Epicardial Coronary Stenosis Research Articles

Development and Management of No-Reflow in a Patient Performed Coronary Angiography for Acute Coronary Syndrome: Case Report

Despite eliminating epicardial coronary artery stenosis or occlusion, insufficient myocardial perfusion is called “no-reflow.” While the no-reflow phenomenon is defined as coronary flow below increased thrombolysis (TIMI) 3 in myocardial infarction in some sources, TIMI is defined as 0–1 flow in some sources. In addition, some publications refer to TIMI 2 flow as slow coronary flow. However, the general view is that TIMI 0–1 coronary flow without severe residual stenosis, spasm, thrombus, or dissection is called no-reflow. The no-reflow phenomenon is a condition in which blood flow is significantly reduced in the ischemic myocardium despite percutaneous coronary intervention. So far, no standard treatment has been established to cure this condition. In this case, we present an interesting case that demonstrates a practical approach to the no-reflow phenomenon.

The functional importance of the left atrium in patients with coronary slow flow phenomenon

The coronary slow flow phenomenon (CSFP) is relatively common in patients scheduled for coronary angiography, characterized by the delayed distal vessel opacification of contrast in the absence of significant epicardial coronary stenosis

Relationship between epicardial adipose tissue and coronary artery stenoses on computed tomography in patients scheduled for carotid artery revascularization

BackgroundWe aimed to clarify the relationship between epicardial adipose tissue (EAT) volume and the presence of severe stenoses (SS) on coronary computed tomography angiography (CTA) for risk stratification of the patients with carotid artery stenoses. MethodsWe prospectively performed CTA for 125 consecutive patients (72.4 ± 8.1 years, 85% men) without a history of coronary artery disease (CAD), who were scheduled for carotid artery revascularization from 2014 to 2020. SS was defined as ≥70% luminal stenosis on CTA. EAT was quantified automatically as the total volume of tissue with -190 to -30 HU. ResultsOf 125 patients, 76 had SS. Between the patients with and without SS, there were significant differences in coronary artery calcium score (CACS), left ventricular ejection fraction (LVEF), dyslipidemia, and EAT, despite no differences in carotid echocardiography findings. After adjustment for age, gender, and dyslipidemia, EAT was an independent factor associated with SS (p=0.011), as well as CACS and LVEF. The addition of EAT to a baseline model including age, gender, dyslipidemia, LVEF, and CACS achieved both net reclassification improvement (0.505, p=0.003) and integrated discrimination improvement (0.059, p=0.003). ConclusionsIn patients with carotid stenoses, EAT is associated with CAD and is useful for additional risk stratification. Epicardial fat may have a specific role in the development of CAD in patients with suspected systemic atherosclerosis.

Left Atrial Dysfunction in Patients with Coronary Slow Flow

The coronary slow flow phenomenon (CSFP) is relatively common in patients scheduled for coronary angiography, characterized by delayed distal vessel opacification of contrast in the absence of significant epicardial coronary stenosis.

Safety of low-dose dobutamine stress test in coronary slow flow phenomenon

Purpose: To investigate the feasibility and safety of a low-dose dobutamine stress test in coronary slow flow phenomenon (CSFP) patients.Methods: One hundred and forty-two CSFP patients, and forty-four patients without CSFP or significant epicardial coronary stenosis who served as the control group, were retrospectively reviewed. All patients were infused intravenously with dobutamine at an initial infusion rate of 5 μg/kg/min which was then increased at 8-min intervals to 10, 15, and 20 μg/kg/min. Symptoms and echocardiography were monitored simultaneously.Results: Patient tolerance decreased as the doses of dobutamine increased. No termination of the test occurred without dobutamine or at the infusion rate of 5 μg/kg/min. Nonetheless, when the infusion rates were adjusted to 15 and 20 μg/kg/min, the incident of side effects reached up to 30.9 %, and a few patients experienced ST-segment depression in precordial electrocardiographic leads. There were no induced arrhythmias without dobutamine, while the incidence of arrhythmias was highest at the infusion rate of 20 μg/kg/min. Malignant arrhythmias such as ventricular fibrillation and sustained ventricular tachycardia, were not detected. No significant differences were showed in echocardiogram result for left ventricular ejection fraction (LVEF) between CSFP and control group (63.7±7.9 in the CSFP group, versus 64.3±7.2 in the control group; p = 0.63).Conclusion: A low-dose dobutamine stress test is safe and feasible in CSFP patients.

