing at least 50% stenosis was identified in 11% of patients. 4.5% of these patients required revascularisation, 17 of whom underwent Percutaneous Coronary Intervention (PCI) with a further 13 being referred for Coronary Artery Bypass Grafting. A positive family history was the most dominant risk factor associated with significant CAD. An equivalent number of males to females were referred for CTCA, however, men were more than 7 times more likely to have severe disease. (12% vs 88%). All patients referred for CTCA via the chest pain pathway were followed up by the Emergency Cardiology ANP/CNS in a virtual clinic, delivering risk factor modification advice and preventative therapies, when indicated. There was no evidence of any major adverse cardiovascular events within a 30-day period for this patient cohort. Conclusion The integration of CTCA into an adapted HEART pathway has resulted a safe and timely discharge for patients presenting to ED with acute chest pain, of possible cardiac origin. CTCA offers excellent early detection of coronary artery disease in this patient cohort with normal ECGs and cardiac biomarkers, but with a history of chest pain suggestive of CAD.

Case report: A case of an anomalous right coronary artery arising from the left coronary cusp.

Abstract
 An anomalous origin of the right coronary artery is usually asymptomatic. It is mostly found incidentally on an invasive diagnostic angiogram. It does lead to an increased risk of sudden cardiac death, especially in younger patients. We present a case of a 41-year-old who had presented to the hospital with complaints of chest pain. The patient was evaluated by cardiology who performed an angiography that identified an anomalous origin of the right coronary artery arising from the left coronary cusp but no evidence of coronary artery disease. Once identified, these anomalous vessels should be corrected surgically, as these conditions increase the risk of sudden cardiac death arrhythmia and ischemic events.
 
 INTRODUCTION
 Anomalous aortic origin of the right coronary artery (AAORCA) is an uncommon congenital malformation with varying clinical presentations ranging from asymptomatic to sudden cardiac death (SCD). Those with symptoms or high-risk lesions are usually managed by unroofing or reimplantation, coronary artery bypass graft (CABG), AAORCA treated with right internal memory artery graft with proximal RCA ligation.
 
 CASE DESCRIPTION
 A 41-year-old female patient with obesity and hypertension presented with a 1-year history of intermittent exertional substernal pressure radiating to left shoulder and back. The pain, which lasted about 10 minutes per episode, had been more frequent and intense over the past week.Upon initial evaluation, she was hypertensive at 150/90 mmHg and heart rate 60 bpm. Blood work was unremarkable, including negative serial troponin levels. Electrocardiography showed sinus bradycardia without ischaemic changes. Anomalous origin of RCA was incidentally discovered from computed tomography (CT) of the chest. Coronary angiography and ascending aortography were then performed, which revealed a patent RCA originating from the left coronary cusp (Fig. 1A). CT heart angiography with reconstruction revealed the RCA ostium in the left coronary cusp with a malignant course between the aorta and pulmonary artery and without an obvious intramural segment
 Discussion:
 
 An anomalous origin of the right coronary artery (RCA) is a rare congenital anomaly that was first described in 1948 by White and Edwards. After carrying out angiography in 126,595 patients, Yamanaka and Hobbs reported the incidence of anomalous origin of the right and left coronary arteries as 136 (0.107%) and 22 (0.017%), respectively. The prevalence of an anomalous origin of RCA (ARCA) arising from the left coronary cusp with an inter-arterial course varies between 0.026% and 0.25%. An ARCA is more common than the anomalous origin of the left coronary artery (ALCA), but the latter is shown to be responsible for up to 85% of sudden cardiac deaths (SCD) related to the anomalous origins of arteries. Most coronary anomalies are detected incidentally on diagnostic angiography and are clinically insignificant; some, however, have been associated with an increased risk of SCD. It is second only to hypertrophic cardiomyopathy as a leading cause of SCD in young athletes. Mechanical compression of the RCA by the great vessels, which dilate and compress the RCA during periods of increased stroke volume, is the usual explanation for coronary ischemia. Patients usually have no ischemic changes on an electrocardiogram (ECG) at rest; however, multi-detector computed tomography (MDCT) is being used to evaluate the course of anomalous vessels outlying their relative positions to the aorta and the pulmonary artery. It also gives additional information regarding any stenotic lesion in these anomalous vessels. Echocardiography (Echo), magnetic resonance angiography (MRA), MCDT, and cardiac catheterization are all complementary diagnostic tools for evaluating anomalous coronary arteries [10]. While it is agreed that surgical correction is the standard of care for ALCA, when found, the management for right ARCA is more complicated. Treatment options for these patients include observation with medical therapy, percutaneous intervention (stenting), or surgery. Early diagnosis of coronary artery anomalies based on the patients’ symptoms can help decrease the incidence of sudden cardiac deaths, fatal arrhythmias, and ischemic events in the high-risk population.
 
