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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible virus with significant global impact, morbidity, and mortality. The SARS-CoV-2 virus may result in widespread organ manifestations including acute respiratory distress syndrome, acute renal failure, thromboembolism, and myocarditis. Virus-induced endothelial injury may cause endothelial activation, increased permeability, inflammation, and immune response and cytokine storm. Endothelial dysfunction is a systemic disorder that is a precursor of atherosclerotic vascular disease that is associated with cardiovascular risk factors and is highly prevalent in patients with atherosclerotic cardiovascular and peripheral disease. Several studies have associated various viral infections including SARS-CoV-2 infection with inflammation, endothelial dysfunction, and subsequent innate immune response and cytokine storm. Noninvasive monitoring of endothelial function and identification of high-risk patients who may require specific therapies may have the potential to improve morbidity and mortality associated with subsequent inflammation, cytokine storm, and multiorgan involvement.

Bacteriophages are generally specific, and a cocktail of phages is needed to combat different bacterial targets. Their production usually requires pathogenic isolation hosts. We identified a novel strain, Escherichia coli ST155, that could serve as a production host for three different polyvalent phages (ϕPh_SE03, ϕPh_SD01, and ϕPh_EC01), thus superseding the use of individual isolation hosts. Upon propagation in E. coli ST155, the phages demonstrated differential intergeneric infectivity against Salmonella enterica, E. coli OP50, Shigella dysenteriae, E. coli MDR, and Acinetobacter baumannii. Phages were characterised based on morphology, latent period, burst size, the efficiency of plating, and restriction enzyme profile. Survival assay on Caenorhabditis elegans, the absence of Shiga toxin, and enterotoxigenic E. coli virulence genes indicated that E. coli ST155 could be non-pathogenic. Lack of antibiotic resistance and absence of functional prophages rendered the host suitable for environmental applications. As a proof-of-concept, phage ϕPh_SE03 was produced in ST155 by employing a unique Bacteriophage Amplification Reactor-Lytics Broadcasting System and was simultaneously disseminated into S. enterica augmented wastewater, which resulted in a 3-log reduction in 24 h. The study establishes the potential of E. coli ST155 as a phage production host thereby minimising the possibility of accidental release of pathogenic hosts into wastewater.

Background and Purpose: XO (xanthine oxidase) is a key enzyme of uric acid metabolism and is thought to contribute to oxidative pathways that promote atherosclerotic plaque progression, yet its role in plaque destabilization is not well elucidated. We hypothesized that XO is expressed in carotid plaque from symptomatic patients in association with cardiovascular risk factors. Methods: Patients were stratified by symptoms, defined as presentation with an ipsilateral cerebral ischemic event. Carotid atherosclerotic plaques were obtained from 44 patients with symptomatic plaque and 44 patients without ischemic cerebral events. Protein expression of XO was evaluated by immunohistochemical staining and the percentage of cells expressing XO and CD68 (macrophage marker) compared between the groups. Biochemical and demographic cardiometabolic risk factors of study participants also were measured. Results: Carotid atherosclerotic plaques from symptomatic patients were associated with significantly higher XO expression versus asymptomatic plaque (median [interquartile range]: 1.24 [2.09] versus 0.16 [0.34]; P P P =0.010, r =−0.30) and directly with circulating uric acid levels ( P r =0.45). The average percentage of macrophages that expressed XO was significantly higher in symptomatic versus asymptomatic plaques (median [interquartile range]: 93.37% [25] versus 46.15% [21], respectively; P Conclusions: XO overexpression in macrophages is associated with increased serum uric acid and low high-density lipoproteins cholesterol levels and may potentially have a mechanistic role in carotid plaque destabilization. The current study supports a potential role for uric acid synthesis pathway as a target for management of carotid atherosclerosis in humans.

Background: Uric acid (UA) concentration within carotid plaque and its association with cerebrovascular events have not been detected or quantified. Systemically, serum UA is a marker of inflammation and risk factor for atherosclerosis. However, its association with carotid plaque instability and stroke pathogenesis remains unclear. In patients undergoing carotid endarterectomy, we aimed to determine whether UA is present differentially in symptomatic versus asymptomatic carotid plaques and whether serum UA is associated with cerebrovascular symptoms (stroke, transient ischemic attack, or amaurosis fugax). Methods: Carotid atherosclerotic plaques were collected during carotid endarterectomy. The presence of UA was assessed using Gomori methenamine silver staining as well as anti-UA immunohistochemical staining and its quantity measured using an enzymatic colorimetric assay. Clinical information was obtained through a retrospective review of data. Results: UA was more commonly detected in symptomatic (n=23) compared with asymptomatic (n=9) carotid plaques by Gomori methenamine silver (20 [86.9%] versus 2 [22.2%]; P =0.001) and anti-UA immunohistochemistry (16 [69.5%] versus 1 [11.1%]; P =0.004). UA concentration was higher in symptomatic rather than asymptomatic plaques (25.1 [9.5] versus 17.9 [3.8] µg/g; P =0.021). Before carotid endarterectomy, serum UA levels were higher in symptomatic (n=341) compared with asymptomatic (n=146) patients (5.9 [interquartile range, 4.6–6.9] mg/dL versus 5.2 [interquartile range, 4.6–6.2] mg/dL; P =0.009). Conclusions: The current study supports a potential role of UA as a potential tissue participant and a systemic biomarker in the pathogenesis of carotid atherosclerosis. UA may provide a mechanistic explanation for plaque instability and subsequent ischemic cerebrovascular events.

Objectives To describe hemodynamic efficacy and clinical outcomes of Impella percutaneous left ventricular assist device (pLVAD) in patients with cardiogenic shock (CS). Background Percutaneous LVADs are increasingly used in CS management. However, device-related outcomes and optimal utilization remain active areas of investigation. Methods All CS patients receiving pLVAD as mechanical circulatory support (MCS) between 2011 and 2017 were identified. Clinical characteristics and outcomes were analyzed. A multivariable logistic regression model was created to predict MCS escalation despite pLVAD. Outcomes were compared between early and late implantation. Results A total of 115 CS patients (mean age 63.6 ± 13.8 years; 69.6% male) receiving pLVAD as MCS were identified, the majority with CS secondary to acute myocardial infarction (AMI; 67.0%). Patients experienced significant cardiac output improvement (median 3.39 L/min to 3.90 L/min, p = .002) and pharmacological support reduction (median vasoactive-inotropic score [VIS] 25.4 to 16.4, p = .049). Placement of extracorporeal membrane oxygenation (ECMO) occurred in 48 (41.7%) of patients. Higher pre-pLVAD VIS was associated with subsequent MCS escalation in the entire cohort and AMI subgroup (OR 1.27 [95% CI 1.02-1.58], p = .034 and OR 1.72 [95% CI 1.04-2.86], p = .035, respectively). Complications were predominantly access site related (bleeding [9.6%], vascular injury [5.2%], and limb ischemia [2.6%]). In-hospital mortality was 57.4%, numerically greater survival was noted with earlier device implantation. Conclusions Treatment with pLVAD for CS improved hemodynamic status but did not uniformly obviate MCS escalation. Mortality in CS remains high, though earlier device placement for appropriately selected patients may be beneficial.