Rational and design of ST-segment elevation not associated with acute cardiac necrosis (LESTONNAC). A prospective registry for validation of a deep learning system assisted by artificial intelligence

BackgroundPatients with chest pain and persistent ST segment elevation (STE) may not have acute coronary occlusions or serum troponin curves suggestive of acute necrosis. Our objective is the validation and cost-effectiveness analysis of a diagnostic model assisted by artificial intelligence (AI). MethodsProspective multicenter registry in two groups of patients with STE: I) coronary arteries without significant lesions and without serum troponin curve suggestive of acute necrosis, II) myocardial infarction with acute coronary occlusion. The inclusion criteria are the following: 1) age ≥ 18 years, 2) chest pain or symptoms suggestive of myocardial ischemia, 3) STE at point J in two contiguous leads ≥0.1 mV, in V2 and V3 ≥ 0,2 mV and 4) signature of informed consent. The exclusion criteria are the following: 1) left bundle branch block, 2) acute cardiac necrosis in the absence of significant epicardial coronary artery stenosis, 3) STE ≤ 0.1 mV with pathologic Q wave, 4) severe anemia (hemoglobin <8.0 g/dl). For each patient without acute cardiac necrosis, the next patient from that center of the same sex and similar age (± 5 years) with myocardial infarction and acute coronary occlusion will be included. A manual centralized electrocardiographic analysis and another by deep learning AI will be performed. ConclusionsThe results of the study will provide new information for the stratification of patients with STE. Our hypothesis is that an AI analysis of the surface electrocardiogram allows a better distinction of patients with STE due to acute myocardial ischemia, from those with another etiology.

Myocardial injury in stress echocardiography: comparison of dobutamine, dipyridamole and dynamic stress echocardiography – single centre study

Abstract Background Stress echocardiography (SE) plays important role in investigation of the patients with chest pain. Adverse events rate is higher in dobutamine stress echocardiography on comparison to dobutamine stress echocardiography (ExSE) or dipyridamole stress echocardiography (DIP). Dynamic stress (ExSE) is recommended as the first-choice method according to the current guidelines. Purpose Response to the different stressors was studied in several studies with controversial results. This study aimed to investigate myocardial injury during stress echocardiography measured by the serum high sensitivity troponin (hsTnT) in a low risk population and whether there is a difference in hsTnT response between various stressors. Methods 135 patients (DSE n=46, ExsE n=46, Dip n=43) investigated for chest pain with suspicion on angina with negative diagnostic stress echocardiography were enrolled in the study. HsTnT was measured before and at 180 min. after the test was terminated. Patients with baseline elevated hsTnT levels (≥14 pg/ml), impaired LV EF (&amp;lt;50%), regional wall motion abnormalities, previous acute coronary syndrome and/or revascularisation, known epicardial coronary artery stenosis &amp;gt;50%, diabetes, prediabates (fasting glycemia at the day of the test ≥5,6 mmol/l, left ventricle hypertrophy &amp;gt;13 mm, baseline uncontrolled hypertension (BP &amp;gt;160/100 mmHg), estimated systolic pulmonary pressure &amp;gt;45 mmHg, more than moderate valvular disease, and patient who experienced dobutmine side effect (hypotension, atrial fibrillation) were excluded from the study. Results HsTnT increased in DSE and ExSE, but not in DIP group [9,4 (1,5–58,6), 1,1 (−0,9–15,7), −0,1 (−1,4–2,1) ng/L, p&amp;lt;0,001]. Similar result was found In DSE and ExSE subgroups without atropine [5,3 (0,4–45,3) vs 1,1 (−1,1–15,7) ng/L, p&amp;lt;0,001]. Adding atropine during SE triggered much greater hsTnT release in DSE [40,1 (3,7–160,3) vs 5,3 (0,4–45,3) ng/L, p&amp;lt;0,001], but not in ExSE group [0,6 (−0,9–22,7) vs 1,1 (−1,1–15,7) ng/L, p=0,786]. Moderate correlation of hsTnT rise with DSE length was observed (r=0,43). Conclusions DSE leads to significant myocardial injury multiplied when atropine is used. No injury was observed in DIP and only mild was revealed in ExSE. This finding support ExSE as the preferred stress echocardiography method. Whether significant myocardial injury is causative of the higher adverse event rates in DSE remains to be determined. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): University Hospital Hradec Kralove, Czech RepublicFaculty of Medicine Hradec Kralove, Charles University, Czech Republic hsTnT change 0–180 min. the whole grouphsTnT change 0–180 min. w/wo atropine

Atherosclerosis in Fabry Disease-A Contemporary Review.

