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BACKGROUND: We investigated the usefulness of invasive coronary function testing to diagnose the cause of angina in patients with no obstructive coronary arteries. METHODS: Outpatients referred for coronary computed tomography angiography in 3 hospitals in the United Kingdom were prospectively screened. After coronary computed tomography angiography, patients with unobstructed coronary arteries, and who consented, underwent invasive endotyping. The diagnostic assessments included coronary angiography, fractional flow reserve (patient excluded if ≤0.80), and, for those without obstructive coronary artery disease, coronary flow reserve (abnormal <2.0), index of microvascular resistance (abnormal ≥25), and intracoronary infusion of acetylcholine (0.182, 1.82, and 18.2 μg/mL; 2 mL/min for 2 minutes) to assess for microvascular and coronary spasm. Participants were randomly assigned to disclosure of the results of the coronary function tests to the invasive cardiologist (intervention group) or nondisclosure (control group, blinded). In the control group, a diagnosis of vasomotor angina was based on medical history, noninvasive tests, and coronary angiography. The primary outcome was the between-group difference in the reclassification rate of the initial diagnosis on the basis of coronary computed tomography angiography versus the final diagnosis after invasive endotyping. The Seattle Angina Questionnaire summary score and Treatment Satisfaction Questionnaire for Medication were secondary outcomes. RESULTS: Of 322 eligible patients, 250 (77.6%) underwent invasive endotyping; 19 (7.6%) had obstructive coronary disease, 127 (55.0%) had microvascular angina, 27 (11.7%) had vasospastic angina, 17 (7.4%) had both, and 60 (26.0%) had no abnormality. A total of 231 patients (mean age, 55.7 years; 64.5% women) were randomly assigned and followed up (median duration, 19.9 [12.6-26.9] months). The clinician diagnosed vasomotor angina in 51 (44.3%) patients in the intervention group and in 55 (47.4%) patients in the control group. After randomization, patients in the intervention group were 4-fold (odds ratio, 4.05 [95% CI, 2.32-7.24]; P<0.001) more likely to be diagnosed with a coronary vasomotor disorder; the frequency of this diagnosis increased to 76.5%. The frequency of normal coronary function (ie, no vasomotor disorder) was not different between the groups before randomization (51.3% versus 50.9%) but was reduced in the intervention group after randomization (23.5% versus 50.9%, P<0.001). At 6 and 12 months, the Seattle Angina Questionnaire summary score in the intervention versus control groups was 59.2±24.2 (2.3±16.2 change from baseline) versus 60.4±23.9 (4.6±16.4 change) and 63.7±23.5 (4.7±14.7 change) versus 66.0±19.3 (7.9±17.1 change), respectively, and not different between groups (global P=0.36). Compared with the control group, global treatment satisfaction was higher in the intervention group at 12 months (69.9±22.8 versus 61.7±26.9, P=0.013). CONCLUSIONS: For patients with angina and no obstructive coronary arteries, a diagnosis informed by invasive functional assessment had no effect on long-term angina burden, whereas treatment satisfaction improved. [ABSTRACT FROM AUTHOR]

Background: Pulsed field ablation (PFA) has a unique safety profile when used to treat atrial fibrillation, largely related to its preferentiality for myocardial tissue ablation, in particular, esophageal sparing. A pentaspline catheter was the first such PFA system studied clinically for atrial fibrillation ablation; in these initial regulatory trials, the catheter was used for pulmonary vein isolation and left atrial posterior wall ablation. Since its regulatory approval in Europe, in clinical practice, physicians have ablated beyond pulmonary vein isolation and left atrial posterior wall ablation to expanded lesion sets in closer proximity to coronary arteries. This is an unstudied important issue because preclinical and clinical data have raised the potential for coronary arterial spasm. Herein, we studied the vasospastic potential of PFA lesion sets, both remote from and adjacent to coronary arteries. Methods: During routine atrial fibrillation ablation using the pentaspline PFA catheter, coronary angiography was performed before, during, and after pulsed field applications. The lesion sets studied included: (1) those remote from the coronary arteries such as pulmonary vein isolation (n=25 patients) and left atrial posterior wall ablation (n=5), and (2) ablation of the cavotricuspid isthmus (n=20) that is situated adjacent to the right coronary artery. Results: During pulmonary vein isolation and left atrial posterior wall ablation, coronary spasm did not occur, but cavotricuspid isthmus ablation provoked severe subtotal vasospasm in 5 of 5 (100%) consecutive patients, and this was relieved by intracoronary nitroglycerin in 5.5±3.5 minutes. ST-segment elevation was not observed. However, no patient (0%, P =0.004) had severe spasm if first administered parenteral nitroglycerin, either intracoronary (n=5) or intravenous (n=10), before treatment. Conclusions: Coronary vasospasm was not provoked during PFA at locations remote from coronary arteries, but when the energy is delivered adjacent to a coronary artery, PFA routinely provokes subclinical vasospasm. This phenomenon is attenuated by nitroglycerin, administered either post hoc to treat spasm or as prophylaxis. [ABSTRACT FROM AUTHOR]

