Addition of Blood Pressure and Weight Transmissions to Standard Remote Monitoring of Implantable Defibrillators and its Association with Mortality and Rehospitalization.

BACKGROUND: Among patients with implantable defibrillators (ICD), use of remote patient monitoring (RPM) is associated with lower risk of death and rehospitalization. Standard ICD RPM can be supplemented with weight and blood pressure data. It is not known whether standard RPM plus routine weight and blood pressure transmission (RPM+) is associated with better outcomes. METHODS AND RESULTS: RPM+ patients (n=4106) were compared with patients who only transmitted standard ICD RPM data (n=14 183). Logistic regression models identified patient, physician, and hospital characteristics associated with RPM+ utilization. Mortality and rehospitalization were examined using landmark analyses at 180 days after ICD implant in Medicare fee-for-service patients. In these analyses, we examined the independent association between RPM+ utilization and times to events up to 3 years after device implantation with Cox regression models. We further examined whether the association between RPM+ and outcomes varied by frequency or type of transmissions. Determinants of RPM+ utilization included impaired ejection fraction, cardiac resynchronization therapy, and institutional practice. The risk of mortality of RPM+ patients was similar to standard ICD RPM patients (hazard ratio, 1.06; 95% confidence interval, 0.94-1.19; P=0.34). RPM+ patients also had similar risks of all-cause hospitalization (subdistribution hazard ratio, 1.03; 95% confidence interval, 0.94-1.14; P=0.52), cardiovascular hospitalization (subdistribution hazard ratio, 0.92; 95% confidence interval, 0.83-1.02; P=0.15), or heart failure hospitalizations (subdistribution hazard ratio, 0.90; 95% confidence interval, 0.78-1.05; P=0.18). RPM+ transmission frequency was not associated with outcomes. CONCLUSIONS: In patients using standard ICD RPM, the added transmission of weight and blood pressure data was not associated with improved outcomes.

Traditional heart failure medications and sudden cardiac death prevention: a review.

Sudden cardiac death (SCD) is still a major public health issue with an estimated annual incidence ranging from 184,000 to > 400,000 per year. The ACC/AHA/ESC 2006 guidelines define SCD as "death from an unexpected circulatory arrest, usually due to a cardiac arrhythmia occurring within an hour of the onset of symptoms". A recent study of sudden cardiac death using multiple sources of ascertainment found that coronary artery disease was present in more than 50% of patients older than 35 years who died suddenly and underwent autopsy. Antiarrhythmic drugs have failed to show any mortality benefit even when compared to placebo or implantable cardiovertor defibrillators (ICDs). While patients with systolic heart failure are at higher risk of dying suddenly, most of the patients experiencing sudden cardiac death have left ventricular ejection fraction (LVEF) > 50%. ß-blockers, Angiotensin enzymes (ACE) inhibitors as well as aldosterone antagonists prevent ischemia and remodelling in the left ventricle especially in post myocardial infarction (MI) patients and in patients with systolic heart failure. This article will review the data on the effects of traditional heart failure medications, especially ß-blockers, Renin Angiotensin system blockers, as well as Statin therapy on sudden cardiac death in post MI patients and in patients with systolic heart failure.

Epicardial Fat and Atrial Fibrillation: A Review.

Atrial fibrillation (AF) is a progressive disorder that increases with age. Obesity is an important risk factor for AF. Pericardial fat is an active adipose tissue in close proximity to the heart and has been shown to be a risk factor for structural as well as coronary artery disease independent of body mass index. Recent studies suggest a role of epicardial fat in atrial remodeling as well as AF burden. This review will summarize the recent evidence linking epicardial fat and AF.

Pericardial fat is independently associated with human atrial fibrillation.

OBJECTIVES: The purpose of this study was to investigate the association between atrial fibrillation (AF) and pericardial fat. BACKGROUND: Pericardial fat is visceral adipose tissue that possesses inflammatory properties. Inflammation and obesity are associated with AF, but the relationship between AF and pericardial fat is unknown. METHODS: Pericardial fat volume was measured using computed tomography in 273 patients: 76 patients in sinus rhythm, 126 patients with paroxysmal AF, and 71 patients with persistent AF. RESULTS: Patients with AF had significantly more pericardial fat compared with patients in sinus rhythm (101.6 +/- 44.1 ml vs. 76.1 +/- 36.3 ml, p < 0.001). Pericardial fat volume was significantly larger in paroxysmal AF compared with the sinus rhythm group (93.9 +/- 39.1 ml vs. 76.1 +/- 36.3 ml, p = 0.02). Persistent AF patients had a significantly larger pericardial fat volume compared with paroxysmal AF (115.4 +/- 49.3 ml vs. 93.9 +/- 39.1 ml, p = 0.001). Pericardial fat volume was associated with paroxysmal AF (odds ratio: 1.11; 95% confidence interval: 1.01 to 1.23, p = 0.04) and persistent AF (odds ratio: 1.18, 95% confidence interval: 1.05 to 1.33, p = 0.004), and this association was completely independent of age, hypertension, sex, left atrial enlargement, valvular heart disease, left ventricular ejection fraction, diabetes mellitus, and body mass index. CONCLUSIONS: Pericardial fat volume is highly associated with paroxysmal and persistent AF independent of traditional risk factors including left atrial enlargement. Whether pericardial fat plays a role in the pathogenesis of AF requires future investigation.

