Genomic and functional analyses of Rhodococcus equi phages ReqiPepy6, ReqiPoco6, ReqiPine5, and ReqiDocB7.

The isolation and results of genomic and functional analyses of Rhodococcus equi phages ReqiPepy6, ReqiDocB7, ReqiPine5, and ReqiPoco6 (hereafter referred to as Pepy6, DocB7, Pine5, and Poco6, respectively) are reported. Two phages, Pepy6 and Poco6, more than 75% identical, exhibited genome organization and protein sequence likeness to Lactococcus lactis phage 1706 and clostridial prophage elements. An unusually high fraction, 27%, of Pepy6 and Poco6 proteins were predicted to possess at least one transmembrane domain, a value much higher than the average of 8.5% transmembrane domain-containing proteins determined from a data set of 36,324 phage protein entries. Genome organization and protein sequence comparisons place phage Pine5 as the first nonmycobacteriophage member of the large Rosebush cluster. DocB7, which had the broadest host range among the four isolates, was not closely related to any phage or prophage in the database, and only 23 of 105 predicted encoded proteins could be assigned a functional annotation. Because of the relationship of Rhodococcus to Mycobacterium, it was anticipated that these phages should exhibit some of the features characteristic of mycobacteriophages. Traits that were identified as shared by the Rhodococcus phages and mycobacteriophages include the prevalent long-tailed morphology and the presence of genes encoding LysB-like mycolate-hydrolyzing lysis proteins. Application of DocB7 lysates to soils amended with a host strain of R. equi reduced recoverable bacterial CFU, suggesting that phage may be useful in limiting R. equi load in the environment while foals are susceptible to infection.

Effects of verapamil on the extracellular K+ rise during myocardial ischaemia in dogs.

The effects of verapamil on the [K+]o rise produced by myocardial ischaemia were assessed in 26 open chest mongrel dogs. Ischaemia was produced by intermittent occlusion of the LAD artery (15 dogs) or by reduction of flow of the cannulated LAD (11 dogs). Specially constructed valinomycin K+ sensitive electrodes were inserted into the mid myocardium in the central zone of ischaemia (CZ); in the margin (MZ) and in the nonischaemic zone (NZ). Occlusion of the coronary artery under controlled conditions produced significant [K+]o rise, greater in the CZ than in the MZ. During the infusion of verapamil the ischaemic [K+]o rise was substantially reduced in both zones. During controlled 75% reduction of coronary flow the [K+]o reached a plateau that remained stable until reperfusion was re-established. During verapamil infusion, the plateau showed a steady decline, both in the CZ and in the MZ. The changes in [K+]o produced by verapamil, during myocardial ischaemia are probably due to: coronary dilatation of the marginal arteries and+or to a reduction of the late cellular K+ conductance due to a decrease in the intracellular Ca2+, produced by verapamil.

Transesophageal echocardiography in the diagnosis of left atrial appendage aneurysm.

Intrapericardial left atrial appendage aneurysm is rare. We describe the transthoracic and transesophageal echocardiographic findings in a 42-year-old man with atrial arrhythmia and an abnormal left atrial appendage on chest roentgenogram. Presence of an intrapericardial left atrial appendage aneurysm was confirmed at surgery.

Angiotensin-converting enzyme inhibition in myocardial infarction--Part 1: Clinical data.

There is an increasing body of clinical trial evidence to support the use of angiotensin-converting enzyme (ACE) inhibitors in the management of patients following myocardial infarction (MI). Enthusiasm for the use of ACE inhibitors in the acute phase of MI had previously been tempered by the adverse results of an early trial. However, exciting new information is available from several large, randomized studies that has not only quelled those initial concerns but also attests to the efficacy of using this class of medication in the first 24 h after an acute MI. A Canadian National Opinion Leader Symposium was held in November 1995 to review the results of the major ACE inhibitor clinical trials and to discuss key issues and controversies surrounding their use in acute MI. The focus of this paper, the first of two parts, is on the results of the major ACE inhibitor clinical trials.

Angiotensin-converting enzyme inhibition in myocardial infarction--Part 2: Clinical issues and controversies.

