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The Bayesian brain hypothesis is one of the most influential ideas in neuroscience. However, unstated differences in how Bayesian ideas are operationalized make it difficult to draw general conclusions about how Bayesian computations map onto neural circuits. Here, we identify one such unstated difference: some theories ask how neural circuits could recover information about the world from sensory neural activity (Bayesian decoding), whereas others ask how neural circuits could implement inference in an internal model (Bayesian encoding). These two approaches require profoundly different assumptions and lead to different interpretations of empirical data. We contrast them in terms of motivations, empirical support and relationship to neural data. We also use a simple model to argue that encoding and decoding models are complementary rather than competing. Appreciating the distinction between Bayesian encoding and Bayesian decoding will help to organize future work and enable stronger empirical tests about the nature of inference in the brain.

Optical atomic clocks are the most accurate measurement devices ever constructed and have found many applications in fundamental science and technology1–3. The use of highly charged ions (HCI) as a new class of references for highest-accuracy clocks and precision tests of fundamental physics4–11has long been motivated by their extreme atomic properties and reduced sensitivity to perturbations from external electric and magnetic fields compared with singly charged ions or neutral atoms. Here we present the realization of this new class of clocks, based on an optical magnetic-dipole transition in Ar13+. Its comprehensively evaluated systematic frequency uncertainty of 2.2 × 10−17is comparable with that of many optical clocks in operation. From clock comparisons, we improve by eight and nine orders of magnitude on the uncertainties for the absolute transition frequency12and isotope shift (40Ar versus 36Ar) (ref. 13), respectively. These measurements allow us to investigate the largely unexplored quantum electrodynamic (QED) nuclear recoil, presented as part of improved calculations of the isotope shift, which reduce the uncertainty of previous theory14by a factor of three. This work establishes forbidden optical transitions in HCI as references for cutting-edge optical clocks and future high-sensitivity searches for physics beyond the standard model.

For this article, the literature on the pathophysiology, clinical features, natural history, prognosis, and management of the Eisenmenger syndrome in adults was reviewed. English-language articles from 1966 to the present were identified through a search of the MEDLINE database by using the terms Eisenmenger, congenital heart disease, and pulmonary hypertension. Selected cross-referenced articles were also included. Articles on the pathophysiology, clinical presentation, evaluation, natural history, complications, and treatment of the Eisenmenger syndrome in adults were selected, and descriptive and analytical data relevant to the practicing physician were manually extracted. The Eisenmenger syndrome is characterized by elevated pulmonary vascular resistance and right-to-left shunting of blood through a systemic-to-pulmonary circulation connection. Most patients with the syndrome survive for 20 to 30 years. The hemostatic changes associated with the syndrome may lead to thromboembolic events, cerebrovascular complications, or the hyperviscosity syndrome. Erythrocytosis is present in most patients, but excessive phlebotomy may cause microcytosis and exacerbate the symptoms of hyperviscosity. Other complications associated with the Eisenmenger syndrome include hemoptysis, gout, cholelithiasis, hypertrophic osteoarthropathy, and decreased renal function. Pregnancy or noncardiac surgery is associated with a high mortality rate in patients with the Eisenmenger syndrome. Because most pediatric patients with the Eisenmenger syndrome survive to adulthood, primary care physicians should have a thorough understanding of the syndrome; its associated complications; and medical and surgical management, especially with regard to the appropriate timing of phlebotomy and lung or heart-lung transplantation. In addition, patients with the syndrome should undergo routine follow-up at a tertiary care center that has physicians and nurses with special expertise in congenital heart disease. In patients with the Eisenmenger syndrome who are pregnant or require noncardiac surgery, a multidisciplinary approach should be used to reduce the excessive mortality associated with these conditions., A review of the causes and treatment of Eisenmenger syndrome is presented. This syndrome is usually caused by an abnormal opening between the right and left sides of the heart which causes blood to pass from the right side to the left. This causes un-oxygenated blood to travel through the body, which leads to low oxygen levels and an increase in the number of red blood cells. This causes blood to become thick, which can cause abnormal blood clotting and other complications. Treatment includes removing small amounts of blood and heart-lung transplantation.

