2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines.

AIM: The "2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease" provides an update to and consolidates new evidence since the "2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease" and the corresponding "2014 ACC/AHA/AATS/PCNA/SCAI/STS Focused Update of the Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease." METHODS: A comprehensive literature search was conducted from September 2021 to May 2022. Clinical studies, systematic reviews and meta-analyses, and other evidence conducted on human participants were identified that were published in English from MEDLINE (through PubMed), EMBASE, the Cochrane Library, Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline. STRUCTURE: This guideline provides an evidenced-based and patient-centered approach to management of patients with chronic coronary disease, considering social determinants of health and incorporating the principles of shared decision-making and team-based care. Relevant topics include general approaches to treatment decisions, guideline-directed management and therapy to reduce symptoms and future cardiovascular events, decision-making pertaining to revascularization in patients with chronic coronary disease, recommendations for management in special populations, patient follow-up and monitoring, evidence gaps, and areas in need of future research. Where applicable, and based on availability of cost-effectiveness data, cost-value recommendations are also provided for clinicians. Many recommendations from previously published guidelines have been updated with new evidence, and new recommendations have been created when supported by published data.

Indoor particulate matter concentrations and air cleaner intervention association with biomarkers in former smokers with COPD.

BACKGROUND: Indoor pollutants have been associated with worse clinical outcomes in chronic obstructive pulmonary disease (COPD). Elevated biomarkers are associated with ambient pollution exposure, however the association with indoor pollution remains unclear. METHODS: Former smokers with spirometry-confirmed COPD were randomized to portable air cleaner or placebo. Indoor particulate matter (PM2.5, PM10, and ultrafine particles [UFP; PM<0.1]) and biomarkers were measured longitudinally at pre-specified intervals and course PM fraction (PM10-2.5) was calculated. Biomarkers were categorized based on associations with biologic mechanisms: inflammation (white blood cell count, interleukin [IL]-6, IL-8, IL-1ß, tumor necrosis factor-α, interferon-γ, serum amyloid A), platelet activation (P-selectin, CD40 ligand [CD40L], 11-dehdydro-thromboxane-B2 [11dTxB2]), endothelial dysfunction (Vascular Cell Adhesion Molecule [VCAM]-1, Intercellular Adhesion Molecule [ICAM]-1), and oxidative stress (thiobarbituric acid reactive substances [TBARS], 8-hydroxydeoxyguanosine, 8-isoprostane). Associations between PM concentrations and each biomarker were analyzed using multivariable linear mixed models. An intention-to-treat analysis was performed to evaluate the air cleaner intervention on the biomarker levels longitudinally. RESULTS: Fifty-eight participants were randomized to each group. Finer PM was more strongly associated with higher IL-8 (mean difference per doubling: UFP 13.9% [p = 0.02], PM2.5 6.8% [p = 0.002], PM10-2.5 5.0% [p = 0.02]) while interferon-γ was associated with UFP and IL-1ß with PM10-2.5. UFP and PM2.5 were associated with elevated levels of the oxidative stress biomarkers TBARS and 8-isoprostane respectively. For platelet activation markers, UFP was associated with higher 11dTxB2 while PM2.5 was associated with higher P-selectin and CD40L. Pollutants were not associated with biomarkers of endothelial dysfunction. In intention-to-treat analysis there was no association of the air cleaner intervention with any of the biomarkers. DISCUSSION: Among former smokers with COPD, elevated levels of indoor air pollutants, particularly ultrafine particles (PM<0.1), were associated with elevated biomarkers of inflammation, platelet activation, and oxidative stress. However, an air cleaner intervention that reduced PM did not significantly reduce biomarker levels.

What Is the Optimal Duration of Antiplatelet Therapy for Patients with Coronary Heart Disease?