Fabry disease (FD) is a lysosomal storage disorder characterised by a deficiency in the enzyme α-galactosidase A resulting in sphingolipid deposition which causes progressive cardiac, renal, and cerebral manifestations. The case illustrates a patient with FD who died suddenly, and medical examination demonstrated myocardial scarring and prior infarction. Angina is a frequent symptom in FD. Our own data are consistent with registry data indicating a high prevalence of risk factors for coronary artery disease (CAD) in FD that may accelerate conventional atherosclerosis. Patients with FD also have a higher high-density lipoprotein (HDL)/total cholesterol (T-Chol) ratio which may further accelerate atherosclerosis through expression of early atherosclerotic markers. Patients with FD may develop CAD both via classical atherosclerosis and through formation of thickened fibrocellular intima containing fibroblasts with storage of sphingolipids. Both mechanisms occurring together may accelerate coronary stenosis, as well as alter myocardial blood flow. Our data supports limited data that, although coronary flow may be reduced, the prevalence of epicardial coronary stenosis is low in FD. Microvascular dysfunction and arterial wall stress from sphingolipid deposition may form reactive oxygen species (ROS) and myeloperoxidase (MPO), key atherosclerotic mediators. Reduced myocardial blood flow in FD has also been demonstrated using numerous imaging modalities suggesting perfusion mismatch. This review describes the above mechanisms in detail, highlighting the importance of modifying cardiovascular risk factors in FD patients who likely develop accelerated atherosclerosis compared to the general population.

Physiological significance of pericoronary inflammation in epicardial functional stenosis and global coronary flow reserve

Both fractional flow reserve (FFR) and global coronary flow reserve (g-CFR) provide prognostic information in patients with stable coronary artery disease (CAD). Inflammation plays a vital role in impaired endothelial dysfunction and atherosclerotic progression, potentially predicting cardiovascular mortality. This study aimed to evaluate the physiological significance of pericoronary adipose tissue inflammation assessed by CT attenuation (PCATA) in epicardial functional stenosis severity and g-CFR in patients with CAD. A total of 131 CAD patients with a single de novo epicardial coronary stenosis who underwent coronary CT-angiography (CCTA), phase-contrast cine-magnetic resonance imaging (PC-CMR) and FFR measurement were studied. PCATA was assessed using the mean CT attenuation value. G-CFR was obtained by quantifying absolute coronary sinus flow (ml/min/g) by PC-CMR at rest and during maximum hyperemia. Median FFR, g-CFR, and PCATA values were 0.75, 2.59, and − 71.3, respectively. Serum creatinine, NT-proBNP, left ventricular end-diastolic volume, and PCATA were independently associated with g-CFR. PCATA showed a significant incremental predictive efficacy for impaired g-CFR (< 2.0) when added to the clinical risk model. PCATA was significantly associated with g-CFR, independent of FFR. Our results suggest the pathophysiological mechanisms linking perivascular inflammation with g-CFR in CAD patients.

Invasive Assessment of Microvascular Resistance in Hypertrophic Cardiomyopathy With Echocardiographic Correlates