2022; 24:, 1256-1266. doi: 10.1093/europace/euac050 10 Ruwald M, Johannessen A, Hansen M, Work R, Hansen J. Pulsed field ablation of the cavotricuspid isthmus using a multispline-electrode pulsed field ablation catheter. Keywords: Editorials; atrial fibrillation; catheter ablation EN Editorials atrial fibrillation catheter ablation 1820 1822 3 12/15/22 20221213 NES 221213 B Article, see p 1808 b Atrial fibrillation (AF) increases the risk of stroke and heart failure while decreasing functional capacity and quality of life.[[1], [3]] A strategy of rhythm control is recommended for symptomatic AF patients.[[1], [3]] Robust evidence supports cost-effective reduction in AF recurrence and improvement in quality of life with ablation compared with antiarrhythmic drug therapy for rhythm control.[4] AF ablation no longer represents a therapy of last resort for highly symptomatic patients with drug refractory AF. Despite this acute success, AF recurrence is common, occurring in up to 50% of patients at 4 years.[3] Further reducing procedural complications and AF recurrence remain major challenges for radiofrequency and cryoablation. [Extracted from the article]

Background: Cardiac injury is common in patients who are hospitalized with coronavirus disease 2019 (COVID-19) and portends poorer prognosis. However, the mechanism and the type of myocardial damage associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain uncertain.Methods: We conducted a systematic pathological analysis of 40 hearts from hospitalized patients dying of COVID-19 in Bergamo, Italy, to determine the pathological mechanisms of cardiac injury. We divided the hearts according to presence or absence of acute myocyte necrosis and then determined the underlying mechanisms of cardiac injury.Results: Of the 40 hearts examined, 14 (35%) had evidence of myocyte necrosis, predominantly of the left ventricle. Compared with subjects without necrosis, subjects with necrosis tended to be female, have chronic kidney disease, and have shorter symptom onset to admission. The incidence of severe coronary artery disease (ie, >75% cross-sectional narrowing) was not significantly different between those with and without necrosis. Three of 14 (21.4%) subjects with myocyte necrosis showed evidence of acute myocardial infarction, defined as ≥1 cm2 area of necrosis, whereas 11 of 14 (78.6%) showed evidence of focal (>20 necrotic myocytes with an area of ≥0.05 mm2 but <1 cm2) myocyte necrosis. Cardiac thrombi were present in 11 of 14 (78.6%) cases with necrosis, with 2 of 14 (14.2%) having epicardial coronary artery thrombi, whereas 9 of 14 (64.3%) had microthrombi in myocardial capillaries, arterioles, and small muscular arteries. We compared cardiac microthrombi from COVID-19-positive autopsy cases to intramyocardial thromboemboli from COVID-19 cases as well as to aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19-infected patients presenting with ST-segment-elevation myocardial infarction. Microthrombi had significantly greater fibrin and terminal complement C5b-9 immunostaining compared with intramyocardial thromboemboli from COVID-19-negative subjects and with aspirated thrombi. There were no significant differences between the constituents of thrombi aspirated from COVID-19-positive and -negative patients with ST-segment-elevation myocardial infarction.Conclusions: The most common pathological cause of myocyte necrosis was microthrombi. Microthrombi were different in composition from intramyocardial thromboemboli from COVID-19-negative subjects and from coronary thrombi retrieved from COVID-19-positive and -negative patients with ST-segment-elevation myocardial infarction. Tailored antithrombotic strategies may be useful to counteract the cardiac effects of COVID-19 infection. [ABSTRACT FROM AUTHOR]

