Impact of acute left ventricular apical thrombus on cardioversion for atrial fibrillation.

Among patients undergoing cardioversion for atrial fibrillation, the presence of left ventricular thrombus is a relatively uncommon and challenging clinical dilemma. While left atrial appendage thrombus is a contraindication to cardioversion, there is paucity of data regarding the safety of cardioversion in with the presence of left ventricular apical thrombus. Also, thrombus characteristics such as protrusion and mobility on echocardiography are known risk factors for systemic embolism. In this article, we present a case highlighting the management of atrial fibrillation in the setting of left ventricular dysfunction, acute heart failure, and echocardiographic evidence of acute left ventricular apical thrombus.

Brief report: rheumatoid arthritis is associated with left ventricular concentric remodeling: results of a population-based cross-sectional study.

OBJECTIVE: To study left ventricular (LV) geometry in patients with rheumatoid arthritis (RA) and no history of heart failure compared with that in subjects with neither RA nor a history of heart failure, and to determine the impact of RA on LV remodeling. METHODS: A cross-sectional, community-based study was conducted among adult (age ≥50 years) patients with RA and age- and sex-matched subjects with neither RA nor a history of heart failure. All participants underwent standard 2-dimensional Doppler echocardiography. LV geometry was classified into the following 4 categories based on relative wall thickness and sex-specific cutoffs for the LV mass index: concentric remodeling, concentric hypertrophy, eccentric hypertrophy, or normal geometry. RESULTS: Among 200 patients with RA and 600 age- and sex-matched subjects without RA, the mean age was 65 years, and 74% of the individuals in both cohorts were female. Compared with subjects without RA, patients with RA were significantly more likely to have abnormal LV geometry (odds ratio [OR] 1.44, 95% confidence interval [95% CI] 1.03-2.00), even after adjusting for cardiovascular risk factors and comorbidities. Among subjects with abnormal LV geometry, the odds of concentric LV remodeling were significantly increased in patients with RA (OR 4.73, 95% CI 2.85-7.83). In linear regression analyses, the LV mass index appeared to be lower in patients with RA who were currently receiving corticosteroids (ß ± SE -0.082 ± 0.027, P = 0.002), even after adjusting for cardiovascular risk factors and comorbidities. CONCLUSION: RA was strongly associated with abnormal LV remodeling (particularly concentric LV remodeling) among RA patients without heart failure. This association remained significant after adjustment for cardiovascular risk factors and comorbidities. RA disease-related factors may promote changes in LV geometry. The biologic mechanisms underlying LV remodeling warrant further investigation.

Artificial Intelligence-Enhanced Electrocardiogram for the Early Detection of Cardiac Amyloidosis.

OBJECTIVE: To develop an artificial intelligence (AI)-based tool to detect cardiac amyloidosis (CA) from a standard 12-lead electrocardiogram (ECG). METHODS: We collected 12-lead ECG data from 2541 patients with light chain or transthyretin CA seen at Mayo Clinic between 2000 and 2019. Cases were nearest neighbor matched for age and sex, with 2454 controls. A subset of 2997 (60%) cases and controls were used to train a deep neural network to predict the presence of CA with an internal validation set (n=999; 20%) and a randomly selected holdout testing set (n=999; 20%). We performed experiments using single-lead and 6-lead ECG subsets. RESULTS: The area under the receiver operating characteristic curve (AUC) was 0.91 (CI, 0.90 to 0.93), with a positive predictive value for detecting either type of CA of 0.86. By use of a cutoff probability of 0.485 determined by the Youden index, 426 (84%) of the holdout patients with CA were detected by the model. Of the patients with CA and prediagnosis electrocardiographic studies, the AI model successfully predicted the presence of CA more than 6 months before the clinical diagnosis in 59%. The best single-lead model was V5 with an AUC of 0.86 and a precision of 0.78, with other single leads performing similarly. The 6-lead (bipolar leads) model had an AUC of 0.90 and a precision of 0.85. CONCLUSION: An AI-driven ECG model effectively detects CA and may promote early diagnosis of this life-threatening disease.

Increased prevalence of diastolic dysfunction in rheumatoid arthritis.

OBJECTIVE: To compare the prevalence of left ventricular (LV) diastolic dysfunction in subjects with and without rheumatoid arthritis (RA), among those with no history of heart failure (HF), and to determine risk factors for diastolic dysfunction in RA. METHODS: A cross-sectional, community-based study comparing cohorts of adults with and without RA and without a history of HF was carried out. Standard two-dimensional/Doppler echocardiography was performed in all participants. Diastolic dysfunction was defined as impaired relaxation (with or without increased filling pressures) or advanced reduction in compliance or reversible or fixed restrictive filling. RESULTS: The study included 244 subjects with RA and 1448 non-RA subjects. Mean age was 60.5 years in the RA cohort (71% female) and 64.9 years (50% female) in the non-RA cohort. The vast majority (>98%) of both cohorts had preserved ejection fraction (EF> or =50%). Diastolic dysfunction was more common in subjects with RA at 31% compared with 26% (age and sex adjusted) in non-RA subjects (OR=1.6; 95% CI 1.2 to 2.4). Patients with RA had significantly lower LV mass, higher pulmonary arterial pressure and higher left atrial volume index than non-RA subjects. RA duration and interleukin 6 (IL-6) level were independently associated with diastolic dysfunction in RA even after adjustment for cardiovascular risk factors. CONCLUSION: Subjects with RA have a higher prevalence of diastolic dysfunction than those without RA. RA duration and IL-6 are independently associated with diastolic dysfunction, suggesting the impact of chronic autoimmune inflammation on myocardial function in RA. Clinical implications of these findings require further investigation.