OBJECTIVES We sought to assess in-hospital and long-term outcomes of retrograde compared with antegrade-only percutaneous coronary intervention for chronic total occlusion (CTO PCI). BACKGROUND Procedural and clinical outcomes following retrograde compared with antegrade-only CTO PCI remain unknown. METHODS Using the core-lab adjudicated OPEN-CTO registry, we compared the outcomes of retrograde to antegrade-only CTO PCI. Primary endpoints included were in-hospital major adverse cardiac and cerebrovascular events (MACCE) (all-cause death, stroke, myocardial infarction [MI], emergency cardiac surgery, or clinically significant perforation) and MACCE at 1-year (all-cause death, MI, stroke, target lesion revascularization, or target vessel reocclusion). RESULTS Among 885 single CTO procedures from the OPEN-CTO registry, 454 were retrograde and 431 were antegrade-only. Lesion complexity was higher (J-CTO score: 2.7 vs. 1.9; p

BACKGROUND We aimed to test the hypothesis that peripheral endothelial dysfunction induced by mental stress may predict cardiovascular events after acute coronary syndrome beyond traditional cardiovascular disease risk factors. METHODS This was a prospective study in which 417 patients who had acute coronary syndrome were enrolled in two sites at the US and Qatar. Cardiovascular disease risk factors such as past medical history, blood pressure, heart rate, peripheral endothelial dysfunction, and response to three different mental stress examinations (Stroop Color Word, Arithmetic, and Spiral Omnibus) as assessed by ratio of reactive hyperemia tonometry (EndoPAT) with stress over EndoPAT at rest were obtained at baseline. Major adverse cardiac events were then recorded at 1 year after the index event. RESULTS There were no differences in baseline peripheral endothelial dysfunction or vascular response to mental stress between the US vs. Qatar patients. Women were more likely to experience major adverse cardiac events in the year following acute coronary syndrome (relative risk 2.42, 95% confidence interval 1.53-3.84, P = 0.044), and had a significantly lower mental stress ratio compared to women who did not (1.0 ± 0.17 vs. 1.20 ± 0.17, P = 0.04). In multivariate analyses stratified by sex, baseline peripheral endothelial dysfunction (EndoPAT < 1.7) (χ = 8.0, P = 0.005) and mental stress ratio (χ = 7.7, P = 0.006), were independently predictive of major adverse cardiac events in women, but not men. CONCLUSION The current study demonstrates that in women both baseline endothelial function and vascular function in response to mental stress ratio are predictive of worse cardiovascular disease outcomes 1 year after acute coronary syndrome. The study may suggest an important mechanism for adverse clinical outcomes in women following acute coronary syndrome.

Background: There are limited data describing gender differences in patients undergoing chronic total occlusion (CTO) percutaneous coronary interventions (PCI). Methods: We compared baseline clinical and angiographic characteristics and procedural outcomes between men and women among 9457 CTO PCIs performed at 38 centers between 2012 and 2022. Results: A total of 7687 (81%) men and 1770 (19%) women were treated. Women were older, more likely to have comorbidities such as diabetes, hypertension and peripheral arterial disease, and had higher left ventricular ejection fraction. The most common CTO target vessel was the right coronary artery for both men (53%) and women (52%), although the left anterior descending artery was more frequently the target vessel among women (31% vs. 25%; p < 0.001). The J‐CTO score (2.4 ± 1.3 vs. 2.2 ± 1.2; p < 0.001) as well as the PROGRESS‐CTO score (1.3 ± 1.0 vs. 1.1 ± 1.0; p < 0.001) were higher among men. In female patients, antegrade wiring was more frequently the initial crossing strategy (87.6% vs. 82.4%; p < 0.001) and was more successful in crossing the target lesion (62.7% vs. 54.0%; p < 0.001) compared with men. Interventions in men required longer procedure time and fluoroscopy time, as well as higher air kerma radiation dose and contrast volume when compared to women. Technical (89% vs. 86%; p < 0.001) and procedural (87% vs. 84%; p = 0.003) success rates were higher among women. In‐hospital major adverse cardiovascular events (MACE) were also higher in women (2.9% vs. 1.8%; p < 0.001). Conclusions: Women undergoing CTO PCI had higher technical and procedural success rates, but also higher in‐hospital MACE compared with men.

Women presenting to the cardiac catheterization laboratory with normal coronary arteries without significant atherosclerotic disease is a common presentation. In such patients, it is important to maintain a wide differential and consider alternate diagnoses. We present two cases of women presenting with chest pain found to have severe coronary vasospasm in the setting of recent initiation of phentermine. Phentermine may have vasospastic proprieties which are important to consider when prescribing to patients.

Symptomatic non-obstructive coronary artery disease (NOCAD) is an increasingly recognised entity that is associated with poor cardiovascular outcomes. Nearly half of those undergoing coronary angiography for appropriate indications, such as typical angina, or a positive stress test have no obstructive lesion. There are no guideline recommendations as to how to care properly for these patients. Physiologic assessment of the coronary arteries beyond two-dimensional angiography is not standardised, yet it can provide valuable information in patients presenting with typical angina in the setting of NOCAD. In this consensus document, we detail steps for the interventional cardiologist to evaluate the patient with symptomatic NOCAD in the cardiac catheterisation laboratory, first with the assessment of coronary flow reserve (CFR), and then with delineation of deficiencies in non-endothelium-dependent CFR (CFRne) versus endothelium-dependent CFR (CFRe) using provocative agents such as adenosine and acetylcholine, respectively, followed by the evaluation of smooth muscle function with nitroglycerine (NTG). Once the mechanism behind the anginal symptoms is established, one can identify the appropriate treatment strategies to address the physiologic deficiency that is present. Despite an established safety profile, a comprehensive assessment may be considered for selected patients which requires an understanding of the appropriate invasive evaluation by the practising interventional cardiologist when evaluating not only patients with obstructive CAD but also those with NOCAD.