PURPOSE: Nicotine replacement therapy has become a popular therapy for smokers attempting to stop smoking. Unfortunately, some subjects continue to smoke while receiving it. Since nicotine is believed to be the primary constituent of cigarette smoke responsible for its acute adverse effects on myocardial oxygen supply and demand, concomitant nicotine replacement therapy and smoking theoretically could provoke a marked decrease in myocardial oxygen supply and increase in demand. This study was performed to assess the effects of cigarette smoking with and without concomitant intranasal nicotine spray on: (a) myocardial oxygen demand, (b) coronary arterial dimensions, and (c) the development of acute cardiovascular tolerance. PATIENTS AND METHODS: In 19 smokers referred for cardiac catheterization for the evaluation of chest pain, we assessed the effects of cigarette smoking with and without concomitant intranasal nicotine spray on. (a) heart rate-systolic arterial pressure product lan estimate of myocardial oxygen demand), (b) coronary arterial dimensions (measured with computer-assisted quantitative arteriography), and (c) the development of acute cardiovascular tolerance. RESULTS: Smoking a first cigarette increased rate pressure product (P

Background: Cocaine and ethanol are often abused concomitantly, and this combination may be more lethal than either substance alone. Although previous studies showed that cocaine causes coronary arterial vasoconstriction, the combined effect of cocaine and ethanol on the coronary vasculature in humans is unknown. Thus, we assessed the effects of intranasal cocaine, intravenous ethanol, or a cocaine-ethanol combination on heart rate, systemic arterial pressure, and coronary arterial dimensions in humans. Methods: Thirty-four subjects with chest pain (27 men and seven women, aged 34 to 67 years) who were referred for catheterization received one of the following pharmacologic interventions: (1) intranasal (2 mL) and intravenous (5 mL/kg) saline (n = 8 [group A]); (2) intranasal cocaine (2 mg/kg) and intravenous saline (5 mL/kg) (n = 9 [group B]); (3) intranasal saline (2 mL) and intravenous 10% ethanol (5 mL/kg) (n = 9 [group C]); or (4) intranasal cocaine (2 mg/kg) and intravenous 10% ethanol (5 mL/kg) (n = 8 [group D]). Heart rate, systemic arterial pressure, left coronary arterial dimensions (by computer-assisted quantitative angiography), as well as blood cocaine, ethanol, and cocaine metabolite concentrations were measured before and 30, 60, and 90 minutes after initiation of the intravenous infusions. Results: No hemodynamic or angiographic changes were observed in the group A (saline) subjects. In the group B (cocaine) subjects, the heart rate--systolic arterial pressure product increased by 5% and 10% at 30 and 90 minutes, respectively, and coronary arterial diameter decreased by 14% at these times. In the group C (ethanol) subjects, no hemodynamic changes were noted, but coronary arterial diameters increased by 12%, 11%, and 12% at 30, 60, and 90 minutes, respectively. In the group D (cocaine-ethanol) patients, rate-pressure product increased by 17%, 10%, and 16%, and coronary arterial diameters increased by 7%, 12%, and 13%, at 30, 60, and 90 minutes, respectively. Conclusion: The combination of intranasal cocaine and intravenous ethanol causes an increase in the determinants of myocardial oxygen demand. However, it also causes a concomitant increase in epicardial coronary arterial diameter. (Arch Intern Med. 1995;155:1186-1191)

In patients with acute myocardial infarction, percutaneous transluminal coronary angioplasty (PTCA) may be used (1) to restore antegrade flow in the infarct artery (so called 'primary' PTCA) instead of thrombolytic therapy, (2) to establish antegrade coronary flow after unsuccessful thrombolytic therapy (so called 'rescue' or 'salvage' PTCA), and (3) to reduce the residual infarct artery stenosis after successful thrombolysis. This review examines the prospective, randomized studies that have addressed the use of PTCA for each of these purposes. In selected circumstances, PTCA is a reasonable alternative to thrombolytic therapy in patients with evolving or recent Q-wave myocardial infarction. In those patients with acute myocardial infarction complicated by cardiogenic shock, PTCA may be the preferred treatment. After thrombolytic therapy, the use of PTCA in the absence of spontaneous or provocable ischemia offers no benefit with regard to left ventricular function or survival. in this circumstance, its use is associated with an excessive risk of bleeding, transfusions, and emergent coronary artery bypass surgery when performed within hours of infarction.

PURPOSE: As cocaine abuse has become widespread, catastrophic cocaine-associated cardiovascular events have been noted with increasing frequency. Although these incidents are thought to be caused by drug-induced vasoconstriction and/or arterial thrombosis, the influence of cocaine on the plasma constituents involved in endogenous thrombosis and thrombolysis has not been characterized. PATIENTS AND METHODS: In 22 patients (8 men, 14 women, ages 32 to 62 years) undergoing cardiac catheterization, blood samples were procured before and 15 minutes after the administration intranasal saline (n = 8, controls) or cocaine, 2 mg/kg (n = 14), and the plasma concentrations of fibrinogen, plasminogen, and lipoprotein(a), as well as tissue plasminogen activator activity and plasminogen activator inhibitor (PAI-1) activity, were measured. RESULTS: No variable changed with the use of intranasal saline, whereas the use of cocaine resulted in an increase in PAI-I activity (0.48 + 0.06 (mean + SD] nmol\L at baseline, 0.53 + 0.05 nmol/L after cocaine, P = 0.011). CONCLUSION: Intranasal cocaine administration is associated with an increase in plasma PAI-1 activity. This may be important in recreational users of cocaine who experience vascular thrombosis.