 Conclusions 
 
 Coronary anomalies should be suspected in symptomatic young patients with a normal cardiac workup. Non-invasive imaging modalities such as a CTCA can help establish the diagnosis

Difficulties in myocarditis diagnosis: a case report

Myocarditis is often difficult to diagnose. The diagnostic difficulties include nonspecific symptoms or a “vague” clinical picture, absence of pathognomonic signs during physical examination, and endomyocardial biopsy, which is the “gold standard” of diagnosis of myocarditis, being an invasive procedure that is performed under strict indications in certain patients. Nevertheless, as radiology is rapidly developing, clinicians are now able to noninvasively diagnose symptoms of inflammatory myocardial damage, including edema and myocardial fibrosis, using cardiac magnetic resonance imaging. This article presents the clinical case of a young patient with symptoms of acute coronary syndrome, who showed no evidence of coronary artery disease. Myocarditis was suspected because of increased activity of cardiospecific enzymes and high levels of inflammatory markers, pronounced electrocardiography changes with positive dynamics, and recent infection. Magnetic resonance imaging was used to confirm myocarditis diagnosis. Thus, this case study demonstrates the role of imaging techniques in the differential diagnosis of ischemic and inflammatory heart diseases.

Non-Obstructing Coronary Artery Ischemia, An Underdiagnosed Silent Killer

Dear Madam, Ischemia due to Non-Obstructing Coronary Arteries (INOCA), formerly known as Prinzmetal Angina, is a condition that affects a significant number of people, especially in Pakistan. I have encountered several cases where patients exhibit stable angina symptoms, despite having normal or near-normal coronary angiograms. Among about 400,000 patients with suspected ischemic heart disease, the American College of Cardiology National Cardiovascular Data Registry found that only 37.6% had obstructive coronary artery disease, and 39.2% had no evidence of coronary artery disease. The exact prevalence of INOCA is not well-known. (1) Moreover, a prior research study found that heart failure patients of South Asian origin had a higher prevalence of INOCA compared to other populations. (2) A recent meta-analysis revealed that approximately 50% of the patients with nonobstructive coronary artery disease had coronary microvascular disease (CMD) and/or coronary artery spasms, suggesting that a significant number of INOCA patients are not appropriately diagnosed in routine clinical practice. (3) This shows us the importance of INOCA and also suggests that we need to improve the diagnosis protocols that Pakistani physicians commonly use. INOCA and myocardial infarction with non-obstructive coronary artery disease (MINOCA) are underrecognized and underdiagnosed conditions with cardiovascular health implications. These conditions are associated with a higher risk of death from cardiovascular causes in Pakistan, as well as a greater burden on the healthcare system, due to frequent hospital admissions for persistent chest pain and invasive coronary angiographies that often yield negative results. We have to dive more into Invasive coronary angiography by doing the Comprehensive Physiologic Assessment, using a pressure sensing guidewire to measure FFR (Fractional Flow reserve) and CFR (Coronary Flow Reserve) to evaluate Epicardial Stenosis and Microvascular Angina respectively. Later on, CFT can also be performed to confirm the diagnosis of coronary microvascular dysfunction. (4) To ensure that we do not miss INOCA, we should also consider other tests that do not involve inserting a catheter into the heart. These tests include Transthoracic echocardiography, Cardiac MRI, and Cardiac PET. By doing these tests, we can determine if the patient has INOCA and what type of INOCA they have. These will help us to tailor our management plan in the best possible way and also help us to guide the patients on how to reduce their risk factors.

Differences in left anterior descending coronary artery disease in participants without standard modifiable cardiovascular risk factors: the Multi-Ethnic Study of Atherosclerosis (MESA)

