Clinical Approach to Post-acute Sequelae After COVID-19 Infection and Vaccination.

The spike protein of SARS-CoV-2 has been found to exhibit pathogenic characteristics and be a possible cause of post-acute sequelae after SARS-CoV-2 infection or COVID-19 vaccination. COVID-19 vaccines utilize a modified, stabilized prefusion spike protein that may share similar toxic effects with its viral counterpart. The aim of this study is to investigate possible mechanisms of harm to biological systems from SARS-CoV-2 spike protein and vaccine-encoded spike protein and to propose possible mitigation strategies. We searched PubMed, Google Scholar, and 'grey literature' to find studies that (1) investigated the effects of the spike protein on biological systems, (2) helped differentiate between viral and vaccine-generated spike proteins, and (3) identified possible spike protein detoxification protocols and compounds that had signals of benefit and acceptable safety profiles. We found abundant evidence that SARS-CoV-2 spike protein may cause damage in the cardiovascular, hematological, neurological, respiratory, gastrointestinal, and immunological systems. Viral and vaccine-encoded spike proteins have been shown to play a direct role in cardiovascular and thrombotic injuries from both SARS-CoV-2 and vaccination. Detection of spike protein for at least 6-15 months after vaccination and infection in those with post-acute sequelae indicates spike protein as a possible primary contributing factor to long COVID. We rationalized that these findings give support to the potential benefit of spike protein detoxification protocols in those with long-term post-infection and/or vaccine-induced complications. We propose a base spike detoxification protocol, composed of oral nattokinase, bromelain, and curcumin. This approach holds immense promise as a base of clinical care, upon which additional therapeutic agents are applied with the goal of aiding in the resolution of post-acute sequelae after SARS-CoV-2 infection and COVID-19 vaccination. Large-scale, prospective, randomized, double-blind, placebo-controlled trials are warranted in order to determine the relative risks and benefits of the base spike detoxification protocol.

Retrospective Study of Outcomes and Hospitalization Rates of Patients in Italy with a Confirmed Diagnosis of Early COVID-19 and Treated at Home Within 3 Days or After 3 Days of Symptom Onset with Prescribed and Non-Prescribed Treatments Between November 2020 and August 2021.

BACKGROUND This retrospective study aimed to investigate outcomes and hospitalization rates in patients with a confirmed diagnosis of early COVID-19 treated at home with prescribed and non-prescribed treatments. MATERIAL AND METHODS The medical records of a cohort of 158 Italian patients with early COVID-19 treated at home were analyzed. Treatments consisted of indomethacin, low-dose aspirin, omeprazole, and a flavonoid-based food supplement, plus azithromycin, low-molecular-weight heparin, and betamethasone as needed. The association of treatment timeliness and of clinical variables with the duration of symptoms and with the risk of hospitalization was evaluated by logistic regression. RESULTS Patients were divided into 2 groups: group 1 (n=85) was treated at the earliest possible time (<72 h from onset of symptoms), and group 2 (n=73) was treated >72 h after the onset of symptoms. Clinical severity at the beginning of treatment was similar in the 2 groups. In group 1, symptom duration was shorter than in group 2 (median 6.0 days vs 13.0 days, P<0.001) and no hospitalizations occurred, compared with 19.18% hospitalizations in group 2. One patient in group 1 developed chest X-ray alterations and 2 patients experienced an increase in D-dimer levels, compared with 30 and 22 patients, respectively, in group 2. The main factor determining the duration of symptoms and the risk of hospitalization was the delay in starting therapy (P<0.001). CONCLUSIONS This real-world study of patients in the community showed that early diagnosis and early supportive patient management reduced the severity of COVID-19 and reduced the rate of hospitalization.

Vitamin D deficiency in association with endothelial dysfunction: Implications for patients with COVID-19.

