Risk of pocket hematoma in patients on chronic anticoagulation with warfarin undergoing electrophysiological device implantation: a comparison of different peri-operative management strategies.

OBJECTIVE: Periprocedural management of warfarin remains challenging in patients requiring electrophysiological device surgery. For patients at high risk of thromboembolic events, guidelines recommend bridging therapy with heparin; however, this strategy is associated with a high risk of pocket hematoma. This paper systematically reviews studies appraising the risk of pocket hematoma with different perioperative anticoagulation strategies. METHODS: All relevant studies identified in MEDLINE/PubMed, The Cochrane Collaboration CENTRAL, clinicaltrials.org and in bibliographies of key articles. Estimates were combined using a fixed effects model. Heterogeneity was assessed by p values of χ2 statistics and I2. Publication bias was assessed by visual examination of funnel plots and by Egger test. Fifteen studies enrolling 5911 patients met all inclusion criteria and were included in this review. RESULTS: Heparin bridging compared with no heparin was associated with increased risk of pocket hematoma (OR = 4.47, 95% CI 3.21-6.23, p < 0.00001), and prolonged hospital stay (9.13 ± 1.9 days vs. 5.11 ± 1 .39 days, p < 0.00001). Warfarin continuation was not associated with increased pocket hematoma compared to warfarin discontinuation (p = 0.38), but was associated with reduced risk of pocket hematoma compared with heparin bridging (OR = 0.37, 95% CI 0.2-0.69, p = 0.002). Thromboembolic complications were reduced with heparin bridging vs. no heparin (0.50% vs.1.07%, p = 0.02), and no significant differences were reported between heparin bridging vs. warfarin continuation (p = 0.83). CONCLUSIONS: Heparin bridging is associated with a higher risk of pocket hematoma and a prolonged hospital stay. Perioperative continuation of warfarin reduces the occurrence of pocket hematoma compared with heparin bridging without any significant differences in thromboembolic complications.

Defibrillation testing at the time of ICD insertion: an analysis from the Ontario ICD Registry.

BACKGROUND: increasingly, ICD implantation is performed without defibrillation testing (DT). OBJECTIVES: To determine the current frequency of DT, the risks associated with DT, and to understand how physicians select patients to have DT. METHODS: between January 2007 and July 2008, all patients in Ontario, Canada who received an ICD were enrolled in this prospective registry. RESULTS: a total of 2,173 patients were included; 58% had new ICD implants for primary prevention, 25% for secondary prevention, and 17% had pulse generator replacement. DT was carried out at the time of ICD implantation or predischarge in 65%, 67%, and 24% of primary, secondary, and replacement cases respectively (P = <0.0001). The multivariate predictors of a decision to conduct DT included: new ICD implant (OR = 13.9, P < 0.0001), dilated cardiomyopathy (OR = 1.8, P < 0.0001), amiodarone use (OR = 1.5, P = 0.004), and LVEF > 20% (OR = 1.3, P = 0.05). A history of atrial fibrillation (OR = 0.58, P = 0.0001) or oral anticoagulant use (OR = 0.75, P = 0.03) was associated with a lower likelihood of having DT. Age, gender, NYHA class, and history of stroke or TIA did not predict DT. Perioperative complications, including death, myocardial infarction, stroke, tamponade, pneumothorax, heart failure, infection, wound hematoma, and lead dislodgement, were similar among patients with (8.7%) and without (8.3%) DT (P = 0.7) CONCLUSIONS: DT is performed in two-thirds of new ICD implants but only one-quarter of ICD replacements. Physicians favored performance of DT in patients who are at lower risk of DT-related complications and in those receiving amiodarone. DT was not associated with an increased risk of perioperative complications.

Increased titres of anti-human heat shock protein 60 predict an adverse one year prognosis in patients with acute cardiac chest pain.

OBJECTIVE: To assess whether antibodies to human heat shock protein 60 (anti-huhsp60) or to mycobacterial heat shock protein 65 (anti-mhsp65) predict an adverse one year prognosis in patients admitted with acute cardiac chest pain. DESIGN: Prospective observational study. SETTING: Teaching hospital. PATIENTS: 588 consecutive emergency admissions of patients with acute chest pain of suspected cardiac origin. MAIN OUTCOME MEASURES: Anti-huhsp60 and anti-mhsp65 titres were assayed on samples drawn on the morning after admission. The end points after discharge were coronary heart disease death, non-fatal myocardial infarction, coronary artery bypass grafting, percutaneous transluminal coronary angioplasty, angiogram, or readmission with further cardiac ischaemic chest pain. RESULTS: During follow up after discharge (mean of 304 days, range 1-788 days), 277 patients had at least one of the study outcomes. Patients with increased titres of anti-huhsp60 had an adverse prognosis (hazard ratio 1.56 (95% confidence interval 1.09 to 2.23) comparing highest versus lowest quartiles, p = 0.015). Anti-mhsp65 titres were not predictive. CONCLUSIONS: Patients admitted with acute cardiac chest pain and increased titres of anti-huhsp60 had an adverse one year prognosis.

