Safe Triage of STEMI Patients to General Telemetry Units After Successful Primary Percutaneous Coronary Intervention.

OBJECTIVE: To analyze outcomes of patients with ST-segment elevation myocardial infarction (STEMI) after successful primary percutaneous coronary intervention (PCI) triaged to the cardiac intensive care unit (CICU) vs a general telemetry unit by a Zwolle risk score-based algorithm. METHODS: We introduced a quality improvement protocol in 2014 encouraging admission of STEMI patients with Zwolle score of 3 or less to general telemetry units unless they were hemodynamically unstable. We subsequently conducted a retrospective single-center cohort study of consecutive STEMI patients who had undergone primary PCI from January 1, 2014, to December 31, 2018. Outcomes studied include immediate complications, need for urgent unplanned intervention, need for CICU care, length of hospitalization, and survival. RESULTS: We identified 547 patients, 406 with a Zwolle score of 3 or less. Of these, 192 (47.3%) were admitted to general telemetry and 214 (52.7%) to the CICU. Reasons for CICU admission included persistent chest pain, late presentation, and procedural complications. The average hospital length of stay was 2.1±1.4 days for non-CICU patients and 3.3±2.8 days for low-risk CICU patients (P<.001). Two patients initially admitted to general telemetry required transfer to the CICU. There were 26 patients who required unplanned cardiovascular intervention within 30 days, 5 from the general telemetry unit; 540 patients survived to discharge. One in-hospital death occurred among those initially triaged to the general telemetry unit, and this was due to a noncardiac cause. CONCLUSION: A Zwolle score-based algorithm can be used to safely triage post-PCI STEMI patients to a general telemetry unit.

Clinical Outcomes of Various Management Strategies for Symptomatic Bradycardia.

OBJECTIVE: To determine clinical outcomes of various management strategies for reversible and irreversible causes of symptomatic bradycardia in the inpatient setting. DESIGN: Retrospective observational study. SETTING: Emergency room and inpatient. PARTICIPANTS: Patients presenting to the emergency department with symptomatic bradycardia. METHODS: We retrospectively reviewed electronic health records of 518 patients from two Mayo Clinic campuses (Rochester and Phoenix) who presented to the emergency department with symptomatic bradycardia (heart rate ≤50 beats/minute) from January 1, 2010 through December 31, 2015. Sinus bradycardia was excluded. The following management strategies were compared: observation, non-invasive management (medications with/without transcutaneous pacing), early permanent pacemaker (PPM) implantation (≤2 days), and delayed PPM implantation (≥3 days). Study endpoints included length of stay and adverse events related to bradycardia (syncope, central line-associated bloodstream infections, cardiac arrest, and in-hospital mortality). Patients who received a PPM were further stratified by weekend hospital admission. RESULTS: Heart block occurred in 200 (38.6%) patients, and atrial arrhythmias with slow ventricular response occurred in 239 (46.1%) patients. Reversible causes of bradycardia included medication toxicity in 22 (4.2%) patients and hyperkalemia in 44 (8.5%) patients. Adverse events were similar in patients who underwent early compared to delayed PPM implantation (6.6% vs 12.5%, P=.20), whereas adverse events were higher in patients who received temporary transvenous pacing (19.1% vs 3.4%, P<.001). Weekend admissions were associated with increased temporary transvenous pacing, prolonged median time to PPM implantation by 1 day, and prolonged median length of stay by 2 days. CONCLUSIONS: Delayed PPM implantation was not associated with an increase in adverse events. Weekend PPM implantation should be considered to reduce temporary transvenous pacing and shorten length of stay.

Thrombocytopenia independently predicts death in idiopathic PAH.

BACKGROUND: Pulmonary arterial hypertension (PAH) is a progressive vascular disorder with a high mortality. Clinical experience and small case series suggest thrombocytopenia may be frequent in this population and associated with a poor prognosis. We sought to estimate the prevalence of thrombocytopenia in patients with PAH and characterize its association with disease characteristics and patient outcome. METHODS: Single center cohort study of 714 incident adult patients with Group 1 PH who were evaluated for baseline platelet count at the time of diagnosis. Pts were stratified into three groups: normal platelet count (>150 × 109/L), Grade 1 thrombocytopenia (75-149 × 109/L) and Grade 2-4 thrombocytopenia (<75 × 109/L). RESULTS: The median platelet count was 209 × 109/L (IQR 163, 264). There were 572 (80%) pts without thrombocytopenia, 107 (15%) with Grade 1 and 35 (5%) with Grade 2-4 thrombocytopenia. The median pt age was 55 years (IQR 44-65) with no difference between platelet groups (p = 0.85). Men were more likely to have thrombocytopenia (62, 34%) than women (80, 15%, p < 0.0001). Thrombocytopenia was frequent with portopulmonary PAH (84%) as opposed to idiopathic PAH (iPAH; 14%) or connective tissue disease associated PAH (12%). Platelet counts were not associated with functional class symptoms, the degree of right ventricular enlargement or dysfunction or tricuspid regurgitation by echocardiography. Invasive hemodynamics of right atrial pressure, mean pulmonary artery pressure and pulmonary vascular resistance were also similar between platelet groups. Thrombocytopenia was associated with higher mortality in iPAH patients (age- and sex-adjusted 5 year mortality [HR 1.95 (1.20, 3.08) p = 0.008] but not in other etiology groups. In a multivariate model of iPAH patients (adjusted for age, sex, DLCO, PVR, creatinine and 6MW distance) thrombocytopenia was most predictive of 5-year mortality [HR 1.68 (1.32, 2.12), p < 0.0001]. CONCLUSION: Thrombocytopenia in the context of iPAH portends a poor prognosis and is a simple independent factor to consider in judging severity of disease.