There is emerging evidence to suggest that vitamin D deficiency is associated with adverse outcomes in COVID-19 patients. Conversely, vitamin D supplementation protects against an initial alveolar diffuse damage of COVID-19 becoming progressively worse. The mechanisms by which vitamin D deficiency exacerbates COVID-19 pneumonia remain poorly understood. In this review we describe the rationale of the putative role of endothelial dysfunction in this event. Herein, we will briefly review (1) anti-inflammatory and anti-thrombotic effects of vitamin D, (2) vitamin D receptor and vitamin D receptor ligand, (3) protective role of vitamin D against endothelial dysfunction, (4) risk of vitamin D deficiency, (5) vitamin D deficiency in association with endothelial dysfunction, (6) the characteristics of vitamin D relevant to COVID-19, (7) the role of vitamin D on innate and adaptive response, (8) biomarkers of endothelial cell activation contributing to cytokine storm, and (9) the bidirectional relationship between inflammation and homeostasis. Finally, we hypothesize that endothelial dysfunction relevant to vitamin D deficiency results from decreased binding of the vitamin D receptor with its ligand on the vascular endothelium and that it may be immune-mediated via increased interferon 1 α. A possible sequence of events may be described as (1) angiotensin II converting enzyme-related initial endothelial injury followed by vitamin D receptor-related endothelial dysfunction, (2) endothelial lesions deteriorating to endothelialitis, coagulopathy and thrombosis, and (3) vascular damage exacerbating pulmonary pathology and making patients with vitamin D deficiency vulnerable to death.

Clinical outcomes after early ambulatory multidrug therapy for high-risk SARS-CoV-2 (COVID-19) infection.

There is an emergency need for early ambulatory treatment of Coronavirus Disease 2019 (COVID-19) in acutely ill patients in an attempt to reduce disease progression and the risks of hospitalization and death. Such management should be applied in high-risk patients age > 50 years or with one or more medical problems including cardiovascular disease. We evaluated a total of 922 outpatients from March to September 2020. All patients underwent contemporary real-time polymerase chain reaction (PCR) assay tests from anterior nasal swab samples. Patients age 50.5 ± 13.7 years (range 12 to 89), 61.6% women, at moderate or high risk for COVID-19 received empiric management via telemedicine. At least two agents with antiviral activity against SARS-CoV-2 (zinc, hydroxychloroquine, ivermectin) and one antibiotic (azithromycin, doxycycline, ceftriaxone) were used along with inhaled budesonide and/or intramuscular dexamethasone consistent with the emergent science on early COVID-19 treatment. For patients with high severity of symptoms, urgent in-clinic administration of albuterol nebulizer, inhaled budesonide, and intravenous volume expansion with supplemental parenteral thiamine 500 mg, magnesium sulfate 4 grams, folic acid 1 gram, vitamin B12 1 mg. A total of 320/922 (34.7%) were treated resulting in 6/320 (1.9%) and 1/320 (0.3%) patients that were hospitalized and died, respectively. We conclude that early ambulatory (not hospitalized, treated at home), multidrug therapy is safe, feasible, and associated with low rates of hospitalization and death. Early treatment should be considered for high-risk patients as an emergency measure while we await randomized trials and guidelines for ambulatory management.

A Call to Action to Develop Integrated Curricula in Cardiorenal Medicine.

With the adoption of the new definition and classification of cardiorenal syndrome (CRS) and its relevant subtypes, much attention has been placed on elucidating the mechanisms of heart and kidney interactions. The pathophysiologic pathways are of great interest by which acute heart failure may result in acute kidney injury (AKI; type 1), chronic heart failure accelerates the progression of chronic kidney disease (CKD; type 2), AKI provokes cardiac events (type 3), and CKD increases the risk and severity of cardiovascular disease (type 4). A remarkable interest has also been placed on the acute and chronic systemic conditions, such as sepsis and diabetes, that simultaneously affect heart and kidney function (type 5). Furthermore, the physiology of acute and chronic heart-kidney crosstalk is drawing attention to hemodynamics (fluids, pressures, flows, resistances, perfusion), physiochemical (electrolytes, pH, toxins) and biologic (inflammation, immune system activation, neurohormonal signals) processes. Common clinical scenarios call for recognition, knowledge, and skill in managing CRS. There is a clear need for medical and surgical specialists who are well versed in the pathophysiology and clinical manifestations that arise in the setting of CRS. With this editorial, we make a call to action to encourage universities, medical schools, and teaching hospitals to create a core curriculum for cardiorenal medicine to better equip the physicians of the future for these common, serious, and frequently fatal syndromes.

Use of Oral Anticoagulation in the Management of Atrial Fibrillation in Patients with ESRD: Pro.

