Longitudinal analysis of thoracic aortic expansion in non-syndromic real-world patients.

Remodeling of the thoracic aorta is commonly seen and viewed as a precursor to an aortic aneurysm. However, while aneurysms have been shown to expand at a rate of approximately 1 mm annually, the expansion of the pre-aneurysmal aorta is poorly characterized, especially in relation to age, gender, and aortic size per se. We identified patients that had undergone echocardiography at least twice at a large university medical center. Diagnosis codes, medications, and blood test results were obtained from hospital records. Syndromic patients were excluded (e.g., Marfan's syndrome, bicuspid aortic valve). Final population comprised n = 24,928 patients (median age 61.2 years (inter-quartile range (IQR): 50.6-71.5); 55.8% males) that had undergone a median of 3 echocardiograms (2-4; range 2-27) during a median of 4.0 years (IQR: 2.3-6.2). Hypertension was present in 39.6% of patients and diabetes in 20.7%, median LV ejection fraction was 56.0% (IQR: 41.0-62.0). Aortic size measurements were analyzed in mixed models while clustering on individual patients. Mean expansion was determined for sinus of Valsalva as 1.93 (95% confidence interval; CI95: 1.87-1.99) mm per decade, and for ascending aorta as 1.76 (CI95: 1.70-1.82) mm per decade. Faster expansion was found in males, with larger aortic size, and younger age (p for interaction <0.05 for all). In conclusion, expansion of the thoracic aorta, in real world, non-syndromic patients, is slow and averages <2 mm per decade. This will help to inform management of this large patient group.

Impact of Chronic Kidney Disease on Outcomes in Transcatheter Aortic Valve Implantation.

INTRODUCTION: Chronic kidney disease (CKD) is a significant comorbidity in aortic stenosis (AS) patients. We examined the impact of baseline CKD, postoperative acute kidney injury (AKI) and CKD progression on clinical outcomes in patients who underwent transcatheter aortic valve implantation (TAVI). MATERIALS AND METHODS: Consecutive patients with severe AS who underwent TAVI were classified into CKD stages 1-2 (≥60 mL/min/1.72m2), 3 (30-59 mL/min/1.73m2) and 4-5 (<30 mL/min/1.73m2 or dialysis) based on estimated glomerular filtration rate (eGFR). Primary outcome was mortality and secondary outcomes included 1-year echocardiographic data on aortic valve area (AVA), mean pressure gradient (MPG) and aortic regurgitation (AR). RESULTS: A total of 216 patients were included. Higher eGFR was associated with lower overall mortality (adjusted hazards ratio [AHR] 0.981, 95% confidence interval [CI] 0.968-0.993, P = 0.002). CKD 4-5 were associated with significantly higher mortality from non-cardiovascular causes (P <0.05). Patients with CKD 3-5 had higher incidence of moderate AR than those with CKD 1-2 (P = 0.010); no difference in AVA and MPG was seen. AKI patients had higher mortality (P = 0.008), but the effect was attenuated on multivariate analysis (AHR 1.823, 95% CI 0.977-3.403, P = 0.059). Patients with CKD progression also had significantly higher mortality (AHR 2.969, 95% CI 1.373-6.420, P = 0.006). CONCLUSION: CKD in severe AS patients undergoing TAVI portends significantly higher mortality and morbidity. Renal disease progression impacts negatively on outcomes and identifies a challenging subgroup of patients for optimal management.

Clinical Updates on the Diagnosis and Management of Chronic Thromboembolic Pulmonary Hypertension.

INTRODUCTION: Chronic thromboembolic pulmonary hypertension (CTEPH) is a known sequela after acute pulmonary embolism (PE). It is a debilitating disease, and potentially fatal if left untreated. This review provides a clinically relevant overview of the disease and discusses the usefulness and limitations of the various investigational and treatment options. METHODS: A PubMed search on articles relevant to PE, pulmonary hypertension, CTEPH, pulmonary endarterectomy, and balloon pulmonary angioplasty were performed. A total of 68 articles were found to be relevant and were reviewed. RESULTS: CTEPH occurs as a result of non-resolution of thrombotic material, with subsequent fibrosis and scarring of the pulmonary arteries. Risk factors have been identified, but the underlying mechanisms have yet to be fully elucidated. The cardinal symptom of CTEPH is dyspnoea on exertion, but the diagnosis is often challenging due to lack of awareness. The ventilation/perfusion scan is recommended for screening for CTEPH, with other modalities (eg. dual energy computed tomography pulmonary angiography) also being utilised in expert centres. Conventional pulmonary angiography with right heart catheterisation is important in the final diagnosis of CTEPH. CONCLUSION: Operability assessment by a multidisciplinary team is crucial for the management of CTEPH, as pulmonary endarterectomy (PEA) remains the guideline recommended treatment and has the best chance of cure. For inoperable patients or those with residual disease post-PEA, medical therapy or balloon pulmonary angioplasty are potential treatment options.