Hypertrophic cardiomyopathy (HCM) is often associated with ischaemia despite lack of focal epicardial coronary stenosis. Our aim was to assess invasive coronary microvascular circulation and correlate findings with echocardiography. We prospectively enrolled patients with HCM and controls who were referred for diagnostic coronary angiography. A pressure-temperature sensor coronary guidewire was used with intracoronary injections of room-temperature saline to measure mean coronary transit time during rest and hyperaemia induced with intravenous adenosine. The index of microvascular resistance (IMR) was calculated. Left ventricular mass was calculated during echocardiographic studies. Patients with HCM (n=12) and controls (n=7), had similar demographics. Left ventricular ejection fraction was higher in HCM (76.7%±11.0% vs 55.0%±15.9%, p=0.003). IMR was non-significantly higher in HCM (21.7±10.2 vs 15.3±4.8, p=0.16). Only patients with HCM had abnormal IMR (>25). Coronary flow reserve was non-significantly higher in HCM (2.7±1.6 vs 2.1±1.2, p=0.34). IMR correlated with left ventricular mass in hypertrophic cardiomyopathy subjects (Pearson r=0.68, p=0.02). Microvascular dysfunction as assessed by IMR may be abnormal in HCM and is correlated with left ventricular mass.

Role of Fibroblast Growth Factor-23 in Coronary Slow Flow Phenomenon Pathogenesis

The phenomenon of angina chest pain without significant epicardial coronary artery stenosis, but accompanied by a slowdown in coronary blood flow is often found in patients with symptoms of acute coronary syndrome who undergoing invasive coronary angiography. This phenomenon of slow coronary blood flow is then called the coronary slow flow phenomenon (CSFP). The pathogenesis mechanism of CSFP remains unclear. The pathogenesis of CSFP is thought to be multifactorial. Endothelial dysfunction, small vessel disease, inflammation, renin system angiotensin aldosterone, atherosclerosis are thought to be involved in the pathogenesis of CSFP. Cardiovascular disease incidence and death were associated with elevated levels of Fibroblast growth factor-23 (FGF-23). High levels of FGF-23 can lead to formation of blood vessel calcification, left ventricular hypertrophy, arterial stiffness, endothelial dysfunction, increased inflammatory markers and elevated levels of angiotensin II. It is suspected that FGF-23 has a role in this event other than as a regulator of bone and mineral metabolism. This literature review aims to determine the relationship between fibroblast growth factor-23 and the pathophysiology of CSFP. Based on the broad role of FGF-23, it is possible that FGF-23 is involved in the pathogenesis of CSFP.

Coronary microvascular adaptations distal to epicardial artery stenosis.

Until recently, epicardial coronary stenosis has been considered the primary outcome of coronary heart disease, and clinical interventions have been dedicated primarily to the identification and removal of flow-limiting stenoses. However, a growing body of literature indicates that both epicardial stenosis and microvascular dysfunction contribute to damaging myocardial ischemia. In this review, we discuss the coexistence of macro- and microvascular disease, and how the structure and function of the distal microcirculation is impacted by the hemodynamic consequences of an epicardial, flow-limiting stenosis. Mechanisms of endothelial dysfunction as well as alterations of smooth muscle function in the coronary microcirculation distal to stenosis are discussed. Risk factors including diabetes, metabolic syndrome, and aging exacerbate microvascular dysfunction in the myocardium distal to a stenosis, and our current understanding of the role of these factors in limiting collateralization and angiogenesis of the ischemic myocardium is presented. Importantly, exercise training has been shown to promote collateral growth and improve microvascular function distal to stenosis; thus, the current literature reporting the mechanisms that underlie the beneficial effects of exercise training in the microcirculation distal to epicardial stenosis is reviewed. We also discuss recent studies of therapeutic interventions designed to improve microvascular function and stimulate angiogenesis in clinically relevant animal models of epicardial stenosis and microvascular disease. Finally, microvascular adaptation to removal of epicardial stenosis is considered.

From anatomy to function and then back to anatomy: invasive assessment of myocardial ischemia in the catheterization laboratory based on anatomy-derived indices of coronary physiology.

For many decades, the severity of coronary artery disease (CAD) and the indication to proceed with either percutaneous coronary intervention (PCI) or surgical revascularization has been based on anatomically derived parameters of vessel stenosis, and typically on the percentage of lumen diameter stenosis (DS%) as determined by invasive coronary angiography (CA). However, it is currently a well-accepted concept that pre-specified thresholds of DS% have a weak correlation with the ischemic and functional potential of an epicardial coronary stenosis. In this regard, the introduction of fractional-flow reserve (FFR) has represented a paradigm-shift in the understanding, diagnosis, and treatment of CAD, but the adoption of FFR into the clinical practice remains surprisingly limited and sub-standard, probably because of the inherent drawbacks of pressure-wire-based technology such as additional costs, prolonged procedural time, invasive instrumentation of the target vessel, and use of vaso-dilatory agents causing side effects for patients. For this reason, new modalities are under development or validation to derive FFR from computational fluid dynamics (CFD) applied to a three-dimensional model (3D) of the target vessel obtained from CA, intravascular imaging, or coronary computed tomography angiography. The purpose of this review was to describe the technical details of these anatomy-derived indices of coronary physiology with a special focus on summarizing their workflow, available evidence, and future perspectives about their application in the clinical practice.