Warfarin has had a thin margin of benefit over risk for the prevention of stroke and systemic embolism in patients with ESRD because of higher bleeding risks and complications of therapy. The successful use of warfarin has been dependent on the selection of patients with nonvalvular atrial fibrillation at relatively high risk of stroke and systemic embolism and lower risks of bleeding over the course of therapy. Without such selection strategies, broad use of warfarin has not proven to be beneficial to the broad population of patients with ESRD and nonvalvular atrial fibrillation. In a recent meta-analysis of use of warfarin in patients with nonvalvular atrial fibrillation and ESRD, warfarin had no effect on the risks of stroke (hazard ratio, 1.12; 95% confidence interval, 0.69 to 1.82; P=0.65) or mortality (hazard ratio, 0.96; 95% confidence interval, 0.81 to 1.13; P=0.60) but was associated with increased risk of major bleeding (hazard ratio, 1.30; 95% confidence interval, 1.08 to 1.56; P<0.01). In pivotal trials, novel oral anticoagulants were generally at least equal to warfarin for efficacy and safety in nonvalvular atrial fibrillation and mild to moderate renal impairment. Clinical data for ESRD are limited, because pivotal trials excluded such patients. Given the very high risk of stroke and systemic embolism and the early evidence of acceptable safety profiles of novel oral anticoagulants, we think that patients with ESRD should be considered for treatment with chronic anticoagulation provided that there is an acceptable bleeding profile. Apixaban is currently indicated in ESRD for this application and may be preferable to warfarin given the body of evidence for warfarin and its difficulty of use and attendant adverse events.

Nutritional Deficiencies and Sarcopenia in Heart Failure: A Therapeutic Opportunity to Reduce Hospitalization and Death.

There is an expanding prevalence pool of heart failure (HF) due to the increasing prevalence of survivors of myocardial infarction, diabetes, hypertension, chronic kidney disease, and obesity. There is increasing interest in the role of nutrition in all forms of HF, given observations concerning micro- and macronutrient deficiencies, loss of lean body mass or sarcopenia, and their relationships with hospitalization and death. This review examines the relationships among loss of lean body mass, macro- and micronutrient intake, and the natural history of HF, particularly in the elderly, in whom the risks for all-cause rehospitalization, infection, falls, and mortality are increased. These risks are potentially modifiable through strategies that improve nutrition in this vulnerable population.

Acute and chronic cardiovascular effects of hyperkalemia: new insights into prevention and clinical management.

The plasma pool of potassium is a partial reflection of the overall body, transient cellular shifts, and potassium elimination regulated by the kidneys. Potassium concentrations elevating above the upper limit of normal (> 5.0 mEq/L) have become more common in cardiovascular practice due to the growing population of patients with chronic kidney disease and the broad applications of drugs that modulate potassium excretion by either reducing production of angiotensin II (angiotensin-converting enzyme inhibitors, direct renin inhibitors, beta-adrenergic receptor antagonists), blocking angiotensin II receptors (angiotensin receptor blockers), or antagonizing the action of aldosterone on mineralocorticoid receptors (mineralocorticoid receptor antagonists). In addition, acute kidney injury, critical illness, crush injuries, and massive red blood cell transfusions can result in hyperkalemia. Progressively more severe elevations in potassium are responsible for abnormalities in cardiac depolarization and repolarization and contractility. Untreated severe hyperkalemia results in sudden cardiac death. Traditional management steps have included reducing dietary potassium and discontinuing potassium supplements; withdrawal of exacerbating drugs; acute treatment with intravenous calcium gluconate, insulin, and glucose; nebulized albuterol; correction of acidosis with sodium bicarbonate for short-term shifts out of the plasma pool; and, finally, gastrointestinal ion exchange with oral sodium polystyrene sulfonate in sorbitol, which is mainly used in the hospital and is poorly tolerated due to gastrointestinal adverse effects. This review explores hyperkalemia as a complication in cardiovascular patients and highlights new acute, chronic, and preventative oral therapies (patiromer calcium, cross-linked polyelectrolyte, ZS-9) that could potentially create a greater margin of safety for vulnerable patients with combined heart and kidney disease.

No independent association of serum phosphorus with risk for death or progression to end-stage renal disease in a large screen for chronic kidney disease.

