Person:

Steigner, Michael

Background: We aimed to assess the feasibility of 3 dimensional (3D) respiratory and ECG gated, gadolinium enhanced magnetic resonance angiography (MRA) on a 3 Tesla (3 T) scanner for imaging pulmonary veins (PV) and left atrium (LA). The impact of heart rate (HR) and rhythm irregularity associated with atrial fibrillation (AF) on image and segmentation qualities were also assessed. Methods: 101 consecutive patients underwent respiratory and ECG gated (ventricular end systolic window) MRA for pre AF ablation imaging. Image quality (assessed by PV delineation) was scored as 1 = not visualized, 2 = poor, 3 = good and 4 = excellent. Segmentation quality was scored on a similar 4 point scale. Signal to noise ratios (SNRs) were calculated for the LA, LA appendage (LAA), and PV. Contrast to noise ratios (CNRs) were calculated between myocardium and LA, LAA and PV, respectively. Associations between HR/rhythm and quality metrics were assessed. Results: 35 of 101 (34.7%) patients were in AF at time of MRA. 100 (99%) patients had diagnostic studies, and 91 (90.1%) were of good or excellent quality. Overall, mean ± standard deviation (SD) image quality score was 3.40 ± 0.69. Inter observer agreement for image quality scores was substantial, (kappa = 0.68; 95% confidence interval (CI): 0.46, 0.90). Neither HR adjusting for rhythm [odds ratio (OR) = 1.03, 95% CI = 0.98,1.09; p = 0.22] nor rhythm adjusting for HR [OR = 1.25, 95% CI = 0.20, 7.69; p = 0.81] demonstrated association with image quality. Similarly, SNRs and CNRs were largely independent of HR after adjusting for rhythm. Segmentation quality scores were good or excellent for 77.3% of patients: mean ± SD score = 2.91 ± 0.63, and scores did not significantly differ by baseline rhythm (p = 0.78). Conclusions: 3D respiratory and ECG gated, gadolinium enhanced MRA of the PVs and LA on a 3 T system is feasible during ventricular end systole, achieving high image quality and high quality image segmentation when imported into electroanatomic mapping systems. Quality is independent of HR and heart rhythm for this free breathing, radiation free, alternative strategy to current MRA or CT based approaches, for pre AF ablation imaging of PVs and LA.

Background: Sleep apnea (SA) is associated with an increased risk of atrial fibrillation (AF). We sought to determine the effect of SA on cardiac structure in patients with AF, whether therapy for SA was associated with beneficial cardiac structural remodelling, and whether beneficial cardiac structural remodelling translated into a reduced risk of recurrence of AF after pulmonary venous isolation (PVI). Methods and Results: A consecutive group of 720 patients underwent a cardiac magnetic resonance study before PVI. Patients with SA (n=142, 20%) were more likely to be male, diabetic, and hypertensive and have an increased pulmonary artery pressure, right ventricular volume, atrial dimensions, and left ventricular mass. Treated SA was defined as duration of continuous positive airway pressure therapy of >4 hours per night. Treated SA patients (n=71, 50%) were more likely to have paroxysmal AF, a lower blood pressure, lower ventricular mass, and smaller left atrium. During a follow‐up of 42 months, AF recurred in 245 patients. The cumulative incidence of AF recurrence was 51% in patients with SA, 30% in patients without SA, 68% in patients with untreated SA, and 35% in patients with treated SA. In a multivariable model, the presence of SA (hazard ratio 2.79, CI 1.97 to 3.94, P<0.0001) and untreated SA (hazard ratio 1.61, CI 1.35 to 1.92, P<0.0001) were highly associated with AF recurrence. Conclusions: Patients with SA have an increased blood pressure, pulmonary artery pressure, right ventricular volume, left atrial size, and left ventricular mass. Therapy with continuous positive airway pressure is associated with lower blood pressure, atrial size, and ventricular mass, and a lower risk of AF recurrence after PVI.

