Zian H. Tseng

Sudden cardiac death in patients with human immunodeficiency virus infection.

OBJECTIVES The aim of this study was to determine the incidence and clinical characteristics of sudden cardiac death (SCD) in patients with human immunodeficiency virus (HIV) infection. BACKGROUND As the HIV-infected population ages, cardiovascular disease prevalence and mortality are increasing, but the incidence and features of SCD have not yet been described. METHODS The records of 2,860 consecutive patients in a public HIV clinic in San Francisco between April 2000 and August 2009 were examined. Identification of deaths, causes of death, and clinical characteristics were obtained by search of the National Death Index and/or clinic records. SCDs were determined using published retrospective criteria: 1) the International Classification of Diseases-10th Revision, code for all cardiac causes of death; and (2) circumstances of death meeting World Health Organization criteria. RESULTS Of 230 deaths over a median of 3.7 years of follow-up, 30 (13%) met SCD criteria, 131 (57%) were due to acquired immune deficiency syndrome (AIDS), 25 (11%) were due to other (natural) diseases, and 44 (19%) were due to overdoses, suicides, or unknown causes. SCDs accounted for 86% of all cardiac deaths (30 of 35). The mean SCD rate was 2.6 per 1,000 person-years (95% confidence interval: 1.8 to 3.8), 4.5-fold higher than expected. SCDs occurred in older patients than did AIDS deaths (mean 49.0 vs. 44.9 years, p = 0.02). Compared with AIDS and natural deaths combined, SCDs had a higher prevalence of prior myocardial infarction (17% vs. 1%, p < 0.0005), cardiomyopathy (23% vs. 3%, p < 0.0005), heart failure (30% vs. 9%, p = 0.004), and arrhythmias (20% vs. 3%, p = 0.003). CONCLUSIONS SCDs account for most cardiac and many non-AIDS natural deaths in HIV-infected patients. Further investigation is needed to ascertain underlying mechanisms, which may include inflammation, antiretroviral therapy interruption, and concomitant medications.

Intracardiac and extracardiac markers of inflammation during atrial fibrillation

BACKGROUND A decrease in inflammation after cure of atrial arrhythmias suggests that such arrhythmias are proinflammatory, and lower inflammatory marker levels in the coronary sinus suggest that atrial arrhythmias result in intracardiac appropriation of inflammatory cytokines. OBJECTIVE The purpose of this study was to investigate the effect of atrial fibrillation on inflammatory markers drawn from intracardiac and extracardiac chambers. METHODS We performed a case-control study of 167 AF patients and 207 controls. Blood from intracardiac and extracardiac sites was obtained from a subset of patients undergoing curative AF ablation (n = 46). RESULTS No significant differences in C-reactive protein (CRP) or interleukin-6 (IL-6) levels were seen between patients with and those without a history of AF. Both levels were significantly higher when blood was drawn during AF than during sinus rhythm: median CRP 3.1 mg/dL (interquartile range [IQR] 1.0-6.0) versus 1.7 mg/dL (IQR 0.7-3.9, P = .0005); median IL-6 2.3 ng/mL (IQR 1.5-3.9) versus 1.5 ng/mL (IQR 0.7-2.5, P = .007). This finding persisted after adjusting for potential confounders. AF ablation patients in AF exhibited a positive median left atrial minus coronary sinus gradient CRP (0.3 mg/dL, IQR -0.03-1.1), whereas those in sinus rhythm had a negative median left atrial minus coronary sinus gradient CRP (-0.2, IQR -0.8-[-0.02], P = .01). Femoral artery minus femoral vein gradients in AF versus sinus rhythm did not show any differences. CONCLUSION AF at the time of the blood draw, rather than a history of AF, was independently associated with inflammation. Differences in transcardiac gradients suggest that AF results in sequestration of inflammatory cytokines in the heart.