Chronic total occlusions remain among the most technically challenging lesions to treat percutaneously. Limitations of 2-dimensional angiography may further hinder successful treatment of these lesions. Intrasvascular ultrasound has a key role in percutaneous recanalization for a chronic total occlusion by providing key lesion characteristics, facilitating guidewire crossing, elucidating the intraplaque or extralaque path of the guidewire, optimizing lesion preparation, guiding stenting and identifying suboptimal results. Live visualization of the guidewire during crossing may reduce extraplaque wire tracking. This review describes the practical uses of intravascular imaging for commonly encountered scenarios when treating chronic total occlusions.

Contains fulltext : 220910.pdf (Publisher’s version ) (Closed access) Cardiovascular disease is the leading cause of morbidity and mortality in women. We suggest the need to develop a paradigm that connects sex- and age-specific nontraditional risk factors that serve as a common mechanism ultimately leading to an increased risk of cardiovascular events. Vascular injury with abnormal repair leading to functional, rather than structural, abnormalities can be regarded as accelerated vascular aging. It emerges as a common feature that can trigger the early diagnosis and risk stratification for cardiovascular disease in women. We discuss sex-specific risk factors that can contribute to vascular injury with age, and these might not always be considered by cardiovascular physicians. It is important for the primary physician to be aware of these risk factors to enable more intensified management of this at-risk population. Novel technologies that allow the assessment of vascular function noninvasively can serve as key diagnostic and therapeutic tools with which we can identify such individuals and target therapy to manage this important patient population appropriately and effectively. We hope that this article will stimulate interest in this field and encourage further research in these important areas.

BACKGROUND Cardiac allograft vasculopathy (CAV) is a major complication after heart transplantation (HT). Uric acid (UA) may play a role in CAV due to its role in stimulating T-cell-mediated immunity. Sirolimus is associated with CAV attenuation through a number of mechanisms, including immune-mediated effects. We aimed to determine whether UA is an independent predictor of CAV and whether conversion to sirolimus as primary immunosuppression modulates UA levels. METHODS We retrospectively analyzed a cohort of 224 patients who underwent HT between 2004 and 2015 and had serial coronary intravascular ultrasound (IVUS) studies. Serum UA levels were measured at baseline and last follow-up IVUS in all participants. CAV progression was assessed by measuring the change in plaque volume (ΔPV) and plaque index (ratio of plaque volume to vessel volume [ΔPI]) between last follow-up and baseline IVUS after correction for time of follow-up. RESULTS Patients with high (≥7 mg/dl) compared with low ( 0.50 mm3/mm) (hazard ratio 2.2, 95% confidence interval 1.1 to 4.6; p = 0.037). Sirolimus resulted in decreased UA levels (5.8 ± 1.4 vs 5.2 ± 1.5; p = 0.002) and patients converted to sirolimus and had low UA levels had the least CAV progression (p < 0.001). After adjustment for potential confounders, change in UA level was also an independent predictor of CAV progression. CONCLUSIONS UA is an independent predictor of CAV after HT. Sirolimus is associated with decreased UA levels and may explain one of the mechanisms by which sirolimus attenuates CAV progression.

Background Lipoprotein-associated phospholipase A2 (Lp-PLA2) may play a role in plaque progression and vulnerability. We aimed to define plaque characteristics on multimodality intravascular imaging in patients with coronary endothelial dysfunction in response to long-term inhibition of Lp-PLA2 by darapladib. Patients and methods This is a double-blinded, randomized study screening 70 patients, and enrolling 54 patients with suspected ischemia, without obstructive disease on angiography and with coronary endothelial dysfunction by invasive assessment. Patients were randomized to receive darapladib or placebo for 6 months. Forty patients underwent multimodality intravascular imaging at baseline and after 6 months of therapy. Several parameters of plaque vulnerability were measured, including maximum value of lipid core burden index for any of the 4-mm segment (maxLCBI4 mm) by near-infrared spectroscopy. Microchannels and macrophages were assessed using optical coherence tomography and necrotic core volume by virtual histology intravascular ultrasound. Results There was no significant difference in maxLCBI4 mm [64.56 (7.74, 128.56) vs. 22.43 (0, 75.63), P=0.522] or in macrophage images angle [-9.5° (-25.53°, 12.68°) vs. -16.7° (-28.6°, -4.8°), P=0.489] between groups. There was a trend toward shorter microchannel length in the darapladib arm [0, (-4.4, 0.2) mm vs. 0.8 (-0.15, 1.9) mm, P=0.08]. Percentage of necrotic core volume was not significantly different. Conclusion Thus, long-term inhibition of endogenous Lp-PLA2 activity with darapladib was not associated with a change in plaque progression and vulnerability indices after 6 months of therapy, and the endogenous Lp-PLA2 pathway may not play a direct role in the progression of early atherosclerosis in humans.

Endothelial function is a marker for cardiovascular risk. Thus, abnormal endothelial function may be associated with adverse 1-year outcome in patients presenting to the emergency department chest pain unit (CPU).Following endothelial function testing, using EndoPAT 2000 in 300 consecutive subjects with chest pain and no history of coronary artery disease (CAD) presenting to CPU, patients underwent coronary computerized tomographic angiography (CCTA) or single-photon emission computed tomography according to availability.Mean 10-year Framingham risk score (FRS) was 6.6±5.9%, median reactive hyperemia index (RHI) as a measure of endothelial function 2.08 and mean was 2.0±0.4. During a 1-year follow-up, the 20 (6.6%) patients who developed major adverse cardiovascular end-points (MACE), including all-cause mortality, non-fatal myocardial infarction, hospitalization for heart failure or angina pectoris, stroke, coronary artery bypass grafting and percutaneous coronary interventions, had higher 10-year FRS (10.5±8.2% vs 6.3±5.7%; p0.001), lower baseline RHI (1.43±0.41 vs 2.10±0.44; p0.001) and a greater extent of coronary atherosclerosis lesions (70% vs 3.9%, p0.001) in the CPU CCTA, compared to those without MACE. RHI≤the median was associated with higher 1-year MACE (13% vs 0.7%, p0.001) compared to RHIthe median. Multivariate analysis demonstrated that RHI≤the median is an independent predictor of coronary atherosclerosis lesions in the CPU CCTA (OR 5.98, 95% CI 03.29-10.88; p0.001) and 1-year MACE (OR 15.207, 95% CI 2.00-115.33; p0.01).Our findings suggest that non-invasive endothelial function testing may have clinical utility in triaging patients in the CPU and in predicting 1-year MACE.