Aims The impact of coronary computed tomographic angiography (CTA) on management of anomalous origin of the coronary artery arising from the opposite sinus (ACAOS) remains uncertain. We examined the prevalence, anatomical characterization, and outcomes of ACAOS patients undergoing CTA. Methods and results Among 5991 patients referred for CTA at two tertiary hospitals between January 2004 and June 2014, we identified 103 patients (1.7% prevalence) with 110 ACAOS vessels. Mean age was 52 years (range 5–83, 63% male), with 55% previously known ACAOS and 45% discovered on CTA. ACAOS subtypes included: 39% interarterial (n = 40 anomalous right coronary artery, n = 3 anomalous left coronary artery), 38% retroaortic, 15% subpulmonic, 5% prepulmonic, and 2% other. ACAOS patients were assessed for symptoms, ischaemic test results, revascularization, all-cause or cardiovascular (CV) death, and myocardial infarction. CTAs were reviewed for ACAOS course, take-off height and angle, length and severity of proximal narrowing, intramural course, and obstructive coronary artery disease (CAD). In follow-up (median 5.8 years), there were 20 surgical revascularizations and 3 CV deaths. After adjusting for obstructive CAD (n = 21/103, 20%), variables associated with ACAOS revascularization included the following: CV symptoms, proximal vessel narrowing ≥50%, length of narrowing >5.4 mm, and an interarterial course. Conclusion The prevalence of ACAOS on CTA was 1.7%, including 45% of cases discovered incidentally. CTA provided excellent characterization of ACAOS features associated with coronary revascularization, including the length and severity of proximal vessel narrowing.

The aim of this study was to investigate the association between major adverse cardiovascular events (MACEs) and inducible ischemia on regadenoson cardiac magnetic resonance (CMR) myocardial perfusion imaging (MPI) performed at 3.0 T. Regadenoson stress CMR MPI is increasingly used to assess patients with suspected ischemia; however, its value in patient prognostication and risk reclassification is only emerging. A total of 346 patients with suspected ischemia who were referred for regadenoson CMR were studied. The prognostic association of presence of inducible ischemia by CMR with MACEs was determined. In addition, we assessed the extent of net reclassification improvement by CMR beyond a clinical risk model. There were 52 MACEs during a median follow-up period of 1.9 years. Patients with inducible ischemia were fourfold more likely to experience MACEs (hazard ratio, 4.14, 95% confidence interval 2.37 to 7.24, p <0.0001). In the best overall model, presence of inducible ischemia conferred a 2.6-fold increased hazard for MACEs adjusted to known clinical risk markers (adjusted hazard ratio 2.59, 95% confidence interval 1.30 to 5.18, p = 0.0069). Patients with no inducible ischemia experienced a low rate of cardiac death and myocardial infarction (0.6% per patient-year), whereas those with inducible ischemia had an annual event rate of 3.2%. Net reclassification improvement across risk categories (low <5%, intermediate 5% to 10%, and high >10%) by CMR was 0.29 (95% confidence interval 0.15 to 0.44), and continuous net reclassification improvement was 0.58. In conclusion, in patients with clinical suspicion of myocardial ischemia, regadenoson stress CMR MPI provides robust risk stratification. CMR MPI negative for ischemia was associated with a very low annual rate of hard cardiac events. In addition, CMR MPI provides effective risk reclassification in a substantial proportion of patients.

Background

While pulmonary vein isolation (PVI) has become a mainstream therapy for selected patients with atrial fibrillation (AF), late recurrent AF is common and its risk factors remain poorly defined. The purpose of our study was to test the hypothesis that reduced left atrial passive emptying function (LAPEF) as determined by cardiac magnetic resonance (CMR) has a strong association with late recurrent AF following PVI.

Methods and Results

346 AF patients referred for CMR PV mapping prior to PVI were included. Maximum LA volumes (VOLmax) and volumes before atrial contraction (VOLbac) were measured; LAPEF was calculated as (VOLmax − VOLbac)/VOLmax × 100. Kaplan-Meier curves were constructed to determine late recurrent AF stratified by LAPEF quintile. Cox proportional hazards regression was used to adjust for known markers of recurrence. Over a median follow-up of 27 months, 124 patients (35.8%) experienced late recurrent AF. Patients with recurrence were more likely to have non-paroxysmal AF (75.8% vs. 51.4%, P<0.01), higher mean VOLmax (60.2 ml/m2 vs. 52.8 ml/m2, P<0.01), and lower mean LAPEF (19.1% vs. 26.0%, P<0.01). Patients in the lowest LAPEF quintile were at highest risk of developing recurrent AF (two-year recurrence lowest vs. highest: 60.5% vs. 17.3%, P<0.01). After adjusting for known predictors of recurrence, patients with low LAPEF remained significantly more likely to recur (HR lowest vs. highest quintile = 3.92, 95% CI 2.01–7.65).

