Assessment of pericardial constraint: the relation between right ventricular filling pressure and pericardial pressure measured after pericardiocentesis

Experimental studies have shown that right ventricular filling pressure (that is, intracavitary diastolic pressure) approximates pericardial surface pressure but, in many patients after removal of pericardial effusion, right ventricular filling pressure has been found to markedly exceed pericardial pressure recorded by an open catheter. The aim of this study was to determine whether this apparent contradiction was related to the technique of pericardial pressure measurement. Nine patients with chronic pericardial effusion were studied and, although these pressures diverged to varying degrees in individual patients, the previous observation was confirmed in that, although initially similar, right ventricular filling pressure and pericardial pressure (measured by means of an open catheter) tended to diverge during removal of the effusate; when the evacuation was as complete as possible pericardial pressure was 2.1 +/- 1.0 (mean +/- SE), while right ventricular filling pressure was 8.7 +/- 1.7 mm Hg (p less than 0.01). In six open chest, anesthetized, volume-loaded dogs with pericardial effusion (50 ml), right ventricular filling pressure and pericardial pressures measured with both open catheter and flat balloon were all equal. With decreasing volume of pericardial fluid, right ventricular filling pressure and pericardial pressure (by catheter) diverged as had been observed in patients. However, pericardial pressure (balloon) continued to be equal to right ventricular filling pressure. (With 0 ml in the pericardium, right ventricular filling pressure = 12.9 +/- 0.9 mm Hg, pericardial pressure [catheter] = 1.4 +/- 1.9 mm Hg and pericardial pressure [balloon] = 12.4 +/- 1.5 mm Hg.) Thus, these observations support the use of right ventricular filling pressure as an estimate of pericardial constraint in patients.     

Prolonged QTc interval and risk of sudden cardiac death in a population of older adults.

OBJECTIVES: This study sought to investigate whether prolongation of the heart rate-corrected QT (QTc) interval is a risk factor for sudden cardiac death in the general population. BACKGROUND: In developed countries, sudden cardiac death is a major cause of cardiovascular mortality. Prolongation of the QTc interval has been associated with ventricular arrhythmias, but in most population-based studies no consistent association was found between QTc prolongation and total or cardiovascular mortality. Only very few of these studies specifically addressed sudden cardiac death. METHODS: This study was conducted as part of the Rotterdam Study, a prospective population-based cohort study that comprises 3,105 men and 4,878 women aged 55 years and older. The QTc interval on the electrocardiogram was determined during the baseline visit (1990 to 1993) and the first follow-up examination (1993 to 1995). The association between a prolonged QTc interval and sudden cardiac death was estimated using Cox proportional hazards analysis. RESULTS: During an average follow-up period of 6.7 years (standard deviation, 2.3 years) 125 patients died of sudden cardiac death. An abnormally prolonged QTc interval (>450 ms in men, >470 ms in women) was associated with a three-fold increased risk of sudden cardiac death (hazard ratio, 2.5; 95% confidence interval, 1.3 to 4.7), after adjustment for age, gender, body mass index, hypertension, cholesterol/high-density lipoprotein ratio, diabetes mellitus, myocardial infarction, heart failure, and heart rate. In patients with an age below the median of 68 years, the corresponding relative risk was 8.0 (95% confidence interval 2.1 to 31.3). CONCLUSIONS: Abnormal QTc prolongation on the electrocardiogram should be viewed as an independent risk factor for sudden cardiac death.     

Drug-induced atrial fibrillation

Atrial fibrillation (AF) is the most common sustained rhythm disorder observed in clinical practice and predominantly associated with cardiovascular disorders such as coronary heart disease and hypertension. However, several classes of drugs may induce AF in patients without apparent heart disease or may precipitate the onset of AF in patients with preexisting heart disease. We reviewed the literature on drug-induced AF, using the PubMed/Medline and Micromedex databases and lateral references. Successively, we discuss the potential role in the onset of AF of cardiovascular drugs, respiratory system drugs, cytostatics, central nervous system drugs, genitourinary system drugs, and some miscellaneous agents. Drug-induced AF may play a role in only a minority of the patients presenting with AF. Nevertheless, it is important to recognize drugs or other agents as a potential cause, especially in the elderly, because increasing age is associated with multiple drug use and a high incidence of AF. This may contribute to timely diagnosis and management of drug-induced AF.     