Uric acid is a risk factor for coronary artery disease in postmenopausal women, but the association with inflammation and coronary endothelial dysfunction (CED) is not well defined. The aim of this study was to determine the relationship of serum uric acid (SUA), inflammatory markers, and CED. In this prospective cohort study, SUA, high-sensitivity C-reactive protein levels, and neutrophil count were measured in 229 postmenopausal women who underwent diagnostic catheterization, were found to have no obstructive coronary artery disease, and underwent coronary microvascular function testing, to measure coronary blood flow response to intracoronary acetylcholine. The average age was 58 years (interquartile range, 52–66 years). Hypertension was present in 48%, type 2 diabetes mellitus in 5.6%, and hyperlipidemia in 61.8%. CED was diagnosed in 59% of postmenopausal women. Mean uric acid level was 4.7±1.3 mg/dL. Postmenopausal women with CED had significantly higher SUA compared with patients without CED (4.9±1.3 versus 4.4±1.3 mg/dL; P =0.02). There was a significant correlation between SUA and percent change in coronary blood flow to acetylcholine ( P =0.009), and this correlation persisted in multivariable analysis. SUA levels were significantly associated with increased neutrophil count ( P =0.02) and high-sensitivity C-reactive protein levels ( P =0.006) among patients with CED, but not among those without CED. SUA is associated with CED in postmenopausal women and may be related to inflammation. These findings link SUA levels to early coronary atherosclerosis in postmenopausal women.

BACKGROUND Surgical revascularization is associated with improved ventricular function and clinical outcomes among patients with ischemic cardiomyopathy. There are less extensive data on changes in ventricular function among patients with ischemic cardiomyopathy undergoing percutaneous coronary intervention (PCI). Accordingly, we sought to assess the extent and predictors of change in left ventricular ejection fraction (ΔLVEF) among patients undergoing hemodynamically-supported PCI. METHODS We assessed ΔLVEF following hemodynamically-supported PCI (with Impella or intra-aortic balloon counterpulsation) among patients enrolled in the PROTECT II trial and cVAD registry. The ΔLVEF was compared among patients with paired echocardiography at baseline and at least 30 days of follow-up. Independent correlates of ΔLVEF (modeled continuously and with an absolute ΔLVEF≥5%) were assessed using multivariable models. RESULTS Among the 689 patients with paired echocardiographic data included in the analysis, the mean LVEF improved from 24.8 ± 9.9% to 31.4 ± 13.3% after PCI, for a net increase of 6.5 ± 10.8% (p

CD34+ cells are haematopoietic stem cells used therapeutically in patients undergoing radiation or chemotherapy due to their regenerative potential and ability to restore the haematopoietic system. In animal models, CD34+ cells have been associated with therapeutic angiogenesis in response to ischaemia. Several trials have shown the potential safety and efficacy of CD34+ cell delivery in various cardiovascular diseases. Moreover, Phase III trials have now begun to explore the potential role of CD34+ cells in treatment of both myocardial and peripheral ischaemia. CD34+ cells have been shown to be safe and well-tolerated in the acute myocardial infarction (AMI), heart failure, and angina models. Several studies have suggested potential benefit of CD34+ cell therapy in patients with coronary microvascular disease as well. In this review, we will discuss the therapeutic potential of CD34+ cells, and describe the pertinent trials that have used autologous CD34+ cells in no-options refractory angina, AMI, and heart failure. Lastly, we will review the potential utility of autologous CD34+ cells in coronary endothelial and microvascular dysfunction.

Background Women with non‐obstructive coronary artery disease have increased cardiovascular morbidity. The role of risk factors in this population has yet to be established. We aimed to study the predictive effect of triglycerides and the triglyceride/high‐density lipoprotein ratio on major adverse cardiovascular events (MACE) in patients with non‐obstructive coronary artery disease, and to explore the role of lipid lowering therapy in modifying this risk. Methods and Results This is a prospective cohort study enrolling patients with anginal symptoms referred to the cardiac catheterization laboratory for suspected ischemia, who were subsequently diagnosed with non‐obstructive coronary artery disease, defined as no stenosis >20% on angiography. All patients had baseline laboratory testing and were followed for 7.8±4.3 years for the development of major adverse cardiovascular events. We performed Cox proportional hazard testing to determine the effect of triglycerides on risk of major adverse cardiovascular events among men and women by baseline statin use. A total of 462 patients were included. Median age was 53 (Q1, Q3: 45, 62) years. In a Cox proportional hazard model stratified by statin use adjusting for confounders, among those not on baseline statins, triglycerides were independently predictive of major adverse cardiovascular events in women (per 50 mg/dL risk ratio: hazard ratio 1.25 [95% CI : 1.06, 1.47]; P =0.01). This was not true among men. The interaction between triglycerides and sex, and triglycerides and statin was statistically significant. Conclusions Triglyceride levels may play a key role in predicting cardiovascular‐specific risk in women, and statin use may be protective. Further investigation is necessary to better delineate the role of statin use in preventing cardiovascular risk.

The decision requires balancing the risk of thrombosis against the risk of bleeding. A cardiologist can help.

Background: Whether revascularization improves prognosis in stable ischemic heart disease is controversial. Methods: Individual patient-level data from 19 prospective, randomized stent trials were pooled. Rates of 5-year major adverse cardiovascular events (MACE; a composite of cardiac death, myocardial infarction, or ischemia-driven target lesion revascularization) were assessed and compared after percutaneous coronary intervention with bare-metal stents (BMS) and first-generation and second-generation drug-eluting stents (DES1 and DES2, respectively). Poisson multivariable regression analysis was performed to identify predictors of adverse events. Results: Among 10 987 patients treated with percutaneous coronary intervention for stable ischemic heart disease, 1550, 2776, and 6661 received BMS, DES1, and DES2, respectively. The 5-year rates of MACE progressively declined with evolution in stent technology (BMS: 24.1% versus DES1: 17.9% versus DES2: 13.4%, P P =0.02). Conclusions: Patients with stable ischemic heart disease remain at substantial risk for long-term MACE after revascularization with percutaneous coronary intervention, even with contemporary DES. New approaches to reduce the ongoing risk of MACE beyond 1 year after stent implantation are necessary.

