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Aim: To evaluate the potential impact of preemptive multigene pharmacogenomic (PGx) testing on medication prescribing in real-world clinical settings. Patients & methods: Prescription frequencies for 65 medications with actionable PGx recommendations were collected in 215 percutaneous coronary intervention (PCI) and 131 allogeneic hematopoietic cell transplant (allo-HCT) patients. A simulation projected the number of PGx-guided prescribing opportunities. Results: In PCI and allo-HCT patients, respectively, 66.5 and 90.1% were prescribed at least one medication with actionable PGx prescribing recommendations. Simulations projected 26.5 and 41.2 total PGx-guided prescribing opportunities per 100 PCI and allo-HCT patients, respectively, if multigene PGx results were available. Conclusion: A multigene PGx testing strategy offers potential to optimize medication prescribing beyond clopidogrel and tacrolimus in PCI and allo-HCT patients.

Background: Accurate blood pressure (BP) measurement is critical for optimal cardiovascular risk management. Age-related trajectories for cuff-measured BP accelerate faster in women compared with men, but whether cuff BP represents the intraarterial (invasive) aortic BP is unknown. This study aimed to determine the sex differences between cuff BP, invasive aortic BP, and the difference between the 2 measurements. Methods: Upper-arm cuff BP and invasive aortic BP were measured during coronary angiography in 1615 subjects from the Invasive Blood Pressure Consortium Database. This analysis comprised 22 different cuff BP devices from 28 studies. Results: Subjects were 64±11 years (range 40–89) and 32% women. For the same cuff systolic BP (SBP), invasive aortic SBP was 4.4 mm Hg higher in women compared with men. Cuff and invasive aortic SBP were higher in women compared with men, but the sex difference was more pronounced from invasive aortic SBP, was the lowest in younger ages, and the highest in older ages. Cuff diastolic blood pressure overestimated invasive diastolic blood pressure in both sexes. For cuff and invasive diastolic blood pressure separately, there were sex*age interactions in which diastolic blood pressure was higher in younger men and lower in older men, compared with women. Cuff pulse pressure underestimated invasive aortic pulse pressure in excess of 10 mm Hg for both sexes in older age. Conclusions: For the same cuff SBP, invasive aortic SBP was higher in women compared with men. How this translates to cardiovascular risk prediction needs to be determined, but women may be at higher BP-related risk than estimated by cuff measurements.

Numerous algorithms are available to predict short-term mortality in ST elevation myocardial infarction (STEMI) but none are focused on elderly patients or include invasive hemodynamics. A simplified risk score (LASH score) including left ventricular end diastolic pressure > 20 mm Hg, age > 75 years, systolic blood pressure < 100 mm Hg and heart rate > 100 bpm was tested in a retrospective, single-center study of 346 patients ≥ 60 years old who underwent primary percutaneous coronary intervention (PPCI). The median age was 70 years [IQR: 64, 79], 60.1% were men, and 77.8% identified as White. In-hospital all-cause mortality was 10.1%. Patients with a LASH score ≥ 3 (n = 34) had an in-hospital mortality rate of 44.1% compared to 6.4% for LASH score ≤ 2 (p < 0.0001). The odds ratio for in-hospital mortality for patients with LASH score ≥ 3 was 13.2 (95% CI 5.3-33.1) compared to patients with a LASH score ≤ 2 when adjusted for sex, cardiac arrest, heart failure, and prior cerebrovascular event. The LASH score had an area under the ROC curve for predicting in-hospital mortality of 0.795 [CI 0.716-0.872], as compared to TIMI-STEMI (0.881, CI 0.829-0.931; p = 0.01), GRACE (0.849, CI 0.778-0.920; p = 0.19), shock index (0.769, CI 0.667-0.871; p = 0.51) and modified shock index (0.765, CI 0.716-0.873; p = 0.48). In summary, a simplified, easy to calculate risk score that incorporates age and invasive hemodynamics predicts in-hospital mortality in patients ≥ 60 years old undergoing PPCI for STEMI.