Whether higher serum phosphorus levels are associated with a higher risk for death and/or progression of chronic kidney disease (CKD) is not well established, and whether the association is confounded by access and barriers to care is unknown. To answer these questions, data of 10,672 individuals identified to have CKD (estimated glomerular filtration rate <60 ml/min per 1.73 m(2)) from those participating in a community-based screening program were analyzed. Over a median follow-up of 2.3 years, there was no association between quartiles of serum phosphorus and all-cause mortality (adjusted hazards ratio for serum phosphorus over 3.3 to 3.7, over 3.7 to 4.1, and over 4.1 mg/dl, respectively: 1.22 (0.95-1.56), 1.00 (0.76-1.32), and 1.00 (0.75-1.33); reference, serum phosphorus of 3.3 mg/dl and below). Individuals in the highest quartile for serum phosphorus had a significantly higher risk for progression to end-stage renal disease (ESRD) (unadjusted hazards ratio, 6.72 (4.16-10.85)); however, the risk became nonsignificant on adjustment for potential confounders. There was no appreciable change in hazards ratio with inclusion of variables related to access and barriers to care. Additional analyses in subgroups based on 12 different variables yielded similar negative associations. Thus, in the largest cohort of individuals with early-stage CKD to date, we could not validate an independent association of serum phosphorus with risk for death or progression to ESRD.

The association of parathyroid hormone with ESRD and pre-ESRD mortality in the Kidney Early Evaluation Program.

CONTEXT: Studies have suggested that PTH may influence mortality and progression of chronic kidney disease. However, the development of either event may influence the development of the other as a competing risk. OBJECTIVE: The objective of the study was to examine the association of PTH with end-stage renal disease (ESRD) and pre-ESRD death using a competing risk survival model. DESIGN, SETTING, AND PATIENTS: A total of 10,823 participants in the Kidney Early Evaluation Program with chronic kidney disease (estimated glomerular filtration rate < 60 ml/min per 1.73 m(2)) were examined from 2005 to 2010. MAIN OUTCOME MEASURES: The association of PTH levels with ESRD and pre-ESRD mortality was ascertained by linking Kidney Early Evaluation Program data to the Social Security Administration Death Master File and the U.S. Renal Data System. RESULTS: Among the cohort, the incidence of ESRD and pre-ESRD mortality was 6.4 and 20.1 events per 1000 person-years. Higher PTH levels were associated with increasing age, black race, lack of a high school education, cardiovascular disease, hypertension, and lower glomerular filtration rate. The incidence of ESRD and pre-ESRD mortality was lowest among participants in the second PTH quintile. After multivariate adjustment, as compared with the second quintile, the risk of pre-ESRD mortality was higher in the third [subhazard ratio (SHR) 1.52 (95% confidence interval 1.04-2.22)], fourth [SHR 1.73 (95% confidence interval 1.19-2.52)], and fifth [SHR 1.86 (1.28-2.52)] quintiles, respectively. Conversely, PTH was not associated with ESRD after multivariate adjustment. The association was not modified by diabetic status, gender, race, or glomerular filtration rate status. CONCLUSIONS: Elevated PTH levels are associated with increased pre-ESRD mortality but not with ESRD.

Nutritional and micronutrient determinants of idiopathic dilated cardiomyopathy: diagnostic and therapeutic implications.

Idiopathic dilated cardiomyopathy (IDCM) is the term used to describe a group of myocardial diseases of unknown cause whose common clinical presentation is heart failure. The prevalence of IDCM is estimated to be between 7 and 13% of patients with systolic heart failure. Throughout medical history, several nutrient-deficient states have been identified as the root cause of IDCMs, Keshan's disease being one such example, where selenium deficiency-induced heart failure is now well documented. This raises the question of whether a micro- or macro-nutrient imbalance can provide the milieu for inefficient energy expenditure and cardiac metabolism in the context of IDCMs, either causing or exacerbating the condition. To date, there is insufficient evidence in the literature to support this theory, although numerous studies suggest a link between nutrient deficiencies, inefficient energy expenditure and subsequent heart failure. Given the unique metabolic needs of the failing heart, the role of micronutrient testing and supplementation in IDCMs warrants further well-designed studies.

Identification and management of chronic kidney disease complications by internal medicine residents: a national survey.