Gemella morbillorum prosthetic valve endocarditis.

The authors describe a case of prosthetic valve infective endocarditis (IE) caused by Gemella morbillorum (GM), a gram-positive coccus that grows slowly in culture and occasionally causes a subacute to chronic form of IE. To the author's knowledge, this is the third case of GM prosthetic valve IE to be reported. Subacute to chronic IE caused by slow-growing organisms can be subtle in presentation and should be suspected in patients who have prosthetic valves presenting with worsening heart failure.

Electroanatomic mapping of postpacing intervals clarifies the complete active circuit and variants in atrial flutter.

BACKGROUND: Typical atrial flutter is characterized by cavotricuspid isthmus dependence and activation sequentially around the tricuspid annulus (TA), usually counterclockwise. However, analysis of the upper portion of the annulus by postpacing interval after entrainment sometimes suggests it is outside the circuit. Details on the true active circuit are limited, particularly in the upper portions. OBJECTIVE: The purpose of this study was to define the full active circuit in atrial flutter. METHODS: In 26 patients with isthmus-dependent atrial flutter, we created detailed electroanatomic maps of postpacing intervals throughout the entire right atrium. Postpacing intervals within 20 ms of the flutter cycle length were defined as within the circuit. RESULTS: Creating postpacing interval maps allowed characterization of the full active circuit in all patients, and revealed significant variations despite similar counterclockwise or clockwise patterns with activation mapping. In 8, the active circuit was solely around the TA. In 14, an oblique course between the anterior and posterior borders was found, with the upper circuit off the annulus, posterior to the right atrial appendage base. Of these, 8 coursed anterior to the SVC, 5 behind the SVC and 1 bifurcated the SVC. In 4 others, bifurcation of the upper circuit was seen around the right atrial appendage (n = 3), or around the combined right atrial appendage-superior vena cava (n = 1). CONCLUSION: Despite similar activation around the TA, creating electroanatomic postpacing interval maps distinguishes the active flutter circuit from passively activated myocardium. Significant variability exists in the active circuit, with only a minority around the TA. Most commonly, the circuit courses not around a single barrier but obliquely between anterior and posterior borders.

Endothelial dysfunction in heart failure identifies responders to cardiac resynchronization therapy.

BACKGROUND: The presence of endothelial dysfunction is associated with increased heart failure mortality. Cardiac resynchronization therapy (CRT) improves heart failure outcomes; however, current guidelines do not adequately identify responders to CRT. OBJECTIVE: The purpose of this study was to determine whether endothelial dysfunction can predict response to CRT. METHODS: Brachial artery flow-mediated dilation, a measure of endothelial function, was measured at baseline preimplant and 90 days postimplant in 33 patients undergoing CRT (age 64.2 +/- 16.8 years, left ventricular ejection fraction [LVEF] 25% +/- 9%, QRS duration 158 +/- 25 ms, New York Heart Association class III-IV). RESULTS: Of the 33 patients, 19 (58%) were responders to CRT. Baseline flow-mediated dilation was 4.6% +/- 4.5% in responders and 8.6% +/- 4.2% in nonresponders (P <.01). After 90 days of CRT, responders had significant improvement in LVEF (23% +/- 8% to 30% +/- 9%, P = .03), 6-minute walk distance (756 +/- 213 feet to 1,089 +/- 242 feet, P = .04), and quality of life (52 +/- 22 to 31 +/- 28, P <.005), whereas nonresponders did not show improvement in these measures. The presence of baseline endothelial dysfunction correlated with impaired baseline functional capacity (r = 0.39, P = .03), and improvement in flow-mediated dilation correlated with improvement in 6-minute walk distance (r = 0.34, P = .05). Logistic regression analysis showed that every 1% reduction in baseline flow-mediated dilation correlated with an approximately 5% increased likelihood of response to CRT. The predictive value of baseline endothelial dysfunction was independent of QRS duration, LVEF, or dyssynchrony and provided additive prognostic value. CONCLUSION: The presence of endothelial dysfunction independently identifies CRT responders and provides additive prognostic value for predicting response over current criteria. Addition of endothelial function assessment to current selection criteria may improve the ability to identify CRT responders.

The effects of statins and renin-angiotensin system blockers on atrial fibrillation recurrence following antral pulmonary vein isolation.

