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Occupational doses from fluoroscopy-guided interventional procedures are the highest ones registered among medical staff using x-rays. The aim of the present study was to evaluate the order of magnitude of cancer risk caused by professional radiation exposure in modern invasive cardiology practice. From the dosimetric Tuscany Health Physics data bank of 2006, we selected dosimetric data of the 26 (7 women, 19 men; age 46 ± 9 years) workers of the cardiovascular catheterization laboratory with effective dose >2 mSv. Effective dose (E) was expressed in milliSievert, calculated from personal dose equivalent registered by the thermoluminescent dosimeter, at waist or chest, under the apron, according to the recommendations of National Council of Radiation Protection. Lifetime attributable risk of cancer was estimated using the approach of Biological Effects of Ionizing Radiation 2006 report VII. Cardiac catheterization laboratory staff represented 67% of the 6 workers with yearly exposure >6 mSv. Of the 26 workers with 2006 exposure >2 mSv, 15 of them had complete records of at least 10 (up to 25) consecutive years. For these 15 subjects having a more complete lifetime dosimetric history, the median individual effective dose was 46 mSv (interquartile range = 24-64). The median risk of (fatal and nonfatal) cancer (Biological Effects of Ionizing Radiation 2006) was 1 in 192 (interquartile range = 1 in 137-1 in 370). Cumulative professional radiological exposure is associated with a non-negligible Lifetime attributable risk of cancer for the most exposed contemporary cardiac catheterization laboratory staff.

Patients with dilated cardiomyopathy whose symptoms and cardiac function have recovered often ask whether their medications can be stopped. The safety of withdrawing treatment in this situation is unknown. We did an open-label, pilot, randomised trial to examine the effect of phased withdrawal of heart failure medications in patients with previous dilated cardiomyopathy who were now asymptomatic, whose left ventricular ejection fraction (LVEF) had improved from less than 40% to 50% or greater, whose left ventricular end-diastolic volume (LVEDV) had normalised, and who had an N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) concentration less than 250 ng/L. Patients were recruited from a network of hospitals in the UK, assessed at one centre (Royal Brompton and Harefield NHS Foundation Trust, London, UK), and randomly assigned (1:1) to phased withdrawal or continuation of treatment. After 6 months, patients in the continued treatment group had treatment withdrawn by the same method. The primary endpoint was a relapse of dilated cardiomyopathy within 6 months, defined by a reduction in LVEF of more than 10% and to less than 50%, an increase in LVEDV by more than 10% and to higher than the normal range, a two-fold rise in NT-pro-BNP concentration and to more than 400 ng/L, or clinical evidence of heart failure, at which point treatments were re-established. The primary analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT02859311. Between April 21, 2016, and Aug 22, 2017, 51 patients were enrolled. 25 were randomly assigned to the treatment withdrawal group and 26 to continue treatment. Over the first 6 months, 11 (44%) patients randomly assigned to treatment withdrawal met the primary endpoint of relapse compared with none of those assigned to continue treatment (Kaplan-Meier estimate of event rate 45·7% [95% CI 28·5–67·2]; p=0·0001). After 6 months, 25 (96%) of 26 patients assigned initially to continue treatment attempted its withdrawal. During the following 6 months, nine patients met the primary endpoint of relapse (Kaplan-Meier estimate of event rate 36·0% [95% CI 20·6–57·8]). No deaths were reported in either group and three serious adverse events were reported in the treatment withdrawal group: hospital admissions for non-cardiac chest pain, sepsis, and an elective procedure. Many patients deemed to have recovered from dilated cardiomyopathy will relapse following treatment withdrawal. Until robust predictors of relapse are defined, treatment should continue indefinitely. British Heart Foundation, Alexander Jansons Foundation, Royal Brompton Hospital and Imperial College London, Imperial College Biomedical Research Centre, Wellcome Trust, and Rosetrees Trust.

Antibody-Associated Cardiac Amyloid RegressionThe investigators describe antibodies that bound amyloid in three patients with transthyretin amyloidosis. Spontaneous regression of cardiomyopathy occurred in all three patients.