The prognostic significance of tricuspid valve regurgitation in pulmonary arterial hypertension.

INTRODUCTION: Tricuspid valve regurgitation (TR) is a frequent finding in patients with pulmonary arterial hypertension (PAH). However, its prognostic significance and relation to PAH, while suspected, are poorly understood. We assessed 727 consecutive patients with newly diagnosed PAH who underwent transthoracic echocardiographic evaluation of tricuspid valve function. OBJECTIVES: The study objective was to determine the association of TR presence and severity with patient characteristics, pulmonary artery hemodynamics and outcome. METHODS: Consecutive patients with newly diagnosed PAH (N = 727 with group 1 pulmonary hypertension) underwent transthoracic echocardiographic evaluation of tricuspid valve function at diagnosis. The primary study end point was all-cause mortality or lung transplantation. RESULTS: In this population, 702 patients (96.5%) had TR; in 165 patients (23%), TR was severe. Compared with those with no or mild TR by echocardiography criteria, patients with severe TR had shorter mean (SD) 6-minute walk distances (285 [125] m vs 360 [121] m; P = .02) and higher levels of B-type natriuretic peptide (695 [672] pg/dL vs 328 [300] pg/dL; P < .05). Severe TR was associated with greater right atrial dilatation (91% vs 47%; P = .004) and right ventricular (RV) dilatation (92% vs 51%; P = .008), greater right atrial pressure (mean [SD] 15 [7] mm Hg vs 10 [6] mm Hg; P < .001) and lower cardiac index (mean [SD], 2.2 [0.7] L/min/m2 vs 2.8 [0.9] L/min/m2; P < .001). Severe TR was strongly predictive of greater 5-year mortality risk after adjustment for age, sex, functional class, 6-minute walk distance, diffusing capacity, RV size and pulmonary vascular resistance index (adjusted hazard ratio, 1.83; 95% CI, 1.38-2.41; P < .001). CONCLUSIONS: Severe TR was a significant predictor of long-term mortality rate in PAH, and TR severity correlated with PAH severity.

Multimodal Imaging of Anomalous Left Coronary Artery from the Pulmonary Artery in a 75-Year-Old Woman.

Anomalous origin of the left coronary artery from the pulmonary artery is rare and typically results in mitral regurgitation, ventricular arrhythmias, heart failure, and sudden death. The condition most often manifests itself in early childhood, but some individuals are diagnosed much later. We describe the case of a 75-year-old woman with heart failure in whom stepwise multimodal imaging revealed anomalous origin of the left coronary artery from the pulmonary artery.

Side Effects of CV Medications Following Hospitalization for ACS Are Associated With More Frequent Health-Care Contacts.

BACKGROUND: Patients hospitalized for first acute coronary syndrome (ACS) are frequently discharged on multiple new medications. The short-term tolerability of these medications is unknown. METHODS: This single-center cohort study assessed 30-day health-care utilization and how it may be impacted by medication prescribing trends. We included Olmsted County patients presenting with ACS and previously undiagnosed coronary artery disease in 2008 to 2009. All health-care contacts were reviewed 30 days after index hospital discharge for potential adverse medication effects including documented hypotension or bradycardia, or symptoms likely attributed to the medications. RESULTS: The study included 86 patients; their mean age was 63 (standard deviation: 15.5 years). Antianginal or antihypertensive cardiovascular (CV) medications were prescribed to 98% of patients at discharge; 76% were prescribed 2 or more. There were 233 health-care contacts in 30 days; 90 (39%) of these contacts were unscheduled. More CV medications tended to be prescribed to patients with unscheduled contacts, both pre-ACS ( P = .045) and upon hospital discharge ( P = .051). Hypotension and/or bradycardia at follow-up occurred in 52 patients (60%). Surprisingly, there was no association between hypotension and/or bradycardia at follow-up and increased health-care utilization ( P = .12). Potential adverse drug effects were reported in 34 (40%) patients. These patients had significantly more total health-care contacts ( P < .001) and unscheduled health-care contacts (median 0 vs 1.5; P < .001). CONCLUSIONS: Symptoms of adverse drug effects were associated with more frequent health-care utilization after ACS. Clinicians need to consider this while striving to increase patient compliance with post-ACS medications and optimize care transitions.