Abstract Background/Introduction The development of coronary artery disease (CAD) and myocardial infarction (MI) in the absence of standard modifiable cardiovascular risk factors (SMuRFs) has been highlighted as an unmet clinical need, accounting for between 10-27% of ST elevation MI and associated with higher 30-day mortality. One potential contributor to the early mortality is the higher observed rates of LAD territory culprit lesions in SMuRFless patients compared to those with at least one SMuRF. Purpose To characterise the differential proportion of LAD disease in an asymptomatic population with no prior cardiovascular disease (CVD) history, comparing individuals with CAD despite no SMuRFs to those with at least one SMuRF in the Multi-Ethnic Study of Atherosclerosis (MESA). Methods A MESA sub-cohort with a baseline coronary artery calcium score (CACS) >0 Agatston units (AU) was prepared. SMuRF status was assigned by self-report, treatment, or biomarkers for hypertension, hypercholesterolaemia, diabetes, and smoking. Proportion of disease in the left main, LAD, circumflex, and right coronary arteries were calculated by the vessel CACS divided by the total CACS. Standard descriptive statistics were used to characterise baseline differences. Group comparisons were completed with Wilcoxon rank sum for continuous measures and Chi-square for categorical. Results A CAC positive cohort of 3,417 participants was prepared from participants with SMuRF and CT imaging data, 14.3% of whom were considered SMuRFless. Total CACS was lower in SMuRFless participants compared to those with ≥1 SMuRF (58 AU vs. 102 AU, p<0.0001). However, proportion of calcium burden in the LAD was significantly higher in SMuRFless participants with CAD (74.2% vs. 56.8%, p<0.0001). When considering clinically significant CACS strata, proportion of LAD calcium burden was not significantly different between SMuRFless vs. ≥1 SMuRF participants with a total CACS of 1-99 AU (93.7% vs. 80.0%). However, statistically significant differences in LAD calcium proportion were observed between SMuRFless vs. ≥1 SMuRF participants with a total CACS 100-400 AU (69.5% vs. 57.8%) and CACS>400AU (45.2% vs. 40.5%). This difference remained significant during multivariate modelling, including consideration of absolute CACS. Conclusion Of patients with evidence of CAD (CACS>0) in the MESA cohort, SMuRFless status was associated with a higher proportion of LAD disease compared to participants with ≥1 SMuRF. This adds to previous observations in STEMI cohorts suggesting a heightened susceptibility to atherosclerosis development in the LAD territory against a lower traditional risk burden, and highlights the need for consideration of distinct biology and clinical significance in future studies.Fig. 1Fig. 2

Abstract 12588: A Hyperactive Heart: A Case of Adderall-Induced Cardiomyopathy

Introduction: Stimulants are commonly used in the treatment of attention deficit hyperactivity disorder (ADHD). Cardiomyopathy is a rare but serious potential side effect of long-term stimulant use, even when done so for therapeutic purposes. Case: We present a 56-year-old female with ADHD and long-term high dose Adderall use who presented for progressively worsening dyspnea over the course of 1 year. Labs were notable for peak hs-troponin 246ng/L and pro-BNP 6598pg/mL. On admission, echocardiogram was notable for reduced left ventricular (LV) ejection fraction (EF) of 20-25% with normal LV wall thickness and mild-moderate valvular disease. ECG showed sinus rhythm 97 bpm, bi-atrial enlargement, normal voltage and no evidence of conduction delay. A left heart catheterization demonstrated no evidence of coronary artery disease. Cardiac MRI at 1.5T was notable for LVEF 18%, severe LV dilation (EDV 189mL/m2), severe right ventricular (RV) dilation (EDV 131mL/m2) with RVEF 26%, native T1 1099 msec, ECV 41%, normal T2*, and a very thin circumferential subendocardial late gadolinium enhancement involving the apical and mid segments (6% of LV mass). TSH, Vitamin B1, and selenium levels were normal, and there was no evidence of tachyarrhythmia throughout her admission. She denied significant alcohol use, illicit substance use, or family history of cardiomyopathy. The absence of paraprotein gap and other stigmata lowered suspicion for amyloidosis. Due to the results of her workup, her Adderall was discontinued as this was thought to be the likely cause of her newly discovered cardiomyopathy. She was discharged home on GDMT with close follow up with advanced heart failure. Discussion: The association between long-term stimulant use and cardiomyopathy is known, but not well described. Common cardiac effects of stimulants include tachycardia, hypertension and increased risk of arrhythmias, all of which are associated with increased workload on the heart and therefore contribute to the development of cardiomyopathy. Although generally rare, long-term use of prescription stimulant medications can contribute to the development of cardiomyopathy and should therefore be used sparingly and for the shortest period possible when necessary for the treatment of ADHD.

RELATIONSHIP BETWEEN CAROTID ARTERY DISEASE EVALUATED BY ULTRASOUND AND CORONARY ARTERY DISEASE EVALUATED BY CORONARY COMPUTED TOMOGRAPHY

