Search

The purpose of this study is to investigate the viability of transcatheter aortic valve replacement (TAVR) for severe symptomatic aortic stenosis (AS) in patients with prior chest radiation therapy (cXRT).Since patients with prior cXRT perform poorly with surgical aortic valve replacement, TAVR can be a viable alternative. However, clinical outcomes after TAVR in this patient population have not been well studied.From the pooled registry of the placement of aortic transcatheter valves II trial, we identified patients with and without prior cXRT who underwent TAVR (n = 64 and 3923, respectively). The primary outcome was a composite of all-cause death and any stroke at 2 years. Time to event analyses were shown as Kaplan-Meier event rates and compared by log-rank testing. Hazard ratios (HRs) were estimated and compared by Cox proportional hazards regression model.There was no significant difference in the primary outcome between the patients with and without prior cXRT (30.7% vs. 27.0%; p = 0.75; HR, 1.08; 95% confidence interval, 0.66-1.77). Rates of myocardial infarction, vascular complications, acute kidney injury, or new pacemaker implant after TAVR were not statistically different between the two groups. The rate of immediate reintervention with a second valve for aortic regurgitation after TAVR was higher among the patients with prior cXRT. However, no further difference was observed during 2 years follow-up after discharge from the index-procedure hospitalization.TAVR is a viable alternative for severe symptomatic AS in patients who had cXRT in the past.

Infective endocarditis (IE) is associated with marked morbidity and mortality in the United States and parallels the opioid pandemic. Few studies explore this interaction and its effect on clinical outcomes. We analyzed contemporary patients admitted with IE to determine predictors of readmission in the United States. The 2017 National Readmission Database was used to identify index admissions in adults with the diagnosis of IE, based on the International Classification of Disease, 10th Revision codes. The primary outcome of interest was 30-day readmission. Secondary outcomes were mortality, hospital charges, and predictors of hospitalization readmission. Of 40,413 index admissions for IE, 5,558 patients (13.8%) were readmitted within 30 days. Patients who were readmitted were younger (55 ± 20 vs 61 ± 19 years, p0.001) and more likely to have end-stage renal disease (12.2% vs 10.5%, p0.001), hepatitis C virus (19.4% vs 12.6%, p0.001), HIV (1.8% vs 1.2%, p = 0.001), opioid abuse (23.9% vs 15%, p0.001), cocaine use (7.3% vs 4.4%, p0.001), and other substance abuse (8.5 vs 5.6, p0.001). Patients readmitted were less likely to have diabetes mellitus (27.8% vs 29.4%, p = 0.01), hypertension (56.9% vs 64%, p0.001), heart failure (37.7% vs 40%, p0.001), chronic kidney disease (31.2% vs 32%, p0.001), and peripheral vascular disease (3.6% vs 4.6%, p = 0.001). The median cost of index admission for the total cohort was $84,325 (39,922 to 190,492). After adjusting for age, diabetes mellitus, heart failure, hypertension, and end-stage renal disease, opioid abuse (odds ratio [OR] 1.34; 95% confidence interval [CI] 1.23 to 1.46; p0.001), cocaine use (OR 1.32; 95% CI 1.17 to 1.48; p0.001), other substance abuse (OR 1.16; 95% CI 1.04 to 1.30; p = 0.008), and hepatitis C virus (OR 1.32; 95% CI 1.21 to 1.43; p0.001) correlated with higher odds of 30-day readmission. These factors may present targets for future intervention.