PURPOSE OF REVIEW: Optimal duration of antiplatelet therapy continues to attract extensive debates and has been progressively adjusted in the setting of advancements in stent design and assessment of patient clinical characteristics. Given the ever-changing landscape of antiplatelet therapy and the multitude of clinical trials that have examined this duration, there are varying scenarios for optimal duration based on patient presentation and risk profile. This review highlights the current concepts and recommendations regarding duration of antiplatelet therapy in coronary heart disease. RECENT FINDINGS: In particular, we review the current data on the use of dual antiplatelet therapy in the different clinical scenarios. Relatively longer dual antiplatelet therapy is perhaps limited to patients with higher risk for cardiovascular events and/or high-risk lesions and shorter durations of dual antiplatelet therapy have been shown to reduce bleeding complications at the same time as stabilization of ischemic endpoints. More recent trials have demonstrated the safety of shorter durations of dual antiplatelet therapy in appropriate patients with coronary heart disease.

Center Variation in Use of Preoperative Dual Antiplatelet Therapy and Platelet Function Testing at the Time of Coronary Artery Bypass Grafting in Maryland.

BACKGROUND: Patients presenting with acute coronary syndrome are administered a P2Y 12 inhibitor and aspirin before coronary catheterization to prevent further myocardial injury from thrombosis. Guidelines recommend a standard waiting period between the time patients are administered dual antiplatelet therapy (DAPT) and elective cardiac surgery. Since 25% to 30% of the population may be considered nonresponders to clopidogrel, platelet function testing can be utilized for timing of surgery and to assess bleeding risks. The extent to which a standard waiting period or platelet function testing is used across centers is not established, representing an important opportunity to standardize practice. METHODS: We conducted a retrospective cohort study from 2011 to 2020 using data from the Maryland Cardiac Surgical Quality Initiative, a consortium of all 10 hospitals in the state performing cardiac surgery. The proportion of patients administered DAPT within 5 days of surgery was examined by hospital over the time period. Mixed-effects multivariable logistic regressions were used to examine the association of preoperative DAPT with ischemic and bleeding outcomes. Centers were surveyed on use or nonuse of preoperative platelet function testing, and bleeding outcomes were compared. RESULTS: There was significant heterogeneity of preoperative DAPT usage across centers ranging from 2% to 54% ( P < .001). DAPT within 5 days of isolated coronary artery bypass grafting (CABG) was associated with higher odds of reoperation for bleeding (odds ratio [OR], 1.55; 95% confidence interval [CI], 1.19-2.01; P = .001), >2 units of red blood cells (RBCs) transfused (OR, 1.62; 95% CI, 1.44-1.81; P < .001), and >2 units of non-RBCs transfused (OR, 1.79; 95% CI, 1.60-2.00; P < .001). In the 5 hospitals using preoperative platelet function testing to guide timing of surgery, there were greater odds for DAPT within 5 days (OR, 1.33; 95% CI, 1.22-1.45; P < .001), fewer RBCs >2 units transfusions (22% vs 33%; P < .001), and non-RBCs >2 units (17% vs 28%; P < .001) transfusions within DAPT patients. CONCLUSIONS: There is significant variability in DAPT usage within 5 days of CABG between hospital centers. Preoperative platelet function testing may allow for earlier timing of surgery for those on DAPT without increased bleeding risks.

Platelet Serotonin Signaling in Patients With Cardiovascular Disease and Comorbid Depression.

OBJECTIVE: Depression in patients with cardiovascular disease is associated with increased risk of adverse clinical outcomes. Investigators have searched for potential biobehavioral explanations for this increased risk. Platelet activation and response to serotonin is an attractive potential mechanism. The aim of the study was to examine platelet serotonin signaling in a group of patients with coronary artery disease (CAD) and comorbid depression to define the relationship between platelet serotonin signaling and cardiovascular complications. METHODS: A total of 300 patients with CAD were enrolled (145 with acute coronary syndrome and 155 with stable CAD). Depression was assessed using the Structured Clinical Interview for DSM-IV as well as Beck Depression Inventory II in a dichotomous and continuous manner. Platelet serotonin response was measured by serotonin augmented aggregation, direct platelet serotonin activation, platelet serotonin receptor density, and platelet serotonin uptake. Cardiovascular outcomes were assessed at 12-month follow-up. RESULTS: One third of enrolled participants had at least minimal depressive symptoms and 13.6% had major depressive disorder. Depressed cardiovascular patients had significantly higher incidence of major (odds ratio = 3.43, 95% confidence interval = 1.49-7.91, p = .004) and minor (odds ratio = 2.42, 95% confidence interval = 1.41-4.13, p = .001) adverse cardiac events. Platelet serotonin response was not significantly different in patients with depression. Participants with major depressive disorder had higher serotonin receptor density (997.5 ± 840.8 vs 619.3 ± 744.3 fmol/ug, p = .009) primarily found in ACS patients. Depressed patients with minor adverse cardiac events had increased platelet response to serotonin. CONCLUSIONS: Depressed cardiovascular patients had higher serotonin receptor density and significantly higher incidence of major and minor cardiac adverse events. Future studies with larger sample sizes including patients with more severe depression are needed to expand on the present hypothesis-generating findings.