PURPOSE: To assess the coronary anatomy and prognosis of young, asymptomatic survivors of myocardial infarction. PATIENTS AND METHODS: The records Of all 5,316 patients who underwent cardiac catheterization at Parkland Memorial Hospital from July 1978 to December 1992 were reviewed to identify those patients 40 years old and younger who were catheterized within 60 days of a first myocardial infarction. Of 129 such patients, 48 had no indication for catheterization other than age (group I), and 81 were catheterized for spontaneous or provocable ischemia (group II). Extent of coronary artery disease and long-term follow-up were examined to ascertain the utility of cardiac catheterization in the asymptomatic patients. Results: The 2 groups were similar with respect to clinical variables. The asymptomatic survivors of infarction (group I) had fewer diseased coronary arteries than did those with post-infarction ischemia (group II) (1.0 [+ or -] 0.7 versus 1.5 [+ or -] 1.0 [mean + or -] SD] diseased coronary arteries, respectively; P = 0.002) and were less likely to have left-main or 3-vessel coronary artery disease (4% versus 20%, respectively; P = 0.027). Eight-three percent of the group I patients had one diseased coronary artery, or less, and no patient underwent angioplasty or coronary bypass grafting on the basis of catheterization. After 71 [+ or -] 44 months of follow-up, only 5 (10%) had died of a coronary-related event. CONCLUSIONS: Asymptomatic survivors of myocardial infarction who are 40 years of age or less rarely have left-main or 3-vessel coronary artery disease, and their long-term prognosis with conservative therapy is good. Routine catheterization in these patients is not warranted and should be reserved for those who manifest spontaneous or provocable post-infarction ischemia.

Cocaine use has been associated with a number of cardiovascular complications, including angina pectoris, myocardial infarction and sudden cardiac death.[1-4] Previous studies in humans have shown that cocaine causes epicardial coronary vasoconstriction, which is mediated, at least in part, by [alpha]-adrenergic stimulation.[5-10] Studies in experimental animals have suggested that cocaine may also cause vasoconstriction by altering calcium transport in vascular smooth muscle,[11] and this can be attenuated by calcium channel blockade. The present study was performed to assess the effect of verapamil, a calcium antagonist, on cocaine-induced coronary vaso-constriction in humans.

To assess the incidence, pathophysiology and influence on operative outcome of a depressed left ventricular (LV) ejection fraction (EF) in patients with mitral stenosis (MS), demographic, hemodynamic and cineangiographic data on 72 patients (16 men, 56 women, aged 19 to 75 years) with isolated MS were reviewed. Of the 45 who had mitral commissurotomy or replacement, operative course and functional class before and after surgery were assessed. Of the 72 patients, 21 (29%) had an LVEF [is less than or equal to]0.50. These 21 were similar to the 51 with an LVEF >0.50 in age, gender, heart rate, intracardiac pressures, transvalvular gradient and valve area, but they had larger LV end-diastolic (79 [+ or -] 19 [mean [+ or -] SD] vs 59 [+ or -] 15 ml/[m.sup.2], p 0.50. (Am J Cardiol 1994;73:65-69)

The hydrogen inhalation technique is easily performed and exquisitely sensitive for detecting intracardiac left-to-right shunting. Previous studies of this technique relied heavily on data from infants and children, and the distinction between 'normal' and 'abnormal' was imprecise and somewhat arbitrary. The present study was done to assess the results of hydrogen inhalation in adults with and without intracardiac left-to-right shunting. In 45 adult subjects (15 men, 30 women, aged 18 to 72 years) (18 without and 27 with intracardiac left-to-right shunting), the elapsed time from hydrogen inhalation to its appearance in the pulmonary artery was measured. The 18 patients without shunting had an appearance time of 12 [+ or -] 3 (mean [+ or -] SD) seconds, and it was [greater than or equal to]9 seconds in all. In contrast, the 27 subjects with shunting had an appearance time of 1.5 [+ or -] 0.7 second, with only 1 of 27 being [greater than or equal to]3 seconds. There was no relation between the magnitude of left-to-right shunting and the hydrogen appearance time. Thus, the hydrogen inhalation technique easily and reliably separates adult subjects with and without intracardiac left-to-right shunting, with no overlap between the 2 groups.