Introduction: Transthyretin cardiac amyloidosis (ATTR-CM) is an important comorbidity associated with aortic stenosis. Multiple studies have shown that the prevalence of ATTR-CM in severe AS is 15-20%. Concomitant AS and ATTR-CM confers worse outcomes than lone AS. Hypothesis: The purpose of this quality improvement project is to raise awareness of ATTR-CM in patients TAVR amongst the provider and patients. Methods: We retrospectively reviewed TAVR cases performed at our institution in 2019 (Total cases 87). We interrogated the presence of predefined high-risk features for ATTR-CM based on prior literature and guidelines. We subsequently contacted the identified subjects to discuss our suspicion of ATTR-CM and offered clinical referral to a cardiac amyloid specialist. Results: Of the total of 87 patients who underwent TAVR in 2019, 12 patients were deceased at time of chart review. We reviewed 75 patient medical records, of which 50 patients (66.7%) had high-risk features of ATTR-CM. Total of 19 patients (38%) agreed to being referred to a cardiac amyloid specialist. In addition, 7 more patients were found to be deceased on phone call (total 19 patients deceased), 18 patients could not be reached, and 6 patients declined referral. Conclusions: Comprehensive risk assessment approach in patients with severe AS may disclose otherwise unsuspected ATTR-CM and allow earlier diagnosis and treatment. These findings served as the basis for implementation of a prospective screening process for ATTR-CM utilizing pyrophosphate nuclear scanning in select patients referred for TAVR in our institution.

A patient’s supine posture redistributes plasma into the vascular space, leading to dilution of blood constituents. The extent to which posture may influence identification of hospital-acquired anemia is unknown. Patients in this quasi-experimental study had blood obtained for hemoglobin measurement while recumbent for at least 6 hours, and then again after sitting upright for at least 1 hour. Of the 35 patients who completed the study, 13 were women (37%). Patients had a median increase in hemoglobin of 0.60 g/dL (range, –0.6 to 1.4 g/dL) with sitting, a 5.2% (range, (–4.5% to 15.1%) relative change (P < .001). Ten of 35 patients (29%) exhibited an increase in hemoglobin of 1.0 g/dL or more. Posture influences hemoglobin levels in hospitalized patients on general medicine wards; this knowledge may help curb unnecessary testing to evaluate small changes in hemoglobin concentration.

Coronary computed tomography angiography (CCTA) offers high-resolution anatomic characterization of the coronary vasculature but may be suboptimal for lesions dependent on real-time visualization of flow including chronic total occlusion (CTO). In CTOs, heavy calcification and distal vessel opacification from collateralization may confound luminal assessment. Several studies have examined the role of CCTA in characterizing known CTOs to guide percutaneous coronary intervention (PCI). However, the efficacy of CCTA in the de novo diagnosis of CTOs prior to coronary angiography (CAG) has not been demonstrated. A total of 233 consecutive patients who presented for CAG within a 3-month period of having CCTA were retrospectively reviewed. Those patients with prior diagnosis of CTO or prior bypass of the occluded vessels were excluded. Sensitivity and specificity analysis of CCTA in identifying CTOs using CAG as the gold standard was performed. The prevalence of CTO was 21.11% in the population that met criteria for analysis (n = 199). The sensitivity of CCTA in predicting CTO was 57.1%, while the specificity was 96.8%. The positive predictive value and negative predictive value of CCTA in detection of CTO were 82.8 and 89.4%, respectively. Our study shows that CCTA has excellent specificity but poor sensitivity in the detection of CTO thus limiting its clinical use in de novo diagnosis. Further studies to determine the effect of de novo CTO diagnosis on clinically important procedural factors, such as radiation exposure, contrast use, and need for repeat procedures, are warranted and may implicate a role for CCTA in this setting.

Atrial fibrillation (AF) in the setting of malignancy poses a unique challenge given the confluent pathologies and risks of current treatments. Oral anticoagulation is recommended to reduce the risk of systemic thromboembolism in high-risk individuals with AF. The ‘Watchman’ device for left atrial appendage closure has shown comparable efficacy compared with anticoagulation with warfarin; however, patients with cancer were not included in trials testing Watchman safety and efficacy. We present the current treatment approaches for the management of AF in patients with malignancy. We review contemporary guidelines and propose a novel clinical decision tree by which physicians can consider left atrial appendage closure in cancer patients, and at last, suggest future investigation that might further clarify the clinical benefit of this approach.