Do platelet-derived microparticles play a role in depression, inflammation, and acute coronary syndrome?

BACKGROUND: Major depression is an independent predictor of increased mortality in patients presenting with acute coronary syndromes (ACS). There have been several mechanisms proposed to explain the link between depression and ischemic heart disease. Both abnormal platelet physiology and inflammation have been suggested as potential confounding variables. OBJECTIVE: We set out to examine platelet activation, inflammation, and levels of depression in hospitalized patients presenting with ACS. METHODS: We enrolled 28 patients with ACS and assessed levels of depression by PHQ-9. Platelet activation was assessed by the measurement of platelet microparticle levels and platelet aggregation to adenosine diphosphate and serotonin. Inflammatory markers were assessed by the measurement of TNF alpha, IL-6, and CRP. RESULTS: We found that ACS patients with moderate depressive symptoms who had higher TNF alpha, IL-6, and CRP levels had higher levels of platelet microparticles. We also found that ACS patients with PHQ-9 ≥ 10 had higher platelet aggregation to ADP. CONCLUSION: Our results suggest that patients hospitalized for the treatment of an ACS who have moderate depression have increased platelet aggregation. These patients also have a positive association between elevated inflammatory markers and platelet activation, thus suggesting a pro-inflammatory component in ACS patients with depressive symptoms that may alter platelet function. These results are intriguing in that a potential pathway to explain the connection between depression, inflammation, and increased cardiovascular thrombosis might be found when both platelet activation and inflammation are measured.

Urine and Plasma Markers of Platelet Activation and Respiratory Symptoms in COPD.

Introduction: Antiplatelet therapy has been associated with fewer exacerbations and reduced respiratory symptoms in chronic obstructive pulmonary disease (COPD). Whether platelet activation is associated with respiratory symptoms in COPD is unknown. Methods: Former smokers with spirometry-confirmed COPD had urine 11-dehydro-thromboxane B2 (11dTxB2), plasma soluble CD40L (sCD40L), and soluble P-selectin (sP-selectin) repeatedly measured during a 6- to 9-month study period. Multivariate mixed-effects models adjusted for demographics, clinical characteristics, and medication use evaluated the association of each biomarker with respiratory symptoms, health status, and quality of life. Results: Among 169 participants (average age 66.5±8.2 years, 51.5% female, 47.5±31 pack years, forced expiratory volume in 1 second percent predicted 53.8±17.1), a 100% increase in 11dTxB2 was associated with worse respiratory symptoms reflected by higher scores on the COPD Assessment Test (ß 0.77, 95% confidence interval [CI]: 0.11-1.4) and Ease of Cough and Sputum Clearance Questionnaire ß 0.77, 95%CI: 0.38-1.2, worse health status (Clinical COPD Questionnaire ß 0.13, 95%CI: 0.03-0.23) and worse quality of life (St George's Respiratory Questionnaire ß 1.9, 95%CI: 0.39-3.4). No statistically significant associations were observed for sCD40L or sP-selectin. There was no consistent statistically significant effect modification of the relationship between urine 11dTxB2 and respiratory outcomes by history of cardiovascular disease, subclinical coronary artery disease, antiplatelet therapy, or COPD severity. Conclusions: In stable moderate-severe COPD, elevated urinary11dTxB2, a metabolite of the platelet activation product thromboxane A2, was associated with worse respiratory symptoms, health status, and quality of life.