In survivors of acute myocardial infarction (AMI), the restoration of anterograde flow in the infarct artery, even if accomplished beyond the time for myocardial salvage, may reduce the frequency of subsequent arrhythmic events and sudden death. Twelve subjects (8 men and 4 women, aged 39 to 69 years) with a first AMI, signal-averaged electrocardiographic late potentials, and an occluded infarct artery were prospectively identified. Seven (group I) had successful coronary angioplasty 6 to 15 days after AMI, and 5 (group II) were managed conservatively. Follow-up signal-averaged electrocardiography was performed 3 to 7 months later. From baseline to follow-up, the 7 group I subjects had a significant change in QRS duration (117 [+ or -] 13 [mean + SD] to 102 [+ or -] 10 ms), root-mean-square voltage (10.4 [+ or -] 4.7 to 31.0 [+ or -] 7.6 [Micro]V), and low-amplitude signal duration (47.5 [+ or -] 8.5 to 32.4 [+ or -] 5.2 ms) (p [less than or equal to]0.05 for all 3 variables). No group I patient had a late potential at follow-up. In contrast, the 5 group II patients showed no change in QRS duration or low-amplitude signal duration from baseline to follow-up, and all 5 had a late potential at follow-up. At follow-up, the root-mean-square voltage was significantly greater and the low-amplitude signal and QRS durations significantly less in group I than in group II (p (Am J Cardiol 1992;70:1515-1519)

This study was done to compare single and biplane left ventriculography in quantitating left ventricular (LV) volumes and ejection fraction. LV volumes and ejection fraction were measured from a 30 [degrees] right anterior oblique single plane ventriculogram and a 30 [degrees] right anterior oblique 60 [degrees] left anterior oblique biplane ventriculogram in 152 men (aged 59 [+ or -] 9 [mean [+ or -] standard deviation] years), of whom 102 had hypokinesia, akinesia, or dyskinesia. There was excellent agreement between the results of single and biplane ventriculography with respect to LV end-diastolic volume (r = 0.96), end-systolic volume (r = 0.98) and ejection fraction (r = 0.97). The end-diastolic and end-systolic volumes measured by biplane ventriculography were consistently slightly larger than those measured by single plane, whereas ejection fractions measured by the 2 techniques were remarkably similar, even for the 46 patients with biplane ejection fractions

* Background. - Clinically, ischemic and nonischmeic (idiopathic) dilated cardiomyopathy may be difficult to distinguish. Radionuclide ventriculography and exercise testing with thallium-201 scintigraphy are often used in attempt to differentiate them noninvasively. With these techniques, the presence of (1) left ventricular (LV) regional asynergy, (2) depressed LV systolic function with normal right ventricular function, and/or (3) thallium-201 perfusion abnormalities traditionally has been regarded as evidence of ischemic heart disease. We assessed the incidence with which these abnormalities occur in patients with nonischemic-dilated cardiomyopathy. Methods. - Seventy-six patients (45 men, 31 women, aged 18 to 74 years) with invasively proven nonischemic-dilated cardiomyopathy underwent radionuclide ventriculography (n = 75) and provocative thallium-2011 perfusion imaging (n = 17). Results. - Regional LV wall abnormalities were noted in 48% of patients, and 54% had LV systolic dysfunction without concomitant right ventricular dysfunction. Reversible and/or fixed exercise-induced thallium-2011 perfusion abnormalities occurred in 94% of the patients studied. Conclusions. - Radionuclide ventriculography and exercise testing with thallium perfusion imaging cannot be used reliably to differentiate ischemic from nonischemic dilated cardiomyopathy, since many patients with the latter have radionuclide evidence of LV segmental wall motion selective LV systolic dysfunction, and segmental perfusion abnormalities. (Arch Intern Med. 1992; 152;769-772)

* Objective: To define the temporal characteristics of cocaine-induced coronary vasoconstriction in humans and to assess the relation between cocaine-induced coronary vasoconstriction and the blood concentration of cocaine and its main metabolites. * Design: Randomized, double-blind, controlled clinical trial. * Setting: Cardiac catheterization laboratory of a large teaching hospital. * Patients: Eighteen patients (16 men and 2 women, 37 to 65 years of age) having catheterization for evaluation of chest pain. * Measurements: At catheterization, patients received intranasal saline (8 patients) or cocaine, 2 mg/kg body weight (10 patients). Cineangiographic examination of the left coronary artery and quantitation of the blood concentration of cocaine and its metabolites were done before (baseline) and 30, 60, and 90 minutes after administration of intranasal saline or cocaine. * Results: In response to cocaine, proximal coronary arterial diameter decreased from 2.4 [+ or -] 1.6 mm (mean [+ or -] SD) at baseline to 2.0 [+ or -] 1.4 mm at 30 minutes (P < 0.05). This change corresponded temporarily to the peak blood concentration of cocaine. At 60 minutes, the cocaine concentration decreased and coronary artery diameter returned to baseline (2.3 [+ or -] 1.6 mm) (P = > 0.05 compared with baseline). At 90 minutes, all patients had recurrent vasoconstriction (1.0 [+ or -] 1.4 mm, P < 0.05) despite a further decrease in the blood cocaine concentration. This vasoconstriction corresponded temporarily with an increasing blood concentration of cocaine's main metabolites, benzoylecgonine and ethyl methyl ecgonine. No changes were observed in the control group. * Conclusion: Intranasal cocaine causes recurrent coronary vasoconstriction, which may be due to its metabolites.