Congenital Heart Disease in the Older Adult A Scientific Statement From the American Heart Association

The population of adults with congenital heart disease (ACHD) has increased dramatically over the past few decades, with many people who are now middle-aged and some in the geriatric age range. This improved longevity is leading to increased use of the medical system for both routine and episodic care, and caregivers need to be prepared to diagnose, follow up, and treat the older adult with congenital heart disease (CHD). The predictable natural progression of CHD entities and sequelae of previous interventions must now be treated in the setting of late complications, acquired cardiac disease, multiorgan effects of lifelong processes, and the unrelenting process of aging. Despite the advances in this field, death rates in the population from 20 to >70 years of age may be twice to 7 times higher for the ACHD population than for their peers.1 This American Heart Association (AHA) scientific statement will focus on the older adult (>40 years old) with CHD. It is meant to be complementary to the 2008 American College of Cardiology (ACC)/AHA guidelines for ACHD and orient the reader to the natural history, ramifications of childhood repair, and late initial diagnosis of CHD in the older adult. This population with CHD is unique and distinct from both the pediatric and young adult populations with CHD. Much of the information we provide is from scientific research combined with clinical experience from longitudinal care. We emphasize that this is the beginning of a discussion regarding this rapidly growing population, and continued research aimed at the progression of disease and complications reviewed here is necessary to advance the field of ACHD with the scientific rigor it deserves. ACHD encompass a broad range of presentations. There are people who are diagnosed for the first time in adulthood, as well as those with prior palliative repair …

Markers of inflammation before and after curative ablation of atrial flutter

BACKGROUND Atrial arrhythmias are associated with inflammation. The cause and effect of the association are unknown. OBJECTIVE The purpose of this study was to test the hypothesis that atrial tachyarrhythmias contribute to inflammation. METHODS We performed a prospective observational study wherein C-reactive protein (CRP) and interleukin-6 (IL-6) levels from the femoral vein and coronary sinus (CS) were compared before curative ablation for atrial flutter (AFL; n = 59) and paroxysmal supraventricular tachycardia (SVT; n = 110). Follow-up levels were obtained at 1 and 6 months. RESULTS Peripheral levels of both biomarkers were significantly higher in the AFL group. After multivariate adjustment, only those in the AFL group who presented in AFL or atrial fibrillation (AF) had significantly elevated CRP levels (odds ratio 1.26; P = .033). Levels of each marker were similar in the CS and peripheral blood in the SVT group; in the AFL group, both CRP and IL-6 were significantly lower in the CS than in the periphery (P = .0076 and P = .0021, respectively). CRP was significantly lower a median of 47 days after AFL ablation (from a median of 6.28 mg/L to a median of 2.92 mg/L; P = .028) and remained reduced at second follow-up. IL-6 decreased across three time points after AFL ablation (P = .002). No reduction in inflammatory biomarkers was observed after SVT ablation. CONCLUSIONS CRP and IL-6 levels are elevated in patients presenting in AFL. Given the lower CS values in these patients, their origin appears to be systemic rather than cardiac. Because these levels significantly fall after ablation of AFL, the atrial tachyarrhythmia appears to be the cause (not the effect) of the inflammation.

Repeat Transseptal Catheterization After Ablation for Atrial Fibrillation

Introduction: A substantial number of patients require a second left atrial procedure after ablation for atrial fibrillation (AF), either for left atrial flutter or recurrent AF. The success and complication rates of repeat transseptal catheterization in these patients are unknown. The aim of this study was to determine the difficulty and/or success rates of repeat transseptal catheterization after left atrial ablation for AF.

Impact of Remote Magnetic Catheter Navigation on Ablation Fluoroscopy and Procedure Time

Background: Remote magnetic catheter navigation (RCN) is gaining acceptance in clinical cardiac electrophysiology, but details regarding how RCN affects procedure execution are not well characterized.