The formation of a thrombus in the left ventricle (LV) in patients with normal systolic function is very rare. We report a case and identified 31 other adult patients who had an LV thrombus with normal LV systolic function. The median (IQR) age of these patients was 43 [37,59] years with a slight male predominance (59%). The vast majority of patients presented with embolic complications (28; 88%) with 3 of the other patients presenting with a febrile illness. Most of the cases occurred in the setting of an identifiable medical condition that carries an increased risk of thrombosis including inflammatory diseases, malignancies or hypereosinophilia. Treatment generally included anticoagulation with or without surgical removal or systemic thrombolysis. Recurrence of LV thrombus and/or embolic events have been reported in patients with LV thrombus and normal LV systolic function suggesting that long term anticoagulation may be needed.

Hypercholesterolemia is a well-established risk factor for atherosclerotic cardiovascular disease (ASCVD). Low-density lipoprotein cholesterol (LDL-C) has been labeled as “bad” cholesterol and high-density lipoprotein cholesterol (HDL-C) as “good” cholesterol. The prevailing hypothesis is that lowering blood cholesterol levels, especially LDL-C, reduces vascular deposition and retention of cholesterol or apolipoprotein B (apoB)-containing lipoproteins which are atherogenic. We review herein the clinical trial data on different pharmacological approaches to lowering blood cholesterol and propose that the mechanism of action of cholesterol lowering, as well as the amplitude of cholesterol reduction, are critically important in leading to improved clinical outcomes in ASCVD. The effects of bile acid sequestrants, fibrates, niacin, cholesteryl ester transfer protein (CETP) inhibitors, apolipoprotein A-I and HDL mimetics, apoB regulators, acyl coenzyme A: cholesterol acyltransferase (ACAT) inhibitors, cholesterol absorption inhibitors, statins, and proprotein convertase subtilisin kexin 9 (PCSK9) inhibitors, among other strategies are reviewed. Clinical evidence supports that different classes of cholesterol lowering or lipoprotein regulating approaches yielded variable effects on ASCVD outcomes, especially in cardiovascular and all-cause mortality. Statins are the most widely used cholesterol lowering agents and have the best proven cardiovascular event and survival benefits. Manipulating cholesterol levels by specific targeting of apoproteins or lipoproteins has not yielded clinical benefit. Understanding why lowering LDL-C by different approaches varies in clinical outcomes of ASCVD, especially in survival benefit, may shed further light on our evolving understanding of how cholesterol and its carrier lipoproteins are involved in ASCVD and aid in developing effective pharmacological strategies to improve the clinical outcomes of ASCVD.

Black patients suffer worse outcomes after percutaneous coronary intervention (PCI) than White patients. Inequities in antiplatelet prescribing may contribute to this health disparity. We compared P2Y

Coronary artery disease (CAD) costs healthcare billions of dollars annually and is the leading cause of death despite available noninvasive diagnostic tools.This study aims to examine the usefulness of machine learning in predicting hemodynamically significant CAD using routine demographics, clinical factors, and laboratory data.Consecutive patients undergoing cardiac catheterization between March 17, 2015, and July 15, 2016, at UNC Chapel Hill were screened for comorbidities and CAD risk factors. In this pilot, single-center, prospective cohort study, patients were screened and selected for moderate CAD risk (n = 185). Invasive coronary angiography and CAD prediction with machine learning were independently performed. Results were blinded from operators and patients. Outcomes were followed up for up to 90 days for major adverse cardiovascular and renal events (MACREs). Greater than 70% stenosis or a fractional flow reserve less than or equal to 0.8 represented hemodynamically significant coronary disease. A random forest model using demographic, comorbidities, risk factors, and lab data was trained to predict CAD severity. The Random Forest Model predictive accuracy was assessed by area under the receiver operating characteristic curve with comparison to the final diagnoses made from coronary angiography.Hemodynamically significant CAD was predicted by 18-point clinical data input with a sensitivity of 81% ± 7.8%, and specificity of 61% ± 14.4% by the established model. The best machine learning model predicted a 90-day MACRE with specificity of 44.61% ± 14.39%, and sensitivity of 57.13% ± 18.70%.Machine learning models based on routine demographics, clinical factors, and lab data can be used to predict hemodynamically significant CAD with accuracy that approximates current noninvasive functional modalities.