Previous studies have shown that long-term survival after acute myocardial infarction (AMI) is improved by Beta-adrenergic blockade and anterograde flow in the infarct artery. This study was done to assess the influence of Beta blockade on mortality in survivers of AMI without anterograde flow. Over 9.5 years, 113 subjects (87 men and 26 women, aged 26 to 66 years) with AMI and no anterograde flow in the infarct artery and no disease of the other arteries were medically treated for 48 +/- 28 (mean +/- standard deviation) months. Forty-six patients received long-term P blockade (group 1), whereas 67 did not (group 11). The groups were similar in age, sex, cardioactive medications, left ventricular performance and infarct artery. Of the 46 group 1 subject, 1 (2%) died of cardiac causes; in contrast, 20 30%) of the group 11 patients died of cardiac causes (p = 0.007 compared with group 1). Thus, in survivors of AMI without anterograde flow in the infarct artery, mortality is markedly reduced by long-term Beta blockade. (Am J Cardiol 1991;68:150-154), Acute myocardial infarction (AMI; heart attack) occurs when one or more of the coronary arteries, which supply blood to the heart, become blocked. The subsequent myocardial ischemia (diminished cardiac blood flow) can cause death or permanent cardiac damage. Among AMI survivors, ischemia-induced cardiac arrhythmias, or abnormal heart rhythms, appear to be a significant contributor to cardiovascular mortality. Some studies have reported that arrhythmias are more prevalent among AMI patients in whom there is no anterograde flow in the infarct artery. (That is, abnormal heart rhythms occur more often in AMI patients when blood flow is not reestablished in the occluded artery). Beta adrenergic receptor blockers (beta blockers), a class of drugs with blood pressure-lowering and anti-arrhythmic properties, have been reported effective in reducing mortality among AMI survivors. To test the hypothesis that one mechanism of action through which this is accomplished is suppression of cardiac arrhythmias, a study was done involving 113 subjects (87 men and 26 women between the ages of 26 and 66) who were recovering from AMI, and in whom there was no anterograde flow in the infarct-related coronary artery. Researchers theorized that since these patients are more prone to cardiac arrhythmias, they should be more susceptible to any beneficial effects of beta blocker treatment. Patients were randomly assigned to one of two groups and received either standard medical treatment or the same treatment plus beta blockers. Among the beta blocker-treated patients, only one person (2 percent) died during the course of the 48-month treatment period; 20 patients (30 percent) who did not receive beta blocker treatment died during the same period. Hence, long-term beta blockade therapy significantly reduced mortality in AMI survivors who are prone to cardiac arrhythmias. (Consumer Summary produced by Reliance Medical Information, Inc.)

Cocaine can cause death either by its effects on the brain and spinal cord or by its actions on the heart and the vessels supplying the heart. Cocaine causes an increase in heart rate, blood pressure, and oxygen consumption by the heart, and may decrease blood flow to the heart in persons with diseased heart vessels. Cocaine stimulates the release of noradrenaline (NA) which then acts on both alpha and beta adrenergic receptors, which are proteins that line certain types of cells in the body, to produce the above effects. Beta adrenergic blocking agents ('beta blockers') are drugs that prevent NA from acting on the beta receptor and are used to treat conditions such as high blood pressure and chest pain (angina), which may result from a decrease in blood flow to the heart. Beta blockers have been used to treat patients with cocaine-induced decreases in blood flow to the heart, but the unopposed action of noradrenaline at the alpha adrenergic receptor may constrict the vessels more and worsen the condition. A recent study of 30 patients examined the effects of beta blockers on cocaine-induced constriction of heart vessels. Cocaine decreased the oxygen supply to the heart by constricting the coronary arteries and this effect was significantly exaggerated by the beta blocker propranolol. It is thought that the decreased oxygen supply may lead to chest pain or a heart attack in some people. Since beta blockers worsened this condition, they should be avoided in patients with a history of cocaine use who have angina. (Consumer Summary produced by Reliance Medical Information, Inc.)

I agree with Ben Marcus ['Why Experimental Fiction Threatens to Destroy Publishing, Jonathan Franzen, and Life as We Know It,' Folio, October] that there is a resistance to experimental writing [...]