At presentation, the patient had sinus tachycardia, blood pressure was normal, and the rest of the cardiovascular system examination was unremarkable. DOI: 10.1161/CIRCULATIONAHA.120.052301 198 RESPONSE TO ECG CHALLENGE The ECG shows sinus tachycardia with diffuse ST-segment elevation in all leads and ST-segment depression in lead aVR. During the patient's hospitalization, we observed spontaneous, self-resolving ST-T changes in the ECG suggestive of episodes of coronary vasospasm (Figure 4). [Extracted from the article]

First, Kereiakes et al[10] report the 5-year clinical follow-up results of the well conducted ABSORB III trial, which randomly assigned 2008 patients undergoing percutaneous coronary intervention to either the Absorb BVS or everolimus-eluting stent. The relative hazards for target lesion failure and stent thrombosis changed directionally, consistent with "borderline" I P i values for interaction (target lesion failure, I P i =0.052; stent thrombosis, I P i =0.056). In a recent optical coherence tomography analysis using BIOSOLVE II data, late scaffold recoil emerged as the major driver of Magmaris restenosis rather than neointimal hyperplasia (ie, the typical cause of Absorb BVS and metallic stents restenosis).[18] Late recoil may be the direct consequence of a premature loss of radial strength and seems addressable by device modification. 6 Stone GW, Ellis SG, Gori T, Metzger DC, Stein B, Erickson M, Torzewski J, Williams J Jr, Lawson W, Broderick TM, ABSORB IV Investigators Blinded outcomes and angina assessment of coronary bioresorbable scaffolds: 30-day and 1-year results from the ABSORB IV randomised trial. [Extracted from the article]

The authors found that the TTS patients had reduced left ventricular ejection fraction, increased left ventricular mass, elevated native T1 and T2, and defective myocardial calcium handling in the affected myocardial segments during the acute phase of the disease. Singh et al[1] studied myocardial manganese uptake (mMnUp), via cardiac manganese-enhanced magnetic resonance imaging (cMRI-Mn) in 20 patients with takotsubo syndrome (TTS). (2) What was the mMnUp of the patient imaged at 368 days after onset of TTS symptoms or similar patients imaged late at follow-up?. [Extracted from the article]

Myocardial infarction in the absence of obstructive coronary artery disease is found in ≈5% to 6% of all patients with acute infarction who are referred for coronary angiography. There are a variety of causes that can result in this clinical condition. As such, it is important that patients are appropriately diagnosed and an evaluation to uncover the correct cause is performed so that, when possible, specific therapies to treat the underlying cause can be prescribed. This statement provides a formal and updated definition for the broadly labelled term MINOCA (incorporating the definition of acute myocardial infarction from the newly released "Fourth Universal Definition of Myocardial Infarction") and provides a clinically useful framework and algorithms for the diagnostic evaluation and management of patients with myocardial infarction in the absence of obstructive coronary artery disease. [ABSTRACT FROM AUTHOR]

Coronary artery disease is prevalent in different causes of out-of-hospital cardiac arrest (OHCA), especially in individuals presenting with shockable rhythms of ventricular fibrillation/pulseless ventricular tachycardia (VF/pVT). The purpose of this report is to review the known prevalence and potential importance of coronary artery disease in patients with OHCA and to describe the emerging paradigm of treatment with advanced perfusion/reperfusion techniques and their potential benefits on the basis of available evidence. Although randomized clinical trials are planned or ongoing, current scientific evidence rests principally on observational case series with their potential confounding selection bias. Among patients resuscitated from VF/pVT OHCA with ST-segment elevation on their postresuscitation ECG, the prevalence of coronary artery disease has been shown to be 70% to 85%. More than 90% of these patients have had successful percutaneous coronary intervention. Conversely, among patients resuscitated from VF/pVT OHCA without ST-segment elevation on their postresuscitation ECG, the prevalence of coronary artery disease has been shown to be 25% to 50%. For these patients, early access to the cardiac catheterization laboratory is associated with a 10% to 15% absolute higher functionally favorable survival rate compared with more conservative approaches of late or no access to the cardiac catheterization laboratory. In patients with VF/pVT OHCA refractory to standard treatment, a new treatment paradigm is also emerging that uses venoarterial extracorporeal membrane oxygenation to facilitate return of normal perfusion and to support further resuscitation efforts, including coronary angiography and percutaneous coronary intervention. The burden of coronary artery disease is high in this patient population, presumably causative in most patients. The strategy of venoarterial extracorporeal membrane oxygenation, coronary angiography, and percutaneous coronary intervention has resulted in functionally favorable survival rates ranging from 9% to 45% in observational studies in this patient population. Patients with VF/pVT should be considered at the highest severity in the continuum of acute coronary syndromes. These patients have a significant burden of coronary artery disease and acute coronary thrombotic events. Evidence from randomized trials will further define optimal clinical practice. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 38-year-old black woman with a history of eczema, chronic hypereosinophilia, and temporal artery aneurysm. Topics discussed include laboratory examination included a normal complete metabolic profile and revealed complete blood count; mentions the finding of peripheral eosinophilia is striking and must influence the differential diagnosis; and also mentions the cardiac examination was normal, militating against pericarditis or myopericarditis.

