Comparing the response to acute and chronic exposure to short wavelength lighting emitted from computer screens.

The use of electronic devices with light-emitting screens has increased exponentially in the last decade. As a result, humans are continuously exposed to unintentional artificial light. We explored the effects of acute and chronic exposure to artificial light at night (ALAN) via screen illumination on sleep, circadian rhythms, and related functional outcomes. Nineteen participants (11 female and 8 males, mean age 28.1 ± 7.2 years) underwent a six-night study with three experimental conditions using a repeated-measures design: baseline (first night, no light exposure), acute ALAN exposure (second night), and chronic ALAN exposure (third to sixth nights). Each light exposure lasted for 2 hours (21:00-23:00). Participants underwent an overnight polysomnography at the end of each condition (nights 1, 2, and 6). We collected urine samples (for melatonin metabolite analysis), while body (oral) temperatures were measured before and after exposure. Each morning, the participants filled out questionnaires and conducted a computerized attention test. Both acute and chronic illumination significantly disrupted sleep continuity and architecture and led to greater self-reported daytime sleepiness, negative emotions, and attention difficulties. Both exposure types also altered circadian rhythms, subduing the normal nocturnal decline in body temperature and dampening nocturnal melatonin secretion. In sum, ALAN exposure from electronic screens has an immediate, detrimental, yet stable effect on sleep, circadian regulation, and next-day functional outcomes. Given the widespread use of electronic devices today, our findings suggest that even one night of screen light exposure may be sufficient to cause adverse effects on health and performance.

Evening light exposure to computer screens disrupts human sleep, biological rhythms, and attention abilities.

The use of electronic devices with light-emitting screens has increased exponentially in the last decade. As a result, humans are almost continuously exposed to unintentional artificial light. We explored the independent and combined effects of two aspects of screen illumination, light wavelength, and intensity, on sleep, its biological regulation, and related functional outcomes. The 2 × 2 repeated-measure design included two independent variables: screen light intensity (low ([LI] versus high [HI]) and wavelength (short [SWL] versus long [LWL]). Nineteen participants (11F, 8M; mean age 24.3 [±2.8] years) underwent four light conditions, LI/SWL, HI/SWL, LI/LWL, and HI/LWL, in counterbalanced order. Each light exposure lasted for two hours (21:00-23:00), following which participants underwent an overnight polysomnography. On each experimental night, oral temperature and urine samples (for melatonin analysis) were collected at multiple time points. Each morning, participants filled out questionnaires and conducted a computerized attention task. Irrespective of light intensity, SWL illumination significantly disrupted sleep continuity and architecture and led to greater self-reported daytime sleepiness. SWL light also altered biological rhythms, subduing the normal nocturnal decline in body temperature and dampening nocturnal melatonin secretion. Light intensity seemed to independently affect sleep as well, but to a lesser degree. Both light intensity and wavelength negatively affected morning attention. In sum, light wavelength seems to have a greater influence than light intensity on sleep and a wide-range of biological and behavioral functions. Given the widespread use of electronic devices today, our findings suggest that screen light exposure at evening may have detrimental effects on human health and performance.

Short-term effects of estrogen, tamoxifen and raloxifene on hemostasis: a randomized-controlled study and review of the literature.