The prospective study was conducted in the Department of Cardiology, Nishtar Medical & Institute of Cardiology Hospital from June 2022 to June 2023 to evaluate the association between the severity of CAD and carotid IMT through multi-slice computed tomography (MSCT) scan in symptomatic or asymptomatic patients. Patients with dyspnea, chest pain, or asymptomatic patients with low to moderate pre-test probability of CAD detected by MSCT were included in the study. Mean IMT, presence or absence of plaque, CACS, and any evidence of atherosclerosis were recorded. Of 250 patients, 8% had dyspnea, 14.8% had chest pain, 10.8% had dizziness, 6.4% had palpitations, and 62% were asymptomatic. Corid plaque and higher CAC score (P<0 .0001) had a significant association. 48% (50 of 105) patients with CACS 0 had carotid plaque, while 87.5% (127 of 145) patients with CACS >0 had carotid plaque, which shows the association between higher CACS and carotid plaque (P=0.0001). Similarly, 52.3% (55 of 105) patients without atherosclerosis had carotid plaque, and 85% (119 of 140) patients with atherosclerosis had carotid plaque (P < 0.0001). It is concluded that plaque and carotid IMT are associated with the degree and presence of coronary disease and calcification on CTA. Due to modest correlation, imaging modality should be selected based on the pattern of atherosclerosis and methodological considerations.

Treadmill running intensity and post-exercise increase in plasma cardiac troponin I and T-A pilot study in healthy volunteers.

Plasma concentrations of cardiac troponins increase in healthy individuals after strenuous training, but the response to lower exercise intensities has not been characterized. To determine whether exercise at moderate intensity significantly increases plasma cardiac troponins measured with different assays in healthy recreational athletes. Twenty-four self-reported healthy volunteers were instructed to complete three 60-min bouts of treadmill running at variable intensities: High-intensity training (HIT) including a maximal exercise test and an anaerobic threshold test followed by training at 80%-95% of maximum heart rate (HRmax ), Moderate-intensity training (MIT) at 60%-75% of HRmax , and Low-intensity training (LIT) at 45%-55% of HRmax . Blood samples were collected before and at 2, 4, and 6 h after HIT and 4 h after MIT and LIT. Troponin I and T were measured in plasma samples with assays from Abbot, Siemens, and Roche. Plasma troponins measured with all assays were significantly increased compared to baseline after HIT but not after LIT. After HIT, the fraction of all participants with one or more values above the assay-specific 99th percentiles ranged from 13% to 61%. The biomarker criteria for acute myocardial injury were met after HIT for troponin T in 75% of female participants having no clinical evidence of coronary artery disease. High-intensity, but not moderate- or low-intensity, training for 60 min induced a potentially clinically significant increase in plasma cardiac troponins in healthy volunteers. Results exceeding the population 99th percentiles were most frequent with the troponin T assay.

Peripheral Vascular Disease and Carotid Artery Disease Are Associated with Decreased Bile Acid Excretion.

Low bile acid excretion (BAE) is associated with a higher risk of coronary artery disease (CAD) and cerebrovascular disease (stroke). This study investigated BAE in patients with peripheral vascular disease (PVD) and carotid artery disease (CA) and those without these diseases, compared to patients with CAD, stroke, or no evidence of atherosclerosis. Patients with complaints of chest pain-suspected CAD, syncope, stroke/TIA, severe headache, intermittent claudication, or falls were enrolled. All received a 4-day standard diet with 490 mg of cholesterol and internal standard copper thiocyanate. Fecal BAE was measured using gas-liquid chromatography. One hundred and three patients, sixty-eight (66%) men and thirty-five women (34%), mean age range 60.9 ± 8.9 years, were enrolled in this prospective, 22-year follow-up study. Regression analysis showed that advanced age, total BAE, and excretion of the main fractions were the only significant independent factors that predicted prolonged survival (p < 0.001). Twenty-two years' follow-up revealed only 15% of those with BAE <262.4 mg/24 h survived, compared to >60% of participants without atherosclerosis and a mean BAE of 676 mg/24 h. BAE was lower in patients with polyvascular atherosclerosis than in those with involvement of 1-3 vascular beds. Pearson correlations were found between total BAE and various fractions of BA, as well as HDL cholesterol. BAE and short-term survival were decreased among patients with PVD compared to those with CAD or stroke. Low BAE should be considered a valuable and independent risk factor for PVD.

Marcadores genéticos y séricos relacionados con una rápida progresión clínica de la arteriosclerosis coronaria