Both elevated serum uric acid (SUA) and peripheral endothelial dysfunction (PED) are associated independently with cardiovascular disease (CVD). However, the association between SUA and PED is yet to be established. We hypothesized that high normal range of SUA is associated with PED.We performed a retrospective cross-sectional analysis of patients who were referred to Mayo Clinic between 2006 and 2014 for routine cardiovascular evaluation and who underwent evaluation of Reactive Hyperemia Peripheral Arterial Tonometry (index2 consistent with PED). A high UA was defined as ≥5 mg/dL, in keeping with previous studies evaluating the link between SUA and CVD outcomes.One hundred forty patients were included (mean age 50.7 ± 12.9 years, 86 (61.4%) female). Twenty four patients (17.1%) had pre-existing CVD (8 (9.3%) in females). Thirty patients (21.6%) had a Framingham score 10% (8 (9.4%) in females). Fifty eight (41.4%) had PED and 77 (55.0%) had an elevated SUA. SUA levels were higher in patients with PED compared to those without (5.5 ± 1.4 vs 4.8 ± 1.2 mg/dL; p = 0.004). In an univariate analysis, elevated SUA levels were associated with PED (Odds Ratio (OR): 2.7; 95% confidence interval [CI] 1.33-5.48; p = 0.005). In a multivariate analysis adjusting for age, sex, presence of obstructive CVD and Framingham score10, elevated SUA levels were associated with PED (OR 2.45; 95% CI 1.08-5.52; p = 0.031). After stratifying by sex, this association persisted in females only.High normal SUA levels are associated with PED in women who are otherwise at low risk for CVD. Thus, SUA is a promising circulating biomarker that could be used to assist in risk stratification in female patients with chest pain and/or those undergoing evaluation of CVD risk.

Coronary endothelial dysfunction (CED) is associated with recurrent ischemia. The role of high-sensitivity cardiac troponin I (hscTnI) levels in patients with CED has not been established.Patients with suspected ischemia, who underwent clinically indicated coronary angiography and were found to have non-obstructive coronary artery disease, were included in the study. CED was defined as ≤50% increase in coronary blood flow from baseline and/or a decrease in epicardial coronary artery diameter20% in response to maximal dosages of acetylcholine. HscTnI was measured at the time of the procedure using the Architect hscTnI assay (Abbott).Of 299 patients, 60 had normal endothelial function and 239 patients had abnormal endothelial function. The median age of the population was 52 years (interquartile range [IQR], 45-60 years). Patients with abnormal endothelial function had significantly higher log hscTnI values when compared to patients with normal endothelial function (0.9 ng/L [IQR, 0.7-1.4 ng/L] vs 0.7 ng/L [IQR, 0.7-1.1 ng/L]; P=.04). An hscTnI value12.5 ng/L was 100% specific for the presence of endothelial dysfunction (100% positive predictive value). There were 39 major adverse cardiovascular events during follow-up. In patients with normal endothelial function, hscTnI levels were significantly higher in patients who developed major adverse cardiac events when compared to patients who did not (1.35 ng/L [IQR, 1.1-2.1 ng/L] vs 0.7 ng/L [IQR, 0.7-1.1 ng/L]; P=.02).Our findings suggest that endothelial dysfunction may be associated with higher baseline hscTnI levels, suggesting increased myocardial injury in this population of patients. Additional studies are necessary to further define the role of hscTnI in risk stratification in this population.

The patient’s many problems include ventricular tachycardia, requiring an implanted cardioverter-defi brillator and amiodarone.

Work‐related stress is an example of a psychosocial risk factor that has become of interest in today's ever‐demanding, fast‐paced, and globalized society, although its link to adverse health and in particular coronary heart disease (CHD) is incompletely understood. In this review, we will

Medically refractory angina remains a significant health concern despite major advances in revascularization techniques and emerging medical therapies. We aimed to determine the safety and efficacy of extracorporeal shockwave myocardial therapy (ESMT) in managing angina pectoris.A single-arm multicenter prospective study was designed aiming to determine the safety and efficacy of ESMT. Patients of functional Canadian Cardiovascular Society class II-IV, despite stable and optimal medical management, with documented myocardial segments with reversible ischemia and/or hibernation on the basis of echocardiography/single-photon emission computerized tomography (SPECT) were enrolled from 2010 to 2012. A total of 111 patients were enrolled, 33 from Indonesia, 21 from Malaysia, and 57 from Philippines. Patients underwent nine cycles of ESMT over 9 weeks. Patients were followed up for 3-6 months after ESMT treatment. During follow-up, patients were subjected to clinical evaluation, the Seattle Angina Questionnaire, assessment of nitrate intake, the 6-min walk test, echocardiography, and SPECT.The mean age of the population was 62.9±10.9 years. The summed difference score on pharmacologically induced stress SPECT improved from 9.53±17.87 at baseline to 7.77±11.83 at follow-up (P=0.0086). Improvement in the total Seattle Angina Questionnaire score was seen in 83% of patients (P0.0001). Sublingual nitroglycerin use significantly decreased (1.14±1.01 tablets per week at baseline to 0.52±0.68 tablets per week at follow-up; P=0.0215). There were no changes in left ventricular function on echocardiography (0.33±9.97, P=0.93). The Canadian Cardiovascular Society score improved in 74.1% of patients.This multicenter prospective trial demonstrated that ESMT is both a safe and an efficacious means of managing medically refractory angina.

Lipoprotein-associated phospholipase AFifty-four patients with CED were enrolled in a double-blinded randomized placebo-controlled trial, and were randomized to receive oral darapladib, 160mg daily, or placebo. Coronary angiography and invasive coronary endothelial function assessment were performed at baseline and post-6months of treatment. Primary endpoints were change in coronary artery diameter and coronary blood flow in response to acetylcholine. Additionally, Lp-PLALp-PLANCT01067339.

BACKGROUND: Erectile dysfunction (ED) is associated with an increased risk for cardiovascular disease, stroke, and all-cause mortality, independent of conventional cardiovascular risk factors. Coronary endothelial dysfunction is independently associated with ED in men with early coronary atherosclerosis. We aimed to investigate whether coronary microvascular dysfunction predicts development of ED in patients presenting with coronary atherosclerosis without critical stenoses. PATIENTS AND METHODS: Coronary microvascular function was evaluated in 130 men with coronary atherosclerosis without critical stenoses by administration of intracoronary acetylcholine at the time of diagnostic study. After a mean follow-up of 8.4 years, patients were assessed for the development of ED by administration of a questionnaire. RESULTS: In all, 68 (50%) men had microvascular endothelial dysfunction at baseline; 35 (51%) men with microvascular endothelial dysfunction developed ED on follow-up compared with 19 (31%) men without microvascular endothelial dysfunction. Men who developed ED had a lower coronary blood flow response (% [INCREMENT]CBF) compared with men who did not develop ED, with mean+/-SD of 25.4+/-71.3 versus 81.7+/-120 (P=0.003). In univariate analysis, microvascular endothelial dysfunction was a predictor for the development of ED, with relative risk of 2.4 (1.2-4.9) (P=0.016). In multivariate logistic regression adjusting for traditional cardiovascular risk factors (age, hypertension, hyperlipidemia, diabetes, vascular disease, and family history of coronary artery disease), only microvascular endothelial dysfunction (P=0.027) and age (P=0.044) remained significant predictors of development of ED. CONCLUSION: Coronary microvascular dysfunction is a predictor of the development of ED in men with coronary atherosclerosis without critical stenoses. This study underscores the systemic involvement of the endothelial function in vascular disease.