ECG-gated cardiac CT angiography using 64-MDCT for detection of patent foramen ovale.

OBJECTIVE: The purpose of our study was to show the feasibility of ECG-gated, 64-MDCT cardiac angiography for the detection of patent foramen ovale (PFO). MATERIALS AND METHODS: Chart review was performed on 214 consecutive patients referred for clinically indicated 64-MDCT angiography. The study cohort consisted of 20 patients who had previously undergone transesophageal echocardiography (TEE). Blinded consensus review of each CT angiography was performed by two experienced cardiac radiologists and results were compared with TEE, which served as a reference standard. CT criteria for the diagnosis of PFO were distinct left atrial "flap" in the expected location of the septum primum, continuous column of contrast material connecting this flap to the right atrium, and a "jet" of contrast material from the column into the right atrium. RESULTS: Of the 20 patients who underwent both TEE and cardiac CT angiography, six (30%) were found to have a PFO by TEE. Using the presence of a left atrial flap as the only diagnostic criterion, all six cases of PFO were detected using CT (sensitivity = 100%). Of the 14 patients with no PFO seen on TEE, 12 of these were correctly identified using CT (specificity = 86%). Using all three criteria together, the sensitivity decreased to 66% and the specificity increased to 100%. CONCLUSION: ECG-gated cardiac CT angiography performed with a 64-MDCT scanner can be used to reliably detect PFO.

Dietary sodium modulation of aldosterone activation and renal function during the progression of experimental heart failure.

AIMS: Aldosterone activation is central to the sodium­fluid retention that marks the progression of heart failure (HF). The actions of dietary sodium restriction, a mainstay in HF management, on cardiorenal and neuroendocrine adaptations during the progression of HF are poorly understood. The study aim was to assess the role of dietary sodium during the progression of experimental HF. METHODS AND RESULTS: Experimental HF was produced in a canine model by rapid right ventricular pacing which evolves from early mild HF to overt, severe HF. Dogs were fed one of three diets: (i) high sodium [250 mEq (5.8 g) per day, n =6]; (ii) standard sodium [58 mEq (1.3 g) per day, n =6]; and (iii) sodium restriction [11 mEq (0.25 g) per day, n =6]. During the 38-day study, haemodynamics, renal function, plasma renin activity (PRA), and aldosterone were measured. Changes in haemodynamics at 38 days were similar in all three groups, as were changes in renal function. Aldosterone activation was demonstrated in all three groups; however, dietary sodium restriction, in contrast to high sodium, resulted in early (10 days) activation of PRA and aldosterone. High sodium demonstrated significant suppression of aldosterone activation over the course of HF progression. CONCLUSIONS: Excessive dietary sodium restriction particularly in early stage HF results in early aldosterone activation, while normal and excess sodium intake are associated with delayed or suppressed activation. These findings warrant evaluation in humans to determine if dietary sodium manipulation, particularly during early stage HF, may have a significant impact on neuroendocrine disease progression.

Echocardiographic variables after left ventricular assist device implantation associated with adverse outcome.

BACKGROUND: Operative mortality after left ventricular assist device (LVAD) implantation is heavily influenced by patient selection and the technical difficulty of surgery. However, how we treat our patients and LVAD setting may affect the patient outcome beyond this period. We postulated that the presence of echocardiographic variables 1 month after surgery suggesting appropriate degree of LV unloading and an adequate forward flow would be important in determining clinical outcomes after the initial successful LVAD implantation. METHODS AND RESULTS: We retrospectively analyzed various variables in echocardiographic examinations performed 30 days after LVAD implant in 76 consecutive patients receiving continuous flow device for their association with a compound end point (90-day mortality, readmission for heart failure, or New York Heart Association class III or higher at the end of the 90-day period). The echocardiographic associations examined included estimated LVAD flow, with and without native LV contribution, interventricular septal position, the status of aortic valve opening, an estimated left atrial pressure (ELAP), the mitral flow E-wave deceleration time, and the ratio of deceleration time to E-wave velocity (mitral deceleration index [MDI]). Four patients died during the 30- to 90-day period, 6 patients were readmitted for heart failure, and 25 patients were considered to have New York Heart Association class III or higher at the end of the 90-day period. Variables associated with adverse outcome included increased ELAP (odds ratio, 1.30 [1.16-1.48]; P<0.0001), MDI <2 ms/[cm/s] (odds ratio, 4.4 implantation [1.22-18]; P=0.02) and decreased tricuspid lateral annulus velocity (odds ratio, 0.70 implantation [0.48-0.95]; P=0.02). A leftward deviation of interventricular septum was associated with a worse outcome (odds ratio, 3.03 implantation [1.21-13.3]; P=0.01). CONCLUSIONS: Mortality and heart failure after LVAD surgery appear to be predominantly determined by echocardiographic evidence of inefficient unloading of the left ventricle and persistence of right ventricular dysfunction. Increased estimated LA pressure and short MDI are associated with worse mid term outcome. Leftward deviation of the septum is associated with worse outcome as well.

