Circulation: Clinical Summaries
Original Research Put Into Perspective for the Practicing Clinician
- Incident Atrial Fibrillation Among Asians, Hispanics, Blacks, and Whites
- Uteroplacental Blood Flow, Cardiac Function, and Pregnancy Outcome in Women With Congenital Heart Disease
- Duration of Resuscitation Efforts and Functional Outcome After Out-of-Hospital Cardiac Arrest: When Should We Change to Novel Therapies?
- Cardiopulmonary Resuscitation With Chest Compressions During Sustained Inflations: A New Technique of Neonatal Resuscitation That Improves Recovery and Survival in a Neonatal Porcine Model
- Alloantibody and Complement Promote T Cell–Mediated Cardiac Allograft Vasculopathy Through Noncanonical Nuclear Factor-κB Signaling in Endothelial Cells
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Incident Atrial Fibrillation Among Asians, Hispanics, Blacks, and Whites
Although atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice, the underlying mechanisms responsible for its induction and perpetuation remain incompletely understood. Blacks experience a substantially lower rate of AF compared with whites, and the relative strength of this association suggests the mechanism responsible for the race-AF association plays an important role in disease pathogenesis. Because AF rates have only been rigorously compared between black and white patients, it is unclear whether white race confers elevated AF risk or black race affords arrhythmia protection. The present investigation compared incident AF between whites, blacks, Hispanics, and Asians receiving hospital-based medical care in California. A significantly lower hazard of AF was observed among blacks, Hispanics, and Asians compared with whites both before and after controlling for established risk factors. These findings argue against a protective effect unique to black race and instead suggest an unidentified characteristic inherent to white race increases AF risk. In addition, the difference in AF risk between whites and non-whites was most pronounced in the absence of established AF risk factors. This further suggests that an unknown, alternative disease mechanism is driving these racial differences. As non-white racial and ethnic populations within the United States continue to grow, clinicians should be aware of the importance of race in AF prediction and incorporate this knowledge into their care of patients at risk for this frequently encountered disease. See p 2470.
Uteroplacental Blood Flow, Cardiac Function, and Pregnancy Outcome in Women With Congenital Heart Disease
Women with congenital heart disease (CHD) are not only at risk of maternal cardiovascular complications during their pregnancies, but they also have an increased risk of obstetric and offspring complications. Offspring complications such as small for gestational age and premature birth are related to maternal cardiac function, but the mechanism underlying this relationship is unknown. In this clinical study, in 209 pregnant women with CHD and 70 healthy women, we demonstrated that uteroplacental Doppler flow parameters (uterine and umbilical artery pulsatility and resistance indices) are worse in pregnant women with CHD than in healthy women and are related to maternal cardiovascular function parameters, such as right ventricular function, valvular regurgitation, heart rate, and prepregnancy need for cardiac medication. Uteroplacental flow parameters were related to offspring outcome, as is also known in the general pregnant population. Therefore, we concluded that in women with CHD, uteroplacental flow may be compromised by maternal cardiac dysfunction and that impaired uteroplacental flow may be a key factor in the high incidence of obstetric and offspring complications. Our study improves the understanding of the pathophysiology of offspring events in women with CHD and may also contribute to a better insight into the pathophysiology of offspring complications in the general population. The results of this study are of importance for counseling of women with CHD who are contemplating pregnancy and will improve risk stratification leading to more adequate monitoring of pregnancies in these women. See p 2478.
Duration of Resuscitation Efforts and Functional Outcome After Out-of-Hospital Cardiac Arrest: When Should We Change to Novel Therapies?