INTRODUCTION: Estrogen therapy (ET), tamoxifen and raloxifene are associated with a two- to three-fold increased risk of venous thrombosis (VT); however, the mechanisms by which each drug increases venous thrombosis propensity are not fully understood. The objectives of this investigation were to compare the effects of these three treatments on hemostasis in a head to head randomized placebo-controlled trial. PATIENTS/METHODS: Ninety-four postmenopausal women were assigned to receive oral estrogen (conjugated equine estrogen [CEE] 0.625 mg, n=23), tamoxifen 20 mg (n=24), raloxifene 60 mg (n=24) or placebo (n=23) daily for 6 months. Blood samples were analyzed for procoagulant factors (prothrombin, factors VII [fVII], VIII [fVIII], IX [fIX] and XI [fXI], D-dimer and von Willebrand factor [vWf]), anticoagulant factors (antithrombin [AT], total and free protein S, protein C and activated protein C [APC] resistance) and fibrinolytic factors (thrombin activatable fibrinolysis inhibitor [TAFI] and plasminogen activator inhibitor-1 [PAI-1]), at baseline and at 6 months of treatment. RESULTS: Estrogen increased factor VII and D-dimer, and decreased antithrombin, total and free protein S and PAI-1. Changes with tamoxifen were distinct from estrogen with increases in factors VIII, IX, vWf and free protein S, and decreases in AT, total protein S, protein C and plasminogen activator inhibitor-1. Raloxifene produced similar effects as tamoxifen, but did not increase factor IX or decrease protein C. CONCLUSIONS: Estrogen, tamoxifen and raloxifene affected hemostasis favoring procoagulation and impairing anticoagulation. The biochemical effects of the selective estrogen receptor modulators (SERMs) were distinct from those of estrogen and differed only subtly from each other.

Early administration of nifedipine in suspected acute myocardial infarction. The Secondary Prevention Reinfarction Israel Nifedipine Trial 2 Study.

BACKGROUND: The administration of nifedipine, 30 mg/d, between 7 and 22 days after hospitalization for an acute myocardial infarction (Secondary Prevention Reinfarction Israel Nifedipine Trial study) showed no effect on subsequent mortality and morbidity. Since a possible indication of benefit was observed in patients with a second- or higher-order infarction, a second trial was conducted with a higher dose (60 mg/d), early administration (usually within 3 hours of hospital admission), and in high-risk patients only. METHODS: A total of 1358 men and women with suspected acute myocardial infarction (MI), judged not to require calcium antagonist therapy, were randomized to receive nifedipine, 60 mg/d, or placebo between November 1985 and July 1986. Study medication was discontinued in 352 patients because they did not exhibit study criteria for MI or lacked high-risk criteria, or because they decided to discontinue the study. Thus, the treated high-risk group included 1006 patients, of whom 826 were successfully titrated to the target dose of 60 mg/d and were treated for up to 6 months. RESULTS: In the 1006 patients, mortality was 18.7% among those randomized to nifedipine and 15.6% in the patients randomized to placebo. This reflected an increased mortality of 7.8% as compared with 5.5% during the first 6 days in the nifedipine and placebo groups, respectively (adjusted mortality odds ratio by logistic regression, 1.60; 95% confidence interval, 0.86 to 3.00). Among the 826 patients who continued treatment, mortality was equal in the nifedipine (9.3%) and placebo (9.5%) groups. No differences in the rates of nonfatal MI (5.1% and 4.2% in the nifedipine and placebo groups, respectively), hospitalization due to unstable angina, and frequency of chest pain reported during follow-up were observed. An increased rate of sudden death (4.9%) in the placebo group in comparison with the nifedipine group (2.3%) was not statistically significant on post hoc testing, nor was an effect of nifedipine demonstrable in post hoc analyses by congestive heart failure status of randomized patients. CONCLUSION: Nifedipine as a prophylactic treatment in patients immediately after acute MI or in survivors recovering 1 week or longer after acute MI appears ineffective. Early routine administration of nifedipine in acute MI, other than to patients in whom it may be specifically indicated (eg, those with Prinzmetal's variant angina or severe hypertension) may be hazardous and seems to be contraindicated.

Magnesium in the prevention of lethal arrhythmias in acute myocardial infarction.

Seven of 48 patients (14.6%) with acute myocardial infarction who were given 2.4 g of magnesium sulfate as a single intravenous dose had potentially lethal arrhythmias during the first 24 hours after admission, whereas 16 (34.8%) of 46 patients receiving placebo had similar arrhythmias. In addition, 14 of these 16 patients in the placebo group had their first arrhythmia (in the intensive coronary-care unit) within two hours after the start of the study, whereas in the magnesium-treated group, there were no such arrhythmias until some four hours later. The higher the lymphocyte potassium concentration, the greater the reduction in the incidence of arrhythmias. Serum magnesium levels increased by 16.5% and lymphocyte magnesium concentrations by 72% in the magnesium treated group. Intravenous magnesium reduces the incidence of serious arrhythmias after acute myocardial infarction.