Keywords: myocardial infarction; prognosis; type 1 myocardial infarction; type 2 myocardial infarction EN myocardial infarction prognosis type 1 myocardial infarction type 2 myocardial infarction 2083 2085 3 11/25/20 20201124 NES 201124 The 4th Universal Definition of Myocardial Infarction classifies myocardial infarction (MI) into 5 subtypes, of which types 1 and 2 MI are the most common.[1],[2] Type 1 MI (T1MI) is defined as MI caused by acute coronary atherothrombosis including plaque rupture and erosion. Flowchart showing the placement of myocardial infarction patients following the proposed modification of the 4th Universal Definition of Myocardial Infarction. Myocardial infarction, prognosis, type 1 myocardial infarction, type 2 myocardial infarction. [Extracted from the article]

Keywords: cell- and tissue-based therapy; models, animal; myocardial infarction; stem cells; translational research EN cell- and tissue-based therapy models, animal myocardial infarction stem cells translational research 1037 1039 3 04/20/20 20200324 NES 200324 Cardiac cell therapy using adult cells with stem- or progenitor-like properties has been under clinical investigation for more than 15 years. MNCs were largely absent from all tissues examined, including heart and lung (Figure, C), accounting for less than 3 cells per milligram tissue weight, or roughly 450 MNCs in an entire mouse heart. [Extracted from the article]

Varying results may be realized among higher risk patients with moderate-severe ischemia or patients with myocardial ischemia in specific coronary territories. An important take-home message from the ORBITA trial is that ischemia is an important mediator of improved patient symptoms after PCI, but ischemia is likely not the only variable of importance. [Extracted from the article]

The Universal Definition of Myocardial Infarction (UDMI)[1] classifies myocardial infarction (MI) into 5 subtypes, of which type 1 and type 2 MI are the most common and relevant to practicing clinicians. CAD indicates coronary artery disease; and MI, myocardial infarction. Executive Group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction Fourth Universal Definition of Myocardial Infarction (2018). [Extracted from the article]

Since the late 1990s, there has been a steady decline in cancer-related mortality, in part related to the introduction of so-called targeted therapies. Intended to interfere with a specific molecular pathway, these therapies have, paradoxically, led to a number of effects off their intended cancer tissue or molecular targets. The latest examples are tyrosine kinase inhibitors targeting the Philadelphia Chromosome mutation product, which have been associated with progressive atherosclerosis and acute vascular events. In addition, agents designed to interfere with the vascular growth factor signaling pathway have vascular side effects ranging from hypertension to arterial events and cardiomyocyte toxicity. Interestingly, the risk of cardiotoxicity with drugs such as trastuzumab is predicted by preexisting cardiovascular risk factors and disease, posing the question of a vascular component to the pathophysiology. The effect on the coronary circulation has been the leading explanation for the cardiotoxicity of 5-fluorouracil and may be the underlying the mechanism of presentation of apical ballooning syndrome with various chemotherapeutic agents. Classical chemotherapeutic agents such as cisplatin, often used in combination with bleomycin and vinca alkaloids, can lead to vascular events including acute coronary thrombosis and may be associated with an increased long-term cardiovascular risk. This review is intended to provide an update on the evolving spectrum of vascular toxicities with cancer therapeutics, particularly as they pertain to clinical practice, and to the conceptualization of cardiovascular diseases, as well. Vascular toxicity with cancer therapy: the old and the new, an evolving avenue. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 32-year-old male endurance athlete who developed multiple episodes of chest tightness while training for a triathlon. He had previous seasonal allergic rhinitis and childhood asthma and occasional binge drinking. A left ventricular ejection fraction was revealed in the transthoracic echodiagram. The patient is under observation in a tertiary hospital.