Many patients with chronic kidney disease (CKD) receive care from primary care physicians. Identification and management of CKD complications in primary care is suboptimal. It is not known if current residency curriculum adequately prepares a future internist in this aspect of CKD care. We performed an online questionnaire survey of internal medicine residents in the United States to determine knowledge of CKD complications and their management. Four hundred seventy-nine residents completed the survey with postgraduate year (PGY) distribution 166 PGY1, 187 PGY2, and 126 PGY3. Most of the residents correctly recognized anemia (91%) and bone disease (82%) as complications at estimated glomerular filtration rate less than 60 mL/min/1.73 m; however, only half of the residents identified coronary artery disease (54%) as a CKD complication. For a patient with estimated glomerular filtration rate less than 60 mL/min/1.73 m, two thirds of the residents would workup for anemia (62%), whereas half of them would check for mineral and bone disorder (56%). With regard to anemia of CKD, less than half of the residents knew the CKD goal hemoglobin level of 11 to 12 g/dL (44%); most would supplement iron stores (86%), whereas fewer would consider nephrology referral (28%). For mineral and bone disorders, many residents would recommend dietary phosphorus restriction (68%) and check 25-hydroxyvitamin D (62%); fewer residents would start 1,25-dihydroxyvitamin D (40%) or refer to the nephrologist (45%). Residents chose to discontinue angiotensin-converting enzyme inhibitor for medication-related complication of greater than 50% decline in estimated glomerular filtration rate (68%) and potassium greater than 5.5 mEq/L (93%). Mean performance score improved with increasing PGY (PGY1 59.4% ± 17.6%, PGY2 63.6% ± 15.6%, and PGY3 66.2% ± 16.5%; P = 0.002). Our study identified specific gaps in knowledge of CKD complications and management among internal medicine residents. Educational efforts such as instruction on use of CKD clinical practice guidelines may help raise awareness of CKD complications, benefits of early intervention, and improve CKD management.

Plasma parathyroid hormone level and prevalent cardiovascular disease in CKD stages 3 and 4: an analysis from the Kidney Early Evaluation Program (KEEP).

BACKGROUND: Cardiovascular disease (CVD) is the most common cause of death in patients with chronic kidney disease (CKD). Secondary hyperparathyroidism is common in patients with CKD, and its relationship to CVD is not well defined. This analysis aims to assess whether serum intact parathyroid hormone (PTH) level is an independent risk factor for CVD in patients with CKD stages 3 and 4. METHODS: In this cross-sectional study, medical history surveys, including CVD events, were collected from 4,472 patients with stages 3 and 4 CKD identified by the National Kidney Foundation Kidney Early Evaluation Program (KEEP), which included blood pressure measurement and laboratory testing. Age, hemoglobin level, estimated glomerular filtration rate, serum phosphorus level, and serum calcium level were evaluated as continuous variables, and plasma PTH levels, by tertile: less than 35, 35 to 70, and greater than 70 pg/mL. Multivariate logistic regression was used to estimate odds ratios (ORs) of CVD predictor variables. RESULTS: Mean age was 68.3 +/- 11.8 years. Of the study population, 68% were women, 69% were white, 6% were current smokers, 45% were obese, 46% had diabetes, and 83% had hypertension. A history of CVD was present for 1,972 (44.1%), and plasma PTH level greater than 70 pg/mL, for 2,239 (50.1%). Multivariate logistic regression showed ORs for CVD events increasing with age (OR, 1.03; P < 0.001), male sex (OR, 1.51; P < 0.001), diabetes (OR, 1.73; P < 0.001), hypertension (OR, 1.43; P < 0.001), and intact PTH level greater than 70 pg/mL (OR, 1.51; P < 0.001; reference, <35 pg/mL). CONCLUSIONS: PTH level greater than 70 pg/mL is independently associated with CVD events in patients with CKD stages 3 and 4. No association was observed between serum phosphorus or calcium level and CVD events. These findings provide support for intact PTH testing, along with testing for other indicators of CKD mineral and bone disorders, at earlier CKD stages.

Trends in mineral metabolism: Kidney Early Evaluation Program (KEEP) and the National Health and Nutrition Examination Survey (NHANES) 1999-2004.

