Cardiac MR elastography for quantitative assessment of elevated myocardial stiffness in cardiac amyloidosis.

PURPOSE: To evaluate if cardiac magnetic resonance elastography (MRE) can measure increased stiffness in patients with cardiac amyloidosis. Myocardial tissue stiffness plays an important role in cardiac function. A noninvasive quantitative imaging technique capable of measuring myocardial stiffness could aid in disease diagnosis, therapy monitoring, and disease prognostic strategies. We recently developed a high-frequency cardiac MRE technique capable of making noninvasive stiffness measurements. MATERIALS AND METHODS: In all, 16 volunteers and 22 patients with cardiac amyloidosis were enrolled in this study after Institutional Review Board approval and obtaining formal written consent. All subjects were imaged head-first in the supine position in a 1.5T closed-bore MR imager. 3D MRE was performed using 5 mm isotropic resolution oblique short-axis slices and a vibration frequency of 140 Hz to obtain global quantitative in vivo left ventricular stiffness measurements. The median stiffness was compared between the two cohorts. An octahedral shear strain signal-to-noise ratio (OSS-SNR) threshold of 1.17 was used to exclude exams with insufficient motion amplitude. RESULTS: Five volunteers and six patients had to be excluded from the study because they fell below the 1.17 OSS-SNR threshold. The myocardial stiffness of cardiac amyloid patients (median: 11.4 kPa, min: 9.2, max: 15.7) was significantly higher (P = 0.0008) than normal controls (median: 8.2 kPa, min: 7.2, max: 11.8). CONCLUSION: This study demonstrates the feasibility of 3D high-frequency cardiac MRE as a contrast-agent-free diagnostic imaging technique for cardiac amyloidosis. LEVEL OF EVIDENCE: 2 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2017;46:1361-1367.

Shorter minimum p-wave duration is associated with paroxysmal lone atrial fibrillation.

BACKGROUND AND PURPOSE: Prolonged P-wave dispersion (PWD) and P-wave duration (PWdur) have been found to be associated with common atrial fibrillation (AF), but the association of P-wave indices with lone atrial fibrillation (LAF) is unclear. METHODS: We enrolled 61 paroxysmal LAF cases and 150 controls without AF. P-wave indices were measured from a 12-lead ECG. Multivariable logistic regression was used to assess the association between P-wave indices and LAF. RESULTS: PWD was longer in LAF patients (median, IQR; 54.1 [42.9-63.2] ms) than controls (46.0 [38.5-57.7] ms), P=0.03. MinPWdur was shorter in LAF patients (60.5 [50.7-72.6] ms) than controls (66.0 [55.5-76.4] ms), P=0.03. In multivariable models, only the association between shorter minPWdur and LAF remained statistically significant (OR [95% CI] per tertile increment in minPWdur, 0.64 [0.42-0.95], P=0.03). CONCLUSIONS: Unlike common AF, paroxysmal LAF is independently associated with shorter minPWdur. This finding suggests that both shorter and prolonged PWdur may be associated with increased risk of AF.

Usefulness of Atrial Fibrillation as a Marker for Adverse Cardiovascular Outcomes in Both Primary and Secondary Prevention in Patients With Implantable Cardioverter-Defibrillators.

Whether the risk factors for cardiovascular (CV) outcomes are different in primary versus secondary prevention implantable cardioverter-defibrillator (ICD) patients is unclear. We sought to identify predictors of CV outcomes in ICD recipients for primary (G1) versus secondary prevention (G2). Consecutive patients who had ICD implanted during August 2005 to December 2009 were included. The primary outcome was a composite of appropriate shock, acute coronary syndrome, ischemic stroke, coronary revascularization, heart failure exacerbation, CV hospitalization, or all-cause death. We used Cox proportional hazards model and a stepwise selection method to fit the most parsimonious model to predict the primary outcome in all patients and separately for G1 and G2 patients. We followed 223 (184 G1 and 39 G2, mean age 61 years) patients through December 31, 2012; 141 (63.2%) developed the primary outcome. In all patients, atrial fibrillation (AF; hazard ratio 6.72, 95% CI 4.20 to 10.75; p <0.001), use of antiarrhythmic drug (1.55, 1.02 to 2.36; p = 0.04), and lower estimated glomerular filtration rate (0.99, 0.98 to 0.997; p = 0.01) were associated with increased risk of the primary outcome; the attributable risks were 21.6%, 16.0%, and 15.9%, respectively. In G1, AF, hypertension, and lower estimated glomerular filtration rate were associated with increased risk, whereas in G2, AF, use of antiarrhythmic drug, and nonischemic cardiomyopathy were associated with increased risk. In conclusion, although risk factors are different for primary and secondary prevention patients, AF is a strong and consistent risk factor for adverse outcomes in both populations.

Amino acid substitutions of quinolone resistance determining regions in GyrA and ParC associated with quinolone resistance in Acinetobacter baumannii and Acinetobacter genomic species 13TU.

BACKGROUND AND PURPOSE: Amino acid substitutions in GyrA and ParC are associated with resistance to quinolones in Acinetobacter baumannii (A baumannii), but this association is rarely elucidated in Acinetobacter genomic species (AGS) 13TU. This study aims to compare the association of amino acid substitutions in GyrA and ParC with quinolone resistance in A baumannii and AGS 13TU in Taiwan. METHODS: Eleven representative strains of A baumannii and 13 strains of AGS 13TU were selected from 402 bacteremic isolates. The sequences of quinolone resistance determining regions of gyrA and parC were determined. Minimal inhibitory concentrations (MICs) of nalidixic acid, ciprofloxacin, levofloxacin and moxifloxacin were determined by agar dilution method. RESULTS: Ser83Leu substitution in GyrA in A baumannii (one strain) was associated with resistance to all tested quinolones. This substitution plus a Ser80Leu or Ser80Tyr in ParC in A baumannii (four strains) and AGS 13TU (two strains) were associated with higher MICs of all quinolones. All but one quinolone MICs of A baumannii (one strain) and AGS 13TU (two strains) carrying a single substitution Ser56Asn in ParC remained in the susceptibility breakpoint. The Ser83Leu substitution in GyrA, even with additional Ser56Asn substitution in ParC, was associated with resistance to only nalidixic acid, but not other newer quinolones in AGS 13TU (two strains). CONCLUSION: A baumannii and AGS 13TU possessed similar quinolone resistance associated with amino acid substitutions in GyrA and ParC. Further study with more strains is needed to determine whether a single Ser83Leu substitution in GyrA was associated with a high level of quinolone MIC only in A baumannii, but not in AGS 13TU.