COVID-19 has posed an extraordinary burden on health and the economy worldwide. Patients with cardiovascular diseases are more likely to have severe illness due to COVID-19 and are at increased risk for complications and mortality. We performed a narrative literature review to assess the burden of COVID-19 and cardiovascular morbidity and mortality. Myocardial injury has been reported in 20%–30% of patients hospitalized due to COVID-19 and is associated with a worse prognosis and high mortality (~50%–60%). Proposed mechanisms of myocardial injury include inflammation within the myocardium (due to direct viral infection or cytokine storm), endotheliitis, coronary vasculitis, myocarditis, demand ischemia, plaque destabilization and right ventricular failure. The right ventricle is particularly vulnerable to injury and failure in COVID-19-infected patients, given the hypoxic pulmonary vasoconstriction, pulmonary microthrombi or pulmonary embolism. Echocardiography is an effective and accessible tool to evaluate left and right ventricular functions and risk stratify patients with COVID-19 infection. Cardiac MRI has detected and characterized myocardial injury, with changes compatible with other inflammatory cardiomyopathies. The long-term consequences of these inflammatory changes are unknown, but accumulating data will provide insight regarding the longitudinal impact of COVID-19 infection on cardiovascular morbidity and mortality.

Indwelling pulmonary arterial catheters are often used to monitor and to guide therapy in critically ill patients. The magnitude of the V wave recorded from the pulmonary arterial wedge (PAW) position is sometimes used to assess the presence and severity of mitral regurgitation (MR). The present study was performed to assess the relation (or lack thereof) between a 'prominent' PAW V wave and qualitative and quantitative estimates of MR. in 903 subjects (445 men and 458 women, aged 49 [+ or -] 13 [mean [+ or -] SD] years) referred for cardiac catheterization, an oximetrically confirmed PAW pressure was recorded with a large-lumen stiff catheter, and a left ventriculogram was recorded. In 646 of these subjects (328 men and 318 women, aged 50 [+ or -] 13 years), forward cardiac output was measured by the Fick principle, and a regurgitant fraction was calculated. Prominent PAW V waves--as defined in several ways--were insensitive and had poor positive predictive value in identifying moderate or severe MR. At the same time, the absence of prominent PAW V waves was relatively specific for the absence of moderate or severe MR, and the negative predictive value of small V waves was very good. Thus, the prominence of a PAW V wave cannot be used to assess the presence or severity of MR. (Am J Cardiol 1994;73:S68-570)

PURPOSE: Although labetalol is sometimes given to patients with cocaine-associated chest pain, its influence on cocaine-induced coronary vasoconstriction is unknown. PATIENTS AND METHODS: In 15 patients (7 men, 8 women, aged 40 to 79 years) undergoing catheterization for chest pain, heart rate, mean arterial pressure, and coronary arterial area (by computer-assisted quantitative angiography) were measured (1) at baseline, (2) 15 minutes after intranasal cocaine, 2 mg/kg, then (3) 5 minutes after intravenous saline (n = 6) or labetalol, 0.25 mg/kg (n = 9). RESULTS: Of 40 coronary arterial segments analyzed, cocaine induced a 13% [+ or -] 10% (mean [+ or -] standard deviation) decrease in coronary arterial area in 32. Subsequently, no variable changed after saline administration. Although labetalol reduced mean arterial pressure (117 [+ or -] 14 mm Hg after cocaine, 110 [+ or -] 11 mm Hg after labetalol; p < 0.05), it induced no change in the coronary arterial area (3.47 [+ or -] 1.37 [mm.sup.2] after cocaine, 3.37 [+ or -] 1.32 [mm.sup.2] after labetalol; p = NS). CONCLUSION: Labetalol reverses the cocaine-induced rise in mean arterial pressure, but does not alleviate cocaine-induced coronary vasoconstriction.

In early reports, coronary arteriography in patients with left main (LM) coronary artery disease (CAD) had a substantial risk, but recent reports suggest that arteriography in these subjects is now associated with a low mortality. The present study was performed to examine the periprocedure mortality in patients with LMCAD undergoing catheterization, to compare the periprocedure mortality in these patients with that in subjects with less CAD and to identify the variables associated with pericatheterization mortality in this patient cohort. Of 4,009 patients undergoing elective coronary arteriography from 1978 to 1992, 176 had LMCAD. Of the 10 deaths during or within 24 hours of cathetezation, 5 occured in these 176 subjects. This periprocedure mortality of 2.8% in patients with LMCAD was >20 times that of those without LMCAD (0.13%). In comparison with the 171 patients with LMCAD who survived, the 5 who died were older (67[+ or -]8 vs 58[+ or -]12 years), and had more severe LMCAD (92[+ or -]10% vs 72 :E 16%) and a lower cardiac index (1.9[+ or -]0.4 vs 2.6[+ or -]0.7 liters/min/[m.sup.2]) (p (Am J Cardiol 1992;70:1388-1390)