Intracellular cations and diuretic therapy following acute myocardial infarction.

In a controlled, prospective, randomized study of the effects of diuretic therapy on serum, lymphocyte, and erythrocyte potassium, magnesium, and calcium concentrations, 155 patients were followed up for six months after experiencing acute myocardial infarction. Of these, 48 patients received furosemide and potassium; 37 patients received hydrochlorothiazide and amiloride hydrochloride; and 70 patients did not require diuretics. Lymphocyte and erythrocyte cation concentrations were all statistically significantly lower in the furosemide-treated patients when compared with the patients in the nondiuretic-therapy group or the hydrochlorothiazide-amiloride-treated group, with no change in serum levels. Since the combination of low intracellular potassium and magnesium concentrations in patients with recent myocardial infarction may be of importance in the cause of arrhythmias, we suggest that potassium- (and magnesium-) sparing diuretics be used in the treatment of patients, when necessary, unless their diuretic needs cannot be met by such agents.

Serum, lymphocyte, and erythrocyte potassium, magnesium, and calcium concentrations and their relation to tachyarrhythmias in patients with acute myocardial infarction.

Serum, lymphocyte, and erythrocyte potassium, magnesium, and calcium levels were measured in 215 patients during the five days following acute myocardial infarction. Serum potassium fell from 4.25 +/- 0.05 to 4.08 +/- 0.06 mmol/liter (p less than 0.001), magnesium from 0.93 +/- 0.01 to 0.85 +/- 0.01 mmol/liter (p less than 0.001), and calcium from 2.4 +/- 0.02 to 2.2 +/- 0.08 mmol/liter (p less than 0.001). Lymphocyte potassium increased from 18.1 +/- 1.5 to 51.6 +/- 4.3 pmol/100 cells (p less than 0.001) and magnesium from 2.0 +/- 0.1 to 8.2 +/- 0.8 pmol/100 cells (p less than 0.001), whereas calcium decreased from 2.9 +/- 0.27 to 1.4 +/- 0.25 pmol/100 cells (p less than 0.001). Erythrocyte cations remained constant. There was a larger increase in lymphocyte potassium in patients with tachyarrhythmias than in patients without (70.4 and 46.9 pmol/100 cells, respectively, p less than 0.001), whereas the presence of a high lymphocyte magnesium level was associated with a significant decrease in the development of tachyarrhythmias, despite high potassium concentrations. It is suggested that lymphocyte cation concentrations mirror myocardial interstitial concentrations and that a high interstitial magnesium level has a protective effect on the increased cell excitability due to, and despite, a high interstitial potassium level.

Short- and long-term prognosis of patients with a first acute myocardial infarction with concomitant peripheral vascular disease. SPRINT Study Group.

PURPOSE: The aim of the study was to assess the prevalence and the prognostic impact of concomitant peripheral vascular disease (PVD) in patients developing acute myocardial infarction (AMI). PATIENTS AND METHODS: Four thousand two hundred fifty-eight consecutive patients with a first AMI hospitalized in 13 of 21 operating coronary care units in Israel were screened. Anamnestic, demographic, and medical data were collected from hospitalization charts, and all patients were followed clinically 1 year after discharge and up to 7 years (mean: 5.5 years) for mortality. RESULTS: The prevalence of clinically diagnosed PVD in patients with a first AMI was 6.3% (269 of 4,258), with no difference between men and women. Patients with PVD were older (66.2 years) and included more hypertensive subjects (47.2%), diabetic persons (26.4%), and individuals with a previous history of cerebrovascular accident (CVA) (11.5%) in comparison to counterparts without PVD (61.7 years; 39.4%, 19.9%, and 3.3%, respectively; p < 0.01 for each). On admission to the coronary care units, 36.5% of patients with PVD were in Killip class II, III, or IV versus only 18.0% in the reference group (p < 0.001). During hospitalization, patients with PVD exhibited a significantly higher rate of paroxysmal atrial fibrillation (17.5%), advanced atrioventricular block (15.2%), and cardiogenic shock (11.9%) in comparison to patients without PVD (11.9%, 10.2%, and 5.3%, respectively; p < 0.01 for each). After adjustment for age, gender, hypertension, history of angina, diabetes mellitus, history of CVA, site of infarction, and congestive heart failure on admission, the odds ratio for in-hospital mortality associated with PVD was 1.37 (90% confidence interval 1.01 to 1.83). There was no independent contribution of PVD to long-term (mean: 5.5 years) postdischarge mortality; the odds ratio was 1.02. CONCLUSION: PVD in patients with a first AMI independently increases the risk of in-hospital death but does not affect long-term mortality in survivors.