Platelet activation and endothelial dysfunction biomarkers in acute coronary syndrome: the impact of PCSK9 inhibition.

AIMS: Platelet activation and endothelial dysfunction contribute to adverse outcomes in patients with acute coronary syndromes (ACS). The goals of this study were to assess the impact of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition on markers of platelet activation and endothelial dysfunction in ACS patients and the interaction among PCSK9, platelets, and endothelial cells (ECs) on left internal mammary artery (LIMA) vascular endothelium using specimens obtained during coronary artery bypass surgery (CABG). METHODS AND RESULTS: Acute coronary syndromes patients enrolled in the Evolocumab in ACS trials were randomized to placebo or a single dose of 420 mg evolocumab within 24 h of hospitalization. Serum samples for analysis of platelet factor 4 (PF4) and P-selectin, markers of platelet activation, and von Willebrand factor (vWF), a marker of endothelial dysfunction, were obtained at baseline and 30 days. Additionally, LIMA segments obtained during CABG from patients who were and were not receiving evolocumab were immunostained with PCSK9; CD61, a platelet-specific marker; and CD31, an endothelial cell-specific marker. Forty-six participants were randomized to placebo or to evolocumab. Controlling for baseline levels, PF4 and vWF were significantly lower in the evolocumab, than in the placebo, group at 30 days. Immunostaining of LIMA specimens from twelve participants undergoing CABG revealed colocalization of PCSK9, CD61, and CD31 at the vascular endothelium. Administration of evolocumab was associated with decreased overlap of PCSK9, CD61, and CD31. CONCLUSIONS: Proprotein Convertase Subtilisin/Kexin 9 inhibition decreases markers of platelet activation and endothelial dysfunction in ACS patients. PCSK9 is associated with platelets and vascular ECs in LIMA segments and PCSK9 inhibition decreases that interaction.

2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines.

AIM: The "2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease" provides an update to and consolidates new evidence since the "2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease" and the corresponding "2014 ACC/AHA/AATS/PCNA/SCAI/STS Focused Update of the Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease." METHODS: A comprehensive literature search was conducted from September 2021 to May 2022. Clinical studies, systematic reviews and meta-analyses, and other evidence conducted on human participants were identified that were published in English from MEDLINE (through PubMed), EMBASE, the Cochrane Library, Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline. STRUCTURE: This guideline provides an evidenced-based and patient-centered approach to management of patients with chronic coronary disease, considering social determinants of health and incorporating the principles of shared decision-making and team-based care. Relevant topics include general approaches to treatment decisions, guideline-directed management and therapy to reduce symptoms and future cardiovascular events, decision-making pertaining to revascularization in patients with chronic coronary disease, recommendations for management in special populations, patient follow-up and monitoring, evidence gaps, and areas in need of future research. Where applicable, and based on availability of cost-effectiveness data, cost-value recommendations are also provided for clinicians. Many recommendations from previously published guidelines have been updated with new evidence, and new recommendations have been created when supported by published data.

Persistent high on-treatment platelet reactivity in acute coronary syndrome.

Persistent high on-treatment platelet reactivity in acute coronary syndrome (ACS) patients managed with appropriate antiplatelet therapy has been correlated with increased risk of cardiovascular events; however, the evolution of this phenomenon overtime is not well known. We investigated platelet activity at a three month follow-up after initial presentation with an ACS. We enrolled a total of 124 patients in the study, 65 were diagnosed with ACS and 59 controls who presented with non-cardiac chest pain for baseline comparisons. Of the enrolled patients, we had 25 ACS patients return, in stable condition, three months after their initial presentation for repeat platelet functional testing. Epinephrine (EPI), adenosine diphosphate (ADP), and arachidonic acid induced platelet aggregation were monitored at baseline with repeat measurement of EPI- and ADP-stimulated aggregation at follow-up. In addition, P-selectin and PAC-1 expression were monitored at presentation and at a three month follow-up period. ACS patients were maintained on aspirin therapy during the intervening period. At the three month follow-up visit, ACS patients initiated on aspirin had no significant percentage change in aggregation to submaximal concentrations of EPI and ADP. They also had no significant percentage change in PAC-1 or P-selectin expression. This study demonstrates persistent high on-treatment platelet reactivity in ACS patients at a three month follow-up, which may place these patients at increased risk of recurrent cardiovascular events.