Introduction and objectivesPatients with clinically evident coronary artery disease differ in their rate of progression, which impacts prognosis. We aimed to characterize serum and genetic markers in patients with rapid clinical progression (RCP) of coronary artery disease vs those with long standing stable (LSS) disease. MethodsRetrospective study of cases (RCP) and controls (LSS) (1:2). Patients requiring ≥ 2 revascularizations due to atherosclerotic progression in the 10 years after a first angioplasty were considered to be RCP and those without events during the same period after the first angioplasty were considered to have LSS disease. After patient selection, we analyzed serum values, mRNA expression and genetic polymorphisms of inflammatory markers, including interleukin-6, C-reactive protein, and tumor necrosis factor (TNF)-a, and atherogenic markers consisted of proprotein convertase subtilisin/kexin type 9 (PCSK9), low-density lipoprotein receptor, sterol regulatory element binding transcription factor 2, and apolipoprotein-B. ResultsThe study included 180 patients (58 RCP and 122 LSS). Demographic characteristics, classic risk factors and the extent of coronary disease were similar in the 2 groups. Patients with RCP showed higher serum levels of interleukin-6 and PCSK9 and higher TNF mRNA expression. Interleukin-6 rs180075C, TNF rs3093664 non-G and PCSK9 rs2483205 T alleles conferred a risk of RCP (P<.05 in all cases). Among patients with RCP, 51.7% had all 3 risk alleles vs 18% of those with LSS (P<.001). ConclusionsWe suggest the existence of specific phenotypic and genotypic markers associated with RCP of coronary artery disease that could help to individualize the type and intensity of treatment.

Inter-Arm Blood Pressure Difference an Indicator of Coronary Artery Disease.

Considering the scarcity of the literature on the association between inter-arms blood pressure difference (IABPD) and coronary artery disease (CAD). We performed this study to investigate the prevalence of IABPD within the Jordanian population and to assess if it has an association with CAD. We sampled patients visiting the cardiology clinics at the Jordan University Hospital between October, 2019 and October 2021 into two groups. Participants were divided into two groups; patients with severe CAD and control group who had no evidence of CAD. We measured the blood pressure for a total of 520 patients. Of the included patients, 289 (55.6 %) had CAD while 231 (44.4%) were labeled as controls who were normal. A total of 221 (42.5%) participants had systolic IABPD above 10 mmHg, while 140 (26.9%) had a diastolic IABPD above 10 mmHg. Univariate analysis demonstrated that patients with CAD were significantly more likely to be older (p < 0.001), of the male gender (p < 0.001), hypertensive (p < 0.001), and having dyslipidemia (p < 0.001). Moreover, they had significantly higher IABPD differences in terms of both systolic and diastolic blood pressure (p < 0.001 and p = 0.022, respectively). Multivariate analysis showed that CAD was a positive predictor of abnormal systolic IABPD. In our study, elevated systolic IABPD was associated with a higher prevalence of severe CAD. Patients with abnormal IABPD might be subjected to more specialist investigation as IABPD consistently predicts coronary artery disease, peripheral arterial disease or other vasculopathy throughout the literature.

Gender differences in plasma levels of cardiovascular risk markers and severity indices in Saudi patients with angiographic evidence of coronary artery disease

Gender differences in plasma levels of cardiovascular risk markers and severity indices in Saudi patients with angiographic evidence of coronary artery disease

992-P: Coronary Artery Calcium Scoring to Improve Statin Use in Adults with Type 2 Diabetes Not on Statin Therapy—Anticipated Cost Utility

Background: Statin use in adults with diabetes is sub-optimal. Coronary artery calcium (CAC) scoring can provide a visual quantification of CV risk and may improve statin initiation and long-term use. Objective: Estimate the cost-utility of CAC scoring compared to traditional CV risk counselling only, for improving statin use in adults with diabetes who have not previously had a CV event, and are not on statin therapy. Methods: Probabilistic Markov model from a health system perspective, over a 10-year time horizon. The effectiveness of CAC scoring was obtained from the EISNER trial. Outcomes included acute coronary syndrome (ACS), stroke, heart failure, mortality, and radiation-induced cancer. Outcome rates and costs were obtained from an analysis of Alberta administrative data, and from publicly available sources. The base population modeled was men age 60, with additional analyses for other age, sex-groups and scenarios. Results: CAC scoring increased statin use to 44% vs 25% with traditional CV risk counselling only. There were 8.4 fewer ACS, 5.5 fewer strokes, and 1.6 fewer deaths / 1000 individuals. Costs were slightly lower (-$14, 95% CI [-$402-(+$208)]) (CAD), for a small benefit in quality-adjusted life years (+0.01, [0.00-0.02]), with mean ICER of $7,132 (-$27,828-(+$65,513)) / QALY. At a willingness-to-pay of $50,000 / QALY, CAC was cost-effective in 95% of trials. CAC scoring was not cost-effective in younger men or in women, but could be cost-effective or cost savings in men (age ≥ 40) and older women (age ≥ 60) who refuse statin therapy, but would be persuaded by personalized evidence of coronary artery disease (CAC score &amp;gt; 10). Conclusion: CAC scoring may be cost-effective in older men not receiving statins, and in men or older women who agree to use statins if shown personalized evidence of coronary artery disease. Disclosure D.Lau: None. G.J.Pearson: Advisory Panel; HLS Therapeutics Inc., Novartis Pharmaceuticals Corporation, Pharmacience, Consultant; Trimedic Therapeutics. P.Raggi: None. S.Klarenbach: Research Support; Bayer Inc., Allergan, GlaxoSmithKline plc., CSL Behring, Lundbeck, University Hospital Foundation (University of Alberta), Purdue Canada.