OBJECTIVE To determine whether the use of invasively measured hemodynamics improves the prognostic ability of a shock index (SI). BACKGROUND SI such as Admission-SI, Age-SI, Modified SI (MSI), and Age-MSI predict short-term mortality in ST-elevation myocardial infarction (STEMI). METHODS Single-center study of 510 patients who underwent primary percutaneous coronary intervention. STEMI SI was defined as age × heart rate (HR) divided by coronary perfusion pressure (CPP). RESULTS The mean age was 62 ± 14 years, 66% were males with hypertension (69%), tobacco use (38%), diabetes (28%) and chronic kidney disease (6%). The mean HR, systolic blood pressure (SBP), and CPP were 81 ± 18 bpm, 124 ± 28 mmHg, and 52.8 ± 16.3 mmHg, respectively. Patients with STEMI SI ≥182 (n = 51) were more likely to experience a cardiac arrest in the catheterization laboratory (9.8% vs. 2.0%; p = .001), require mechanical circulatory support (47.1% vs. 8.5%; p

The Age, Body mass index, Chronic kidney disease, Diabetes mellitus, and CYP2C19 GENEtic variants (ABCD-GENE) score was developed to identify patients at risk for diminished antiplatelet effects with clopidogrel after percutaneous coronary intervention (PCI). The objective of this study was to validate the ability of the ABCD-GENE score to predict the risk for atherothrombotic events in a diverse, real-world population of clopidogrel-treated patients who underwent PCI and received clinical CYP2C19 genotyping to guide antiplatelet therapy. A total of 2,341 adult patients who underwent PCI, were genotyped for CYP2C19, and received treatment with clopidogrel across four institutions were included (mean age 64 ± 12 years, 35% women, and 20% Black). The primary outcome was major atherothrombotic events, defined as the composite of all-cause death, myocardial infarction, ischemic stroke, stent thrombosis, or revascularization for unstable angina within 12 months following PCI. Major adverse cardiovascular events (MACE), defined as the composite of cardiovascular death, myocardial infarction, ischemic stroke, or stent thrombosis, was assessed as the secondary outcome. Outcomes were compared between patients with an ABCD-GENE score ≥ 10 vs. 10. The risk of major atherothrombotic events was higher in patients with an ABCD-GENE score ≥ 10 (n = 505) vs. 10 (n = 1,836; 24.6 vs. 14.7 events per 100 patient-years, adjusted hazard ratio (HR) 1.66, 95% confidence interval (CI), 1.23-2.25, P 0.001). The risk for MACE was also higher among patients with a score ≥ 10 vs. 10 (16.7 vs. 10.1 events per 100 patient-years, adjusted HR 1.59, 95% CI 1.11-2.30, P = 0.013). Our diverse, real-world data demonstrate diminished clopidogrel effectiveness in post-PCI patients with an ABCD-GENE score ≥ 10.

Genotyping for CYP2C19 no function alleles to guide antiplatelet therapy after percutaneous coronary intervention (PCI) improves clinical outcomes. Although results for the increased function CYP2C19*17 allele are also reported, its clinical relevance in this setting remains unclear. A collaboration across nine sites examined antiplatelet therapy prescribing and clinical outcomes in 3,342 patients after implementation of CYP2C19-guided antiplatelet therapy. Risk of major atherothrombotic and bleeding events over 12 months after PCI were compared across cytochrome P450 2C19 isozyme (CYP2C19) metabolizer phenotype and antiplatelet therapy groups by proportional hazards regression. Clopidogrel was prescribed to a similar proportion of CYP2C19 normal (84.5%), rapid (82.9%), and ultrarapid metabolizers (80.6%) (P = 0.360). Clopidogrel-treated normal metabolizers (20.4 events/100 patient-years; adjusted hazard ratio (HR) 1.00, 95% confidence interval (CI), 0.75-1.33, P = 0.993) and clopidogrel-treated rapid or ultrarapid metabolizers (19.1 events/100 patient-years; adjusted HR 0.95, 95% CI, 0.69-1.30, P = 0.734) exhibited no difference in major atherothrombotic events compared with patients treated with prasugrel or ticagrelor (17.6 events/100 patient-years). In contrast, clopidogrel-treated intermediate and poor metabolizers exhibited significantly higher atherothrombotic event risk compared with prasugrel/ticagrelor-treated patients (adjusted HR 1.56, 95% CI, 1.12-2.16, P = 0.008). When comparing clopidogrel-treated rapid or ultrarapid metabolizers to normal metabolizers, no difference in atherothrombotic (adjusted HR 0.97, 95% CI, 0.73-1.29, P = 0.808) or bleeding events (adjusted HR 1.34, 95% CI, 0.83-2.17, P = 0.224) were observed. In a real-world setting of genotype-guided antiplatelet therapy, the CYP2C19*17 allele did not significantly impact post-PCI prescribing decisions or clinical outcomes. These results suggest the CYP2C19 *1/*17 and *17/*17 genotypes have limited clinical utility to guide antiplatelet therapy after PCI.