Conclusion

We found a strong association between LAPEF and recurrent AF after PVI that persisted after multivariable adjustment.

Purpose

Coronary Computed Tomography Angiography (CCTA) contrast opacification gradients, or Transluminal Attenuation Gradients (TAG) offer incremental value to predict functionally significant lesions. This study introduces and evaluates an automated gradients software package that can potentially supplant current, labor-intensive manual TAG calculation methods.

Methods

All 60 major coronary arteries in 20 patients who underwent a clinically indicated single heart beat 320×0.5 mm detector row CCTA were retrospectively evaluated by two readers using a previously validated manual measurement approach and two additional readers who used the new automated gradient software. Accuracy of the automated method against the manual measurements, considered the reference standard, was assessed via linear regression and Bland-Altman analyses. Inter- and intra-observer reproducibility and factors that can affect accuracy or reproducibility of both manual and automated TAG measurements, including CAD severity and iterative reconstruction, were also assessed.

Results

Analysis time was reduced by 68% when compared to manual TAG measurement. There was excellent correlation between automated TAG and the reference standard manual TAG. Bland-Altman analyses indicated low mean differences (1 HU/cm) and narrower inter- and intra-observer limits of agreement for automated compared to manual measurements (25% and 36% reduction with automated software, respectively). Among patient and technical factors assessed, none affected agreement of manual and automated TAG measurement.

Conclusion

Automated 320×0.5 mm detector row gradient software reduces computation time by 68% with high accuracy and reproducibility.

Objectives

This study sought to determine feasibility and prognostic performance of stress cardiac magnetic resonance (CMR) in obese patients (body mass index [BMI] ≥30 kg/m2).

Background

Current stress imaging methods remain limited in obese patients. Given the impact of the obesity epidemic on cardiovascular disease, alternative methods to effectively risk stratify obese patients are needed.

Methods

Consecutive patients with a BMI ≥30 kg/m2 referred for vasodilating stress CMR were followed for major adverse cardiovascular events (MACE), defined as cardiac death or nonfatal myocardial infarction. Univariable and multivariable Cox regressions for MACE were performed to determine the prognostic association of inducible ischemia or late gadolinium enhancement (LGE) by CMR beyond traditional clinical risk indexes.

Results

Of 285 obese patients, 272 (95%) completed the CMR protocol, and among these, 255 (94%) achieved diagnostic imaging quality. Mean BMI was 35.4 ± 4.8 kg/m2, with a maximum weight of 200 kg. Reasons for failure to complete CMR included claustrophobia (n = 4), intolerance to stress agent (n = 4), poor gating (n = 4), and declining participation (n = 1). Sedation was required in 19 patients (7%; 2 patients with intravenous sedation). Sixteen patients required scanning by a 70-cm-bore system (6%). Patients without inducible ischemia or LGE experienced a substantially lower annual rate of MACE (0.3% vs. 6.3% for those with ischemia and 6.7% for those with ischemia and LGE). Median follow-up of the cohort was 2.1 years. In a multivariable stepwise Cox regression including clinical characteristics and CMR indexes, inducible ischemia (hazard ratio 7.5; 95% confidence interval: 2.0 to 28.0; p = 0.002) remained independently associated with MACE. When patients with early coronary revascularization (within 90 days of CMR) were censored on the day of revascularization, both presence of inducible ischemia and ischemia extent per segment maintained a strong association with MACE.

Conclusions

Stress CMR is feasible and effective in prognosticating obese patients, with a very low negative event rate in patients without ischemia or infarction.

Objectives

We aimed to identify the frequency, pattern, and prognostic significance of left ventricular (LV) late gadolinium enhancement (LGE) in patients with atrial fibrillation (AF).

Background

There are limited data on the presence, pattern, and prognostic significance of LV myocardial fibrosis in patients with AF. Late gadolinium enhancement during cardiac magnetic resonance (CMR) is a marker for myocardial fibrosis.

Methods

We studied a consecutive group of 664 patients without known prior myocardial infarction being referred for radiofrequency ablation of AF. CMR was requested to assess pulmonary venous anatomy.