Filter run time in CVVH: pre- versus post-dilution and nadroparin versus regional heparin-protamine anticoagulation

BACKGROUND/AIMS: To study the effect of different modes of continuous veno-venous haemofiltration (CVVH) on filter run time (FRT). METHODS: We studied, in two consecutive prospective, randomised and crossover studies, 16 and 15 patients with acute renal failure during critical illness. Study A compared pre- versus post-dilution, and study B compared regional anticoagulation with heparin (pre-filter) and protamine (post-filter) (HP) versus nadroparin (NP) pre-filter. All CVVH sessions were standardised. Analyses were by Wilcoxon rank sum tests. RESULTS: Study A: During pre-dilution the median FRT was 45.7 vs. 16.1 h in post-dilution CVVH (p = 0.005). The median creatinine clearance during pre-dilution was 33 vs. 45 ml/min in post-dilution (p = 0.001). Study B: During NP, median FRT was 39.5 vs. 12.3 h during HP CVVH (p = 0.045). CONCLUSIONS: Pre-dilution CVVH results in the greatest FRT but a lower plasma creatinine clearance compared to post-dilution. Regional anticoagulation with heparin-protamine resulted in a significantly shorter FRT compared to systemic NP anticoagulation.     

Transseptal pressure gradient and diastolic ventricular septal motion in patients with mitral stenosis

Previous studies from our laboratory have shown that the position of the ventricular septum relative to the two ventricles at end-diastole is determined by the instantaneous transseptal pressure gradient (TSG) defined as left ventricular minus simultaneous right ventricular pressure. Since patients with mitral stenosis often have exaggerated leftward (paradoxic) motion of the ventricular septum during early diastole, we studied seven patients with mitral stenosis undergoing cardiac catheterization to determine if position (and therefore motion) of the ventricular septum was determined by TSG throughout diastole. M Mode echocardiograms derived from a two-dimensional parasternal short-axis view were recorded with simultaneous micromanometer measurements of left ventricular and right ventricular pressures. Six of seven patients demonstrated abnormal early diastolic leftward motion of the ventricular septum in at least one cardiac cycle. TSG measured at intervals throughout diastole ranged from -2.5 to +20 mm Hg, with abnormal TSG observed in most of the 40 cardiac cycles selected for analysis. The intracardiac position of the ventricular septum, defined as the distance from the right ventricular epicardium (RVEpi) to the left surface of the ventricular septum normalized for total cardiac dimension (RVEpi-VS), was plotted against left ventricular pressure, right ventricular pressure, and TSG. Linear regression of pooled data from all patients (164 observations) demonstrated a highly significant correlation between the instantaneous TSG and the relative intracardiac position of the ventricular septum (RVEpi-VS = 1.52 TSG + 42.7; r = .79, p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Postural stability and ankle sprain history in athletes compared to uninjured controls

Background

Diminished postural stability is a risk factor for ankle sprain occurrence and ankle sprains result in impaired postural stability. To date, ankle sprain history has not been taken into account as a determinant of postural stability, while it could possibly specify subgroups of interest.

Methods

Postural stability was compared between 18 field hockey athletes who had recovered from an ankle sprain (mean (SD); 3.6 (1.5) months post-injury), and 16 uninjured controls. Force plate and kinematics parameters were calculated during single-leg standing: mean center of pressure speed, mean absolute horizontal ground reaction force, mean absolute ankle angular velocity, and mean absolute hip angular velocity. Additionally, cluster analysis was applied to the ‘injured’ participants, and the cluster with diminished postural stability was compared to the other participants with respect to ankle sprain history.

Findings

MANCOVA showed no significant difference between groups in postural stability (P = 0.68). A self-reported history of an (partial) ankle ligament rupture was typically present in the cluster with diminished postural stability. Subsequently, a ‘preceding rupture’ was added as a factor in the MANCOVA, which showed a significant association between diminished postural stability and a ‘preceding rupture’ (P = 0.01), for all four individual parameters (P: 0.001–0.029; Cohen's d: 0.96–2.23).

Interpretation

Diminished postural stability is not apparent in all previously injured athletes. However, our analysis suggests that an (mild) ankle sprain with a preceding severe ankle sprain is associated with impaired balance ability. Therefore, sensorimotor training may be emphasized in this particular group and caution is warranted in return to play decisions.     