Tachycardiomyopathy: a diagnosis not to be missed.

The prognosis of dilated cardiomyopathy is generally poor. In the vast majority of cases the cause of the ventricular dysfunction is irreversible but occasionally potentially curable causes are identified. Tachycardiomyopathy is a rare and potentially treatable cause of heart failure. A patient with a particularly severe case who had an excellent outcome is presented.

The genetic determination of left ventricular mass in healthy adults.

AIMS: The extent to which left ventricular (LV) mass, an independent cardiovascular risk factor, is determined by genetic factors is unclear. The aim of this study was to assess the heritability of LV mass and its association with three potential candidate genes. METHODS: A population-based adult twin study model was utilized. Echocardiographic assessment of LV mass was performed in 110 twin pairs (mean age 55.9+/-10.9 years). An estimate of genetic determination, heritability, was calculated for the main echocardiographic parameters. The cohort were genotyped for the G-protein beta-3, aldosterone synthase, and beta-1 adrenoceptor genes. RESULTS: The intra-class correlation coefficients for LV mass were 0.69 for monozygotic (r-MZ) twins and 0.32 for dizygotic (r-DZ) twins, P=0.008 (heritability estimate of 0.69). This pattern persisted following correction for known confounding factors. Within-pair differences in the monozygotic, discordant and concordant dizygotic twins showed no differences for the three genes with respect to left ventricular wall thickness or mass. There was a non-significant trend towards a relationship between LV mass and the beta-1 adrenoceptor genotype. CONCLUSION: Within a normal population left ventricular mass has a significant genetic determination. Further investigation of potential candidate genes is required.

The determination of carotid intima medial thickness in adults--a population-based twin study.

INTRODUCTION: Although cardiovascular events are known to cluster in families it is unclear the extent to which atherosclerosis per se is genetically determined. The aim of this study was to assess the heritability of carotid intima media thickness (IMT) measurements, a surrogate marker of early atherosclerosis, using a population-based twin study methodology. METHODS: B-mode carotid artery ultrasound images were acquired on 264 twin subjects (142 monozygotic (MZ); mean age 54.3 years and 122 dizygotic (DZ); mean age 51.7 years). An estimate of genetic determination, heritability, was calculated for the IMT parameters before and after correction for confounding variables. RESULTS: An increased carotid IMT was associated with known cardiovascular risk factors (total cholesterol r=0.24, P<0.001 and systolic blood pressure r=0.42, P<0.001) and with a history of coronary events (0.79+/-0.12 vs. 0.72+/-0.14, P=0.01). Carotid IMT measurements demonstrated a familial influence (intra-class correlation of 0.54 for MZ vs. 0.39 for DZ) but no specific genetic determination (heritability estimate 0.31, P=0.15). CONCLUSION: Within a normal population carotid IMT is under a familial, but not genetic influence. The mechanism of genetic control over cardiovascular events may not be mediated through atherosclerotic load as measured by IMT.

The haemodynamic effect of the 5HT1 agonist BMS-180048: a class effect of triptans?

AIMS: To investigate the effects of an intravenous infusion of BMS-180048, a novel 5HT1-like agonist, on the systemic, pulmonary and coronary circulations in patients undergoing diagnostic cardiac catheterisation. METHODS: Ten patients (mean age 55 years (range 41-65)) were studied during diagnostic cardiac catheterisation. The haemodynamic response to an intravenous (i.v.) infusion for 30 min of BMS-180048 (0.56 mg kg(-1) h(-1) for 10 min and 0.39 mg kg(-1) h(-1) for 20 min) was assessed via a 7F Swan Ganz catheter and thermodilution cardiac output system. Quantitative coronary angiography was performed at 10 min intervals. RESULTS: BMS-180048 caused a significant increase in systemic arterial systolic blood pressure (rise of 32.5 mmHg, 95% CI 24,44.5) P=0.009), pulmonary artery systolic (12.2 mmHg, 95% CI 6.8,18.5; P=0.009) and diastolic pressures (8.5 mmHg, 95% CI 5.0,13.8; P=0.009), right atrial pressure (4 mmHg, 95% CI 1.5,5.2; P=0.013) and pulmonary capillary wedge pressure (9.5 mmHg 95% CI 5.2,14.0; P=0.09). There was no significant change in cardiac output (0.1 l min(-1), 95% CI -0.17,0.57, P>0.05). Mean coronary artery diameter in the proximal coronary segments decreased by 0.73 mm (95% CI -1.22,-0.15; P=0.03) at 35 min. The corresponding reduction in middle segments was 0.26 mm (95% CI -0.395,-0.08; P=0.02). There was a non-significant trend to constriction in the most distal segments of 0.28 mm (95% CI -0.68,0.015); P=0.06). One patient experienced chest pain with ECG changes suggestive of ischaemia. CONCLUSIONS: BMS-180048 displayed a cardiovascular profile similar to that previously reported for sumatriptan. These changes appear to reflect a class effect of these agents.