The Trajectory of Lipoprotein(a) During the Peri- and Early Postinfarction Period and the Impact of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibition.

Lipoprotein(a), or Lp(a), levels and the effect of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition on Lp(a) during the peri-infarction and early postinfarction period are not well characterized. This study aimed to describe the trajectory of Lp(a), as well as the effect of PCSK9 inhibition on that trajectory during the peri-infarction and early postinfarction period. Lp(a) levels were obtained within 24 hours of hospital admission as well as within 24 hours of hospital discharge and at 30 days from 74 participants who presented with a NSTEMI (troponin I >5 ng/ml) or with a STEMI and were enrolled in 2 randomized, double-blind trials of evolocumab and placebo (Evolocumab in Acute Coronary Syndrome [EVACS I]; ClinicalTrials.gov, NCT03515304 and Evolocumab in Patients With STEMI [EVACS II]; ClinicalTrials.gov Identifier: NCT04082442). There was a significant increase from the pretreatment level in the placebo-treated patients, from 64 (41,187) nmol/L to 80 (47, 172) nmol/L at hospital discharge and to 82 (37, 265) at 30 days. This was primarily driven by the results from participants with high Lp(a) at hospital admission (>75 nmol/L) in whom the median increase was 28% as compared with a 10% increase in those with pretreatment Lp(a) of <75 nmol/L. In contrast, there was no significant change from the pretreatment level in the evolocumab-treated patients regardless of pretreatment Lp(a) levels. In conclusion, Lp(a) rises during the peri-infarction and early postinfarction period in patients with acute myocardial infarction. The increase was prevented by a single dose of subcutaneous evolocumab given within 24 hours of hospital admission.

Genetic regulation of platelet receptor expression and function: application in clinical practice and drug development.

Understanding genetic contributions to platelet function could have profound clinical ramifications for personalizing platelet-directed pharmacotherapy, by providing insight into the risks and possible benefits associated with specific genotypes. This article represents an integrated summary of presentations related to genetic regulation of platelet receptor expression and function given at the Fifth Annual Platelet Colloquium in January 2010. It is supplemented with additional highlights from the literature covering (1) approaches to determining and evidence for the associations of genetic variants with platelet hypo- and hyperresponsive phenotypes, (2) the ramifications of these polymorphisms with regard to clinical responses to antiplatelet therapies, and (3) the role of platelet function/genetic testing in guiding antiplatelet therapy.

Racial differences in platelet serotonin polymorphisms in acute coronary syndrome.

INTRODUCTION: Genetic differences between races have been hypothesized to contribute to differences in outcome from acute coronary syndromes (ACS). Our objective was to assess racial differences in genetic variations in the platelet serotonin transporter (5HTT) and receptor in patients with ACS. MATERIALS AND METHODS: 127 consecutive patients, African Americans (AA) = 27; Caucasian (C) =100, admitted with ACS were evaluated for platelet function by serotonin (5HT) induced platelet activation. All patients were genotyped for two polymorphisms in the serotonin-transporter-linked polymorphic region (5-HTTLPR) S/L and LG/LA and one polymorphism of the serotonin 2A receptor (5-HT2A, T102C) gene. All patients were followed for major and minor adverse cardiac events at 12 months. RESULTS: AA when compared to C had a lower prevalence of the HTTLPR S allele (21% vs 45%, p = 0.0003) and a higher prevalence of the LG allele (24% vs 4.5%, p = 0.0001). Allelic frequency of the 5-HT2A T102C allele was not significantly different between the races. Platelet activation was lower in AA compared to C, median EC50 5HT was 12.08 µg vs 2.14 µg (p = 0.001). The 5-HTTLPR and the 5-HT2A polymorphisms were not associated with platelet functional responses to serotonin. There were no significant differences in major or minor adverse cardiac events in patients with serotonin transporter or receptor polymorphisms. CONCLUSION: We found a lower prevalence of the S allele and a higher prevalence of the G allele in AA with ACS. We also found decreased platelet activation in AA which did not correlate with serotonin-related platelet polymorphisms. It is unclear if other contributing factors may explain these platelet functional differences.