INTRODUCTION: Ablation has emerged as a major treatment option for atrial fibrillation (AF). However, this procedure is limited by a significant rate of AF recurrence. We aimed to examine the effects of statins, angiotensin-converting enzyme inhibitors (ACE-I), and angiotensin receptor blockers (ARB) on the recurrence rate of AF following ablation. METHODS: We conducted a retrospective study of 177 consecutive patients (mean age = 56 +/- 11 yrs, 69% males) who underwent ablation for paroxysmal (n = 132) or persistent AF (n = 45). Patients were treated with ACE-I (n = 31) or ARB (n = 18) or statins (n = 50) prior to ablation and for the duration of follow-up. RESULTS: After a mean follow-up of 13.8 +/- 8.6 months, 72% of patients were free of AF. For patients taking statins, 33 of 50 (60%) were free of AF. In patients treated with ACE-I, 17 of 31 (55%) were free from AF, while in the group of patients treated with ARB, 17 of 18 (94%) were free from AF. Using Cox regression analysis to correct for baseline variables, treatment with statins did not decrease the recurrence rate (HR = 1.10 [95% CI: 0.55-2.27] p = 0.79); nor did treatment with renin angiotensin system (RAS) blockers (HR 0.94 [95% CI: 0.46-1.93] p = 0.87). However, subgroup analysis showed that treatment with ARB was associated with a trend towards lower AF recurrence [HR 0.17, (95% CI: 0.02-1.34) p = 0.09]. CONCLUSIONS: Even though statins and RAS blockers possess anti-inflammatory properties, they did not decrease the recurrence of AF following ablation. However, the subset of patients taking ARB exhibited a trend towards lower AF recurrence. Larger, randomized studies are needed to address this observation.

Surface electrocardiographic patterns and electrophysiologic characteristics of atrial flutter following modified radiofrequency MAZE procedures.

INTRODUCTION: The radiofrequency MAZE is becoming a common adjunct to cardiac surgery in patients with atrial fibrillation. While a variety of postoperative arrhythmias have been described following the original Cox-MAZE III procedure, the electrophysiological characteristics and surgical substrate of post-radiofrequency MAZE flutter have not been correlated. We sought to determine the location, ECG patterns, and electrophysiological characteristics of post-radiofrequency MAZE atrial flutter. METHODS: Nine consecutive patients with post-radiofrequency MAZE flutter presented for catheter ablation 9 +/- 10 months after surgery. RESULTS: Only one patient (11%) had an ECG appearance consistent with typical isthmus-dependent right atrial (RA) flutter. However, on electrophysiological study, 3/9 patients (33%) had typical right counter-clockwise flutter entrained from the cavo-tricuspid isthmus, despite description of surgical isthmus ablation. Six patients (67%) had left atrial (LA) circuits. These involved the mitral annulus in 5/6 cases (83%) despite description of surgical mitral isthmus ablation in the majority (60%). LA flutters had a shorter cycle length compared with RA flutters (253 +/- 39 msec and 332 +/- 63 msec respectively, P < 0.05). After a mean of 8 +/- 4 months following ablation, 8/9 patients (89%) were in sinus rhythm. CONCLUSION: Up to one-third of post-radiofrequency MAZE circuits are typical isthmus-dependent RA flutters, despite a highly atypical surface ECG morphology. Therefore, diagnostic electrophysiological studies should commence with entrainment at the cavo-tricuspid isthmus in order to exclude typical flutter, regardless of the surface ECG appearance. Incomplete surgical lesions at the mitral and cavo-tricuspid isthmus likely predispose to the development of post-radiofrequency MAZE flutter.

Myocardial viability testing and the effect of early intervention in patients with advanced left ventricular systolic dysfunction.

BACKGROUND: The clinical value of revascularization and other procedures in patients with severe systolic heart failure is unclear. It has been suggested that assessing ischemia and viability by positron emission tomography (PET) with fluorodeoxyglucose (FDG) imaging may identify patients for whom revascularization may lead to improved survival. We performed a propensity analysis to determine whether there might be a survival advantage from revascularization. METHODS AND RESULTS: We analyzed the survival of 765 consecutive patients (age 64+/-11 years, 80% men) with advanced left ventricular systolic dysfunction (ejection fraction < or =35%) and without significant valvular heart disease who underwent PET/FDG study at the Cleveland Clinic between 1997 and 2002. Early intervention was defined as any cardiac intervention (surgical or percutaneous) within the first 6 months of the PET/FDG study. In the entire cohort, 230 patients (30%) underwent early intervention (188 [25%] had open heart surgery, most commonly coronary artery bypass grafting, and 42 [5%] had percutaneous revascularization); 535 (70%) were treated medically. Using 39 demographic, clinical and PET/FDG variables, we were able to propensity-match 153 of the 230 patients with 153 patients who did not undergo early intervention. Among the propensity-matched group, there were 84 deaths during a median of 3 years follow-up. Early intervention was associated with a markedly lower risk of death (3-year mortality rate of 15% versus 35%, propensity adjusted hazard ratio 0.52, 95% CI 0.33 to 0.81, P=0.0004). CONCLUSIONS: Among systolic heart failure patients referred for PET/FDG, early intervention may be associated with improved survival irrespective of the degree of viability.

53-years-old with mental status changes.

D-lactic acidosis, a complication of short bowel syndrome, presents with a variety of neurological symptoms and metabolic acidosis. Treatment is hydration, replacement of nutritional deficiency replacement, and selective antibiotics. Prevention entails complex carbohydrate diet and vitamin and mineral supplements.