Arrhythmias and Pregnancy: Management of Preexisting and New-Onset Maternal Arrhythmias.

Arrhythmias are the most common cardiovascular complication of pregnancy in women with and without structural heart disease. Appropriate maternal diagnosis and management is of utmost importance to optimize maternal and fetal outcomes. A multidisciplinary care approach with cardiology, maternal fetal medicine, anesthesia, and pediatrics is important for preconceptional, pregnancy, and delivery planning.

Relationship of non-invasive quantification of myocardial blood flow to arrhythmic events in patients with implantable cardiac defibrillators.

BACKGROUND: Ischemia contributes to arrhythmogenesis though its role is incompletely understood. Abnormal myocardial perfusion measured by PET imaging may predict ventricular arrhythmias (VAs) in a high-risk population. METHODS: Patients with implantable cardiac defibrillators who had undergone rubidium-82 cardiac PET imaging were identified. Patients were stratified by median MBF and MFR values for analysis. The Cox proportional hazards model was used to assess the impact of myocardial perfusion on survival free of VT independent of critical covariates. RESULTS: A total of 159 patients (124 (78%) males, median age 65.9 years, IQR [56.76-72.63]) were followed for 1.43 years IQR [0.83-2.21]. VA occurred in 29 patients (23.7%). After adjustment for ejection fraction, age, and sex, impaired stress MBF was associated with an increased risk of VA (adjusted HR per ml/min/g 1.52, 95% CI (1.01-2.31), P = 0.04). Summed rest and stress scores were not predictive of VA. Among patients with severe LV dysfunction, stress MBF remained an independent predictor of VA (adjusted HR per 1 ml/min/g HR 1.69, 95% CI (1.03-11.36), P = 0.03), while residual EF, summed rest, and summed stress scores were not (P > 0.05). CONCLUSIONS: Impaired stress myocardial blood flow was associated with less survival free of ventricular arrhythmias.

Safety of regadenoson stress testing in patients with pulmonary hypertension.

OBJECTIVES: We sought to determine the safety of regadenoson stress testing in patients with PH. BACKGROUND: PH is increasingly recognized at more advanced ages. As many as one-third of patients with PH have coronary artery disease. Because of their physical limitations, patients with PH are unable to adequately exercise. Regadenoson can potentially have an adverse impact due to their tenuous hemodynamics. Current guidelines suggest performing a coronary angiography in patients with PH who have angina or multiple coronary risk factors. METHODS: We identified 67 consecutive patients with confirmed PH by catheterization (mean PA > 25 mmHg not due to left heart disease) who underwent MPI with regadenoson stress. Medical records were reviewed to determine hemodynamic and ECG response to regadenoson. RESULTS: No serious events occurred. Common side effects related to regadenoson were observed, dyspnea being the most common (70.6%). No syncope occurred. Heart rate increased from 74.6 ± 14 to 96.3 ± 18.3 bpm, systolic blood pressure increased from 129.8 ± 20.9 to 131.8 ± 31 mmHg, and diastolic blood pressure decreased from 77.1 ± 11.4 to 72.9 ± 15.3 mmHg. There was no ventricular tachycardia, ventricular fibrillation, or second- or third-degree atrioventricular block. CONCLUSION: Regadenoson stress MPI appears to be well tolerated and safe in patients with PH.

Effect of cytokine hemoadsorption on brain death-induced ventricular dysfunction in a porcine model.