Results

Overall, 73% were male, with an average age of 56 years, and an ejection fraction of 55±10%. Left ventricular LGE was found in 88 patients (13%). The endpoint was all-cause mortality, and in this cohort we observed 68 deaths over a median follow-up period of 42 months. On univariable analysis, age (HR 1.05, CI 1.03–1.08, LRχ2 15.2, p=0.0001), diabetes (HR 2.39, CI 1.41–4.09, LRχ210.3, p=0.001), a history of heart failure (HR 1.78, CI 1.09–2.91, LRχ2 5.37, p=0.02), left atrial dimension (HR 1.04, CI 1.01–1.08, LRχ2 6.47, p=0.01), presence of LGE (HR 5.08, CI 3.08–8.36, LRχ2 28.8, p<0.0001), and LGE extent (HR 1.15, CI 1.10–1.21, LRχ2 35.6, p<0.0001) provided the strongest association with mortality. The mortality rate was 8.1% per patient-years in patients with LGE vs. 2.3% patients without LGE. In the best overall multivariable model for mortality, age and the extent of LGE were independent predictors of mortality. Indeed, each 1% increase in LGE associated with a 15% increased risk of death.

Conclusions

In patients with AF, LV LGE is a frequent finding and is a powerful predictor of mortality.

Background

A recent large-scale clinical trial found that an initial invasive strategy does not improve cardiac outcomes beyond optimized medical therapy in patients with stable coronary artery disease (CAD). Novel methods to stratify at-risk patients may refine therapeutic decisions to improve outcomes.

Methods and Results

In a cohort of 815 consecutive patients referred for evaluation of myocardial ischemia, we determined the net reclassification improvement of the risk of cardiac death or nonfatal MI (MACE) incremental to clinical risk models, using guideline–based low (<1%), moderate (1–3%), and high (>3%) annual risk categories. In the whole cohort, inducible ischemia demonstrated strong association with MACE (hazard ratio 14.66, P<0.0001) with low negative event rates of MACE and cardiac death (0.6% and 0.4%). This prognostic robustness maintained in patients with prior CAD (hazard ratio 8.17, P<0.0001, and 1.3% and 0.6%, respectively). Adding inducible ischemia to the multivariable clinical risk model (age and prior CAD adjusted) improved discrimination of MACE (C-statistic 0.81 to 0.86, P=0.04; Adjusted hazard ratio 7.37, P<0.0001) and reclassified 91.5% of patients at moderate pre-test risk (65.7% to low risk; 25.8% to high risk) with corresponding changes in the observed event rates (0.3%/year and 4.9%/year, for low and high risk post-test, respectively). Categorical net reclassification index was 0.229 (95% CI 0.063–0.391). Continuous NRI was 1.11 (95% CI 0.81–1.39).

Conclusions

Stress CMR effectively reclassifies patient risk beyond standard clinical variables, specifically in patients at moderate to high pre-test clinical risk and in patients with prior CAD.

Background: Treatments for patients with myocardial ischemia in the absence of angiographic obstructive coronary artery disease are limited. In these patients, particularly those with diabetes mellitus, diffuse coronary atherosclerosis and microvascular dysfunction is a common phenotype and may be accompanied by diastolic dysfunction. Our primary aim was to determine whether ranolazine would quantitatively improve exercise‐stimulated myocardial blood flow and cardiac function in symptomatic diabetic patients without obstructive coronary artery disease. Methods and Results: We conducted a double‐blinded crossover trial with 1:1 random allocation to the order of ranolazine and placebo. At baseline and after each 4‐week treatment arm, left ventricular myocardial blood flow and coronary flow reserve (CFR; primary end point) were measured at rest and after supine bicycle exercise using 13N‐ammonia myocardial perfusion positron emission tomography. Resting echocardiography was also performed. Multilevel mixed‐effects linear regression was used to determine treatment effects. Thirty‐five patients met criteria for inclusion. Ranolazine did not significantly alter rest or postexercise left ventricular myocardial blood flow or CFR. However, patients with lower baseline CFR were more likely to experience improvement in CFR with ranolazine (r=−0.401, P=0.02) than with placebo (r=−0.188, P=0.28). In addition, ranolazine was associated with an improvement in E/septal e′ (P=0.001) and E/lateral e′ (P=0.01). Conclusions: In symptomatic diabetic patients without obstructive coronary artery disease, ranolazine did not change exercise‐stimulated myocardial blood flow or CFR but did modestly improve diastolic function. Patients with more severe baseline impairment in CFR may derive more benefit from ranolazine. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01754259.