Utilidad de la reserva de flujo fraccional para guiar la revascularización en paciente con síndrome coronario agudo sin elevación del segmento ST

Fractional flow reserve is the gold standard for evaluating the functional severity of an epicardial coronary stenosis. Coronary physiology-guided revascularization has been shown to be useful in stable heart disease, but also in acute coronary syndrome. We present the case of a 58 year-old patient with acute coronary syndrome, who presented two angiographically significant stenosis. We decided to perform revascularization guided by coronary physiology. Using fractional flow reserve, the need to revascularize only one of the lesions was determined, leading to a change in therapeutic behavior that exemplifies the virtue of having coronary physiology tools for decision-making.

The spectrum of functional responses during ABCDE stress echocardiography

Abstract Background The new methodological standard in stress echo (SE) is the comprehensive approach with ABCDE protocol: step A for regional wall motion abnormalities (RWMA); step B for B-lines by lung ultrasound; step C for left ventricular contractile reserve (LVCR); step D for Doppler-based coronary flow velocity reserve (CFVR) in left anterior descending coronary artery; and step E for imaging-independent EKG-based heart rate reserve (HRR). Purpose To assess the feasibility of ABCDE-SE in a prospective, large scale, multicenter, international, effectiveness study. Methods From September 2016 to December 2019, we enrolled 4,585 all-comers patients (age 63±11 years, 2,566 males, 56%; ejection fraction 61±9%) with known or suspected chronic coronary artery disease referred to clinically-driven SE with exercise (n=1,774, 38.7%), dipyridamole (n=2,403, 52.4%), dobutamine (n=375, 8.2%) or adenosine (n=33, 0.7%). Recruitment involved 13-certified laboratories of 7 countries. All patients underwent ABCDE-SE. The same transducer was used for cardiac and lung scan. Criteria for abnormal response were: stress-induced changes in RWMA in 2 contiguous segments for step A; stress-rest increase in B-lines ≥2 for step B (4-site simplified scan, each site scored from 0= A-lines or black lung to 10= white lung for coalescing B-lines); LVCR ≤2.0 for exercise and dobutamine (≤1.1 for vasodilators) for step C; CFVR in LAD ≤2.0 for step D; HRR (peak/rest heart rate) ≤1.80 for exercise and dobutamine (≤1.22 for vasodilators) for step E. Results Success rate was 98%, 100%, 99%, 86% and 100% for A, B, C, D and E steps, respectively. The positivity rate was 19% for A, 27% for B, 35% for C, 27% for D and 37% for E. All 5 parameters were normal in 1,496 patients (32.6%), all 5 were abnormal in 183 patients (4.0%). Most patients had abnormal response of 1 (n=1,356, 29.6%), 2 (n=788, 17.2%), 3 (n=477, 9.7%) or 4 (n=315, 6.9%) criteria (see Figure). Conclusions ABCDE-SE is extremely feasible, user-friendly, with minimal increase in imaging and off-line analysis time. It allows a comprehensive and personalized functional stratification assessing different vulnerabilities: epicardial coronary artery stenosis (step A), pulmonary congestion (step B), global myocardial dysfunction (step C), coronary microcirculatory dysfunction (step D), and cardiac autonomic nervous system imbalance (step E). The SE response is not only black and white with step A but can be effectively titrated from benign green code (all steps negative) to more functionally malignant red code (at least 3 steps positive). Figure 1 Funding Acknowledgement Type of funding source: None

Diagnostic accuracy of Instantaneous Wave-Free Ratio (iFR) for the assessment of myocardial ischaemia: a comparison with non-invasive stress imaging