Prevalence and prognosis of chronic obstructive pulmonary disease among 5,839 consecutive patients with acute myocardial infarction. SPRINT Study Group.

PURPOSE: The purpose of this study was to report the prevalence and the clinical significance of clinically recognized chronic obstructive pulmonary disease (COPD) during acute myocardial infarction. PATIENTS AND METHODS: During 1981 to 1983, a secondary prevention study with nifedipine (SPRINT) was conducted in Israel among 2,276 survivors of acute myocardial infarction. During the study, demographic, historical, and medical data were collected on special forms for all patients with diagnosed acute myocardial infarction in 13 hospitals (the SPRINT Registry, n = 5,839). Mortality follow-up was completed for 99% of hospital survivors for a mean follow-up of 5.5 years (range: 4.5 to 7 years). RESULTS: The prevalence of COPD was 7% (406 of 5,839). The latter rate increased significantly in men (7.6%), smokers (9.7%), and older patients (70 years or older, 10.0%). Patients with COPD exhibited a complicated hospital course with an in-hospital mortality rate of 23.9%. Subsequent mortality rates in survivors at 1 and 5 years were 12.3% and 35.9%, respectively. Rates at the same time periods in patients without COPD were 17.2%, 9.2%, and 26.9% (p < 0.005 for in-hospital and 5 years). In a multivariate analysis that included age, gender, and history of myocardial infarction and congestive heart failure, COPD was not independently associated with either in-hospital or postdischarge excess fatality rates. CONCLUSION: In this large cohort of consecutive patients with myocardial infarction, the prevalence of COPD was 7% and higher among smokers, men, and elderly patients. Although in-hospital and postdischarge mortality rates were higher among patients with COPD, this condition did not independently increase either the risk of early death or the risk of long-term mortality among survivors of acute myocardial infarction.

Circadian variation and possible external triggers of onset of myocardial infarction. SPRINT Study Group.

PURPOSE: To determine whether a circadian pattern in onset of symptoms existed and possible external triggers were implicated in the precipitation of acute myocardial infarction (AMI). PATIENTS AND METHODS: One thousand eight hundred eighteen consecutive patients with AMI hospitalized in 14 of the 21 existing coronary care units in Israel during the study period were assessed. RESULTS: The frequency of onset of symptoms by 6-hour intervals showed a predominant morning peak (6 AM to noon) (32%, p < 0.01) in comparison with the other three 6-hour intervals of the day. The preponderance of the morning peak persisted for subgroup analysis by gender (males 32%, females 31%); age (less than or equal to 65 years--32%; greater than 65 years--33%); diabetes mellitus (present or absent, 32%). However, patients with peripheral vascular disease and those with stroke in the past had a predominant evening peak. Possible external triggers of onset of AMI were present in 10% of patients. Exceptional heavy physical work, violent quarrel at work or at home, and unusual mental stress were the three most frequent possible external triggers reported immediately before or within the 24 hours preceding pain onset. Patients with possible external triggers were more likely to be males (85%) and were somewhat but not significantly younger (63.1 years) in comparison with patients without external triggers (73% and 64.3 years respectively). CONCLUSIONS: In a large group of consecutive patients with AMI, a predominant cyclic morning peak of pain onset was found in comparison with the other hours of the day. Possible external triggers precipitating AMI were involved in a minority of cases, suggesting that endogenous changes occurring in the morning hours are generally responsible for the increased rate of myocardial infarction occurring after awakening.