To improve resource allocation in face of the COVID‐19 pandemic, hospitals around the country are restricting the performance of elective surgery to preserve ventilators, operating rooms, ICU beds and protect anesthesiologists. For patients with severe aortic stenosis, efforts to bring treatment to symptomatic patients amid this pandemic might lead to favored use of catheter based management using minimalist techniques that do not require these elements. In this context, some patients with well tested surgical indications for valve replacement may be treated by catheter‐based methods. It is important that outcomes for these cases are followed closely both at respective sites and in national registries. As we recover from this pandemic, surgical cases should once again be driven by multi‐disciplinary discussion and clinical trial data, and not a mentality of crisis management.

Background For patients who have an indication for anticoagulation, it is controversial whether dual therapy with an oral anticoagulant and single antiplatelet agent can be used after percutaneous coronary intervention (PCI) or acute coronary syndrome (ACS) instead of triple therapy with an oral anticoagulant and dual antiplatelet therapy. Participants and methods Twelve observational studies and four clinical trials were identified from three electronic databases from their inception to December, 2017. Pooled estimates were calculated using a random-effects model for meta-analysis. Results Compared with the triple therapy, dual therapy was associated with significantly lower risk of major bleeding [relative risk (RR), 0.63; 95% confidence interval (CI), 0.50-0.80] without statistically significant increase in major adverse cardiac events (RR, 1.04; 95% CI, 0.84-1.29), all-cause death (RR, 1.15; 95% CI, 0.77-1.71), cardiac death (RR, 1.04; 95% CI, 0.67-1.61), myocardial infarction (RR, 1.25; 95% CI, 0.98-1.59), stroke (RR, 1.27; 95% CI, 0.79-2.06), stent thrombosis (RR, 1.52; 95% CI, 0.96-2.41), and repeat revascularization (RR, 1.15; 95% CI, 0.87-1.52). Although risks of myocardial infarction and stent thrombosis were marginally higher in the dual therapy group, this trend was attenuated after excluding studies that exclusively included patients undergoing PCI for ACS, but not stable coronary artery disease. Conclusion Dual therapy may be a reasonable alternative to triple therapy after PCI in patients with indication for chronic anticoagulation. However, further studies are needed to investigate efficacy of dual therapy, especially in the patients with higher ischemic risk, such as in ACS.

Despite the landmark release of recent transcatheter aortic valve replacement data, the gold standard of surgical therapy is here to stay. Surgery remains vital in patient populations with low coronary height raising risk of coronary occlusion, aneurysmal ascending aorta, isolated aortic regurgitation, noncalcific disease, bicuspid valves, and multivessel coronary disease, or other structural abnormality requiring cardiac surgery. Consideration of these issues highlights the ongoing importance of multidisciplinary consideration of individual patient cases, careful review of imaging, and preservation of a robust surgical program to complement transcatheter development. As the landscape of valvular heart disease management continues to evolve, the surgeon's role is changing, but by no means diminished and their engagement in heart team decision making remains paramount.

Patients with myocardial bridging are often asymptomatic but few may also experience chronic exertional angina. The population prevalence of Hypertrophic Cardiomyopathy (HCM) is estimated at less than 1%. While mild concentric right ventricular hypertrophy may be common in HCM, severe hypertrophy

Current practice guidelines advocate culprit vessel intervention alone in patients with ST-segment elevation myocardial infarction (STEMI) found to have multivessel coronary disease during primary percutaneous coronary intervention (PCI). The debate on the timing of noninfarct artery intervention has recently been reinvigorated by the PRAMI (Preventive Angioplasty in Acute Myocardial Infarction) trial, in which patients undergoing preventive PCI of significant nonculprit lesions at the time primary PCI for STEMI had reduced rates of cardiac death, nonfatal myocardial infarction, and refractory angina. Given that previous literature has cautioned against multivessel PCI during STEMI, this raises the question of whether technical and pharmacological advances in PCI may have opened the door to safely revisit this issue with additional clinical rigor. The impact of STEMI pathophysiology on nonculprit vessel plaque, how treatment of nonculprit lesions alters the natural history of coronary disease after STEMI, and whether this results in a clinical benefit remain unclear, and much of the existing data are retrospective. Additionally, the PRAMI trial did not include a staged PCI, leaving questions as to how this approach might fare compared with simultaneous preventive PCI. In this review, we discuss the pathophysiology of nonculprit vessel plaque in STEMI, provide a summary of the existing literature on the topic, and discuss the PRAMI trial in the face of previous data and possible future directions for further study.