BACKGROUND: Chronic kidney disease (CKD) is associated with mineral metabolism dysregulation, cardiovascular disease, and premature mortality. No study specifically examined mineral metabolism trends in a generalizable sample of patients at increased CKD risk. METHODS: This cross-sectional analysis from November 1, 2005, to December 31, 2006, of calcium, phosphorus, and parathyroid hormone (PTH) includes 2,646 individuals with estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m(2) in the National Kidney Foundation Kidney Early Evaluation Program (KEEP), a community-based health-screening program targeting individuals 18 years and older with diabetes, hypertension, or family history of kidney disease, diabetes, or hypertension. A parallel analysis of National Health and Nutrition Examination Survey (NHANES) 1999-2004 data was performed. RESULTS: In KEEP, as eGFR decreased from 55 to less than 60 mL/min/1.73 m(2) to less than 30 mL/min/1.73 m(2), calcium level decreased (9.55 +/- 0.47 to 9.34 +/- 0.62 mg/dL; P < 0.001), phosphorus level increased (3.70 +/- 0.59 to 4.15 +/- 0.80 mg/dL; P < 0.001), and PTH level increased (66.3 +/- 36.3 to 164 +/- 109 pg/mL; mean, 80.8 +/- 57.0 pg/mL; P < 0.001). NHANES 1999-2004 showed similar trends, with PTH values not as high. Individuals within opinion-based Kidney Disease Outcomes Quality Initiatives targets from the highest to the lowest eGFR group were as follows: calcium, 93.0% to 92.3% (KEEP) and 97.4% to 89.6% (NHANES); phosphorus, 90.4% to 90.3% (KEEP) and 91.6% to 87.1% (NHANES); and PTH, 46.1% to 31.2% (KEEP) and 56.4% to 36.1% (NHANES). CONCLUSIONS: In a community-based CKD screening population, increased PTH level occurs early in patients with stage 3, typically with normal calcium and phosphorus levels. These findings support the importance of including PTH with calcium and phosphorus monitoring for individuals with eGFR less than 60 mL/min/1.73 m(2).

Determinants of coronary vascular calcification in patients with chronic kidney disease and end-stage renal disease: a systematic review.

BACKGROUND: Vascular calcification (VC) is a recognized process involved in senescence and atherosclerosis. Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are conditions associated with metabolic disorders related to soft tissue calcification. METHODS: We performed a systematic review of the literature confined to patients with CKD or ESRD with clinical observations of VC. Case reports of calciphylaxis were excluded. We identified 30 studies over 20 years: 11 prospective cohort, 7 cross-sectional, 11 case-control, and 1 retrospective cohort; n = 2918 subjects, mean age 51 years, 59% men and 41% women. Imaging methods used included: x-ray 43%, computed tomography 30%, ultrasound 17%, and other methods 10%. RESULTS: The most consistent determinants of VC were older age and dialysis vintage. Eight analyses determined a relationship between VC and measures of calcium-phosphate balance while 20 analyses specifically did not find such a relationship. Three studies suggested the degree of calcium loading, treatment with phosphate binders, or treatment with vitamin D analogues were related to VC. When taken into consideration, the lipid profile (primarily low high-density lipoprotein cholesterol, elevated triglycerides, elevated low-density lipoprotein, and elevated total cholesterol) were predictive factors in four analyses. CONCLUSIONS: VC is a common observation in CKD and ESRD and is mainly related to age, length of time on dialysis therapy, and possibly dyslipidemia. The calcium-phosphorus balance and its related treatments are likely not related to this unique form of vascular calcification. Further research into the determinants and potential treatments for vascular calcification is warranted.

Application of a cardiac arrest score in patients with sudden death and ST segment elevation for triage to angiography and intervention.

The aim of this study was to test a previously validated, prognostic, cardiac arrest score in patients with ST segment elevation acute myocardial infarction (AMI) who suffered a witnessed cardiac arrest and survived to emergency department admission. A consecutive series constructed retrospectively from a sudden death database (n = 22) of patients with ST segment elevation AMI resuscitated from cardiac arrest underwent angiography and angioplasty of the culprit vessel within 24 hours of presentation. A cardiac arrest score was assigned to each case by explicit criteria present on evaluation. Primary outcomes were survival to hospital discharge and the degree of neurological recovery during the hospitalization. All patients underwent successful coronary angioplasty and 77% received adjunctive intraaortic balloon counterpulsation. The overall rate of survival to discharge was 41%. For cardiac arrest scores of 0, 1, 2, and 3, respectively, the rates of neurologic recovery were 0 (0%) of 4 (95% CI 0-53%), 3 (50%) of 6 (95% CI 15-85%), 2 (67%) of 3 (95% CI 13-98%), and 9 (100%) of 9 (95% CI 72-100%), and the rates of survival to discharge were 0 (0%) of 4, (95% CI 0-53%), 2 (33%) of 6 (95% CI 6-74%), 2 (67%) of 3 (95% CI 13-98%), and 9 (100%) of 9 (95% CI 72-100%), P < 0.01 for both outcomes over ascending scores. These results suggest appropriate patients for primary angioplasty after cardiac arrest are those with ST segment elevation AMI and an emergency department cardiac arrest score of > or = 2, thus predicting a 11 (92%) of 12 (95% CI 65-100%) chance of survival to discharge.