In patients undergoing percutaneous coronary intervention (PCI), the standard of care is dual antiplatelet therapy with a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) and aspirin. Current clinical practice guidelines now recommend more potent P2Y12 inhibitors (prasugrel or ticagrelor) over clopidogrel in acute coronary syndrome (ACS). However, clopidogrel remains the most commonly prescribed P2Y12 inhibitor in the setting of PCI and is also the preferred agent in the treatment and secondary prevention of stroke. Clopidogrel is a prodrug that requires bioactivation by the CYP2C19 enzyme. It has been shown that clopidogrel use in patients who are CYP2C19 no function allele carriers are associated with impaired antiplatelet inhibition and a higher risk of major adverse cardiovascular and cerebrovascular events. Compared to clopidogrel, prasugrel and ticagrelor clinical response is not impacted by CYP2C19 genotype. Even with a demonstrated increased risk of adverse outcomes in CYP2C19 no function allele carriers treated with clopidogrel, routine implementation of CYP2C19 genotyping to guide antiplatelet therapy selection has remained controversial and has not been widely adopted. Recent results from multiple prospective randomized and nonrandomized clinical trials investigating the use of CYP2C19 genotype-guided antiplatelet therapy following PCI have advanced the evidence base demonstrating the clinical utility of this strategy. Multiple recent studies have examined the effects of CYP2C19 genotype on clopidogrel outcomes in the setting of stroke and neurointerventional procedures. In this review, we discern the clinical utility of using CYP2C19 genotype testing to guide antiplatelet therapy prescribing by evaluating the impact of CYP2C19 genotype-guided selection of antiplatelet therapy on clinical outcomes, summarizing emerging data from cardiovascular and neurology clinical studies, and discussing implications for clinical practice guidelines, remaining knowledge gaps and future research directions.

OBJECTIVE Study the effect of coronary artery calcium (CAC) on resting coronary physiological indices. BACKGROUND Prior studies found no correlation between angiographic stenosis and fractional flow reserve (FFR) in heavily calcified arteries. METHODS Two hundred consecutive patients undergoing whole-cycle resting Pd/Pa and FFR evaluation of a single lesion of intermediate severity (40-80%) had CAC quantified based upon radiopacities at the site of the stenosis, where 0 = none or mild calcium, 1 = moderate calcium, and 2 = severe calcium. RESULTS Mean age was 61 ± 11 years and 34% were female. The mean degree of stenosis, FFR, and resting Pd/Pa were 60 ± 12%, 0.83 ± 0.08, and 0.93 ± 0.05, respectively. Resting Pd/Pa correlated with degree of angiographic diameter stenosis (DS) as determined by quantitative coronary angiography (QCA) or visual estimation in arteries with calcium score of 0 or 1, but there was no correlation in severely calcified arteries. The diagnostic accuracy of DS ≥70% by QCA to predict hemodynamic significance was 68% with calcium scores of 0/1, but only 43% with calcium score = 2. Resting Pd/Pa was highly correlated with FFR irrespective of the degree of CAC (R2 = 0.68, p

We describe the case of a 42-year-old female with recurrent left ventricular (LV) thrombus and multiple embolic events despite having normal LV systolic function. The clinical presentation, associated conditions, diagnostic evaluation and treatment of patients with LV thrombus in the setting of normal LV systolic function are discussed. (Level of Difficulty: Beginner.), Graphical abstract, We describe the case of a 42-year-old female with recurrent left ventricular (LV) thrombus and multiple embolic events despite having normal…