Acute coronary syndrome (ACS) coinciding with active malignancy presents a unique clinical challenge given intersecting pathophysiology and treatment-related effects. There is little established clinical guidance on management strategies, rendering most treatment approaches anecdotal. We present a case highlighting the complexity of managing a patient being treated for malignancy who concurrently suffers from ACS. We then review the literature on co-management of ACS and malignancy, including reports of specific cancer therapies associated with ACS, unique features of clinical presentation and optimal use of dual antiplatelet therapy to minimize risks of bleeding and thrombosis. We also describe gaps in current literature, challenges in systematically studying the clinical intersection of these disease processes and propose alternative methodologies for further research.

To compare the outcomes of initial one-stent (1S) versus dedicated two-stent (2S) strategies in complex bifurcation percutaneous coronary intervention (PCI) using everolimus-eluting stents (EES).PCI of true bifurcation lesions is technically challenging and historically associated with reduced procedural success and increased restenosis. Prior studies comparing initial one-stent (1S) versus dedicated two-stent (2S) strategies using first-generation drug-eluting stents have shown no reduction in ischemic events and more complications with a 2S strategy.We performed a retrospective study of 319 consecutive patients undergoing PCI at a single referral center with EES for true bifurcation lesions, defined by involvement of both the main vessel (MV) and side branch (SB). Baseline, procedural characteristics, quantitative coronary angiography and clinical outcomes in-hospital and at one year were compared for patients undergoing 1S (n=175) and 2S (n=144) strategies.Baseline characteristics were well-matched. 2S strategy was associated with greater SB acute gain (0.65±0.41 mm vs. 1.11±0.47 mm, p0.0001). In-hospital serious adverse events were similar (9% with 2S vs. 8% with 1S, p=0.58). At one year, patients treated by 2S strategy had non-significantly lower rates of target vessel revascularization (5.8% vs. 7.4%, p=0.31), myocardial infarction (7.8% vs. 12.2%, p=0.31) and major adverse cardiovascular events (16.6% vs. 21.8%, p=0.21).In this study of patients undergoing PCI for true coronary bifurcation lesions using EES, 2S strategy was associated with superior SB angiographic outcomes without excess complications or ischemic events at one year.

Increasing use of the new oral anticoagulants (NOACs) – dabigatran, rivaroxaban, and apixaban – has prompted considerable discussion in the medical community even as warfarin remains the mainstay of therapy. This article raises 10 controversial issues regarding the use of NOACs for stroke prevention in patients with atrial fibrillation, and offers a review of the latest available evidence. We provide a brief overview of the mechanism and dosing of these drugs, as well as a summary of the key clinical trials that have brought them into the spotlight. Comparative considerations relative to warfarin such as NOAC safety, efficacy, bleeding risk, reversibility, drug-transitioning and use in patients well controlled on warfarin are addressed. Use in select populations such as the elderly, those with coronary disease, renal impairment, or on multiple anti-platelet drugs is also discussed. Finally, we consider such specific issues as comparative efficacy, off-label use, cost, rebound and management during events. Ultimately, the rise of the NOACs to mainstream use will depend on further data and clinical experience amongst the medical community.

Atrial fibrillation (AF) imposes an increased risk of thromboembolic events, mainly due to blood stasis in the left atrial appendage (LAA). Anticoagulation (AC) remains the primary treatment modality, even in a burgeoning area of percutaneous LAA occlusion. In rare instances where neither approach

We describe the case of a 68-year-old woman presenting with stress cardiomyopathy (SCM), with concomitant cardiogenic shock, left ventricular outflow tract obstruction, and ventricular septal rupture. These complications have not simultaneously been reported in a single SCM case. The importance of early diagnosis of serial complications of SCM and using mechanical circulatory support as a treatment strategy are highlighted.