Fortilin reduces apoptosis in macrophages and promotes atherosclerosis.

Atherosclerosis, a deadly disease insufficiently addressed by cholesterol-lowering drugs, needs new therapeutic strategies. Fortilin, a 172-amino acid multifunctional polypeptide, binds p53 and blocks its transcriptional activation of Bax, thereby exerting potent antiapoptotic activity. Although fortilin-overexpressing mice reportedly exhibit hypertension and accelerated atherosclerosis, it remains unknown if fortilin, not hypertension, facilitates atherosclerosis. Our objective was to test the hypothesis that fortilin in and of itself facilitates atherosclerosis by protecting macrophages against apoptosis. We generated fortilin-deficient (fortilin(+/-)) mice and wild-type counterparts (fortilin(+/+)) on a LDL receptor (Ldlr)(-/-) apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1 (Apobec1)(-/-) hypercholesterolemic genetic background, incubated them for 10 mo on a normal chow diet, and assessed the degree and extent of atherosclerosis. Despite similar blood pressure and lipid profiles, fortilin(+/-) mice exhibited significantly less atherosclerosis in their aortae than their fortilin(+/+) littermate controls. Quantitative immunostaining and flow cytometry analyses showed that the atherosclerotic lesions of fortilin(+/-) mice contained fewer macrophages than those of fortilin(+/+) mice. In addition, there were more apoptotic cells in the intima of fortilin(+/-) mice than in the intima of fortilin(+/+) mice. Furthermore, peritoneal macrophages from fortilin(+/-) mice expressed more Bax and underwent increased apoptosis, both at the baseline level and in response to oxidized LDL. Finally, hypercholesterolemic sera from Ldlr(-/-)Apobec1(-/-) mice induced fortilin in peritoneal macrophages more robustly than sera from control mice. In conclusion, fortilin, induced in the proatherosclerotic microenvironment in macrophages, protects macrophages against Bax-induced apoptosis, allows them to propagate, and accelerates atherosclerosis. Anti-fortilin therapy thus may represent a promising next generation antiatherosclerotic therapeutic strategy.

Pericardial effusions in pulmonary arterial hypertension: characteristics, prognosis, and role of drainage.

BACKGROUND: The presence and size of a pericardial effusion in pulmonary arterial hypertension (PAH) and its association with outcome is unclear. METHODS: In this single-center cohort study of 577 patients with group 1 PAH seen between January 1, 1995, and December 31, 2005, all patients underwent transthoracic echocardiography and were followed for ≥ 5 years. Echocardiography-guided pericardiocentesis was performed as needed. RESULTS: Pericardial effusions on index echocardiography occurred in 150 patients (26%); 128 patients had small and 22 had moderate-sized or larger effusions. Most of the moderate or greater effusions occurred in patients who had connective tissue disease (82%). Mean right atrial pressure was 13.4 ± 4.4 mm Hg (no effusion), 15.1 ± 4.4 mm Hg (small effusion), and 17.0 ± 4.0 mm Hg (moderate or greater effusion) (P < .0001). Median survival for patients with moderate or greater effusion, mild effusion, or no effusion was 11.3 months, 42.3 months, and 76.5 months, respectively. Four of the 22 patients with moderate or greater pericardial effusions eventually required echocardiography-guided pericardiocentesis because of clinical and echocardiographic evidence of hemodynamic impact. When drained, the effusions were large (858 ± 469 mL) and generally serous. All pericardiocenteses were performed cautiously under echocardiographic guidance by a highly experienced echocardiologist, with low immediate morbidity and mortality. CONCLUSIONS: Pericardial effusions are relatively common but rarely of hemodynamic significance in patients with PAH. However, even modest degrees of pericardial fluid are associated with a significant increase in mortality and appear to reflect the presence of associated collagen vascular disease and high right atrial pressure.

RETRACTED: Syncope in adults with pulmonary arterial hypertension.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the authors, because of a data entry error which is fundamental to the study findings. As background, this was a clinical study where a specific variable was tested in a large database. The process involved merging a variable (presence or absence of syncope) from one electronic source with an alternate electronic database of patients with pulmonary arterial hypertension and assessing associations and outcomes. In proceeding to design a follow-up study to this work Dr. Le, went back to the original source file to abstract new data. In doing this she identified a 'cut-and paste' error in which the column of syncope data was transferred incorrectly where syncope/no syncope variables were assigned to wrong subjects. This led to a critical error that then got carried forward and a fundamental misclassification of syncope in the final study group. This error fundamentally affects the results which now do not fully support the conclusions.