Antiplatelet agents and anticoagulants are a mainstay for the prevention and treatment of thrombosis. However, despite advances in antithrombotic therapy, a fundamental challenge is the side effect of bleeding. Improved understanding of the mechanisms of haemostasis and thrombosis has revealed new targets for attenuating thrombosis with the potential for less bleeding, including glycoprotein VI on platelets and factor XIa of the coagulation system. The efficacy and safety of new agents are currently being evaluated in phase III trials. This Review provides an overview of haemostasis and thrombosis, details the current landscape of antithrombotic agents, addresses challenges with preventing thromboembolic events in patients at high risk and describes the emerging therapeutic strategies that may break the inexorable link between antithrombotic therapy and bleeding risk.

Background: While the benefits of drug-eluting stents (DES) during percutaneous coronary intervention (PCI) are well established, the frequency and timing of repeat revascularization events, particularly early events, is not well described in contemporary clinical practice. Methods: Patients undergoing PCI at two large tertiary centers in a single health system from April 2014 to December 2019 were prospectively enrolled into the NCDR CathPCI Registry. Target vessel revascularization (TVR) and target lesion revascularization (TLR) were defined as a repeat intervention to the index vessel or lesion respectively and determined by linking to subsequent PCI events and CABG admissions in the EMR. Early TVR and TLR rates were identified at 30 days, 90 days, six months, and one year. Logistic regression was used to estimate the association between stent type and TVR/TLR at the pre-specified time points. Generalized estimating equations with nested modeling were used to account for patients with multiple vessels and lesions. Results: Overall, 8,221 PCI procedures were identified in 7,128 patients with 9,558 vessel interventions and 12,019 lesion interventions. There were similar rates of TVR for Zotarolimus eluting durable polymer stents (ZES-DP), Everolimus eluting bioabsorbable polymer stents (EES-BAP), and Everolimus eluting durable polymer stents (EES-DP) at 30 days (p=0.61), 90 days (p=0.79), six months (p=0.58), and one year (p= 0.35). There were similarly no differences in TLR between stent types at each time point (p= 0.57, 0.79, 0.16, 0.13 respectively). The total rates of TLR and TVR progressed linearly throughout the year following PCI with nearly half of all repeat revascularization events occurring within 6 months. Table 1. Conclusions: Within a single health system from 2014 to 2019, ZES-DP, EES-BAP, and EES-DP were associated with similar rates of TVR and TLR. These events appear to occur earlier than typically reported in clinical trials.

The use of catheter-based renal denervation (RD) for the treatment of hypertension showed promise in early proof-of-concept trials; however, enthusiasm to pursue clinical trials outpaced efforts to understand underlying fundamental principles. The Symplicity HTN-3 trial was a randomized, sham-controlled study that found that the effect of RD on blood pressure in patients with resistant hypertension was no different than seen in the control group. Retrospective analyses showed that the therapeutic failure more likely resulted from suboptimal first-generation technology and poor clinical trial design rather than a failure of concept. This led to the development of new catheters which deliver a more consistent ablation to renal nerves. The most recent studies which utilize these new catheters have demonstrated a consistent reduction in blood pressure, and interest in the field has been renewed. In the aftermath of early clinical trials, a reevaluation of the field of RD resulted in recommendations for improved study design, enhanced procedural techniques, and newly developed catheter technologies. These changes have been incorporated into contemporary studies, which have provided consistent evidence that catheter-based RD can cause a significant reduction in blood pressure in patients with hypertension. Recent developments in the field of RD have lent credence to the notion that a procedure-based approach to lower blood pressure may augment current treatment strategies for hypertension. Future research will help to better define its clinical role and utility.