Balloon floatation pulmonary artery catheters (PACs) have been used for hemodynamic monitoring in cardiac, medical, and surgical intensive care units since the 1970s. With the availability of newer noninvasive diagnostic modalities, particularly echocardiography, the frequency of diagnostic pulmonary artery catheterization has declined. In this review, the evolution of PACs, the results of nonrandomized and randomized studies in various clinical conditions, the uses and abuses of bedside hemodynamic monitoring, and current indications for pulmonary artery catheterization are discussed.

The role of inflammation in the propagation of atherosclerosis and susceptibility to cardiovascular (CV) events is well established. Of the wide array of inflammatory biomarkers that have been studied, high-sensitivity C-reactive protein (hsCRP) has received the most attention for its use in screening and risk reclassification and as a predictor of clinical response to statin therapy. Although CRP is involved in the immunologic process that triggers vascular remodeling and plaque deposition and is associated with increased CV disease (CVD) risk, definitive randomized evidence for its role as a causative factor in atherothrombosis is lacking. Whether measurement of hsCRP levels provides consistent, clinically meaningful incremental predictive value in risk prediction and reclassification beyond conventional factors remains debated. Despite publication of guidelines on the use of hsCRP in CVD risk prediction by several leading professional organizations, there is a lack of clear consensus regarding the optimal clinical use of hsCRP. This article reviews 4 distinct points from the literature to better understand the current state and application of hsCRP in clinical practice: 1) the biology of hsCRP and its role in atherosclerosis; 2) the epidemiological association of hsCRP with CVD; 3) the quality of hsCRP as a biomarker of risk; and 4) the use of hsCRP as a tool to initiate or tailor statin therapy. Furthermore, we highlight recommendations from societies and important considerations when using hsCRP to guide treatment decisions in the primary prevention setting.

T he dreaded sheath pull, bane of every interventional fellow’s existence. A maligned but critical necessity, it inevitably engenders a visceral sense of discontent amplified by the fact that nurses are unhappy because it disrupts their workflow and patients are certainly not pleased at the prospect of another 4 to 6 hours of recumbence, having already endured a stranger mashing down on their nether regions for 15 to 30 minutes. The only solace may be the certainty of burning off a few calories in the tetany-charged upper body workout achieved by the process. I was surprised then, to find myself looking forward to pulling the sheath of a particularly ornery patient around 11 PM one evening. My eyelids trying hard to betray me as I drove back to the hospital, I wondered aloud, why? This woman had recently signed out against medical advice, was threatening to sue the staff for defamation (she deemed certain diagnoses offensive), and to be her nurse meant certain accusation of theft. Frankly, it had been difficult to focus on our procedure through her ceaseless diatribe about the individuals who had scarred her life. And did I mention she had Clostridium difficile—equating to a veritable silo of those lovely yellow gowns we so adore. To that end, she was quite adept at calling out the minute her nurse had left the room, degowned and hand-washed. Reentry was met with further caustic autobiographical details and a disheartening sense that you had contributed to her tragic life story. But, could I blame her? Effectively homeless, she had been left penniless by her daughter and sister, was abandoned as a child by her mother, lost contact with her pedophile father at a young age, and had a host of chronic ailments she could not afford to manage. By right, she was angry at a life that had never really given her a chance. And then, came the week just passed: she had been diagnosed with locally invasive lung cancer, had fallen and fractured several thoracic vertebrae, and had amassed a reputation that precluded physicians from believing her back and chest pain were genuine. It was at this juncture that her entire anteroseptal myocardium fell prey to an occlusive coronary thrombus. This pain was real; electrocardiograms rarely lie. That was when I met her. Now, driving back to the hospital, the following questions ricocheted through my mind. What could I tell her? Would I be just another suspect face? Would she respond to encouragement? Would she care that anyone cared? Why should she—who was I to her anyway? We had the ability to treat her heart. But the heart of the matter lay in her broken spirit. Could we do anything for that? She had shouted sincerely at the start of the case that if God wanted to take her, she was ready. And as we wheeled her out after the heart catheterization, she said emphatically, ‘‘I hope God blesses you all.’’ Of course, our role was to fulfill our duties irrespective of what God or fate or the mysteries of physiology had in store for her. Is it not privilege enough to be entrusted with the responsibility of negotiating the fate of another’s life, or being granted the resources to pursue this role with perseverance? Do we need any further blessing? Now at the bedside, I settle into my familiar stance, hands secure over her femoral arteriotomy. ‘‘Ma’am, you wanted God to bless us—I couldn’t help but wonder, despite all that’s happened this week, do you feel blessed too? You had said you were ready to go. Yet, here we are talking to each other because maybe he wasn’t ready for you.’’ I could see her thinking, and continued: ‘‘You had that pain in your chest that led them to find the cancer, which prompted a transfer to our facility. You tried to leave us, but were made to return after fracturing your spine, bed bound, perhaps to assure that you could not escape us again. It was then that you had this massive heart attack just a short elevator ride away from us. The cancer is removable, the spine will heal, the cigarettes you’ve left behind, and social services have found you a roof under which you can mend. But, had you been anywhere else—even at your local hospital for that matter—this heart attack could have killed you. That didn’t happen, did it? Maybe the blessing you sought for us, ma’am, has been bestowed on you too.’’ I gave her a minute to process this internally. ‘‘Tell me, ma’am, what makes you happy? What do you like to do?’’ She started her story again, but this time, the tone was different. She was intently working through several word game books to improve her DOI: http://dx.doi.org/10.4300/JGME-D-15-00192.1