Over the past 10 years, several clinical studies have concluded that, in patients already receiving conventional therapies, angiotensin-converting enzyme (ACE) inhibitors further reduce the risk of death following myocardial infarction (MI). Post-MI ACE inhibitors have proven to be effective as long term therapy in high risk patients as well as when used for much shorter periods in a broad patient population. However, while considerable mortality data have been collected, the effects of ACE inhibitors post-MI on other cardiovascular outcomes have not been as well documented. In addition, a number of issues regarding the most effective use of these agents remain unresolved. This paper, the second of two parts, focuses on the clinical issues and controversies surrounding the use of ACE inhibitors following acute MI. The effects of ACE inhibitors on the outcomes of sudden death, nonsudden death, recurrent angina, mitral regurgitation and left ventricular dysfunction are reviewed and potential mechanisms of action are proposed. In addition, ACE inhibitor therapy is discussed in terms of patient selection criteria, choice of agent, optimal dosing regimen, concomitant use of other therapies and relative costs of treatment. Finally, potential mechanisms of action of ACE inhibitors are proposed for each of the outcomes examined.

Dicrotic pulse after open heart surgery.

Pre- and postoperative echophonocardiograms (EPCGs) and preoperative hemodynamic data of 108 patients who underwent valve replacement were reviewed to establish the frequency and significance of a dicrotic pulse (DP) postoperatively. DP occurred almost exclusively in patients who underwent valve replacement for regurgitant lesions (20 of 28 with aortic regurgitation, nine of 25 with mitral regurgitation, and four of six with both aortic and mitral regurgitation). These patients were divided into dicrotic and nondicrotic groups. Preoperatively, the dicrotic group had significantly larger end-diastolic volumes (p < 0.01) and end-systolic volumes (p < 0.01) and significantly lower ejection fractions (p < 0.01). Echocardiographically, the dicrotic group had larger left ventricular dimensions, both systolic (p < 0.01) and diastolic (p < 0.05), reduced percentage fractional shortening of the left ventricular cavity (p < 0.01) and poor thickening properties of the left ventricular posterior wall (% delta Th-LVPW) (p < 0.01). Postoperatively the dicrotic group had a slightly larger end-diastolic dimension (p = NS) and markedly depressed % delta Th-LVPW (p < 0.001) compared with the nondicrotic group. On follow-up EPCG the persistence of a DP correlated with continued left ventricular dysfunction by echocardiographic and hemodynamic studies and an extremely poor clinical course. DP after valve replacement is therefore an important prognostic sign.

The prevalence of anxiety disorders among patients with mitral valve prolapse syndrome and chest pain.

Nineteen patients from a cardiology practice with complaints of chest pain and with mitral valve prolapse syndrome were compared with 26 patients with chest pain but no discernible cardiac disorder. Instruments included a truncated form of the Diagnostic Interview Schedule, the symptom checklist 90 revised (SCL-90-R), the McGill Pain Questionnaire, and life events, physical activity, and family history questionnaires. Neither panic disorder nor self-rated anxiety were more common in the mitral valve prolapse group. This study failed to confirm the reported high association between mitral valve prolapse syndrome and panic disorder.

The response of plasma fibronectin to acute myocardial infarction in humans.

The purpose of this study was to investigate the plasma fibronectin response to complicated and uncomplicated acute myocardial infarction. All patients admitted to a Coronary Care Unit over a six-month period were prospectively assessed by measuring admission and daily plasma fibronectin levels using an electroimmunoassay. Of 166 patients admitted to the Unit, 66 were diagnosed as having an acute myocardial infarction. Plasma fibronectin levels were significantly lower 48 h after the onset of symptoms in 15 patients with a complicated acute myocardial infarction, compared to fibronectin levels in patients with an uncomplicated course; patients who had received intracoronary streptokinase had consistently higher plasma fibronectin levels than those seen in patients who did not receive this thrombolytic agent. This hepatocyte-derived plasma protein not only has diagnostic potential, but alterations in its levels may also provide insight into the systemic response to acute myocardial injury.

Quantification of mitral valvular incompetence.

The hemodynamic and angiographic data of 147 individuals were analyzed in an attempt to assess the value of three techniques used in the diagnosis of mitral incompetence. One hundred patients had clinical evidence of mitral incompetence (group A) and 47 had normal hemodynamics (group B). The degree of mitral incompetence was assessed in all 147 individuals by two methods: determination of a regurgitant index (RI) using indicator dilution curves and determination of a regurgitant fraction (RF) using left ventricular volumes. In 26 patients of group A and 26 individuals in group B mitral incompetence was also assessed by cineangiocardiography. Each of these methods was compared with the clinical and hemodynamic evidence of mitral valvular incompetence. Both the determination of RI by dye dilution curves and RF by angiocardiography were found to be useful in separating normal individuals from patients with mitral valvular incompetence. Severe mitral incompetence is associated with an RI greater than 35% and with an RF greater than 55%. The degree of incompetence by either method was not well correlated with any independent hemodynamic variable. The use of cine angiocardiography to quantify the degree of mitral incompetence was found to be too subjective, depending on the observer, and thus less useful.