Background Coronary endothelial dysfunction (CED) is an early stage of atherosclerosis and is associated with adverse cardiovascular events. Inflammation may play a role in the development of endothelial dysfunction. To date no study has evaluated the relationship between C-reactive protein and CED. We aimed to determine if C-reactive protein is associated with CED. Methods In 1016 patients (mean age 50.7±12.3years, 34% male) presenting to the catheterization laboratory with chest pain and non-obstructive coronary artery disease, coronary vasoreactivity was assessed by measuring the percent change in coronary blood flow (% Δ CBF) and coronary artery diameter (% Δ CAD) in response to intracoronary acetylcholine. Plasma high sensitivity C-reactive protein (hs-CRP) was measured and patients were divided into 2 groups: hs-CRP≤3.0mg/L (low-intermediate cardiovascular risk n=169) and 3mg/L Results Patients with a high risk hs-CRP had a significantly lower % Δ CBF and % Δ CAD in response to acetylcholine vs. low risk hs-CRP (43.8±6.1 vs. 65.8±4.5, P =.004 and −17.2±1.5 vs. −13.1±0.8, P =.02 respectively). Low risk hs-CRP was associated with significantly higher % Δ CBF and % Δ CAD vs. high risk hs-CRP (27.1±11.0, P =.01 and 4.5±1.9, P =.02 respectively). CED was associated with significantly higher hs-CRP levels and high risk hs-CRP was independently associated with abnormal coronary vasoreactivity, OR 1.82 (95% CI 1.25–2.69). Conclusions Hs-CRP is independently associated with and a strong predictor of abnormal coronary vasoreactivity inpatients with non-obstructive coronary artery disease.

Background Endothelial dysfunction is an early stage of atherosclerosis. Single‐nucleotide polymorphisms ( SNP s) have been associated with vascular dysfunction, cardiac events, and coronary artery remodeling. We aimed to detect SNP s associated with endothelial dysfunction and determine whether these associations are sex specific. Methods and Results Six hundred forty‐three subjects without significant obstructive coronary artery disease underwent invasive coronary endothelial function assessment. We collected data from 1536 SNP s that had previously been associated with vasoreactivity, angiogenesis, inflammation, artery calcification, atherosclerotic risk factors, insulin resistance, hormone levels, blood coagulability, or with coronary heart disease. Coronary vascular reactivity was assessed by the percent change in coronary artery diameter ≤ −20% after an intracoronary bolus injection of acetylcholine on invasive coronary physiology study. SNP s significantly associated with coronary epicardial endothelial dysfunction were ADORA 1 , KCNQ 1 , and DNAJC 4 in the whole cohort, LPA , MYBPH , ADORA 3 , and PON 1 in women and KIF 6 and NFKB 1 in men ( P Conclusions We have identified several significant SNP s that are associated with an increased risk of coronary endothelial dysfunction. These associations appear to be sex specific and may explain gender‐related differences in development of atherosclerosis.

We aimed to assess the utility of changes in systolic and diastolic function by isoproterenol challenge in predicting symptom resolution post-myectomy in selected patients with hypertrophic cardiomyopathy (HCM) and labile obstruction.In a subset of symptomatic HCM patients without resting/provocable obstruction on noninvasive assessment, isoproterenol challenge during hemodynamic catheterization may elicit labile left ventricular outflow tract (LVOT) obstruction, and demonstrate the effect of obstruction on diastolic function. These changes may determine whether patients achieve complete symptom resolution post-myectomy.Between February 2003 and April 2009, 18 symptomatic HCM patients without LVOT obstruction on noninvasive testing underwent isoproterenol provocation and septal myectomy due to presence of provocable gradient and were followed for 4 (IQR 3-7) years.Thirteen (72.2%) had complete symptom resolution, while 5 (27.8%) had improved, but persistent symptoms. Those with provoked gradient100 mm Hg or increase in left atrial pressure (LAP) with isoproterenol had symptom resolution.Symptomatic HCM patients without LVOT gradient on noninvasive testing may demonstrate labile obstruction with isoproterenol. With isoproterenol, patients with high LVOT gradient or increase in LAP concomitant with an increase in gradient achieved complete symptom resolution post-myectomy. Thus, improved diastolic filling as well as outflow gradient production in patients with HCM may predict symptom response to myectomy. © 2016 Wiley Periodicals, Inc.

We have shown previously that inhibition of the p38 mitogen-activated protein kinase (p38MAPK) directs the differentiation of human embryonic stem cell (hESC)-derived cardiomyocytes (hCM). We investigated the therapeutic benefits of intramyocardial injection of hCM differentiated from hESC by p38MAPK inhibition using closed-chest ultrasound-guided injection at a clinically relevant time post-myocardial infarction (MI) in a mouse model.MI was induced in mice and the animals treated at day 3 with: (a) hCM, (b) human fetal fibroblasts (hFF) as cell control, or (c) medium control (n = 10 animals/group). Left ventricular ejection fraction (LVEF) was evaluated post-MI prior to therapy, and at days 28 and 60 post-cell therapy. Hearts were analyzed at day 60 for infarct size, angiogenesis, cell fate and teratoma formation.LVEF was improved in the hCM-treated animals compared with both hFF and medium control-treated animals at day 28 (39.03 ± 1.79% versus 27.89 ± 1.27%, P0.05, versus 32.90 ± 1.46%, P0.05, respectively), with sustained benefit until day 60. hCM therapy resulted in significantly smaller scar size, increased capillary bed area, increased number of arterioles, less native cardiomyocyte (CM) apoptosis, and increased CM proliferation compared with the other two groups. These benefits were achieved despite a very low retention rate of the injected cells at day 60, as assessed by immunohistochemistry and quantitative real-time polymerase chain reaction (qPCR). Therapy with hCM did not result in intramyocardial teratoma formation at day 60.This study demonstrates that hCM derived from p38MAPK-treated hESC have encouraging therapeutic potential.