Predictors and long-term prognostic significance of recurrent infarction in the year after a first myocardial infarction. SPRINT Study Group.

This study was undertaken to examine whether clinical factors predict reinfarction within 1 year of a first acute myocardial infarction (AMI) and to quantify the subsequent influence of reinfarction on long-term mortality. Data from 3,695 patients with a first AMI included in the Secondary Prevention Reinfarction Israeli Nifedipine Trial Registry were analyzed. The 1-year reinfarction incidence was 6.0% (220 of 3,695) and in-hospital mortality during reinfarction was 31%. Patients with reinfarction were older (63.0 vs 60.8 years) at entry. The independent clinical predictors for 1-year reinfarction were (adjusted relative odds): peripheral vascular disease (2.12), anterior location of the first AMI (1.62), angina before the first AMI (1.53), congestive heart failure on admission (1.34), diabetes (1.33), systemic hypertension (1.28) and age increment (1.13). One-year reinfarction rate increased from 4.0% in patients with 0 or 1 risk factor to 23.3% in patients with 5 to 6 risk factors (p < 0.0001). Patients with reinfarction had significantly increased 1- and 5-year mortality compared with those who had no reinfarction (11.8 vs 5.3% and 40.1 vs 20.3%, respectively, p < 0.001). Recurrent AMI within 1 year was the most powerful predictor of long-term (mean 5.5 years) total mortality (adjusted relative risk = 4.76).

Immediate and long-term prognostic significance of a first anterior versus first inferior wall Q-wave acute myocardial infarction. Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) Study Group.

Of 3,981 patients with a first Q-wave acute myocardial infarction (AMI), 1,929 (48%) had an anterior and 1,724 (43%) an inferior wall AMI. These 2 groups were well-matched with respect to age, gender and relevant history. The in-hospital mortality rate was 18%, and the 1- and 5-year post-discharge mortality rates were 9 and 25%, respectively, in patients with anterior wall AMI compared with the corresponding rates of 11, 6 and 19% in those with inferior wall AMI (p < 0.0001 for each category). The frequency of recurrent nonfatal AMI in the year after the index AMI was 8% in the patients with anterior wall AMI compared with 4% in those with inferior wall AMI (p < 0.0001). By multiple logistic regression analysis of events, anterior wall AMI was an independent predictor of in-hospital mortality only. The findings indicate that the anatomic location of a Q-wave AMI influences immediate and short-term survival of patients with a first Q-wave AMI.

Core body temperature and sleep of older female insomniacs before and after passive body heating.

The purpose of this study was to investigate the relationship between core body temperature and sleep in older female insomniacs and changes in that relationship as a result of passive body heating (PBH). An increase in body temperature early in the evening by way of PBH in older female insomniacs increased SWS in the early part of the sleep period and improved sleep continuity. Fourteen older female insomniacs (60-73 years old) participated in at least two consecutive nights of PBH involving hot (40-40.5 degrees C) baths 1.5-2 hours before bedtime. Hot baths resulted in a significant delay in the phase of the core body temperature rhythm compared to baseline nights. This delay in temperature phase paralleled the improvements in sleep quality.

The predictive value of admission heart rate on mortality in patients with acute myocardial infarction. SPRINT Study Group. Secondary Prevention Reinfarction Israeli Nifedipine Trial.