Abstract Background Instantaneous Wave-Free Ratio (iFR) allows for the assessment of the haemodynamic effects of epicardial coronary stenoses without the need for hyperaemia; iFR is currently recommended as a means to evaluate myocardial ischaemia. Purpose To assess the diagnostic accuracy of iFR with respect to the identification of coronary epicardial stenoses causing ischemia. Therefore, we combined anatomical (% stenosis at invasive coronary angiography, ICA) and functional (non-invasive imaging stress test, NIST) information to obtain a “gold standard” for the identification of stenoses causing ischaemia. Methods We enrolled 71 patients (52 male, 19 female; age mean 68.4±8.1 years) with chronic coronary syndrome or low-risk acute coronary syndrome without ST segment elevation who had at least a NIST and who had at least one vessel with a 50%-85% stenosis at ICA. iFR was measured in all coronary arteries with stenosis &amp;gt;50% and categorised according to the 0.89 threshold for ischaemia. Results iFR was assessed in 122 vessels. In a per-vessel analysis, in 56.7% ischaemia was present both at iFR and NIST, in 21.3% ischaemia was absent in both, while in 23.0% ischaemia was found at NIST but not confirmed by iFR. The overall accuracy of iFR with respect to NIST was 90.1%. However, when considering as the “gold standard” for coronary disease causing ischaemia the contemporary presence of an epicardial stenosis &amp;gt;70% at ICA and a positive NIST, the diagnostic accuracy of iFR greatly improved. The sensibility, specificity, PPV, NPV and accuracy were 96.5%, 75.0%, 73.3%, 96.7% and 84.4%, respectively. In case of discordance between NIST and iFR, revascularization was based on iFR. At a mean follow-up of 23±18 months, the composite endpoint of MACE (major adverse cardiac events, defined as the composite of all-cause death, nonfatal MI and unplanned coronary revascularization) occurred in 16.4%, while death/MI occurred in 11.9%. Stratification according to the per-patient concordance between iFR and NIST showed no significant differences in rates of MACE (p=0.50) and death/MI (p=0.20). Stratification based on iFR showed a higher death/MI rate in iFR-positive patients (11.9% vs. 0%, p=0.047) and a trend to higher MACE rate (11.9% vs. 4.47% p=0.14), Conclusions The diagnostic accuracy of iFR is low when compared with NIST as the reference for myocardial ischaemia, but it is very high when compared with the combined presence of epicardial stenosis and positive NIST. Therefore, iFR can accurately guide the decision to treat or defer revascularization of intermediate coronary stenoses, being most useful in patients with multivessel CAD and when non-invasive functional data are lacking or discordant with anatomy. Funding Acknowledgement Type of funding source: None

The Foundational Role of Cardiovascular Imaging in the Characterization of Mental Stress-Induced Myocardial Ischemia in Patients with Coronary Artery Disease.

Mental stress-provoked myocardial ischemia (MSIMI) is an ischemic phenomenon provoked by the experience of psychologically stressful circumstances. While MSIMI was initially identified 50years ago during activities of daily living through the use of wearable Holter monitor, subsequent research utilized the technologies of cardiac imaging-ventriculography and myocardial perfusion-under controlled conditions to pursue an understanding of pathophysiology and prognosis. This work revealed that MSIMI occurs in almost half of patients with stable coronary artery disease (CAD) and is associated with cardiac events and early mortality. We provide a focused review of the instrumental role that cardiac imaging has played in elucidating how stress affects cardiac physiology and how emerging diagnostic techniques will allow for further research on stress-mediated changes in the coronary macro- and microvasculature. Observations about the cardiac response to mental stress diverge from underlying cornerstones of the traditional CAD paradigm which is based upon myocardial oxygen demand and the degree of epicardial coronary stenosis. Evidence from studies utilizing non-invasive and invasive studies of coronary perfusion indicates perturbations in the microvascular compartment in response to mental stress. Cardiovascular imaging enjoined with mental stress provocation may be a commanding tool to advance our understanding of non-obstructive CAD and the coronary microvasculature. This further understanding will facilitate incorporation of mental stress testing in the clinical care of patients with discrepant diagnostic work-up of CAD and in patients who experience anginal symptoms due to non-exertional and/or emotional triggers. Such algorithms will be crucial to identify treatment targets to modify the risk associated with mental stress-associated ischemia and adverse prognosis.