OBJECTIVE: In an effort to expand the cardiac donor pool, we tested the hypothesis that hemoadsorption of cytokines attenuates brain death-induced ventricular dysfunction. METHODS: Eighteen Yorkshire pigs (50-60 kg) were instrumented with a left ventricular conductance catheter. Cytokine expression, preload recruitable stroke work, and the diastolic relaxation constant tau were measured at baseline and at hourly intervals for 6 hours after induction of brain death by intracranial balloon inflation (brain death, n = 6) or sham operation (control, n = 6). In a third group (brain death + hemoadsorption, n = 6), 3 hours after induction of brain death, animals were placed on an extracorporeal circuit containing a cytokine-hemoadsorption device for the remaining 3 hours of the experiment. Myocardial water content was measured after the animals were killed. RESULTS: Six hours after induction of brain death, tumor necrosis factor and interleukin-6 were highest in the brain death group (106 ± 13.1 pg/mL and 301 ± 181 pg/mL, respectively), lowest in controls (68.3 ± 8.55 pg/mL and 37.8 ± 11 pg/mL, respectively), and intermediate in the brain death + hemoadsorption group (81.2 ± 35.2 pg/mL and 94.6 ± 20 pg/mL, respectively). Compared with controls, preload recruitable stroke work was significantly reduced in the brain death group 4 hours after the induction of brain death and was 50% of baseline by 5 hours. In the brain death + hemoadsorption group, preload recruitable stroke work was relatively preserved at 80% of baseline at similar time points. Tau remained unchanged in the control and brain death + hemoadsorption groups, whereas in the brain death group it was significantly elevated versus baseline 5 (139.3% ± 21.5%) and 6 (172% ± 16.1%) hours after induction of brain death. Myocardial water content was significantly greater in the brain death group than in the other 2 groups. CONCLUSIONS: Hemoadsorption of cytokines using an extracorporeal circuit attenuates brain death-induced ventricular dysfunction in a porcine model. Improvement in function generally correlates with trends in cytokine expression, but this relationship requires further investigation.

Role of cytokine hemoadsorption in cardiopulmonary bypass-induced ventricular dysfunction in a porcine model.

Little is known about the effect of cardiopulmonary bypass alone on cardiac function; in an attempt to illuminate this relationship and test a possible mechanism, we used Cytosorb, a device capable of removing virtually all types of circulating cytokines to test the hypothesis that hemoadsorption of cytokines during bypass attenuates bypass-induced acute organ dysfunction. Twelve Yorkshire pigs (50-65 kg) were instrumented with a left ventricular conductance catheter. Baseline mechanics and cytokine expression (tumor necrosis factor [TNF], interleukin-6 [IL-6], and interleukin-10) were measured before and hourly after 1 hour of normothermic cardiopulmonary bypass. Animals underwent bypass without (cardiopulmonary bypass [CPB], n = 6) or with (CPB+HA, n = 6) the CytosorbTM device. Data were compared with "historical" controls (n = 6) that were similarly instrumented but underwent observation instead of bypass. Five hours after separation from bypass (or observation), animals were euthanized. Myocardial water content was determined postmortem. Neither TNF nor IL-6 was significantly elevated in either experimental group versus controls at any time point. Preload recruitable stroke work and dP/dtmax were significantly depressed immediately after separation from bypass in both CPB+HA and CPB and remained depressed for the duration of the experiment. Although Tau remained unchanged, dP/dTmin was significantly diminished in both bypass groups at all time points after separation from bypass. Cytokine hemoadsorption had no effect on any measurable index of function. Differences in postmortem data were not evident between groups. One hour of normothermic CPB results in a significant and sustained decline in left ventricular function that appears unrelated to changes in cytokine expression. Because we did not appreciate a significant change in cytokine concentrations postbypass, the capacity of cytokine hemoadsorption to attenuate CPB-induced ventricular dysfunction could not be assessed.

Antimicrobial effects of nanofiber poly(caprolactone) tissue scaffolds releasing rifampicin.

This study quantified the antibiotic release kinetics and subsequent bactericidal efficacy of rifampicin (RIF) against Gram-positive and Gram-negative bacteria under in vitro static conditions. Antibiotic-loaded scaffolds were fabricated by electrospinning poly(caprolactone) (PCL) with 10% or 20% (w/w) RIF. Scaffold fiber diameter and RIF loading were characterized, and RIF release kinetics were measured. RIF-releasing and RIF-free scaffolds were inoculated with Pseudomonas aeruginosa and Staphylococcus epidermidis, and the suspended concentration live and dead bacteria were determined by fluorescent microscopy. Adherent bacteria and biofilm formation were examined using scanning electron microscopy. Mean fiber diameters were 557 ± 399 nm for RIF-free, 402 ± 225 nm for 10% RIF, and 665 ± 402 nm for 20% RIF scaffolds. RIF release kinetics exhibited a short-burst release during the first hour, followed by a 7 h, zero-order release during which both RIF scaffolds released ~50% of their initial RIF mass loading. P. aeruginosa and S. epidermidis suspended cell populations proliferated in accordance with logarithmic growth models when exposed to control scaffolds; however both RIF-containing scaffolds completely inhibited bacterial growth in suspension and, subsequently, prevented biofilm formation within the scaffolds through the first 6 h.