Biomarker responses during and after treatment with nesiritide infusion in patients with decompensated chronic heart failure.

BACKGROUND: Objective methods to assess the adequacy of medication therapy for patients with advanced heart failure are lacking. Serial measurements of biomarkers might be beneficial. Therapy guided by N-terminal pro-B-type natriuretic peptide (NT-proBNP) might be helpful because NT-proBNP should be lowered by therapies that decrease endogenous BNP secretion. METHODS: NT-proBNP and BNP were measured in a nonconsecutive patient cohort receiving clinically indicated intravenous nesiritide. Blood samples were drawn before, at 6 and 24 h during, and at 6 h after infusion. A reduction in NT-proBNP was defined as a decrease from baseline during infusion ("infusion responders") of >3 SD of the variability of the assay measurement (approximately 20%). Patients with decreases >20% in both NT-pro BNP and BNP at 6 h post infusion were designated "biochemical responders". RESULTS: Forty patients [27 males; mean (SE) age, 68 (2) years; mean (SE) left ventricular ejection fraction, 25 (1.4)%] were studied. All patients improved clinically. Overall, the changes in NT-proBNP were a 18 (4.6)% [mean (SE)] and 19.8% (median) decrease from baseline at 24 h of infusion and a 22 (6.0)% and 17.8% decrease at 6 h post infusion (P <0.001 compared with baseline). In a large number of patients, decreases in NT-proBNP were, however, within the variability of the assay. Subgroup analysis showed that 22 of 40 patients were infusion responders with a >20% decrease from baseline in NT-proBNP during nesiritide infusion, whereas only 12 patients were biochemical responders with >20% decreases from baseline postinfusion for both NT-proBNP and BNP. CONCLUSIONS: In this study, many patients had decreased NT-proBNP and BNP values after therapy with nesiritide, but the majority of patients did not demonstrate biochemically significant decreases in analytes despite a clinical response. Until we know more about the responses of natriuretic peptides to therapies such as nesiritide, a strategy of monitoring NT-proBNP and BNP to guide therapy cannot be universally advocated.

Natriuretic and antialdosterone actions of chronic oral NEP inhibition during progressive congestive heart failure.

BACKGROUND: Neutral endopeptidase (NEP) degrades atrial natriuretic peptide (ANP) that via cyclic guanosine monophosphate (cGMP) is natriuretic and aldosterone-inhibiting. We hypothesized that chronic oral NEP inhibition (NEPI), initiated in early experimental congestive heart failure (CHF), would delay onset of decreases in sodium excretion during the progression of CHF and, in the severe phase, suppress aldosterone activation and reduce the magnitude of sodium retention. We also hypothesized that chronic NEPI during progressive CHF (PCHF) would improve the natriuretic response to acute volume expansion. METHODS: In a novel canine model that progresses over 38 days from early to moderate and finally severe CHF, we defined the actions of chronic NEPI (candoxatril, 10 mg/kg, orally, twice a day) upon cardiorenal and neurohumoral function as well as the clinical well being of treated and untreated dogs in CHF. RESULTS: From baseline through the moderate phase of CHF, NEPI maintained sodium excretion. In contrast, in moderate CHF, sodium excretion was reduced compared to the early phase in the controls. In severe CHF, sodium excretion was higher with NEPI compared to control. Chronic NEPI also resulted in lower plasma aldosterone as compared to controls. In severe CHF, the natriuretic response to acute saline volume expansion was enhanced with oral NEPI as compared to control. CONCLUSION: This study supports the conclusion that chronic oral NEPI delays the onset of reduction in sodium excretion during the transition from early to severe CHF in this model of PCHF. This therapeutic strategy also improved the natriuretic response to acute volume expansion in severe CHF while enhancing ANP and suppressing aldosterone activation. Thus, these studies demonstrated a selective renal and adrenal action of chronic NEPI in heart failure indicating a therapeutic potential.

Mitral regurgitation in patients with advanced systolic heart failure.

BACKGROUND: Mitral regurgitation (MR) may develop in patients with advanced systolic congestive heart failure (CHF) without organic mitral valve disease and contribute to worsening symptoms and survival. Surgical mitral annuloplasty improves symptoms in patients with advanced CHF, and percutaneous approaches to mitral annuloplasty are being developed. Our objective was to define the prevalence, clinical correlates, and prognostic implications of functional MR and the use of mitral annuloplasty in patients with advanced systolic CHF evaluated in a heart failure clinic. METHODS AND RESULTS: We reviewed clinical, echocardiographic, and survival data from all patients with advanced systolic CHF (New York Heart Association class III or IV; ejection fraction