Protracted CRP Elevation after Atrial Fibrillation Ablation

Background: Atrial fibrillation (AF) has been linked to an inflammatory process detected through various biomarkers, including C‐Reactive Protein (CRP). Early recurrence of AF within the first 3 months after curative AF ablation is not felt to reflect success or failure of the procedure. We hypothesized that this early recurrence is due to an inflammatory response to the ablation itself. We therefore sought to evaluate levels of CRP after AF ablation.

Kidney Dysfunction and Sudden Cardiac Death Among Women With Coronary Heart Disease

We evaluated the association between kidney dysfunction and sudden cardiac death risk among ambulatory women with coronary heart disease. The Heart and Estrogen Replacement Study evaluated the effects of hormone treatment on cardiovascular events among 2763 postmenopausal women with coronary heart disease. Kidney dysfunction was categorized by estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease equation. Multivariate proportional hazards models were used to adjust for cardiovascular risk factors, congestive heart failure, and myocardial infarction. At baseline, 37% (n=1027) had an eGFR of >60 mL/min, 54% (n=1503) had an eGFR of 40 to 60 mL/min, and 8% (n=230) had an eGFR of <40 mL/min. During the 6.8-year follow-up period, there were 136 adjudicated sudden cardiac deaths. The rate of sudden cardiac death was higher in those with lower kidney function (0.5% per year among those with an eGFR >60; 0.6% per year with an eGFR between 40 and 60; and 1.7% per year with an eGFR <40 mL/min; P for trend <0.001). After multivariate analysis with baseline risk factors, eGFR at 40 to 60 mL/min was not a significant predictor, but eGFR at <40 mL/min remained strongly associated with sudden cardiac death (hazard ratio: 3.2; 95% CI: 1.9 to 5.3); adjustment for incident congestive heart failure and myocardial infarction during follow-up diminished this association (hazard ratio: 2.3; 95% CI: 1.3 to 3.9), suggesting that congestive heart failure and myocardial infarction mediated only part of the association between kidney dysfunction and sudden cardiac death. Advanced kidney dysfunction is an independent predictor of sudden cardiac death among women with coronary heart disease.

Alcohol Intake is Significantly Associated with Atrial Flutter in Patients under 60 Years of Age and a Shorter Right Atrial Effective Refractory Period

Background: Although evidence suggests that alcohol is associated with atrial fibrillation (AF), the association between alcohol and atrial flutter (AFL) has not been examined. The mechanism connecting alcohol and atrial arrhythmias is unknown.

A first-degree family history in lone atrial fibrillation patients

BACKGROUND Atrial fibrillation (AF) may be due to an inherited trait, particularly in lone AF patients. A family history of AF in lone AF patients has not previously been compared with a family history of patients with AF and established risk factors (non-lone AF). OBJECTIVE The purpose of this study was to compare the frequency of having a first-degree relative with AF in lone and non-lone AF patients. METHODS We performed a case-control study of consecutive subjects presenting to a single electrophysiology laboratory. A convenience sample of subjects with no known arrhythmias was also enrolled. RESULTS Four hundred twenty-nine subjects were enrolled: 136 had AF (54 with lone AF), 84 had atrial flutter, 158 had other supraventricular arrhythmias, and 51 had no known arrhythmias. Significantly more subjects with AF reported a first-degree family history of AF compared with the remainder of the cohort (25% vs. 5%; P <.001). In multivariable analysis adjusting for potential confounders, AF patients had a 6-fold greater odds of having a family member with AF (95% confidence interval [CI] 2.93-12.7; P <.001). Lone AF patients had a first-degree family member with AF substantially more often than those with non-lone AF (41% vs. 14%; P <.001). After adjusting for potential confounders, lone AF patients remained significantly more likely than other AF patients to have a first-degree relative with AF (OR 7.2; 95% CI 2.1-24.7; P = .002). CONCLUSION Lone AF patients have a first-degree family member with AF substantially more often than other AF patients. This suggests that an inherited trait may be particularly important in this subgroup of patients.