Effect of Crizanlizumab, a P-Selectin Inhibitor, in COVID-19: A Placebo-Controlled, Randomized Trial.

COVID-19 is characterized by vascular inflammation and thrombosis, including elevations in P-selectin, a mediator of inflammation released by endothelial cells. We tested the effect of P-selectin inhibition on biomarkers of thrombosis and inflammation in patients with COVID-19. Hospitalized patients with moderate COVID-19 were randomly assigned to receive either placebo or crizanlizumab, a P-selectin inhibitor, in a double-blind fashion. Crizanlizumab reduced P-selectin levels by 89%. Crizanlizumab increased D-dimer levels by 77% and decreased prothrombin fragment. There were no significant differences between crizanlizumab and placebo for clinical endpoints. Crizanlizumab was well tolerated. Crizanlizumab may induce thrombolysis in the setting of COVID-19. (Crizanlizumab for Treating COVID-19 Vasculopathy [CRITICAL]; NCT04435184).

Clopidogrel use in coronary heart disease and percutaneous coronary intervention.

Antiplatelet therapy has proven efficacy in the management of atherothrombosis. Clopidogrel, a thienopyridine, is a potent antiplatelet agent that achieves its antiplatelet effects by inhibiting the binding of adenosine 5' diphosphate to its platelet receptor. Large clinical trials have demonstrated a role for clopidogrel in the management of symptomatic atherosclerosis, acute coronary syndromes, and patients undergoing percutaneous coronary intervention. In this review, we discuss the pharmacology of clopidogrel including the mechanism of action, review the major clinical trials that have defined the current role of clopidogrel in coronary heart disease and percutaneous coronary intervention, and, finally, examine the concept of clopidogrel resistance and its potential clinical implications.

Editor's Choice-The cardiovascular implications of sedatives in the cardiac intensive care unit.

Patients admitted to the cardiac intensive care unit frequently develop multi-organ system dysfunction associated with their cardiac disease. In many cases, invasive mechanical ventilation is required, which often necessitates sedation for patient-ventilator synchrony, reduction of work of breathing, and patient comfort. In this paper, we describe the use of common sedatives available in the endotracheally intubated critically ill patient and emphasize the clinical and cardiovascular effects. We review γ-aminobutyric acid agonists such as etomidate, benzodiazepines, and propofol, the centrally acting α2-agonist dexmedetomidine, and the N-methyl-D-aspartate receptor antagonist ketamine. Additionally, we outline the use of opioids and their role in potentiating other sedatives. We note that some sedatives are associated with increased delirium rates, and emphasize that judicious strategies minimizing sedative use are associated with decreases in morbidity and mortality. We also discuss standardized sedation assessment scales and highlight the importance of sedation weaning. Finally, we offer recommendations for sedation use during therapeutic hypothermia, and discuss the use of adjuvant neuromuscular blocking agents.

The correlation between intensive care unit attending physician continuity of care with financial and clinical outcomes.

PURPOSE: "Attending rotations" on intensive care unit (ICU) services have been in place in most teaching hospitals for decades. However, the ideal frequency of patient care handoffs is unknown. Frequent attending physician handoffs could result in delays in care and other complications, while too few handoffs can lead to provider burnout and exhaustion. Therefore, we sought to determine the correlation between frequency of attending shifts with ICU charges, 30-day readmission rates, and mortality rates. METHODS: We performed a retrospective cohort study at a large, urban, academic community hospital in Baltimore, MD. We included patients admitted into the cardiac or medical ICUs between September 1, 2012, and December 10, 2015. We tracked the number of attending shifts for each patient and correlated shifts with financial outcomes as a primary measure. RESULTS: For any given ICU length of stay, we found no distinct association between handoff frequency and charges, 30-day readmission rates, or mortality rates. CONCLUSIONS: Despite frequent handoffs in care, there was no objective evidence of care compromise or differences in cost. Further validation of these observations in a larger cohort is justified.