The purpose of this study was to assess the predictive value of admission heart rate (HR) for in-hospital and 1 year post-discharge mortality in a large cohort of patients hospitalized for acute myocardial infarction (MI). Data were derived from the SPRINT-2 secondary prevention study population, and included 1044 patients (aged 50-79), hospitalized in 14 coronary care units in Israel with acute MI in the years 1985-1986, before the beginning of thrombolytic therapy in acute MI. Demographic, historical and medical data were collected for each patient. All deaths during initial hospitalization and 1 year post-discharge were recorded. In-hospital mortality was 5.2% for 294 patients with HR < 70 beats/min, 9.5% for 532 patients with HR 70-89 beats/min, and 15.1% for 323 patients with HR > or = 90 beats/min (p < 0.01). One year post-discharge mortality was 4.3% for patients with HR < 70 beats/min, 8.7% for patients with HR 70-80 beats/min and 11.8% for patients with HR > or = 90 beats/min (p < 0.01). An increasing trend of mortality with higher HR was confined to patients with mild CHF (p = 0.02) and likely to patients with absent CHF (p = 0.06), but this post hoc observation requires confirmation in larger groups. The combination of high admission HR (> or = 90 beats/min) and a systolic blood pressure < 120 mmHg was a powerful predictor of in-hospital mortality. Multivariate analysis showed that admission HR was an independent risk factor for in-hospital and 1 year post-discharge mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Complete atrioventricular canal with survival to the eighth decade.

Survival to the eighth decade of patients with atrioventricular canal is extremely rare. A patient is presented with such survival of the complete form of the defect. This possibly represents the first such report in the medical literature. The value of 2-dimensional echocardiography, particularly with venous contrast studies, in establishing the diagnosis, is shown.

Use of pulmonary artery catheters in patients with acute myocardial infarction. Analysis of experience in 5,841 patients in the SPRINT Registry. SPRINT Study Group.

This study analyzes the use of PAC in a registry comprising 5,841 hospitalized patients with AMI. A total of 371 patients received PAC. In-hospital mortality was higher in patients with CHF who received PAC, while there was no difference in patients with cardiogenic shock or persistent hypotension. Mortality in patients receiving PAC was higher irrespective of the presence or absence of "pump failure." A separate analysis of discharge summaries of 364 patients with CHF showed that PAC was used more frequently in sicker patients and that when severity of CHF was assessed, no difference in mortality was found in patients with mild or moderate CHF. We conclude that while a higher in-hospital mortality is found in patients receiving PAC, this excess is likely related to difference in severity of CHF, which had not been assessed in every individual. It is unlikely that PAC increases mortality.

Changes in cognitive function associated with sleep disordered breathing in older people.

OBJECTIVES: Sleep disordered breathing (SDB) is very common in older people and is known to be associated with complaints of impaired daily functioning, including excessive daytime sleepiness and cognitive impairments. As part of a larger study on SDB and aging, it became possible to examine the relationship between SDB and cognition in older men and women. DESIGN: A population-based longitudinal study. SETTING: In-home interviews and home sleep recordings in the greater San Diego area. PARTICIPANTS: Community-dwelling people age 65 and older with high risk for SDB were originally studied from 1981 through 1985 and then followed every 2 years. Data from the 46 subjects who completed Visit 3 and Visit 4 are presented. MEASUREMENTS: Subjects were interviewed in the home about their sleep and medical condition before each visit. Cognitive function was assessed using the Mini-Mental State Examination (MMSE). Daytime sleepiness was based on self-report. Objective sleep was recorded in the home and scored for sleep, apneas and hypopneas, and oximetry variables. RESULTS: Increases in respiratory disturbance index (RDI) (P= .036) and increases in daytime sleepiness (P= .002) were associated with decreases in cognitive performance (i.e., increases in cognitive impairment). Increases in RDI were also associated with increases in daytime sleepiness (P= .012). Change in MMSE scores was therefore regressed onto changes in RDI, daytime sleepiness, age, and education, resulting in decreases in MMSE scores being associated with increases in daytime sleepiness (P= .019) but not with changes in RDI (P= .515). There was no significant relationship between changes in oxygen saturation levels and changes in MMSE. CONCLUSIONS: The results of this study suggest that declining cognitive function is associated primarily with increases in daytime sleepiness. Although cognitive decline was also associated with increases in RDI, this association did not hold in the more inclusive model which also included variable of SDB, oximetry, sleep and subjective report. One theoretical model could suggest that any relationship between SDB and cognitive function may be mediated by the effect of SDB on daytime sleepiness. These results suggest that older patients suffering from mild to moderate SDB may benefit from the treatment of SDB, even if they are not markedly hypoxemic.