PO-03-230 LEFT VENTRICULAR FUNCTION IN SUDDEN CARDIAC DEATH DUE TO ISCHEMIC AND NONISCHEMIC HEART DISEASE

Sudden cardiac death (SCD) remains a major public health problem. Severe left ventricular (LV) dysfunction (EF ≤ 35%) increases the risk of SCD and is the most important indication for prophylactic implantable cardioverter defibrillator (ICD). Previous studies have shown that subjects with EF ≤ 35% represent a minority of all SCD cases. However, it has been unclear whether ischemic and nonischemic cardiac diseases present with different LVEF prior to SCD. We sought to evaluate the spectrum of LVEF among SCD victims with ischemic and nonischemic etiologies. Our study population is drawn from the Fingesture study, which has prospectively collected autopsy and clinical data from consecutive SCD victims from Northern Finland between 1998 and 2017. The cause of death was verified to be of cardiac origin in a medicolegal autopsy in all cases. Cases with ischemic SCD had evidence of coronary artery disease and ischemic cardiomyopathy at autopsy. Electronic health records were examined to identify subjects who underwent evaluation for LV function before SCD. LV function was categorized by quantitative assessment of LVEF as normal (EF ≥ 50%), reduced (50% > EF > 35%), and severely reduced (EF ≤ 35%). In all cases, echocardiography was unrelated to the SCD event. Left ventricular assessment was available in 717 SCD victims. The majority of subjects (n=449, 62.7%) had normal LVEF prior to SCD. The prevalence of reduced LVEF was 21.9%, while severely reduced LVEF was found only in 110 subjects (15.4%). Men were more likely to have LV dysfunction than women (45.9% vs 29.6%; p<0.001). In addition, LVEF was found to be severely reduced more commonly in men compared to women (17.4% vs 10.9% respectively; p<0.001). In SCD victims with ischemic and nonischemic heart disease, LV dysfunction was equally common (37.7% vs 36% respectively; p=0.72). The prevalence of severely reduced LVEF was also similar between ischemic SCD and nonischemic SCD (15.1% vs. 16.3%, respectively; p=0.72). Only one third of SCD cases had ventricular dysfunction and only one in seven had severely reduced LVEF prior to their SCD event, suggesting that only a minority of SCD victims meet the current criteria for primary prevention ICD. We found no difference in the spectrum of LVEF between ischemic and nonischemic heart diseases. However, women were found to have preserved LV function more often than men, highlighting the importance of developing novel SCD risk stratification tools beyond LVEF.

Serum and genetic markers related to rapid clinical progression of coronary artery disease

Introduction and objectivesPatients with clinically evident coronary artery disease differ in their rate of progression, which impacts prognosis. We aimed to characterize serum and genetic markers in patients with rapid clinical progression (RCP) of coronary artery disease vs those with long standing stable (LSS) disease. MethodsRetrospective study of cases (RCP) and controls (LSS) (1:2). Patients requiring ≥ 2 revascularizations due to atherosclerotic progression in the 10 years after a first angioplasty were considered to be RCP and those without events during the same period after the first angioplasty were considered to have LSS disease. After patient selection, we analyzed serum values, mRNA expression and genetic polymorphisms of inflammatory markers, including interleukin-6, C-reactive protein, and tumor necrosis factor (TNF)-a, and atherogenic markers consisted of proprotein convertase subtilisin/kexin type 9 (PCSK9), low-density lipoprotein receptor, sterol regulatory element binding transcription factor 2, and apolipoprotein-B. ResultsThe study included 180 patients (58 RCP and 122 LSS). Demographic characteristics, classic risk factors and the extent of coronary disease were similar in the 2 groups. Patients with RCP showed higher serum levels of interleukin-6 and PCSK9 and higher TNF mRNA expression. Interleukin-6 rs180075C, TNF rs3093664 non-G and PCSK9 rs2483205 T alleles conferred a risk of RCP (P<.05 in all cases). Among patients with RCP, 51.7% had all 3 risk alleles vs 18% of those with LSS (P<.001). ConclusionsWe suggest the existence of specific phenotypic and genotypic markers associated with RCP of coronary artery disease that could help to individualize the type and intensity of treatment.

