Utility of tissue Doppler and strain echocardiography in arrhythmogenic right ventricular dysplasia/cardiomyopathy.

Arrhythmogenic right ventricular dysplasia (ARVD) is a heritable cardiomyopathy characterized by the fibrofatty replacement of right ventricular (RV) myocardium leading to RV failure and arrhythmias. This study evaluated the potential utility of tissue Doppler echocardiography (TDE) and strain echocardiography (SE) to quantitatively assess RV function and their potential role in diagnosing ARVD. Images of 30 patients with ARVD (diagnosed by task force criteria) and 36 healthy controls were obtained. Peak systolic velocity, early diastolic velocity, displacement, strain rate, strain, outflow tract diameter, and fractional RV area change were measured in all subjects. Peak RV systolic velocity (6.4 +/- 2.2 vs 9 +/- 1.6 cm/s, p <0.0001), early diastolic velocity (-6.7 +/- 2.7 vs -9.4 +/- 2 cm/s, p <0.0001), displacement (13.7 +/- 5.8 vs 18.7 +/- 3.5 mm, p <0.0003), strain rate (-1 +/- 0.7 vs -2 +/- 1 s(-1), p = 0.002), and strain (-10 +/- 6% vs -28 +/- 11%, p = 0.001) were significantly lower in patients with ARVD compared with controls, respectively. Sensitivity and specificity, respectively, were 67% and 89% for systolic velocity, 77% and 71% for displacement, 73% and 87% for strain, 50% and 96% for strain rate, 53% and 93% for outflow tract diameter, and 47% and 83% for fractional area change. RV systolic velocity and displacement were significantly lower than in controls, even in the subset of patients with ARVD with apparently normal right ventricles by conventional echocardiography. Inter- and intraobserver agreement was high. In conclusion, TDE and SE enable the detection of ARVD via the quantification of RV function and may have potential clinical value in the assessment of patients with suspected ARVD. Peak RV systolic velocity <7.5 cm/s and peak RV strain <18% best identify patients with ARVD.

Feasibility and variability of three dimensional echocardiography in arrhythmogenic right ventricular dysplasia/cardiomyopathy.

Arrhythmogenic right ventricular dysplasia (ARVD/C) is a genetic cardiomyopathy characterized by fibrous fatty replacement of the right ventricular (RV) myocardium, leading to progressive RV failure and ventricular arrhythmias in young athletes. This study evaluated whether transthoracic, real-time, 3-dimensional echocardiography (3DE) can adequately assess RV morphology and function in ARVD/C by comparing 3DE with cardiac magnetic resonance (CMR), the current reference standard. Three-dimensional echocardiography was prospectively performed in 58 patients (23 with ARVD/C, 20 first-degree relatives with no ARVD/C, 8 with idiopathic ventricular tachycardia with no ARVD/C, and 7 healthy volunteers). All patients, except 15 patients with ARVD/C with implanted defibrillators, also underwent CMR. Three-dimensional echocardiography and CMR-derived RV volumes and ejection fractions were obtained by offline data analysis by blinded, independent observers. The mean age of the study group was 37 +/- 11 years (30 men). The feasibility of 3DE was high, and analyzable images were obtained in all subjects. Three-dimensional echocardiography revealed a wide variety of RV morphologic abnormalities in ARVD/C. There was a good correlation between 3DE and CMR for RV end-systolic volume (r = 0.72, p = 0.0001), RV end-diastolic volume (r = 0.50, p = 0.0001), and the RV ejection fraction (r = 0.88, p = 0.001). We found high intraobserver and moderate interobserver correlations for 3DE estimations of volumes and ejection fractions. In conclusion, 3DE measurements of RV volumes and ejection fractions closely correlate with CMR values and may be useful in the follow-up of patients with ARVD/C.

Arrhythmogenic right ventricular dysplasia/cardiomyopathy.