Association between antibodies to heat shock protein 65 and coronary atherosclerosis. Possible mechanism of action of Helicobacter pylori and other bacterial infections in increasing cardiovascular risk.

INTRODUCTION: There is growing evidence that the immune response is involved in atherosclerosis. Antibodies to heat shock protein 60/65 have been shown to be a risk factor for carotid atherosclerosis and been proposed as a diagnostic marker of atherosclerosis. In addition, it has been suggested that the immune response to heat shock protein 60/65 may be a link between exposure to microorganisms and increased cardiovascular risk. AIMS: (1) To investigate the association between anti-shock protein 65 titre and coronary atherosclerosis. (2) To assess whether anti-mhsp65 titre is a useful diagnostic marker of atherosclerosis; (3) To examine the influence of Helicobacter pylori infection on anti-heat shock protein 65 titre. METHODS AND RESULTS: In the first study we measured anti-heat shock protein 65 titres in 136 consecutive male subjects admitted for routine coronary angiography. Anti-heat shock protein 65 titres correlated with both the severity and extent of coronary atherosclerosis and the relationship remains statistically significant for the presence of atherosclerosis (P = 0.012) after adjustment for possible confounding influences. However the association had insufficient sensitivity to be a useful clinical test. In the second study we recruited 100 patients with confirmed active H. pylori infection and double blindly randomized them to eradication therapy or placebo. Successful eradication of H. pylori led to a significant fall in anti-heat shock protein 65 titres (from a mean of 256.4 AU.ml-1 to 137.5 AU. ml-1. P = 0.033). CONCLUSION: These results raise the possibility that exposure to H. pylori and other micro-organisms lead to an increased risk of clinically manifest coronary artery disease by an autoimmune process.

The haematological management of patients with cyanotic congenital heart disease. A time for consensus?

AIMS: Recurrent venesection of patients with cyanotic congenital heart disease may be detrimental, with an increased risk of cerebrovascular events and symptomatic iron-deficiency. The aim of this study was to determine the venesection policies as practised in hospitals within a U.K. region and to determine if these policies followed current recommendations. METHODS AND RESULTS: Fifty-eight consultants (56% response rate) in cardiac specialties completed self-assessment questionnaires regarding the indications for and practice of venesection. Sixty-one percent of those responding were involved directly in the care of patients with cyanotic congenital heart disease and of these clinicians 97% used venesection. Indications for venesection varied, with 51% of those responding using an elevated haemoglobin per se (6.5-21.0 g. dl-1); 78% an elevated haematocrit (0.55-0.75) and 83% symptoms. Desired maintenance haemoglobin and haematocrit levels also varied greatly. Fifty percent of the consultants responding routinely screened their patients for iron deficiency and 23% felt there was no indication for investigating a low mean corpuscular volume. Only 18% of the policies described followed any evidence based principles. CONCLUSIONS: The practice of venesecting patients with congenital cyanotic heart disease varies greatly. Policies in many hospitals do not reflect the minimal benefits and considerable risks associated with recurrent venesection.

Parvovirus B19 induced red cell aplasia in myelofibrosis.

A 38-year-old female presented with moderate anaemia and a leucoerythroblastic blood film. Subsequent investigation showed myelofibrosis in cellular phase. Her haemoglobin quickly and spontaneously recovered with concurrent serological evidence of recent parvovirus B19 infection. This is the first report in the literature of parvovirus causing red cell aplasia in myelofibrosis.

Primordial germ cells and gonadal development in the golden hamster.

We present results of a light and electron microscopical study of the developing hamster gonad. Two main problems have been examined: the source of somatic cells contributed to the developing gonad and the possible presence of nuage in germ cells. Nuage has been previously reported in hamster oocytes at meiosis; its possible presence at earlier stages and in male germ cells, especially meiotic spermatocytes, was investigated. The mesonephros was found to be the major source of somatic cells to the developing gonad, though a contribution from the coelomic epithelium could not be excluded, and interstitial tissue appeared to arise from mesenchymal cells. The presence of nuage associated with nuclear pores and mitochondria in hamster oocytes from Day 15 p.c. onwards has been confirmed. New findings are the association of nuage with intercellular bridges and its presence at earlier stages, including Day 8 p.c., and in male germ cells especially at the time of the entry to meiosis.