Apolipoprotein E epsilon4 allele is associated with left ventricular systolic dysfunction

Background

Apolipoprotein (APOE) ?4 allele has been associated with cardiac dysfunction in Alzheimer's disease and β-thalassemia. We investigated the association between APOE genotypes and left ventricular dysfunction in a population of community-dwelling elderly subjects.

Methods

This study was performed in the Rotterdam Study, a population-based prospective cohort study among elderly subjects. For 2206 participants, a baseline echocardiogram and blood specimens for APOE typing were available. Cardiac dysfunction was considered present when fractional shortening was ≤25%. Multivariate logistic regression was used to calculate odds ratios (ORs). The ?3/?3 genotype served as a reference category.

Results

In participants who were homozygous for the ?4 allele, the odds of cardiac dysfunction was increased 3-fold (OR, 3.1; 95% CI, 1.2-8.1), whereas the odds of cardiac dysfunction in persons with APOE ?3/?4 was not significantly increased (OR, 1.5; 95% CI, 0.9-2.5). There was a significant allele-effect relationship for the ?4 allele (P-trend <.05). These elevated odds remained after adjustment for cholesterol levels and atherosclerosis parameters. Risks associated with APOE ?4/?4 and APOE ?3/?4 were more pronounced in participants aged ≥65 years.

Conclusion

The APOE ?4 allele is an independent risk factor for cardiac dysfunction in elderly people. Besides well-known effects on atherosclerosis and cholesterol levels, there may be other mechanisms, such as apoptosis, through which this allele exerts negative effects on myocardial performance.     

Effect of progesterone on canine colonic smooth muscle

This study was undertaken to ascertain the effect and mode of action of progesterone on canine colonic smooth muscle in vitro. Circularly orientated strips of smooth muscle exhibited low-amplitude contractions at the slow wave frequency. Longitudinally orientated strips exhibited larger-amplitude contractions that were associated, electrically, with a series of "spikes" superimposed on a high-frequency oscillation in membrane potential. Progesterone reduced the contractile force of both the circularly and longitudinally orientated strips and the contractile frequency of the longitudinally orientated strips in a dose-dependent manner; this inhibitory effect was observed in the presence of tetrodotoxin but not atropine. The stimulatory effects of a high-potassium superfusate were antagonized by progesterone and verapamil, the effect of progesterone being reversed by increasing the calcium concentration of the superfusate. We conclude that progesterone exerts an inhibitory effect on colonic smooth muscle and this may be mediated by changes in the cytoplasmic calcium concentration.     

Does flecainide regain its antiarrhythmic activity after electrical cardioversion of persistent atrial fibrillation?

OBJECTIVES: The purpose of this study was to evaluate the hypothesis that presumed reversion of electrical remodeling after cardioversion of atrial fibrillation (AF) restores the efficacy of flecainide. BACKGROUND: Flecainide loses its efficacy to cardiovert when AF has been present for more than 24 hours. Most probably, the loss is caused by atrial electrical remodeling. Studies suggest electrical remodeling is completely reversible within 4 days after restoration of sinus rhythm (SR). METHODS: One hundred eighty-one patients with persistent AF (median duration 3 months) were included in this prospective study. After failure of pharmacologic cardioversion by flecainide 2 mg/kg IV (maximum 150 mg in 10 minutes) and subsequent successful electrical cardioversion, we performed intense transtelephonic rhythm monitoring three times daily for 1 month. In case of AF recurrence, a second cardioversion by flecainide was attempted as soon as possible. RESULTS: AF recurred in 123 patients (68%). Successful cardioversion by flecainide occurred only when SR had been maintained for more than 4 days (7/51 patients [14%]). Failure to cardiovert was associated with a prolonged duration of the recurrent AF episode and concurrent digoxin use. Multivariate logistic regression confirmed that successful cardioversion was determined by digoxin use (odds ratio [OR] 0.093, P = .047) and by the interaction between the duration of SR and the (inverse) duration of recurrent AF (OR 6.499, P < .001). When flecainide was administered within 10 hours after AF onset and the duration of SR was greater than 4 days, the success rate was 58%. CONCLUSIONS: Flecainide recovers its antiarrhythmic action after cardioversion of AF. However, successful pharmacologic cardioversion occurs only after SR has lasted at least 4 days and is expected only for recurrences having duration of a few hours. Immediate pharmacologic cardioversion of AF recurrence may be a worthwhile strategy for management of persistent AF.