The aim of this study was to define the prevalence of the metabolic syndrome and its component risk factors among individuals of South Asian origin living in the United States.We analyzed baseline data from 1,445 participants enrolled in a cohort study investigating risk factors for cardiovascular disease in South Asians. We defined the metabolic syndrome using the International Diabetes Federation criteria for waist circumference (90 cm for men;80 cm, women), triglycerides (150 mg/dL), high-density lipoprotein cholesterol (HDL-C) (40 mg/dL (men),mg/dL (women)), blood pressure (135/80 mmHg), and fasting glucose (100 mg/dL).The mean age was 43 +/-10 years, and 30% of participants were women. The prevalence of metabolic syndrome was 27% (31% men vs. 17% women, P0.05). Fifty-nine percent of the cohort had high waist circumference (58% men vs. 62% women, P = not significant [N.S.]), 47% had low HDL-C [46% men vs. 48% women (NS)], 19% had elevated triglycerides (23% men vs. 8% women, P0.05), 14% had hypertension (16% men vs. 9% women, P0.05), and 13% had elevated fasting glucose (18% men vs. 11% women, P0.05). The most common metabolic syndrome phenotype is low HDL-C with elevated triglycerides.Although the prevalence of the metabolic syndrome is lower than previous reports of South Asians, the prevalence is still unacceptably high despite the presence of protective demographic factors.

The optimal preoperative cardiac evaluation strategy for patients with end-stage liver disease (ESLD) undergoing liver transplantation remains unknown. Patients are frequently referred for cardiac catheterization, but the effects of coronary artery disease (CAD) on posttransplant mortality are also unknown. We sought to determine the contribution of CAD and multivessel CAD in particular to posttransplant mortality. We performed a retrospective study of ESLD patients undergoing cardiac catheterization before liver transplant surgery between August 1, 2004 and August 1, 2007 to determine the effects of CAD on outcomes after transplantation. Among 83 patients who underwent left heart catheterization, 47 underwent liver transplantation during the follow-up period. Twenty-one of all ESLD patients who underwent liver transplantation (45%) had CAD. Fifteen of the transplant patients with CAD (71%) had multivessel disease. Among transplant patients, the presence of multivessel CAD (versus no CAD) was predictive of mortality (27% versus 4%, P = 0.046), increased length of stay (22 versus 15 days, P = 0.050), and postoperative pressor requirements (27% versus 4%, P = 0.029). Interestingly, neither the presence of any CAD nor the severity of stenosis in any single coronary artery predicted mortality. Furthermore, none of the traditional clinical predictors (age, gender, diabetes, creatinine, ejection fraction, and Model for End-Stage Liver Disease score) were predictive of mortality among transplant recipients. In conclusion, multivessel CAD is associated with higher mortality after liver transplantation when it is documented angiographically before transplantation, even in the absence of severe coronary artery stenosis. This study provides preliminary evidence showing that there may be significant prognostic value in coronary angiography as a part of the pretransplant workup. Liver Transpl 16:1242-1248, 2010. © 2010 AASLD.

Objectives In patients with coronary artery disease (CAD) medically managed according to currently accepted guidelines, we tested whether a 1-month dietary intervention with flavanol-containing cocoa leads to an improvement of endothelial dysfunction and whether this is associated with an enhanced number and function of circulating angiogenic cells (CACs). Background Dietary flavanols can improve endothelial dysfunction. The CACs, also termed endothelial progenitor cells, are critical for vascular repair and maintenance of endothelial function. Methods In a randomized, controlled, double-masked, cross-over trial, 16 CAD patients (64 ± 3 years of age) received a dietary high-flavanol intervention (HiFI [375 mg]) and a macronutrient- and micronutrient-matched low-flavanol intervention (LoFI [9 mg]) twice daily in random order over 30 days. Results Endothelium-dependent vasomotor function, as measured by flow-mediated vasodilation of the brachial artery, improved by 47% in the HiFI period compared with the LoFI period. After HiFI, the number of CD34+/KDR+-CACs, as measured by flow cytometry, increased 2.2-fold as compared with after LoFI. The CAC functions, as measured by the capacity to survive, differentiate, proliferate, and to migrate were not different between the groups. The HiFI led to a decrease in systolic blood pressure (mean change over LoFI: −4.2 ± 2.7 mm Hg), and increase in plasma nitrite level (mean change over LoFI: 74 ± 32 nM). Applying a mixed-effects linear regression model, the results demonstrated a significant increase in flow-mediated vasodilation and a decrease in systolic blood pressure with increasing levels of CD34+/KDR+-CACs. Conclusions Sustained improvements in endothelial dysfunction by regular dietary intake of flavanols are associated with mobilization of functional CACs. (Effect of Cocoa Flavanols on Vascular Function in Optimally Treated Coronary Artery Disease Patients: Interaction Between Endothelial Progenitor Cells, Reactivity of Micro- and Macrocirculation; NCT00553774).

Although recent case reports and one small single-year observational study report a substantially increased rate of perforation with the St. Jude Riata series defibrillator lead, these results have not been externally validated. From 2004 to 2007, 593 implantable cardioverter-defibrillator (ICD) implants were performed by six faculty and 13 fellows at four University of California, San Francisco, CA, USA and affiliate hospitals. An electronic medical records system was systematically searched to identify clinically significant cases of ICD lead dislodgment or perforation. Of 307 (56%) St. Jude leads (all Riata series 6.3- and 7.3-French leads), 188 (29%) Medtronic leads (including 99 Sprint Fidelis 6.6 French leads), and 98 (15%) Guidant/Boston Scientific leads, there were three perforations in 593 cases (0.51%). One perforation occurred with a Medtronic Sprint Fidelis 6949 lead (0.53%), and two with a St. Jude Riata 1581 lead (0.65%). There were no statistically significant differences in perforation or dislodgement rates between manufacturers or lead models (p = NS for all). In both cases of perforation with the St. Jude Riata leads, the lead tip perforated through the pericardium into the pleural space. In our 4-year series of ICD implants, perforation and dislodgement rates were low, similar across all lead makes and models, and well below published and accepted complication rates. Our findings contradict previously-reported higher rates of perforation with the Riata lead. Registry and product performance reports should also classify complications by severity and outcome to provide a more complete assessment of product safety.

Background Normal endothelial function is central to physiologic anticoagulation mechanisms. Endothelial dysfunction may predispose to venous thromboembolism (VTE). We aimed to investigate if coronary endothelial dysfunction (CED) predicts development of VTE in patients presenting with coronary atherosclerosis without critical stenoses. Methods Coronary microvascular function was evaluated in 502 patients with coronary atherosclerosis without critical stenoses by administration of intracoronary acetylcholine at the time of diagnostic study. After a median follow-up of 6.3 years, patients were assessed for the development of VTE by administration of a questionnaire. Coronary microvascular endothelial dysfunction was defined as ≤ 50% increase in coronary blood flow from baseline in response to maximal dose of acetylcholine. Results The median age was 53 years (IQR: 45, 62) 68% were female and CED occurred in 279 (56%) patients. Hypertension (40.8%), diabetes (8.4%), and hyperlipidemia (58.3%) were common risk factors. There were no differences in baseline characteristics between those with and without CED. There were 9 VTE events (6 unprovoked) among patients with CED compared to no events in the control group (P = 0.01). Discussion CED was associated with the development of VTE. Endothelial injury by causing disruption of vascular hemostasis may play a role in predisposing patients to VTE.