Long-term follow-up of sleep disordered breathing in older adults.

OBJECTIVE: The current study was designed to determine whether, with increasing age, sleep apnea improves, becomes worse, or stays the same. BACKGROUND: There is a high prevalence of sleep disordered breathing (SDB) in older adults, but little is known about longitudinal changes. This study followed older adults to examine the natural history of SDB. METHODS: Subjects were randomly selected community-dwelling elderly (n=427). A subset of subjects was studied approximately every 2 years over an 18-year period. Overnight sleep recordings and sleep questionnaires were completed at each time point. RESULTS: Multiple linear regression showed that three variables were associated with change in respiratory disturbance index (RDI):body mass index (BMI) at initial visit (P=0.001), change in BMI (P=0.02), and a consistent self-report of high blood pressure (P=0.005). RDI increase was associated with BMI increase and presence of self-reported high blood pressure. CONCLUSIONS: The changes in RDI that occurred were associated only with changes in BMI and were independent of age. This underscores the importance of managing weight for older adults, particularly those with hypertension.

Prognosis of early versus late ventricular fibrillation complicating acute myocardial infarction.

Earlier studies have suggested that patients exhibiting late (> 24 h) ventricular fibrillation during acute myocardial infarction had a poorer outcome in comparison to myocardial infarction patients with early (< 24 h) ventricular fibrillation. Between August 1981 and July 1983, 5839 consecutive patients with acute myocardial infarction were hospitalized in 13 out of 21 operating coronary care units in Israel. Demographic and medical data were collected from hospitalization charts and during 1 year of follow-up. Mortality assessment was done for 99% of hospital survivors up to mid-1988 (mean, 5.5 years). The incidence of ventricular fibrillation in the SPRINT Registry was 6% (371/5839). Patients with ventricular fibrillation in the setting of cardiogenic shock (n = 107) were excluded from analysis. Patients with late ventricular fibrillation (n = 109; 41%) were older and had a more complicated hospital course than patients with early ventricular fibrillation (n = 155; 59%). In-hospital and 1-year post-discharge mortality were significantly higher in patients with late ventricular fibrillation (63% and 17%) as compared to patients with early ventricular fibrillation (26% and 4%, respectively; P < 0.05 for each). This difference vanished 5 years after hospital discharge. After multiple logistic regression analysis late occurrence of ventricular fibrillation emerged as an independent predictor of increased in-hospital mortality (Odds ratio, 4.29; 95% confidence interval, 2.11-8.74) but not for subsequent death. Patients with late ventricular fibrillation during the hospital course of acute myocardial infarction had a poorer immediate and subsequent outcome in comparison to patients with early ventricular fibrillation.

Early risk stratification of patients with a first inferior wall acute myocardial infarction. SPRINT Study Group.

A prognostic index based on admission characteristics of patients with inferior acute myocardial infarction was developed to predict mortality and other major complications during hospitalization. The study sample included 1841 consecutive patients with a first inferior wall acute myocardial infarction, hospitalized in 13 out of 21 operating coronary care units in Israel. Age, angina in the past, congestive heart failure and blood glucose level > 180 mg/dl were independently associated with higher in-hospital mortality and morbidity. The prognostic weights of these risk factors were determined in a study group which comprised two thirds of the patients (n = 1210) who were randomly selected from the 1841 participants. A prognostic score (range, 0-15) was calculated as the sum of the prognostic weights of the above four risk factors for each patient. These scores were determined in both the study group and in a validation group (the remaining one third of the patients, n = 592). In-hospital mortality in the study group ranged from no death for 102 patients with a prognostic score of 0, to a 37% mortality rate in 106 patients whose prognostic score was > 8. Accordingly, the study group was divided into groups of low-risk (score 0-5), intermediate-risk (score 6-8) and high-risk (score > 8), with in-hospital mortality of 3, 13 and 37%, respectively. In-hospital mortality among patients in the validation group determined to be at low-, intermediate- and high-risk was 3, 13 and 44%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)