Prevalence of Abnormal Coronary Findings on Coronary Computed Tomography Angiography Among Young Adults Presenting With Chest Pain.

We evaluated the prevalence of coronary stenosis on coronary computed tomography angiography (CCTA) in patients aged 18 to 30 years, who presented to the emergency department with chest pain. We also examined the risk factors potentially associated with abnormal coronary findings on CCTA in this age group. A total of 884 patients were retrospectively evaluated. Indication for CCTA was guided by our hospital's chest pain protocol based on ACC/AHA guidelines. These were performed using the standard technique and interpreted based on CAD-RADS guidelines. Scans were identified as abnormal if atherosclerotic coronary artery disease (CAD), myocardial bridging (MB), or any anatomic coronary artery anomaly were present. Twenty-two percent of patients had a coronary abnormality on CCTA. The most common abnormality was MB (17.3%), followed by CAD (4.4%) and coronary anomalies (1.5%). A small minority had stenosis (2.8%), most commonly caused by CAD. Most cases with stenosis were minimal to mild (72%) with 0.8% having coronary stenosis ≥50%. Age and male sex were risk factors for both coronary artery stenosis (odds ratio: 1.32 and 4.50, 95% confidence interval: 1.03-1.69, and 1.23-16.46, P=0.028 and 0.023, respectively) and CAD (odds ratio: 1.52 and 3.67, 95% confidence interval: 1.14-2.04, and 1.26-10.66, P=0.005 and 0.017, respectively). Epicardial coronary stenosis is rarely the cause of chest pain among young adult patients presenting to the emergency department. Age and male sex were both risk factors for coronary artery stenosis/disease in this age group.

Percutaneous Coronary Revascularization in Patients With Single Coronary Artery

IntroductionSingle coronary artery (SCA) is a rare congenital coronary anomaly. Its incidence in various angiographic series is from 0.024% to 0.066%. Percutaneous coronary intervention (PCI) of coronary artery disease (CAD) in these patients is technically challenging. MethodsWe retrospective analyzed the cardiac catheterization procedures of last 15 years and found 12 cases of SCA (incidence 0.084%). To determine the course of anomalous coronaries, angiographic “dot and eye” method and computed tomography (CT) were used. The course of the SCA was classified as per the modified Lipton criteria. PCI was performed as per the standard protocol for a significant epicardial coronary artery stenosis. ResultsOut of total 12 patients of SCA, 9 patients had PCI of significant CAD. The mean age of 9 PCI patients was 63.8 ± 8.2 years (5 males, 4 females). The origin of the SCA was from the right sinus of Valsalva in 6 cases and from left sinus of Valsalva in 3 cases. Eleven successful PCI procedures were performed, which included PCI of left main, coronary bifurcation lesion, chronic total occlusion, and multi-vessel disease. Four patients had intravascular imaging and 3 patients had rotablation of calcified lesions. ConclusionPCI of SCA is technically challenging, which requires considerable expertise and experience. An appropriate selection of hardware along with technical expertise can make the procedure simpler with optimal end results.

Epicardial coronary stenosis severity and myocardial perfusion

Patients suspected of having epicardial coronary disease are often investigated with noninvasive myocardial ischemia tests to establish a diagnosis and guide management. However, the relationship between myocardial ischemia and coronary stenoses is affected by multiple factors, and there is marked biological variation between patients. The ischemic cascade represents the temporal sequence of pathophysiological events that occur after interruption of myocardial oxygen delivery. The earliest part of the cascade is examined via perfusion imaging, and fractional flow reserve (FFR) is a corresponding index which is specific to the coronary artery. Whereas FFR has come to be regarded a clinical reference standard against which other newer invasive and noninvasive tests are validated, the diagnostic FFR threshold for detecting ischemia was established against a combination of noninvasive ischemia tests that assessed different stages of the ischemic cascade. Moreover, the validity of invasive pressure-derived indices of stenosis severity are contingent on the assumption that pressure is proportional to flow if microvascular resistance is constant, a condition induced by pharmacological intervention or by examining specific segments of the cardiac cycle. Furthermore, myocardial perfusion reserve depends on dynamic modulation of microvascular resistance, and dysfunction of the microvasculature can lead to ischemia even in the absence of epicardial coronary disease.