Cardiac amyloidosis (CA) may affect all cardiac structures, including the valves. From 423 patients undergoing a diagnostic workup for CA we selected 2 samples of 20 patients with amyloid transthyretin (ATTR-) or light-chain (AL-) CA, and age- and sex-matched controls. We chose 31 echocardiographic items related to the mitral, aortic and tricuspid valves, giving a value of 1 to each abnormal item. Patients with ATTR–CA displayed more often a shortened/hidden and restricted posterior mitral valve leaflet (PMVL), thickened mitral chordae tendineae and aortic stenosis than those with AL–CA, and less frequent PMVL calcification than matched controls. Score values were 15.8 (13.6–17.4) in ATTR–CA, 11.0 (9.3–14.9) in AL–CA, 12.8 (11.1–14.4) in ATTR–CA controls, and 11.0 (9.1–13.0) in AL–CA controls (p = 0.004 for ATTR- vs. AL–CA, 0.009 for ATTR–CA vs. their controls, and 0.461 for AL–CA vs. controls). Area under the curve values to diagnose ATTR–CA were 0.782 in patients with ATTR–CA or matched controls, and 0.773 in patients with LV hypertrophy. Patients with ATTR–CA have a prominent impairment of mitral valve structure and function, and higher score values. The valve score may help identify patients with ATTR–CA among patients with CA or unexplained hypertrophy.

IntroductionCardiovascular magnetic resonance (CMR) and extracellular volume (ECV) mapping can quantify amyloid burden in patients with cardiac amyloidosis. At present, there is a paucity of data on tracking changes in amyloid deposition in both untreated and treated cohorts with transthyretin (ATTR) disease. Our aim was to use CMR and ECV mapping to characterise the natural history of untreated ATTR amyloidosis, measure the response to treatment with patisiran, and correlate ECV with changes in structural and functional cardiac parameters.Materials and MethodsIn total, 119 untreated patients and 70 patients treated with patisiran were assessed with serial biomarkers, echocardiography and CMR with ECV mapping at baseline, 1 year, and 2 years where possible. CMR response was categorized by changes in ECV as either: disease progression (≥3% increase), stable (<3% change) or regression (≥3% decrease).ResultsIn untreated patients, 57% had disease progression at 1 year which significantly increased to 70% at 2 years (p<0.05). Mean increase in ECV of 4.0% after 1 year and 6.8% after 2 years was observed, and associated with significant worsening in biomarkers, ventricular wall thickness and global longitudinal strain at each timepoint. Left ventricular (LV) ejection fraction, indexed stroke volume and LV mass significantly worsened after 2 years. Following treatment with patisiran, no significant difference in mean ECV was observed at both timepoints. Disease stability was observed in 66% and 64% of patients and ECV regression observed in 17% and 21% of patients after 1 and 2 years of treatment with patisiran respectively. In all patients followed up at 1 year (n=160), reduction in ECV was not associated with a change in biomarkers or imaging parameters. ECV stability or progression was associated with significant worsening in wall thickness, LV volumes and biventricular longitudinal function.ConclusionCMR with ECV mapping demonstrates that cardiac amyloid deposition increases over time in ATTR amyloidosis and is associated with worsening cardiac structure and function. Although treatment with patisiran is associated with disease stability in the majority, stabilisation of cardiac structural and functional parameters is only observed in those with ECV regression, highlighting the importance of achieving a significant treatment response.AcknowledgementsI would like to thank Dr Ana Martinez-Naharro for her contributions to this project, the supervision of both Professor Julian Gillmore and Professor Marianna Fontana, the staff at the CMR unit at the NAC and finally the patients who underwent CMR throughout the study period.

Abnormalities in endothelium-dependent vasodilation may be detected in arteries before the development of overt atherosclerosis, and their presence may predict stress-induced ischemia as assessed by ST-segment depression and/or perfusion defects. Brachial artery ultrasound during reactive hyperemia is a noninvasive method of assessing peripheral vasomotion, measured by flow-mediated vasodilation (FMD). The purpose of the current study was to assess whether endothelium-dependent FMD of the brachial artery, by ultrasound imaging, predicts the presence of angiographically assessed coronary artery disease (CAD). One hundred ninety-eight in-hospital patients (age, 59 ± 9 years; 78 women) with chest pain syndrome and without previous myocardial infarction or revascularization procedures were enrolled in the present study. All of the patients, at testing time, were not receiving nitrate therapy and underwent, on different days, coronary angiography and endothelium-dependent FMD testing of the brachial artery by high-resolution ultrasound. The result of the flow-mediated dilation (%FMD) is defined as the percent change in the internal diameter of the brachial artery during reactive hyperemia related to baseline. A coronary vessel was considered to have a significant obstruction if its diameter was narrowed by 50% or more on quantitative computer-assisted analysis. A prognostically validated angiographic Duke score (from 0 = normal to 100 = severe left main disease) was calculated. The %FMD was lower in patients with (n = 69) compared with those without (n = 129) CAD (4.64% ± 4.36% vs 7.39% ± 5.68%; P = .01). By multivariate analysis, the %FMD ( P = .01; odds ratio [OR], 1.13; 95% confidence interval [CI], 1.05 to 1.23), male sex ( P = .01; OR, 3.47; 95% CI, 1.64 to 7.36), and cigarette smoking habit ( P < .01; OR, 4.00; 95% CI, 2.50 to 6.35) were independent predictors of CAD. %FMD was poorly albeit significantly correlated with the severity of CAD (%FMD Duke score, P < .01, r = −0.25). The receiver operator characteristic curve showed the %FMD optimal cutoff value as ≤8.84, with sensitivity of 90%, specificity of 37%, negative predictive value of 90%, and positive predictive value of 43%. In patients with chest pain, a depressed FMD of the brachial artery was a sensitive indicator of CAD, but it showed poor specificity, and it appeared to be unable to predict both the extent and the severity of angiographically assessed CAD.