Assessment of Postsystolic Shortening and Global Longitudinal Strain Improves the Sensitivity of Dobutamine Stress Echocardiography in End-Stage Liver Disease

Dobutamine stress echocardiography (DSE) remains a widely used method for detection of coronary artery disease (CAD) in patients with end stage liver disease (ESLD) despite low sensitivity. Speckle tracking assessment of strain may enhance the sensitivity of DSE in the general population but the value of strain analysis in ESLD is unknown. DSE with two-dimensional speckle tracking and quantitative coronary angiography were performed in 146 patients with ESLD. Thirty-six patients (25%) had CAD (> 50% diameter stenosis of a major vessel). Global longitudinal strain at rest (GLSr) and at peak stress (GLSp) and an index of post-systolic (PSSi) shortening ([maximal extent of shortening - extent of shortening in systole] / [extent of shortening in systole]) were determined. A PSSi of > 0.25 was considered evidence for CAD. ROC analysis was used to determine the optimal thresholds of GLSr and GLSp for CAD and to assess the diagnostic performance of wall motion assessment (WMA) and strain parameters. The sensitivity and specificity of WMA, GLSr, GLSp and PSSi were compared. Thirty-six patients (25%) had significant CAD. The areas under the curve (AUC) for WMA, GLSr, GLSp, and PSSi were 0.60, 0.72, 0.68, and 0.78, respectively. Visual assessment of wall motion (WMA) had a sensitivity of 28%. The sensitivity of each of the strain parameters, GLSr (53%, p =0.016), GLSp (69%, p =0.004), and PSSi (78%, p <0.001), exceeded the sensitivity for WMA. WMA specificity was 92% which exceeded the specificity for each of the strain parameters (GLSr 82%, p =0.037), GLSp 63%, p <0.001), and PSSi (78%, p = 0.009). Of the strain parameters, PSSi had the best balance between sensitivity and specificity (both 78%). Assessment of GLS and PSSi with DSE yields better sensitivity than WMA in ELSD patients. PSSi had the best diagnostic performance of all parameters in this population with a low prevalence of CAD.

Secondary Pharmacological Prevention of Coronary Artery Disease among Patients Submitted to Clinical Management, Percutaneous Coronary Intervention, or Coronary Artery Bypass Graft Surgery.

Secondary prevention is recommended for patients with evidence of coronary artery disease (CAD) regardless of the indication for treatment by coronary artery bypass graft surgery (CABG) or percutaneous coronary intervention (PCI). This study evaluated whether clinical treatment, PCI or CABG had an influence on adherence to the pharmacological secondary prevention in patients with stable CAD. This cohort included patients aged ≥40 years with stable CAD confirmed by coronary angiography. The decision for medical treatment alone, or additionally with PCI or CABG, was made by the attending physicians. Adherence to the prescribed drugs recommended by the guidelines for secondary prevention (optimal pharmacological treatment), including antiplatelet agents, lipid-lowering drugs, beta-blockers, and renin-angiotensin-aldosterone system blockers, was assessed at follow-up. Differences were considered significant for p values <0.05. From 928 patients enrolled at baseline, 415 had mild CAD and 66 moderate to severe CAD. The average follow-up was 5.2 ± 1.5 years. Patients submitted to CABG were more likely to receive the optimal pharmacological treatment than those submitted to PCI or treated clinically (63.5% versus 39.1% versus 45.7% respectively, p=0.003). Baseline factors independently associated with greater probability of having a prescription of optimal treatment at follow-up were CABG [39% higher (6% - 83%, p=0.017) and diabetes [25% higher (1% - 56%), p=0.042] than their counterparts treated by other methods and participants without diabetes, respectively. Patients with CAD submitted to CABG are more commonly treated with optimal pharmacological secondary prevention than patients treated by PCI or exclusively with medical therapy.

A STUDY TO IDENTIFY THE PRESENCE OF SEVERE CORONARY ARTERY DISEASE IN PATIENTS WITH NO ELECTROCARDIOGRAPHIC, BIOCHEMICAL AND ECHOCARDIOGRAPHIC EVIDENCE OF CAD USING CT CORONARY ANGIOGRAPHY