Background—Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a puzzling clinical entity with no previous evaluation of the literature. This systematic review aims to (1) quantify the prevalence, risk factors, and 12-month prognosis in patients with MINOCA, and (2) evaluate potential pathophysiological mechanisms underlying this disorder. Methods and Results—Quantitative assessment of 28 publications using a meta-analytic approach evaluated the prevalence, clinical features, and prognosis of MINOCA. The prevalence of MINOCA was 6% [95% confidence interval, 5%-7%] with a median patient age of 55 years (95% confidence interval, 51-59 years) and 40% women. However, in comparison with those with myocardial infarction associated with obstructive coronary artery disease, the patients with MINOCA were more likely to be younger and female but less likely to have hyperlipidemia, although other cardiovascular risk factors were similar. All-cause mortality at 12 months was lower in MINOCA (4.7%; 95% confidence interval, 2.6%-6.9%) compared with myocardial infarction associated with obstructive coronary artery disease (6.7%, 95% confidence interval, 4.3%-9.0%). Qualitative assessment of 46 publications evaluating the underlying pathophysiology responsible for MINOCA revealed the presence of a typical myocardial infarct on cardiac magnetic resonance imaging in only 24% of patients, with myocarditis occurring in 33% and no significant abnormality in 26%. Coronary artery spasm was inducible in 27% of MINOCA patients, and thrombophilia disorders were detected in 14%. Conclusions—MINOCA should be considered as a working diagnosis with multiple potential causes that require evaluation so that directed therapies may improve its guarded prognosis. [ABSTRACT FROM AUTHOR]

Background--Coronary spasm can cause myocardial ischemia and angina in patients with and those without obstructive coronary artery disease. However, provocation tests using intracoronary acetylcholine administration are rarely performed in clinical routine in the United States and Europe. Thus, we assessed the clinical usefulness, angiographic characteristics, and safety of intracoronary acetylcholine provocation testing in white patients with unobstructed coronary arteries. Methods and Results--From September 2007 to June 2010, a total of 921 consecutive patients (362 men, mean age 62±12years) who underwent diagnostic angiography for suspected myocardial ischemia and were found to have unobstructed coronary arteries (no stenosis ≥50%) were enrolled. The intracoronary acetylcholine provocation testing was performed directly after angiography according to a standardized protocol. Three hundred forty-six patients (35%) reported chest pain at rest, 222 (22%) reported chest pain on exertion, 238 (24%) reported a combination of effort and resting chest pain, and 41 (4%) presented with troponin-positive acute coronary syndrome. The overall frequency of epicardial spasm (>75% diameter reduction with angina and ischemic ECG shifts) was 33.4%, and the overall frequency of microvascular spasm (angina and ischemic ECG shifts without epicardial spasm) was 24.2%. Epicardial spasm was most often diffuse and located in the distal coronary segments (P<0.01). No fatal or irreversible nonfatal complications occurred. However, 9 patients (1%) had minor complications (nonsustained ventricular tachycardia [n=1], fast paroxysmal atrial fibrillation [n=1], symptomatic bradycardia [n=6], and catheter-induced spasm [n=1]). Conclusions--Epicardial and microvascular spasm are frequently found in white patients with unobstructed coronary arteries. Epicardial spasm is most often diffuse and located in the distal coronary segments. The intracoronary acetylcholine provocation test is a safe technique to assess coronary vasomotor function. [ABSTRACT FROM AUTHOR]