Background Niacin increases fasting glucose levels, and statins modestly increase the rate of new-onset diabetes. The clinical importance and mechanisms of these effects are not fully explored. Objective On the basis of anecdotal observations, we hypothesized that elevated morning fasting glucose may be accompanied by relatively normal hemoglobin A1c (HbA1c) in patients treated with niacin and other lipid-modifying drugs. We conducted a retrospective cohort analysis to test this hypothesis. Methods The Duke Lipid Clinic database (1994–2007) was screened for simultaneous determinations of fasting morning glucose and HbA1c, yielding 1483 data pairs among 554 subjects. Subjects with diabetes, by clinical diagnosis, medication, or any HbA1c ≥6.5%, or nondiabetes were analyzed separately. Repeated-measures linear regression featured glucose as dependent variable and included terms for HbA1c, drug(s), and their interaction. Results Regression lines for glucose on HbA1c had altered slopes in the presence of niacin and/or statin use in normoglycemic subjects. The corresponding interaction terms (drug and HbA1c) were significant (niacin P = .026, statin P = .013). Fibrate use had no effect (interaction P = .49). When modeled together, niacin and statin effects were independent. Regression curves in diabetic patients were not affected by lipid medications. Conclusion Elevated fasting glucose may be accompanied by relatively normal HbA1c in niacin- and statin-treated patients. HbA1c reflects average daily glucose levels and is likely a better measure of the glycemic effect of lipid medications. Because our data were retrospective, confirmation from randomized trials is needed.

Although patients with severe aortic stenosis and prior chest radiation (cXRT) perform poorly with surgical aortic valve replacement (AVR), cXRT is not included in the Society of Thoracic Surgeons (STS) risk score. Differences in characteristics and outcomes in patients undergoing transcatheter AVR

In 1903, Dr. William Osler advocated for reform of medical education to emphasize bedside teaching, recommending “no teaching without a patient for a text and the best teaching is that taught by the patient himself” [(1)][1]. More than a century later, new voices in the profession echo that

Increasing use of the new oral anticoagulants (NOACs) - dabigatran, rivaroxaban, and apixaban - has prompted considerable discussion in the medical community even as warfarin remains the mainstay of therapy. This article raises 10 controversial issues regarding the use of NOACs for stroke prevention in patients with atrial fibrillation, and offers a review of the latest available evidence. We provide a brief overview of the mechanism and dosing of these drugs, as well as a summary of the key clinical trials that have brought them into the spotlight. Comparative considerations relative to warfarin such as NOAC safety, efficacy, bleeding risk, reversibility, drug-transitioning and use in patients well controlled on warfarin are addressed. Use in select populations such as the elderly, those with coronary disease, renal impairment, or on multiple anti-platelet drugs is also discussed. Finally, we consider such specific issues as comparative efficacy, off-label use, cost, rebound and management during events. Ultimately, the rise of the NOACs to mainstream use will depend on further data and clinical experience amongst the medical community.