INTRODUCTION:Acute chest pain is one of the most common reasons for seeking care in the emergency department (ED), accounting for approximately 10% of all visits. The difficulty lies in discriminating patients with ACS or other lifethreatening conditions from those with non-cardiovascular,non-life-threatening chest pain.The diagnosis ofACS is missed in approximately 2%ofpatients.But itis essential to rule out cardiovascular etiology of chestpain to avoidunnecessary cost and complications of investigations and treatment. This study aims at identifying the prevalence of significant coronary artery disease in patients with no electrocardiographic and biochemical evidence of coronary artery disease. AIM OF STUDY: To identifying the presence of severe coronary artery disease in the patients with no electrocardiographic, biochemical and echocardiographic evidence of CAD using CT Coronary Angiography. MATERIAL AND METHODS: The study was conducted on 50 patients during a period of 4 months,admitted with history of chest pain without any ECG evidence of STEMI, negative cardiac markers, no evidence of RWMA on 2D ECHO, or previous history of myocardial infarction.RESULTS: Out of the 50 patients studied, 38 (76%) were males and 12 (24%) were females.A total of 6 patients (12%) were found to have severe stenosis in major coronary arteries (stenosis &gt; 70%) of which 4 were males (10.5%) and 2 were females (16.67%).CADRAD score≥3 was found in 9 patients (18%):6 males (15.78%) and 3 females (12%).Average age of patients who presented with chest pain with no electrocardiographic and biochemical evidence of coronary artery disease was found to be 61.7 years in males and 60.1 in females.66.7% of the female patients and 78.94% of male patients were over the age of 55 years.CONCLUSION: Furtherworkupofpatientswith chestpainwith no electrocardiographic and biochemicalevidenceofcoronaryarterydiseaseisnecessarytoavoidmissingdiagnosisofCAD

Unmasked by Fever: Diagnosing Brugada Syndrome After Ventricular Fibrillation Arrest

A 65-year-old man presented to the emergency department after he was resuscitated from cardiac arrest due to ventricular fibrillation. Coronary angiography demonstrated no evidence of coronary artery disease. Follow-up electrocardiograms (ECGs) were also unremarkable until the patient developed a fever, and a new ECG demonstrated a rapidly upsloping ST-segment followed by a downsloping, coved ST-segment in leads V1-V2. The diagnosis of Brugada syndrome was made after a procainamide challenge. The Brugada pattern on ECG can be transient and can manifest in the setting of fever or after taking medications with sodium channel blocking effects.

Machine learning-based marker for coronary artery disease: derivation and validation in two longitudinal cohorts

Binary diagnosis of coronary artery disease does not preserve the complexity of disease or quantify its severity or its associated risk with death; hence, a quantitative marker of coronary artery disease is warranted. We evaluated a quantitative marker of coronary artery disease derived from probabilities of a machine learning model. In this cohort study, we developed and validated a coronary artery disease-predictive machine learning model using 95 935 electronic health records and assessed its probabilities as in-silico scores for coronary artery disease (ISCAD; range 0 [lowest probability] to 1 [highest probability]) in participants in two longitudinal biobank cohorts. We measured the association of ISCAD with clinical outcomes-namely, coronary artery stenosis, obstructive coronary artery disease, multivessel coronary artery disease, all-cause death, and coronary artery disease sequelae. Among 95 935 participants, 35 749 were from the BioMe Biobank (median age 61 years [IQR 18]; 14 599 [41%] were male and 21 150 [59%] were female; 5130 [14%] were with diagnosed coronary artery disease) and 60 186 were from the UK Biobank (median age 62 [15] years; 25 031 [42%] male and 35 155 [58%] female; 8128 [14%] with diagnosed coronary artery disease). The model predicted coronary artery disease with an area under the receiver operating characteristic curve of 0·95 (95% CI 0·94-0·95; sensitivity of 0·94 [0·94-0·95] and specificity of 0·82 [0·81-0·83]) and 0·93 (0·92-0·93; sensitivity of 0·90 [0·89-0·90] and specificity of 0·88 [0·87-0·88]) in the BioMe validation and holdout sets, respectively, and 0·91 (0·91-0·91; sensitivity of 0·84 [0·83-0·84] and specificity of 0·83 [0·82-0·83]) in the UK Biobank external test set. ISCAD captured coronary artery disease risk from known risk factors, pooled cohort equations, and polygenic risk scores. Coronary artery stenosis increased quantitatively with ascending ISCAD quartiles (increase per quartile of 12 percentage points), including risk of obstructive coronary artery disease, multivessel coronary artery disease, and stenosis of major coronary arteries. Hazard ratios (HRs) and prevalence of all-cause death increased stepwise over ISCAD deciles (decile 1: HR 1·0 [95% CI 1·0-1·0], 0·2% prevalence; decile 6: 11 [3·9-31], 3·1% prevalence; and decile 10: 56 [20-158], 11% prevalence). A similar trend was observed for recurrent myocardial infarction. 12 (46%) undiagnosed individuals with high ISCAD (≥0·9) had clinical evidence of coronary artery disease according to the 2014 American College of Cardiology/American Heart Association Task Force guidelines. Electronic health record-based machine learning was used to generate an in-silico marker for coronary artery disease that can non-invasively quantify atherosclerosis and risk of death on a continuous spectrum, and identify underdiagnosed individuals. National Institutes of Health.