Hypercholesterolemia is a well-established risk factor for atherosclerotic cardiovascular disease (ASCVD). How cholesterol and its carrier lipoproteins are involved in ASCVD is still under extensive investigation. Satins are thus far the best proven class of cholesterol lowering medications to improve the clinical outcomes of ASCVD. Statins specifically inhibit the rate-limiting enzyme 3-hydroxy-3-methylglutaryl-CoA reductase of the mevalonate (MVA) pathway for cholesterol biosynthesis. The widely accepted theory is that statins inhibit the hepatic cholesterol synthesis causing upregulation of hepatocyte low-density lipoprotein (LDL) receptor; receptor mediated LDL uptake and metabolism in the liver results in reduction of circulating LDL cholesterol (LDL-C), which subsequently reduces vascular deposition and retention of cholesterol or LDL in atherogenesis. Nevertheless, cholesterol biosynthesis is ubiquitous, also in extrahepatic cells including those in vascular wall, under tight regulation by sterol regulatory element-binding protein (SREBP), the master gene transcription factor governing cholesterol biosynthesis. Studies have shown that SREBP can be upregulated in vascular wall subject to injury or stent implantation. SREBP can be activated by proinflammatory and mitogenic factors in vascular cells, leading to hyperactive MVA pathway, which promotes vascular cell mobilization, further proinflammatory and mitogenic factor release from vascular cells, and vascular inflammation. In this article, we review the cellular cholesterol homeostasis regulation by SREBP and SREBP-mediated vascular hyperactive cholesterol biosynthesis, we term vascular hypercholesterolism, in the pathogenesis of ASCVD and vasculopathy. SREBP functions as a platform bridging cholesterol, inflammation, and vascular cell mobilization in ASCVD pathogenesis. Targeting vascular hypercholesterolism could open a new avenue in fighting against ASCVD.

We sought to test the hypothesis that patients undergoing ultrasound-assisted catheter-directed thrombolysis (USAT) with standard alteplase and heparin dosing would not develop significant depletion of systemic fibrinogen, which may account for the lower risk of bleeding seen in contemporary trials. We also sought to compare the relative outcomes of individuals with submassive pulmonary embolism (PE) undergoing USAT and anticoagulation alone.Utilizing a single-center prospective registry, we identified 102 consecutive adult patients with submassive PE who were considered for USAT based on a standardized treatment algorithm between November 2016 and May 2019. Patients not receiving USAT therapy were treated with anticoagulation alone.Baseline characteristics were generally similar between groups (n = 51 in each group). Major bleeding rates were not significantly different between groups (2.0% vs 5.9% in USAT vs control, respectively; P=.62). Notably, no USAT patient experienced clinically significant hypofibrinogenemia (mean trough fibrinogen, 369.8 ± 127.1 mg/dL; minimum, 187 mg/dL). The mean trough fibrinogen of patients experiencing any bleeding event (major or minor) was 306.6 mg/dL (SE, 23.9 mg/dL) vs 380.3 mg/dL (SE, 20.4 mg/dL) in those without a bleeding event (P=.02).In this cohort analysis of patients undergoing USAT, there was no evidence for clinically significant depletion of fibrinogen or intracranial hemorrhage. Although our data suggest an association between lower fibrinogen levels and bleeding events, our results are not clear enough to suggest a clinically useful fibrinogen cut-off value. Further study is needed to determine the utility of routine fibrinogen monitoring in this population.

INTRODUCTION: CYP2C19 genotype-guided selection of P2Y12 inhibitor therapy after percutaneous coronary intervention (PCI) is associated with improved clinical outcomes, but clinical utility in older patients in a real-world setting is unknown. OBJECTIVES: To compare the clinical effectiveness of genotype-guided P2Y12 inhibitor selection following PCI in older patients (≥70 years) and younger patients (

