CONTEMPORARY RADIATION DOSES IN INTERVENTIONAL CARDIOLOGY: A NATIONWIDE STUDY OF PATIENT DOSES IN FINLAND.

The amount of interventional procedures such as percutaneous coronary intervention (PCI), transcatheter aortic valve implantation (TAVI), pacemaker implantation (PI) and ablations has increased within the previous decade. Simultaneously, novel fluoroscopy mainframes enable lower radiation doses for patients and operators. Therefore, there is a need to update the existing diagnostic reference levels (DRLs) and propose new ones for common or recently introduced procedures. We sought to assess patient radiation doses in interventional cardiology in a large sample from seven hospitals across Finland between 2014 and 2016. Data were used to set updated national DRLs for coronary angiographies (kerma-air product (KAP) 30 Gycm2) and PCIs (KAP 75 cm2), and novel levels for PIs (KAP 3.5 Gycm2), atrial fibrillation ablation procedures (KAP 25 Gycm2) and TAVI (KAP 90 Gycm2). Tentative KAP values were set for implantations of cardiac resynchronization therapy devices (CRT, KAP 22 Gycm2), electrophysiological treatment of atrioventricular nodal re-entry tachycardia (6 Gycm2) and atrial flutter procedures (KAP 16 Gycm2). The values for TAVI and CRT device implantation are published for the first time on national level. Dose from image acquisition (cine) constitutes the major part of the total dose in coronary and atrial fibrillation ablation procedures. For TAVI, patient weight is a good predictor of patient dose.

Coronary heart disease and cortical thickness, gray matter and white matter lesion volumes on MRI.

Coronary heart disease (CHD) has been linked with cognitive decline and dementia in several studies. CHD is strongly associated with blood pressure, but it is not clear how blood pressure levels or changes in blood pressure over time affect the relation between CHD and dementia-related pathology. The aim of this study was to investigate relations between CHD and cortical thickness, gray matter volume and white matter lesion (WML) volume on MRI, considering CHD duration and blood pressure levels from midlife to three decades later. The study population included 69 elderly at risk of dementia who participated in the Cardiovascular Risk Factors, Aging and Dementia (CAIDE) study. CAIDE participants were examined in midlife, re-examined 21 years later, and then after additionally 7 years (in total up to 30 years follow-up). MRIs from the second re-examination were used to calculate cortical thickness, gray matter and WML volume. CHD diagnoses were obtained from the Finnish Hospital Discharge Register. Linear regression analyses were adjusted for age, sex, follow-up time and scanner type, and additionally total intracranial volume in GM volume analyses. Adding diabetes, cholesterol or smoking to the models did not influence the results. CHD was associated with lower thickness in multiple regions, and lower total gray matter volume, particularly in people with longer disease duration (>10 years). Associations between CHD, cortical thickness and gray matter volume were strongest in people with CHD and hypertension in midlife, and those with CHD and declining blood pressure after midlife. No association was found between CHD and WML volumes. Based on these results, long-term CHD seems to have detrimental effects on brain gray matter tissue, and these effects are influenced by blood pressure levels and their changes over time.

Alterations of motor cortical excitability and anatomy in Unverricht-Lundborg disease.

Unverricht-Lundborg disease is the most common form of progressive myoclonus epilepsies. In addition to generalized seizures, it is characterized by myoclonus, which usually is the most disabling feature of the disease. Classically, the myoclonus has been attributed to increased excitability of the primary motor cortex. However, inhibitory cortical phenomena have also been described along with anatomical alterations. We aimed to characterize the relationship between the excitability and anatomy of the motor cortex and their association with the severity of the clinical symptoms. Seventy genetically verified patients were compared with forty healthy controls. The symptoms were evaluated with the Unified Myoclonus Rating Scale. Navigated transcranial magnetic stimulation was applied to characterize the excitability of the primary motor cortex by determining the motor thresholds and cortical silent periods. In addition, the induced cortical electric fields were estimated using individual scalp-to-cortex distances measured from MRIs. A cortical thickness analysis was performed to elucidate possible disease-related anatomical alterations. The motor thresholds, cortical electric fields, and silent periods were significantly increased in the patients (P < 0.01). The silent periods correlated with the myoclonus scores (r = 0.48 to r = 0.49, P < 0.001). The scalp-to-cortex distance increased significantly with disease duration (r = 0.56, P < 0.001) and correlated inversely with cortical thickness. The results may reflect the refractory nature of the myoclonus and indicate a possible reactive cortical inhibitory mechanism to the underlying disease process. This is the largest clinical series on Unverricht-Lundborg disease and the first study describing parallel pathophysiological and structural alterations associated with the severity of the symptoms.