Somatic DNA damage has been linked to coronary artery disease (CAD). However, whether genetic instability is linked to CAD per se or to concomitant potentially genotoxic metabolic and pharmacological factors remains still unclear. The aim of this study was to evaluate the determinants of somatic DNA damage in a large population of patients undergoing coronary angiography. A total of 278 in-hospital patients (215 men, age 61.8+/-0.7 years) were studied by using micronucleus assay (MN) in human lymphocytes, which is one of the most commonly used biomarker for somatic DNA damage. Significant CAD (>50% diameter stenosis) was present in 210 patients (179 men, age 62.3+/-0.7 years). Normal coronary arteries were observed in 68 patients (35 men, age 60.2+/-1.7 years). There were no significant differences between patients with and without CAD, but patients with multivessel disease had the highest MN levels (P=0.01). MN frequency was also found significantly higher in presence of type 2 diabetes (P<0.0001), dyslipidemia (P=0.048) and nitrate therapy (P=0.0002). A significant additive effect was also observed between diabetes and nitrate therapy (P=0.02). On multivariate logistic regression analysis, diabetes [odds ratio=6.8 (95% confidence interval, 3.2-14.5), P<0.0001] and nitrate therapy [odds ratio=2.4 (95% confidence interval, 1.3-4.7), P=0.01] remained the only significant determinants for the 50th percentile of MN (>12 per thousand). These results indicated that diabetes and, to a lesser extent, chronic nitrate therapy are major determinants of somatic DNA instability in patients with CAD. DNA damage might represent an additional pathogenetic dimension and a possible therapeutic target in the still challenging management of coronary artery disease concerning diabetics.

A 52-year old female cardiologist with 16 year radiation exposure in Cath Lab as an interventional cardiologist developed a multifocal papillary thyroid carcinoma. Dosimetric (below apron) cumulative exposure totalled 56 mSv, corresponding to 2,800 chest radiographs. The patient also carried genetic polymorphisms of genes (XRCC1 and XRCC3) involved in DNA repair, increasing the cancer risk after ionizing radiation exposure. Dose optimization and diligent radioprotection are essential to minimize cancer risk in professionally exposed cardiologist. Good dosimetric practice is essential to establish a legally plausible cause-effect relationship between exposure and damage.

Papillary thyroid carcinoma of an interventional cardiologist. A case report.

Endothelial function is routinely assessed with high frequency ultrasound of the brachial artery. Fixed time points (1' post-occlusion and 3' post-nitrate) are commonly used to assess dynamic changes in brachial artery diameter. The underlying assumption is the lack of variability in temporal response to both endothelium-dependent and -independent stimuli. To evaluate the temporal course of endothelium-dependent (flow-mediated) and endothelium-independent (nitrate-induced) vasodilation of the brachial artery in patients with coronary artery disease (CAD) using high resolution (10 MHz) ultrasound. Thirty-seven patients with angiographically assessed CAD were prospectively enrolled in the study. End-diastolic, two-dimensional, long axis ultrasonographic images of the brachial artery were digitally stored on-line every 10 s, from baseline up to 4' during flow-mediated and up to 7' during 300 micrograms sublingual nitrate-induced vasodilation of the brachial artery. The mean percent endothelium-dependent flow-mediated maximal dilation (FMD) measured at 60 s was lower than the mean peak FMD (4.8 +/- 4.1 vs. 6.6 +/- 5.2%; p < 0.01). By 60 s only eight patients (35%) reached their maximum FMD response. The mean time to reach peak FMD was 87 +/- 33 s. The mean time for the peak nitrate dilation was 291 +/- 73 s. The peak nitrate-induced percent dilation was higher than that measured at 3 min (12.2 +/- 6.7 vs. 5.4 +/- 4.5%; p < 0.001). By 190 s, only four patients (11%) reached their maximum nitrate response. The routinely used measurement time points for evaluation of FMD and endothelium-independent vasodilation may not be adequate to detect the peak responses of individual patients with CAD.