Background--We reported that phospholipase C (PLC)-&dgr;1 activity was enhanced 3-fold in patients with coronary spastic angina. We detected variant PLC-&dgr;1 with replacement of arginine 257 by histidine (R257H) showing increased enzymatic activity. We tested the hypothesis that increased PLC-&dgr;1 activity causes enhanced coronary vasomotility. Methods and Results--We generated transgenic (TG) mice with human R257H variant PLC-&dgr;1 in vascular smooth muscle cells. PLC enzymatic activity in the coronary artery was increased by 2.57 and 1.89 times, respectively, in homozygous and heterozygous TG compared with wild-type (WT) mice. ST elevation after ergometrine occurred in 17 of 18 homozygous TG, 6 of 20 heterozygous TG, and 3 of 22 WT mice (P<0.01, homozygous TG versus WT; P<0.05, homozygous TG versus heterozygous TG; P=NS, heterozygous TG versus WT). ST elevation was associated with bradyarrhythmias in homozygous TG mice. Focal coronary artery narrowing was documented with the microvascular filling technique in 3 of 5 homozygous TG mice after ergometrine but not in any of 7 WT mice (P<0.05). In the isolated Langendorff hearts, coronary perfusion pressure was increased after ergometrine in homozygous TG mice (P<0.01) but not in heterozygous TG or WT mice. Coronary perfusion pressure increase after prostaglandin F2&agr; was similar among homozygous TG, heterozygous TG, and WT mice. Cultured rat aortic smooth muscle cells transfected with variant PLC-&dgr;1 showed a higher PLC activity than those with WT PLC-&dgr;1 (P<0.05) and furthermore showed greater intracellular Ca2+ response to acetylcholine in variant than in WT PLC-&dgr;1 (P<0.05). Conclusions--Increased PLC-&dgr;1 activity enhances coronary vasomotility such as that seen in patients with coronary spastic angina. [ABSTRACT FROM AUTHOR]

We appreciate the interest of Consuegra-Sánchez and colleagues in the MAGSTEMI trial (Magnesium-Based Resorbable Scaffold vs Permanent Metallic Sirolimus-Eluting Stent in Patients With ST-Segment Elevation Myocardial Infarction).[1] Restoration of vasomotion was a putative advantage of bioresorbable scaffold (BRS) over drug-eluting stent. However, endothelial dysfunction was also observed in coronary segments distal from the target sites both in the magnesium-based BRS arm and in the permanent stent group, indicating a systemic nature of this abnormal reaction. [Extracted from the article]

Letter by Consuegra-Sánchez et al Regarding Article, "Magnesium-Based Resorbable Scaffold Versus Permanent Metallic Sirolimus-Eluting Stent in Patients With ST-Segment Elevation Myocardial Infarction: The MAGSTEMI Randomized Clinical Trial" We read with interest the article by Sabaté et al,[1] which showed that in patients with ST-segment-elevation myocardial infarction, the use of magnesium-based resorbable scaffold stents (MgBRS) versus permanent metallic sirolimus-eluting stents (the MAGSTEMI randomized clinical trial [Magnesium-based Bioresorbable Scaffold in ST Segment Elevation Myocardial Infarction]) resulted in improved endothelium-dependent or -independent coronary reactivity, a finding suggestive of arterial wall "healing" (ie, vascular restoration therapy). Patients who received MgBRS treatment showed greater vasodilation in response to nitroglycerine but also greater vasoconstriction in response to acetylcholine compared with the sirolimus-eluting stents group. [Extracted from the article]

The author reflects on coronary vasoconstriction as a cause of angina or chest pain. Topics discussed include several tests to provoke coronary spasm in variant type angina, the causes for coronary spasm, and the safety of the testing procedures especially in diseased vessels. The use of caution in vasomotor function testing especially in high risk patients was also highlighted.

Letter by Tajiri et al Regarding Article, "Myocardial and Systemic Inflammation in Acute Stress-Induced (Takotsubo) Cardiomyopathy" In the study, the authors prospectively evaluated myocardial and systemic inflammation in acute and 5-month convalescent takotsubo cardiomyopathy (TC). Additionally, in the current study,[1] the authors showed that some inflammatory markers were still elevated at the 5-month follow-up of TC patients; however, the baseline (before TC development) inflammatory condition of the patients was not shown. [Extracted from the article]