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is a genetic cardiomyopathy characterized by ventricular arrhythmias and structural abnormalities of the right ventricle (RV). The most important aspect in the treatment of ARVD/C is establishing a correct diagnosis based on the International Task Force criteria. In our experience, cardiologists are not aware of these diagnostic criteria for ARVD/C and place too much importance on the results of magnetic resonance imaging of the RV. Patients with ARVD/C generally all have an abnormal 12-lead electrocardiogram, abnormal echocardiogram, and ventricular arrhythmias with a left bundle branch block morphology. If noninvasive testing suggests ARVD, invasive testing with an RV angiogram, RV biopsy, and electrophysiology study are recommended. We encourage patients to participate in the National Institutes of Health-sponsored multicenter clinical trial of ARVD/C (http://www.ARVD.comorhttp://www.ARVD.org). Once a diagnosis of ARVD/C is established, the main treatment decision involves whether to implant an implantable cardioverter-defibrillator (ICD). ICDs are recommended for patients who have experienced syncope, sudden death, or a sustained ventricular arrhythmia, and also for patients with overt evidence of ARVD, particularly if the electrophysiology study is abnormal or there is a family history of sudden death. We also recommend treatment of patients with ARVD/C with beta blockers and angiotensin-converting enzyme inhibitors, and that all patients with ARVD/C be screened for a mutation in the gene for plakophilin-2, because this is present in more than one third of patients with ARVD/C and may be helpful in the management of first-degree relatives.

A systematic review of venous thromboembolism prophylaxis strategies in patients with renal insufficiency, obesity, or on antiplatelet agents.

BACKGROUND: There is uncertainty about optimal strategies for venous thromboembolism (VTE) prophylaxis among select populations such as patients with renal insufficiency, obesity, or patients taking antiplatelet drugs including aspirin. Their physiologies make prophylaxis particularly challenging. PURPOSE: We performed a comparative effectiveness review of the literature on efficacy and safety of VTE prophylaxis in these populations. DATA SOURCES: We searched MEDLINE, EMBASE, SCOPUS, CINAHL, International Pharmaceutical Abstracts, clinicaltrial.gov, and the Cochrane Library through August 2012. Eligible studies included controlled trials and observational studies. DATA EXTRACTION: Two reviewers evaluated studies for eligibility, serially abstracted data, and independently evaluated the risk of bias and strength of evidence supporting interventions to prevent VTE in these populations. RESULTS: After a review of 30,902 citations, we identified 9 controlled studies, 5 of which were trials, and the other 4 were observational studies. Five articles addressed prophylaxis of patients with renal insufficiency, 2 addressed obese patients, and 2 addressed patients on antiplatelet agents. No study tested prophylaxis in underweight patients or those with liver disease. The majority of observational studies had a high risk of bias. The strength of evidence ranged from low to insufficient regarding the comparative effectiveness and safety of VTE prophylaxis among these patients. CONCLUSION: The current evidence is insufficient regarding optimal VTE prophylaxis for patients with renal insufficiency, obesity, or those who are on antiplatelet drugs including aspirin. High-quality studies are needed to inform clinicians about the best VTE prophylaxis for these patients.

Pharmacologic and mechanical strategies for preventing venous thromboembolism after bariatric surgery: a systematic review and meta-analysis.

We sought to assess the comparative effectiveness and safety of pharmacologic and mechanical strategies to prevent venous thromboembolism (VTE) in patients undergoing bariatric surgery. We searched (through August 2012) for primary studies that had at least 2 different interventions. Of 30,902 citations, we identified 8 studies of pharmacologic strategies and 5 studies of filter placement. No studies randomized patients to receive different interventions. One study suggested that low-molecular-weight heparin is more efficacious than unfractionated heparin in preventing VTE (0.25% vs 0.68%, P < .001), with no significant difference in bleeding. One study suggested that prolonged therapy (after discharge) with enoxaparin sodium may prevent VTE better than inpatient treatment only. There was insufficient evidence supporting the hypothesis that filters reduce the risk of pulmonary embolism, with a point estimate suggesting increased rates with filters (pooled relative risk [RR], 1.21 95% CI, 0.57-2.56). There was low-grade evidence that filters are associated with higher mortality (pooled RR, 4.30 95% CI, 1.60-11.54) and higher deep vein thrombosis rates (2.94 1.35-6.38). There was insufficient evidence to support that augmented subcutaneous enoxaparin doses (>40 mg daily or 30 mg twice daily) are more efficacious than standard dosing, with a trend toward increased bleeding. Of note, for both filters and augmented pharmacologic dosing strategies, patients at highest risk for VTE were more likely to receive more intensive interventions, limiting our ability to attribute outcomes to prophylactic strategies used.