Background— Re-endothelialization is delayed after drug-eluting stent (DES) implantation. In this setting, neointima is more prone to become lipid laden and develop neoatherosclerosis (NA), potentially increasing plaque vulnerability. Methods and Results— Optical coherence tomography and near-infrared spectroscopy with intravascular ultrasound were used to characterize NA in 65 (51 DES and 14 bare-metal stents) consecutive symptomatic patients with in-stent restenosis. Median duration poststent implantation was 33 months. Optical coherence tomography–verified NA was observed in 40 stents with in-stent restenosis (62%), was more prevalent in DES than bare-metal stents (68% versus 36%; P =0.02), and demonstrated significantly higher prevalence of thin-cap neoatheroma (47% versus 7%; P =0.01) in DES. Near-infrared spectroscopy assessment demonstrated that the total lipid core burden index (34 [interquartile range, 12–92] versus 9 [interquartile range, 0–32]; P P P =0.01) and in areas of the stented segment without significant in-stent restenosis (71%). Periprocedural myocardial infarction occurred only in DES (11 versus 0; P =0.05), of which 6 (55%) could be attributed to segments with >70% in-stent restenosis. By logistic regression, prior DES was the only independent predictor of both NA (odds ratio, 7.0; 95% confidence interval, 1.7–27; P =0.006) and periprocedural myocardial infarction (odds ratio, 1.8; 95% confidence interval, 1.1–2.4; P =0.05). Conclusions— In-stent thin-cap neoatheroma is more prevalent, is distributed more diffusely across the stented segment, and is associated with increased periprocedural myocardial infarction in DES compared with bare-metal stents. These findings support NA as a mechanism for late DES failure.

The role of inflammation in the propagation of atherosclerosis and susceptibility to cardiovascular (CV) events is well established. Of the wide array of inflammatory biomarkers that have been studied, high-sensitivity C-reactive protein (hsCRP) has received the most attention for its use in screening and risk reclassification and as a predictor of clinical response to statin therapy. Although CRP is involved in the immunologic process that triggers vascular remodeling and plaque deposition and is associated with increased CV disease (CVD) risk, definitive randomized evidence for its role as a causative factor in atherothrombosis is lacking. Whether measurement of hsCRP levels provides consistent, clinically meaningful incremental predictive value in risk prediction and reclassification beyond conventional factors remains debated. Despite publication of guidelines on the use of hsCRP in CVD risk prediction by several leading professional organizations, there is a lack of clear consensus regarding the optimal clinical use of hsCRP. This article reviews 4 distinct points from the literature to better understand the current state and application of hsCRP in clinical practice: 1) the biology of hsCRP and its role in atherosclerosis; 2) the epidemiological association of hsCRP with CVD; 3) the quality of hsCRP as a biomarker of risk; and 4) the use of hsCRP as a tool to initiate or tailor statin therapy. Furthermore, we highlight recommendations from societies and important considerations when using hsCRP to guide treatment decisions in the primary prevention setting.

Coronary computed angiography (CCTA) offers high-resolution anatomic characterization of the coronary vasculature but may be sub-optimal for lesions dependent on real-time visualization of flow - including chronic total occlusions (CTO). In CTO lesions, heavy calcification and distal vessel