Endovascular repair is increasingly being adopted as the treatment of choice for many thoracic aortic conditions. The easy-to-handle, low-invasiveness, and inexpensive therapy with AMD3100 that we proposed in the present study can avoid the above-described hurdles to be cleared in clinical trials for cell therapy. Clinical trials of autologous stem/progenitor cell therapy are ongoing, and positive outcomes have emerged, specifically in nonoption patients suffering from severe cardiovascular disease. Our data suggest that AMD3100, an endogenous stem/progenitor cell mobilizer, has the potential to be a simple but promising additional therapy, taking the place of stem/progenitor cell transplantation therapy for ischemic heart diseases. [Extracted from the article]

Introduction: Post cardiopulmonary resuscitation (CPR) ST elevation is usually a sign of an urgent need for cardiac catheterization (CC), especially in the setting of shockable rhythm cardiac arrest. Post CPR ST elevation can be attributed to pericarditis, early repolarization or acute myocardial infarction. CC is mandated in this situation to rule out acute coronary syndrome. Hypothesis: We report a case of post CPR inferior ST elevation that is likely to be related to escalation of vasopressors which lead to generalized coronary vasospasm. There are few cases that report epinephrine-induced ST-elevation myocardial infarction during anaphylactic shock or septoplasty. To our knowledge, this is the first case report of a typical inferior ST elevation in post CPR that was due to vasospasm secondary to vasopressor escalation. Case: A 47 years old male with a history of malignant hypertension and end stage renal disease who presented to the hospital with cardiac arrest (pulseless electrical activity (PEA) and VT/VF). Initial electrocardiogram (EKG) post return of spontaneous circulation did not show acute ischemic changes but on a later repeat, it showed ST elevations in the inferior leads with ST depression in AVR consistent with possible inferior myocardial infarction. The patient was taken emergently to coronary angiogram which demonstrated severe diffuse vasospasm in all three coronary arteries that were completely reversed with intracoronary vasodilator injection. No definite obstructive coronary artery disease was found. The decision was to de-escalate vasopressors doses and follow up EKG demonstrated resolved EKG ischemic changes. Conclusions: Post CPR ST elevation EKG changes can be attributed to vasopressor induced coronary vasospasm without underlying obstructive coronary artery disease. Vasopressor's dose should be adjusted in this setting to avoid inducing myocardial infarction secondary to severe and prolonged coronary vasospasm. [ABSTRACT FROM AUTHOR]

Background: Most acute coronary syndrome (ACS) patients are caused by rupture of preexisting lipid core plaque (LCP). Furthermore, such LCP may be prone to distal embolization which is associated with poor prognosis after percutaneous coronary intervention (PCI). Recently, near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) has emerged as a novel imaging tool for the prediction of LCP. We aimed to assess the comparison of NIRS-IVUS derived LCP composition and reduction during PCI between patients with ACS and stable angina pectoris (sAP). Methods: We studied 85 patients with ACS (n= 25) and sAP (n= 60) undergoing culprit vessel NIRS-IVUS before and after PCI procedure. The ACS group was subdivided into patients with as ST elevation myocardial infarction (STEMI group; n= 10) or unstable AP / non-ST elevation myocardial infarction group (NSTEMI group; n= 15). The parameters measured by NIRS-IVUS at the culprit lesion were compared among the groups. Results: The baseline maximal lipid core burden index (LCBI) score for each of the 4-mm longitudinal segments in the culprit lesion (maxLCBI4mm) was 640.3 ± 184.1, 579.3 ± 225.9, and 360.0 ± 237.1 in STEMI, NSTEMI, and sAP groups (p < 0.001). Similarly, post-procedural maxLCBI4mm was significantly difference among the groups (233.4 ± 183.9, 284.1 ± 142.5, and 128.7 ± 155.3; p = 0.002, respectively). Notably, STEMI group had significantly greater delta-LCBI (defined as maxLCBI4mm at baseline - maxLCBI4mm after PCI) compared with NSTEMI and sAP groups (406.9 ± 231.0 vs. 295.3 ± 201.9 and 231.3 ± 199.5; p = 0.038, respectively), and no reflow/ slow flow phenomenon during PCI was more frequent in STEMI patients (40.0% vs. 13.3% and 1.7%; p < 0.001, respectively). Conclusions: Culprit lesions with STEMI, NSTEMI and sAP display different plaque characteristics assessed by NIRS-IVUS and difference in peri-procedural risk of complications. [ABSTRACT FROM AUTHOR]