Previous studies showed that long-term morbidity and mortality after acute myocardial infarction (AMI) are influenced by the presence or absence of anterograde flow in the infarct artery. In comparison with patients with anterograde flow, those whose infarct artery remains occluded are more likely to have unstable angina, recurrent AMI, congestive heart failure and sudden death. This study was performed to assess the influence of collateral filling of the infarct artery on long-term morbidity and mortality in surviving patients of initial AMI in whom the infarct artery was occluded. Over a 12.5-year period, 146 subject (108 men and 38 women, aged 25 to 76 years) with AMI, no anterograde flow in the infarct artery, and no disease of other coronary arteries were medically treated and followed for 42 [+ or -] 28 (mean [+ or -] standard deviation) months. Of these subjects, 120 had angiographic evidence of collateral filling of the infarct artery (group I), whereas the remaining 26 did not (group II). The groups were similar in age, sex, cardioactive medications, left ventricular performance and infarct artery. They were also similar in incidence of unstable angina (19% of group I, 31% of group II; p = not significant [NS]), recurrent AMI (12% of group I, 8% of group II; p = NS), congestive heart failure (16% of group I, 12% of group II; p = NS) and cardiac death (16% of group I, 19% of group II; p = NS). Thus, angiographic evidence of collateral filling of the infarct artery in surviving patients of AMI exerts no demonstrable influence (beneficial or detrimental) on long-term morbidity or mortality.

Background: Chronic total occlusion (CTO) of a coronary artery is defined as an occluded segment with no antegrade flow and a known or estimated duration of at least 12 weeks. Objective: We considered the current literature describing the indications and clinical outcomes for denovo CTO- percutaneous coronary intervention (PCI), and discuss the role of CTO-PCI and future directions for this procedure. Methods: Databases (PubMed, the Cochrane Library, Embase, EBSCO, Web of Science, and CINAHL were searched and relevant studies of CTO-PCI were selected for review. Results: The prevalence of coronary artery CTO's has been reported to be ~ 20% among patients undergoing diagnostic coronary angiography for suspected coronary artery disease. Revascularization of any CTO can be technically challenging and a time-consuming procedure with relatively low success rates and may be associated with a higher incidence of complications, particularly at non-specialized centers. However, with an increase in experience and technological advances, several centers are now reporting success rates above 80% for these lesions. There is marked variability among studies in reporting outcomes for CTO-PCI with some reporting potential mortality benefit, better quality of life and improved cardiac function parameters. Anecdotally, properly selected patients who undergo a successful CTO-PCI most often have profound relief of ischemic symptoms. Intuitively, it makes sense to revascularize an occluded coronary artery with the goal of improving cardiovascular function and patient quality of life. Conclusion: CTO-PCI is a rapidly expanding specialized procedure in interventional cardiology and is reasonable or indicated if the occluded vessel is responsible for symptoms or in selected patients with silent ischemia in whom there is a large amount of myocardium at risk and PCI is likely to be successful.

Questioning basic assumptions about the structure of space and time has greatly enhanced our understanding of nature. State-of-the-art atomic clocks1–3make it possible to precisely test fundamental symmetry properties of spacetime and search for physics beyond the standard model at low energies of just a few electronvolts4. Modern tests of Einstein’s theory of relativity try to measure so-far-undetected violations of Lorentz symmetry5; accurately comparing the frequencies of optical clocks is a promising route to further improving such tests6. Here we experimentally demonstrate agreement between two single-ion optical clocks at the 10−18level, directly validating their uncertainty budgets, over a six-month comparison period. The ytterbium ions of the two clocks are confined in separate ion traps with quantization axes aligned along non-parallel directions. Hypothetical Lorentz symmetry violations5–7would lead to periodic modulations of the frequency offset as the Earth rotates and orbits the Sun. From the absence of such modulations at the 10−19level we deduce stringent limits of the order of 10−21on Lorentz symmetry violation parameters for electrons, improving previous limits8–10by two orders of magnitude. Such levels of precision will be essential for low-energy tests of future quantum gravity theories describing dynamics at the Planck scale4, which are expected to predict the magnitude of residual symmetry violations.

The authors conducted a survey of recent MBA graduates of 12 of the nation's leading business schools to find the answers to these questions. INSETS: Scope of the survey;Factors influencing turnover;A model for salaries. [ABSTRACT FROM PUBLISHER]

We devise a laser-controlled adaptive optical element that operates intracavity under high-intensity radiation. This element substitutes a conventional mechanically deformable mirror and is free of critical heat-sensitive components and electronics. The deformation mechanism is based on the projection of a continuous-wave control laser onto a specially designed mirror. Mounted to a water-cooled heat sink, the mirror can handle laser radiation beyond 3  MW/cm^2. The properties of the adaptive optical element, including the maximum correctable wavefront pitch of 800 nm, are discussed. The successful implementation in a multi-pass thin-disk amplifier is presented. An improvement of the beam quality by a factor of three is achieved. We identify measures to enhance the performance of the adaptive optics towards efficient operation in a high-power laser system.