Takotsubo cardiomyopathy (TTC) is an acute and reversible cardiomyopathy commonly precipitated by emotional or physical stress. The clinical presentation is similar to the acute coronary syndrome, manifesting as chest pain in association with mild cardiac enzyme elevation and electrocardiographic (EKG) changes in the absence of obstructive lesions on coronary angiography [1, 2]. Increasingly, cases are being described in the setting of acute neurological illnesses, including malignancy, and seizures [3–6]. Compared with typical TTC, seizure-induced TTC confers a higher mortality, thus necessitating prompt recognition and investigation [7]. A 76-year-old female with recurrent malignant meningioma presented to the emergency department following a generalized tonic–clonic seizure (GTCS). The patient’s history was significant for multiple cranial resections (the most recent one-month prior), two previous seizures, hypercholesterolemia, hypertension and chronic bradycardia. On admission, the patient received intravenous lorazepam 1 mg and dexamethasone 10 mg. She was hemodynamically stable and blood glucose was 147 mg/dl. A noncontrast CT-brain revealed bilateral vasogenic edema corresponding to previous resection sites. EEG demonstrated sharp waves in the right parietal region with associated diffuse generalized slowing. Following admission, the patient had witnessed a 30 s GTCS and was admitted to the neurosurgical intensive care unit and administered dexamethasone. Here she reported chest pain, despite post-ictal confusion. Subsequent troponin was 2.7 ng/ml, peaking at 2.9 ng/ml (n \ 0.1 ng/ml), and an EKG showed ST-changes concerning for ischemia. Given a diagnosis of non-STsegment elevation myocardial infarction (NSTEMI), aspirin, clopidogrel and atorvastatin were promptly initiated. Coronary angiography was performed but revealed no culprit lesion. Left ventriculography demonstrated an impaired left ventricular ejection fraction (25 %) and a hyperkinetic base with severe hypokinesis of the anterolateral, diaphragmatic and apical segments, consistent with a diagnosis of TTC. This was confirmed on echocardiography (Fig. 1). The patient was commenced on lisinopril and carvedilol, and clopidogrel was ceased. Once stable, she was discharged home with scheduled cardiac followup. At 1 month, repeat EKG and echocardiogram were performed, revealing resolution of ischemic and structural changes. We describe the case of a 76-year-old woman suffering from seizure-related TTC. This case is remarkable for the patient’s symptomatic presentation, history of multiple brain surgeries, and the absence of the classical echocardiographic finding of apical ballooning. A number of mechanisms have been proposed to explain the relationship between seizures and TTC. The level of circulating catecholamines has been demonstrated to spike in the 30-minutes following a GTCS [8]. This excessive release of catecholamines can cause damage to cardiac muscle, leading to ventricular dysfunction [3, 7, 9]. In addition, the circulatory complications of seizures, including ventricular arrhythmias, metabolic disturbances and hemodynamic compromise, can provide sufficient physical stress to precipitate TTC in certain patients [7, J. Warren U. Baber B. Mohanty S. K. Sharma A. Kini R. Mehran (&) Mount Sinai Medical Center, 1 Gustave L. Levy Place, Box 1030, New York, NY 10029, USA e-mail: roxana.mehran@mountsinai.org

Background— Using a resolution 1000-fold higher than prior studies, we studied (1) the degree to which late gadolinium-enhancement (LGE) cardiac magnetic resonance tracks fibrosis from chronic myocardial infarction and (2) the relationship between intermediate signal intensity and partial volume averaging at distinct “smooth” infarct borders versus disorganized mixtures of fibrosis and viable cardiomyocytes. Methods and Results— Sprague-Dawley rats underwent myocardial infarction by coronary ligation. Two months later, rats were euthanized 10 minutes after administration of 0.3 mmol/kg intravenous gadolinium. LGE images ex vivo at 7 T with a 3D gradient echo sequence with 50×50×50 μm voxels were compared with histological sections (Masson trichrome). Planimetered histological and LGE regions of fibrosis correlated well ( y =1.01 x −0.01; R 2 =0.96; P P Conclusions— These data provide important validation of LGE at nearly the cellular level for detection of fibrosis after myocardial infarction. Although LGE can detect heterogeneous patches of fibrosis and viable cardiomyocytes as patches of intermediate signal intensity, the percentage of intermediate signal intensity voxels is resolution dependent. Thus, at clinical resolutions, distinguishing the peri-infarct border zone from partial volume averaging with LGE is challenging.

Percutaneous coronary intervention (PCI) of complex true coronary bifurcation lesions is challenging and whether to stent side branch dedicatedly is still debatable. To date there is no published study showing the safety and efficacy of the Everolimus-eluting stent (EES) in true bifurcation lesions