Introduction: Patients with gastroesophageal reflux disease (GERD) exhibit GERD-related chest pain as an extra-esophageal symptom that sometimes mimics angina pectoris. We have occasionally experienced some patients with a medical history of GERD, who were suspected with coronary artery disease (CAD). Hypothesis: However, the clinical characteristics of such patients are still unclear. Therefore, this study aimed to investigate the clinical characteristics of such patients. Methods: We enrolled 236 patients (mean age, 67 years; males, 155) who underwent coronary angiography (CAG) for the first time during CAD evaluation. Medical history of each patient was assessed, considering esophageal and stomach diseases such as peptic ulcers (PU) and GERD. Cases with GERD included those with erosive esophagitis and non-erosive reflux disease. If organic coronary stenosis was absent following CAG, spasm provocation test (SPT) was performed to confirm the presence of vasospastic angina (VSA). Organic CAD (o-CAD) was defined as significant (>50%) coronary stenosis. VSA was defined as >90% narrowing of the epicardial coronary arteries, as observed using angiography during SPT with ergotamine maleate or acetylcholine, along with characteristic chest pain and/or ST segment deviation observed using electrocardiography. Patients were divided into three groups based on their CAG results: group I, patients with o-CAD (n = 141); group II, patients with VSA but without organic coronary stenosis (n = 52), and group III, patients without organic coronary stenosis or VSA (n = 43). Results: Group I included more males (p < 0.05). Frequencies of lipid disorder and diabetes mellitus were higher in group I than in other groups (p < 0.05). GERD frequency was significantly higher in group II (21%) than in groups I (3%) and III (7%, p < 0.0001). However, the groups did not differ with regard to the presence of PU. Logistic regression analysis demonstrated that the presence of GERD (odds: 8.3, p < 0.05) was one of the factors associated with the presence of VSA. Conclusions: These findings suggest that patients with medical history of GERD and chest pain have more frequent incidences of VSA and indicate that medical history of GERD may be one of the important factors in differentiating VSA from CAD. [ABSTRACT FROM AUTHOR]

Introduction: Coronary spasm (CS) has been speculated to affect the coronary vasculature; it is also considered to be a cause of acute coronary syndrome. Additionally, the frequency of patients with vasospastic angina (VSA) developing intracoronary erosion and thrombus has been clarified. Hypothesis: To confirm the relationship between CS and intracoronary erosion and thrombus, we assessed the internal aspects of coronary arteries using coronary angioscopy (CAS) in patients with VSA. Methods: The study included 43 patients with VSA who underwent coronary angiography (CAG), spasm provocation test (SPT), and CAS. In all patients, acetylcholine was infused in the left coronary artery and right coronary artery (RCA). Based on SPT results, the vessels were classified into spastic vessels (SVs) and non-spastic vessels (N-SVs). Furthermore, SVs were divided into the following subgroups: 1) vessels with CS occurrence from the proximal to mid-portion and CAS observability within the spastic segments (SV1s) and 2) vessels with distal CS occurrence and CAS observability only within the non-spastic segments (SV2s). In addition, CS was classified into focal and diffuse types according to the length of CS. CAS was performed in the RCA and left anterior descending coronary artery to determine the presence of erosion and thrombus. Results: We identified 31 patients with SV1 and 12 patients with SV2. Among the 31 patients with SV1, erosion and thrombus were detected in 7 (23%) and 8 (26%), respectively, and total intracoronary abnormalities were observed in 12 (39%). Such intracoronary abnormalities tended to be less frequently observed in patients with taking a calcium-channel blocker (CCB) before the STP (18% vs. 50% in patients without taking a CCB, p = 0.0818). Among the 70 vessels observed using CAS, 34 SV1s, 21 SV2s, and 15 N-SVs were identified. Notably, all abnormal findings were observed in SV1 (35%, p < 0.01), and none were observed in SV2 and N-SV. Furthermore, such abnormalities were more frequently observed at the focal spasm segments than at the diffuse spasm segments of the vessels (31% vs. 9%, p < 0.05). Conclusions: Our results suggest that erosion and thrombus are observed in approximately 40% of patients with VSA. Such intracoronary abnormalities may be partly affected by the CS type. [ABSTRACT FROM AUTHOR]