Despite advances in systematic postresuscitation care, only 5% to 15% of out-of-hospital cardiac arrest victims survive to hospital discharge. Few interventions have proven benefit in cardiac arrest resuscitation, and the typical strategy for patients without rapid return of spontaneous circulation is to repeat failed interventions. No additional resources are brought to bear. Novel approaches to treating out-of-hospital cardiac arrest, such as extracorporeal life support, have yielded neurologically favorable survival in select patients in whom traditional resuscitation fails. We investigated the relationship between the duration of cardiopulmonary resuscitation and neurological outcome after cardiac arrest to identify the duration of cardiopulmonary resuscitation beyond which repeating traditional resuscitation measures does not result in incremental neurologically favorable survival. Our findings suggest that conventional resuscitation is the most effective within the first 10 to 15 minutes, by which time 75% of patients with favorable neurological recovery had achieved rapid return of spontaneous circulation. The probability of favorable neurological recovery fell to 2% beyond this point. Cardiopulmonary resuscitation duration was independently associated with favorable neurological outcome, adjusting for prehospital and inpatient covariates. Alternative strategies to traditional resuscitation should be tested immediately after cardiac arrest, rather than after the failure of traditional cardiopulmonary resuscitation. See p 2488.
Cardiopulmonary Resuscitation With Chest Compressions During Sustained Inflations: A New Technique of Neonatal Resuscitation That Improves Recovery and Survival in a Neonatal Porcine Model
Delivery room cardiopulmonary resuscitations are an infrequent event in newborn infants and associated with high rates of neurodevelopmental impairment and mortality. The poor prognosis associated with delivery room resuscitations raises questions as to whether specifically tailored neonatal cardiopulmonary resuscitations could improve outcomes. Current neonatal resuscitation guidelines recommend a ratio of 90 chest compressions and 30 ventilations per minute; however, the most effective ratio remains controversial. In our porcine model of neonatal hypoxia-asphyxia, we were able to passively ventilate the lung while providing chest compressions. To achieve passive ventilation, we applied airway pressure of 30 cm H2O, which was sustained for the duration of the chest compressions. This novel approach significantly improved the return of spontaneous circulation and survival in newborn piglets. We observed improved lung aeration, which resulted in marked increases in pulmonary blood flow. An increase in oxygenated blood flow returning from the lungs restores cardiac function, resulting in increased systemic and pulmonary blood pressure and carotic blood flow during resuscitation. With the use of this new technique, significantly fewer piglets required supplemental oxygen and none required intravenous epinephrine administration. This may be of clinical relevance because hyperoxia can lead to the generation of oxygen-free radicals, a major cause in reperfusion injury after asphyxia. Our results are of considerable clinical relevance, because improved respiratory and hemodynamic parameters potentially minimize morbidity and mortality in newborn infants. See p 2495.
Alloantibody and Complement Promote T Cell–Mediated Cardiac Allograft Vasculopathy Through Noncanonical Nuclear Factor-κB Signaling in Endothelial Cells
Cardiac allograft vasculopathy (CAV), characterized by widespread narrowing of the blood vessels in a transplanted heart, is the leading cause of late graft loss. There are no medical therapies for CAV, and the immunological mechanisms that cause it are unclear. Several studies have implicated host T cells within the graft blood vessel wall that secrete interferon-γ, a cytokine that causes vascular stenosis, as the mediators of CAV. In other studies, host antibodies reactive with HLA antigens, molecules expressed primarily on graft endothelial cells, have been shown to increase the likelihood of developing CAV. In a novel preclinical model of CAV, we treated human endothelial cells with anti-HLA antibodies to activate the complement system. Complement, in turn, activated a signaling pathway in the endothelial cells, known as noncanonical nuclear factor-κB, that increased expression of proinflammatory genes in endothelial cells with protein products that promote T cell binding and induce T cells to make more interferon-γ. We detected noncanonical nuclear factor-κB signaling and target gene expression in kidney biopsies from patients with chronic antibody-mediated rejection and in endothelial cells lining human coronary arteries implanted into immunodeficient mice and then treated with anti-HLA antibodies. Strikingly, such arteries developed more CAV when exposed to human T cells. We conclude that anti-HLA antibodies can promote CAV by activating complement on and noncanonical nuclear factor-κB signaling in graft endothelial cells, linking antibody and complement activation to pathogenic T-cell activation. This pathway may be a target for new drugs to prevent CAV in heart transplantation patients. See p 2504.
- © 2013 American Heart Association, Inc.
- Incident Atrial Fibrillation Among Asians, Hispanics, Blacks, and Whites
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