Hydration is recommended to prevent contrast associated-acute kidney injury (CA-AKI) but interactions between blood pressure, left ventricular end diastolic pressure (LVEDP) and hydration status on CA-AKI are incompletely understood. This analysis presents the results of a single-center prospective study of patients undergoing coronary angiography with a predicted risk of CA-AKI >14%. 146 patients were enrolled with a mean (±SD) age of 71 ± 11 years; 94 (64.4%) were men, 142 (97.3%) had hypertension, 96 (65.8%) had diabetes mellitus and the mean (SD) serum creatinine was 1.21 ± 0.36 mg/dl. CA-AKI occurred in 31 (21%) patients. There were no significant differences in demographics, comorbidities, renal function, LVEDP, systolic blood pressure, diastolic blood pressure, heart rate, mean arterial pressure or pulse pressure in patients who developed versus those who did not develop CA-AKI. There was no association between the amount of peri-procedure intravenous fluids and change in creatinine postprocedure. In multivariate analysis, hemoglobin, the time that the patient was fasting from solids (NPO time), and contrast volume were associated with the development of CA-AKI. There was a highly significant interaction (p = 0.0028) between the amount of intravenous fluids, NPO time and contrast volume and changes in postprocedure creatinine. In summary, hemoglobin, NPO time and contrast volume, but not hemodynamic variables, correlated with worsening renal function following coronary angiography in this population of high-risk patients. Results suggested that intravenous hydration is important in subgroups of patients depending on NPO time and contrast volume.

[Figure][1] ![Figure][1] ![Figure][1] ![Figure][1] Beginning in 2016, the American College of Cardiology (ACC) Board of Governors and the Section Steering Committee petitioned the ACC Board of Trustees to allow domestic state chapters and member sections to jointly

Purpose To evaluate the frequency and clinical impact of switches in antiplatelet therapy following implementation of CYP2C19 genotyping after percutaneous coronary intervention (PCI). Methods The frequency of escalation (clopidogrel switched to prasugrel/ticagrelor) and de-escalation (prasugrel/ticagrelor switched to clopidogrel) was evaluated in 1063 PCI patients who underwent CYP2C19 genotyping. Risk of major adverse cardiovascular or cerebrovascular (MACCE) and bleeding events over one-year was evaluated. Results Antiplatelet therapy switches were common (19%), with escalation (101/115: 88%) and de-escalation (77/84: 92%) occurring predominantly in patients with and without a CYP2C19 nonfunctional allele, respectively. Nonfunctional allele carriers initiated and continued on clopidogrel had a significantly higher risk of experiencing either a MACCE or bleeding event compared to those escalated to prasugrel/ticagrelor (52 vs. 19 events/100 patient-years; adjusted hazard ratio [HR] 2.89 [1.44–6.13], p=0.003). Patients without a nonfunctional allele de-escalated to clopidogrel had no difference in risk compared to those initiated and continued on prasugrel/ticagrelor (21 vs. 19 events/100 patient-years; adjusted HR 1.13 [0.51–2.34], p=0.751). Conclusions CYP2C19-guided escalation and de-escalation is common in a real-world setting. Continuation of clopidogrel in nonfunctional allele carriers is associated with adverse outcomes. De-escalation to clopidogrel in patients without a nonfunctional allele appears safe and warrants prospective study.

ST elevation myocardial infarction (STEMI) occurring in patients hospitalized for a noncardiac condition is associated with a high mortality rate and thus we sought to determine the mechanisms underlying STEMI in this patient population. This is a single center retrospective study of 70 patients who had STEMI while hospitalized on a noncardiac service and underwent coronary angiography. Thrombotic in-hospital STEMI was defined by angiographic or intravascular imaging evidence of intracoronary thrombus, plaque rupture, or stent thrombosis. Thirty-six (51%) inpatient STEMIs developed in the operating room or various postoperative stages and 6 (9%) after endoscopy or a percutaneous procedure. Thrombotic etiologies were found in 39 (56%) patients. Nonthrombotic etiologies included vasospasm, supply-demand mismatch, and takotsubo cardiomyopathy. Patients in the thrombotic group were more likely to have antiplatelet medications discontinued on admission, had higher peak troponin levels and were more likely to undergo percutaneous coronary intervention than patients in the nonthrombotic group. Exposure to vasopressors, time from ECG to angiography, post-STEMI ejection fraction, length of stay, and in-hospital mortality were similar in both groups. There was no difference in the use of percutaneous coronary intervention in patients but longer ECG to coronary angiography times and fivefold higher in-hospital mortality in thrombotic inpatient STEMI compared with 643 patients who presented with an out-of-hospital STEMI during the same time period. In conclusion, thrombotic and nonthrombotic mechanisms cause STEMI in hospitalized patients and are associated with a high mortality.