Autoimmune rheumatic diseases can affect the cardiac vasculature, valves, myocardium, pericardium, and conduction system, leading to a plethora of cardiovascular manifestations that can remain clinically silent or lead to substantial cardiovascular morbidity and mortality. Although the high risk of cardiovascular pathology in patients with autoimmune inflammatory rheumatological diseases is not owing to atherosclerosis alone, this particular condition contributes substantially to cardiovascular morbidity and mortality-the degree of coronary atherosclerosis observed in patients with rheumatic diseases can be as accelerated, diffuse, and extensive as in patients with diabetes mellitus. The high risk of atherosclerosis is not solely attributable to traditional cardiovascular risk factors: dysfunctional immune responses, a hallmark of patients with rheumatic disorders, are thought to cause chronic tissue-destructive inflammation. Prompt recognition of cardiovascular abnormalities is needed for timely and appropriate management, and aggressive control of traditional risk factors remains imperative in patients with rheumatic diseases. Moreover, therapies directed towards inflammatory process are crucial to reduce cardiovascular disease morbidity and mortality. In this Review, we examine the multiple cardiovascular manifestations in patients with rheumatological disorders, their underlying pathophysiology, and available management strategies, with particular emphasis on the vascular aspects of the emerging field of 'cardiorheumatology'.

Aims Metabolic syndrome has been associated with increased risk of cardiovascular disease. We aimed to determine the effectiveness of a community-based screening program in identifying cardiovascular risk factors in healthy young South Asian population. Materials and Methods Between 2006 and 2011, 3314 patients of all ages were recruited as a part of a prospective cohort study investigating cardiovascular risk in South Asians. We analyzed 1537 patients between the ages of 18 and 40. Demographic and baseline characteristics including baseline laboratory markers and blood pressures were obtained at initial visit. Results The total cohort of 1537 patients was 66.5% male, and the mean age was 35 ± 5 years. Among participants who denied a history of hypercholesterolemia, 62% had elevated LDL-C (>100 mg/dL), and 8% had markedly elevated LDL-C (>160 mg/dL). Overall, diabetes was present in 4%, hypertension was present in 12% and hyperlipidemia was present in 46%. Low HDL-C (50% of men, 52% of women) and elevated triglycerides (44% of men, 18% of women) were the most prevalent components of metabolic syndrome. Metabolic syndrome was present in 14% of men and 8% of women and one-third (30%) of men and one-fifth (19%) of women had at least two component risk factors. Conclusions This is the largest study to date assessing effectiveness of a community based screening program aiming to identify cardiovascular risk in young South Asians. We note significant modifiable risk at a young age. Such community based interventions can be effective at detecting and managing risk factors early in this vulnerable population.

Spontaneous coronary artery dissection (SCAD) is a cause of acute coronary syndrome, often occurring in young women. The utility of comprehensive imaging and clinical significance of detected vascular abnormalities have yet to be determined. We hypothesized that extracoronary vascular abnormalities (EVAs) are common in SCAD and aimed to study the prevalence and distribution of these findings. We enrolled 115 patients with confirmed SCAD who were evaluated at the Mayo Clinic SCAD Clinic from February 2010 to May 2014 and prospectively underwent comprehensive computed tomography angiography imaging of the neck, chest, abdomen, and pelvis (SCAD computed tomography angiography protocol, n = 95) or had retrospective review of outside studies (n = 20) including head imaging (n = 40). Follow-up was determined by last clinical visit or study correspondence and included review of recurrent SCAD or myocardial infarction, congestive heart failure, and death. We reported EVAs in 66% of patients with SCAD, most frequently in the abdomen (36%), pelvis (28%), and neck (27%). Only 1 patient had EVA in the chest (aortic dissection and Marfan's). Fibromuscular dysplasia (FMD) (exclusively multifocal) was the most common type of EVA (45%). Vascular abnormalities in those with head imaging included intracranial aneurysms (n = 9) and FMD (n = 3). There were no deaths at median follow-up of 21 months (Q1 to Q3 7.7 to 55). The presence of FMD was not associated with SCAD recurrence (relative risk [RR] 1.2; confidence interval [95% CI] 0.60, 2.5), congestive heart failure (RR 0.66; 95% CI 0.20, 2.3), or myocardial infarction (RR 1.34; 95% CI 0.69, 2.6). In conclusion, EVAs including FMD, dissections, aneurysms, and dilation are common in patients with SCAD and occur in a wide anatomic distribution. The presence of EVAs and/or FMD did not correlate with the risk of subsequent clinical events, but future studies with increased power and longer follow-up will be important to further assess the role of EVAs in patients with SCAD.

To determine the feasibility of automated co-registration of angiography and intravascular ultrasound (IVUS) to facilitate integration of these two imaging modalities in a synchronous manner.IVUS provides cross-sectional imaging of coronary arteries but lacks overview of the vascular territory provided by angiography. Co-registration of angiography and IVUS would increase utility of IVUS in the clinical setting.Forty-nine consecutive patients undergoing surveillance for cardiac allograft vasculopathy with angiography and IVUS of the left anterior descending artery (LAD) were enrolled. A pre-IVUS angiogram of the LAD was performed followed by an ECG-triggered fluoroscopy (ECGTF) during IVUS pullback at 0.5 mm/s using an automatic pullback device. ECGTF was used to track the IVUS catheter during pullback and establish a spatial relationship to the pre-IVUS angiogram. Angio-IVUS co-registration was performed with a research prototype (Siemens Healthcare, Germany) and accuracy was evaluated by distance mismatch between angiography and IVUS images at vessel bifurcations.Median age was 54 (44.5, 67) years. The population was 82.6% male with minimal risk factors. The median (IQR) co-registration distance mismatch measured at 108 bifurcations in 42 (85%) patients was 0.35 (0.00-1.16) mm. Seven patients were excluded due to inappropriate data acquisition (n = 3) and failure of tracking (n = 4), e.g., due to overlapping sternal wires. Estimated effective radiation dose for ECGTF was 0.09 mSv.This study demonstrates the feasibility of angio-IVUS co-registration which may be used as a clinical tool for localizing IVUS cross-sections along an angiographic roadmap. © 2015 Wiley Periodicals, Inc.