Sleep disordered breathing and cardiovascular risk in older patients initiating dialysis in the United States: a retrospective observational study using medicare data.

BACKGROUND: Sleep disordered breathing (SDB) such as sleep apnea is associated with cardiovascular disease in the general population. However, little is known about the cardiovascular risks of SDB in patients with end-stage renal disease (ESRD). METHODS: We identified Medicare fee-for-service beneficiaries aged ≥67 years initiating dialysis between 2004 and 2009. Outcomes of interest included all-cause mortality, incident myocardial infarction, ischemic stroke, and atrial fibrillation. We compared patients with and without diagnosed SDB using Cox proportional hazards regression. RESULTS: Between 2004 and 2009, 184,217 older patients developed ESRD, of whom 15,121 (8.2 %) were previously diagnosed with SDB. Patients diagnosed with SDB were younger, more likely to be male and Caucasian, less Medicaid eligible, had more non-Nephrology clinic visits, higher body mass index, and more comorbidity. In analyses adjusting for demographics and BMI, diagnosed SDB was associated with higher risk of death and atrial fibrillation, but not associated with myocardial infarction or ischemic stroke risk. After further adjustment for all baseline characteristics, diagnosed SDB was associated with slightly lower risks of death (hazard ratio [HR]: 0.93, 95 % confidence interval [CI]: 0.91-0.96), myocardial infarction (HR: 0.92, CI: 0.87-0.98), and ischemic stroke (HR: 0.90, 95 % CI: 0.82-0.98), and not associated with atrial fibrillation (HR: 1.02, CI: 0.98-1.07). CONCLUSIONS: In older patients initiating dialysis in the U.S., diagnosed SDB was weakly associated with lower risks of death and important cardiovascular outcomes, thus adding to the list of established risk factors that are paradoxically associated with cardiovascular outcomes in the ESRD population.

Systematic review: benefits and harms of in-hospital use of recombinant factor VIIa for off-label indications.

BACKGROUND: Recombinant factor VIIa (rFVIIa), a hemostatic agent approved for hemophilia, is increasingly used for off-label indications. PURPOSE: To evaluate the benefits and harms of rFVIIa use for 5 off-label, in-hospital indications: intracranial hemorrhage, cardiac surgery, trauma, liver transplantation, and prostatectomy. DATA SOURCES: Ten databases (including PubMed, EMBASE, and the Cochrane Library) queried from inception through December 2010. Articles published in English were analyzed. STUDY SELECTION: Two reviewers independently screened titles and abstracts to identify clinical use of rFVIIa for the selected indications and identified all randomized, controlled trials (RCTs) and observational studies for full-text review. DATA EXTRACTION: Two reviewers independently assessed study characteristics and rated study quality and indication-wide strength of evidence. DATA SYNTHESIS: 16 RCTs, 26 comparative observational studies, and 22 noncomparative observational studies met inclusion criteria. Identified comparators were limited to placebo (RCTs) or usual care (observational studies). For intracranial hemorrhage, mortality was not improved with rFVIIa use across a range of doses. Arterial thromboembolism was increased with medium-dose rFVIIa use (risk difference [RD], 0.03 [95% CI, 0.01 to 0.06]) and high-dose rFVIIa use (RD, 0.06 [CI, 0.01 to 0.11]). For adult cardiac surgery, there was no mortality difference, but there was an increased risk for thromboembolism (RD, 0.05 [CI, 0.01 to 0.10]) with rFVIIa. For body trauma, there were no differences in mortality or thromboembolism, but there was a reduced risk for the acute respiratory distress syndrome (RD, -0.05 [CI, -0.02 to -0.08]). Mortality was higher in observational studies than in RCTs. LIMITATIONS: The amount and strength of evidence were low for most outcomes and indications. Publication bias could not be excluded. CONCLUSION: Limited available evidence for 5 off-label indications suggests no mortality reduction with rFVIIa use. For some indications, it increases thromboembolism.

Use of Intraoperative Dobutamine Stress Echocardiography on Outcomes of Septal Myectomy.

Septal myectomy is the standard treatment for obstructive hypertrophic cardiomyopathy. We studied the impact of intraoperative pre- and postprocedure dobutamine stress transesophageal echocardiography on surgical planning and outcomes of septal myectomy. We identified 55 patients undergoing septal myectomy over a 24-month period. All patients underwent resting and dobutamine stress (20-40 mcg/kg/min) echocardiography after induction of anesthesia pre- and postprocedure. Demographic, clinical, and imaging data were prospectively collected. Mean age was 59 (42-68). A total of 69% of patients were New York Heart Association Class III/IV. During outpatient evaluation, peak preoperative resting left ventricular outflow tract gradient was 91.6 mm Hg and 94% (50/53) had severe stress-induced mitral regurgitation (MR). After induction, peak resting gradient fell to 47.8 mm Hg and 43% (24/55) had improved gradients (<30 mm Hg). With stress, preprocedure left ventricular outflow gradient increased to 130 mm Hg and all occult gradients were unmasked. Postprocedure, peak resting and stress gradients were substantially reduced (10.2 ± 6.8 mm Hg and 23.6 ± 8.5 mm Hg, respectively). With stress, 84% (42/50) demonstrated reduction in severity of MR to none and/or mild with no patients having greater than moderate. Postprocedure stress echocardiography identified 3 patients with residual gradients, which led to return to bypass for additional procedures and resulted in resolution of elevated residual gradients. Postoperative 60-day stress echocardiography showed sustained resolution of gradients and MR. In this series, 43% of patients had occult left ventricular outflow gradients after induction of anesthesia. Intraoperative stress echocardiography during septal myectomy is useful to unmask occult gradients and confirm adequate myectomy. This imaging strategy is associated with reliable relief of obstruction and MR as demonstrated at 60-day follow-up.

Hypertrophic cardiomyopathy: the future of treatment.

Hypertrophic cardiomyopathy (HCM) is a heterogeneous genetic disorder most often caused by sarcomeric mutations resulting in left ventricular hypertrophy, fibrosis, hypercontractility, and reduced compliance. It is the most common inherited monogenic cardiac condition, affecting 0.2% of the population. Whereas currently available therapies for HCM have been effective in reducing morbidity, there remain important unmet needs in the treatment of both the obstructive and non-obstructive phenotypes. Novel pharmacotherapies directly target the molecular underpinnings of HCM, while innovative procedural techniques may soon offer minimally-invasive alternatives to current septal reduction therapy. With the advent of embryonic gene editing, there now exists the potential to correct underlying genetic mutations that may result in disease. This article details the recent developments in the treatment of HCM including pharmacotherapy, septal reduction procedures, mitral valve manipulation, and gene-based therapies.