PURPOSE: Contrast-induced renal dysfunction has been reported to occur in 15% to 42% of patients with underlying azotemia, but there is disagreement as to whether its incidence is reduced by limiting the amount of contrast material. To adjust the amount of contrast material to the severity of azotemia, we have utilized the following formula to calculate a contrast material 'limit' in patients with renal disease: Contrast material limit = 5 mL of contrast/kg body weight (maximum, 300 mL). / serum creatinine (mg/dL) PATIENTS AND METHODS: Over a 10-year period, 115 patients (53 men, 62 women, aged 61 [+ or -] 11 [mean [+ or -] SD] years) with renal dysfunction (baseline serum creatinine level greater than or equal to 1.8 mg/dL) underwent cardiac catheterization and angiography, after which the level of serum creatinine was measured daily for five days. The amount of contrast material that was given adhered to the limit in 86 patients (Group I) and exceeded it in 29 (Group II). RESULTS: Contrast-induced renal dysfunction (an increase in serum creatinine greater than or equal to 1.0 mg/dL) occurred in two (2%) patients in Group I and in six (21%) patients in Group II (p CONCLUSIONS: Thus, contrast-induced renal dysfunction occurs infrequently if the amount of contrast material is limited in accordance with the degree of azotemia. Diabetic patients have a high incidence of contrast nephropathy, particularly when they receive an excessive amount of contrast. In patients with diabetes and renal impairment, it may be preferable to perform angiography as a staged procedure or to utilize alternative (non-contrast) techniques to obtain the desired information rather than to exceed the prescribed contrast limit.

The restoration of anterograde coronary flow during the hours to days after acute myocardial infarction (AMI) may be beneficial independent of an effect on left ventricular function. This study was done to assess the influence of residual anterograde coronary perfusion on long-term morbidity and mortality in patients after AMI. Over a 10-year period, 179 subjects (132 men, 47 women, aged 25 to 66 years) with infarction and angiographic evidence of disease of only 1 coronary artery were followed for 47 [+ or -] 29 (mean [+ or -] standard deviation) months. All were receiving medical therapy. Sixty-four patients had partial or complete anterograde perfusion of the infarct artery (group I), whereas the other 115 had no or minimal anterograde perfusion (group II). The 2 groups were similar in age, sex, risk factors for atherosclerotic cardiovascular disease, duration of follow-up, maintenance medications and left ventricular function. In group I, unstable angina and congestive heart failure each occurred in [is less than or equal to] 10%, and none died. In marked contrast, the 115 patients in group II frequently had unstable angina (25%) and congestive heart failure (17%) (p [is less than or equal to] 0.05 for both vs group I), and 21 (18%) died suddenly (p

Cardiac output (CO) is a measure of the volume of blood that the heart pumps per minute, evenly split between blood pumped to the lungs for oxygenation and systemic circulation. Accurate measurement of cardiac output is important for assessing the health of the cardiovascular system. The conventional CO measurement is indirectly measured by measuring oxygen consumption and the difference in oxygen concentration between arterial and venous blood. The patient exhales into a 'Douglas' bag and the oxygen concentration in this volume of exhaled air is measured. The method is fraught with difficulties and accurate measurements can only be achieved with careful attention to technical details. A newer and simpler method of measuring oxygen consumption involves the MRM-2, an electrical oxygen consumption meter produced by Waters Instruments. The device has recently been introduced as a replacement for the Douglas bag. The efficiency of the MRM-2 for measuring CO was assessed. Experimentation has shown that the MRM-2 values for oxygen consumption are consistently lower than those determined by the use of a Douglas bag. Thus the device is, despite its widespread use, less accurate.

Case Report This 48-year-old man was in good health until April 1988, when he noted the onset of exertional chest pain. One month later, he underwent cardiac catheterization, which revealed [...]

Dear editor: Wichita Pride would like to thank Side Street, performers and everyone else who helped with the successful Mama's Comedy Night for Pride on April 5. Pride would also [...]

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The year 2014 marked the 20th anniversary of the coining of the term proteomics. The purpose of this scientific statement is to summarize advances over this period that have catalyzed our capacity to address the experimental, translational, and clinical implications of proteomics as applied to cardiovascular health and disease and to evaluate the current status of the field. Key successes that have energized the field are delineated; opportunities for proteomics to drive basic science research, facilitate clinical translation, and establish diagnostic and therapeutic healthcare algorithms are discussed; and challenges that remain to be solved before proteomic technologies can be readily translated from scientific discoveries to meaningful advances in cardiovascular care are addressed. Proteomics is the result of disruptive technologies, namely, mass spectrometry and database searching, which drove protein analysis from 1 protein at a time to protein mixture analyses that enable large-scale analysis of proteins and facilitate paradigm shifts in biological concepts that address important clinical questions. Over the past 20 years, the field of proteomics has matured, yet it is still developing rapidly. The scope of this statement will extend beyond the reaches of a typical review article and offer guidance on the use of next-generation proteomics for future scientific discovery in the basic research laboratory and clinical settings.

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