The purpose of this study was to determine the effect of patisiran on the cardiac amyloid load as measured by cardiac magnetic resonance and extracellular volume (ECV) mapping in cases of transthyretin cardiomyopathy (ATTR-CM).
 
  Administration of patisiran, a TTR-specific small interfering RNA (siRNA), has been shown to benefit neuropathy in patients with hereditary ATTR amyloidosis, but its effect on ATTR-CM remains uncertain.
 
  Patisiran was administered to 16 patients with hereditary ATTR-CM who underwent assessment protocols atthe UK National Amyloidosis Centre.  https://www.selleckchem.com/products/camostat-mesilate-foy-305.html  Twelve of those patients concomitantly received diflunisal as a "TTR-stabilizing"drug. Patients underwent serial monitoring using cardiac magnetic resonance, echocardiography, cardiac biomarkers,bone scintigraphy, and 6-min walk tests (6MWTs). Findings of amyloid types and extracellular volumes werecompared with those of 16 patients who were retrospectively matched based on cardiac magnetic resonance results.
 
  Patisiran was well tolerated. Median serum TTR knockdown among treated patients was 86% (interquartile range [IQR] 82% to 90%). A total of 82% of cases showed >80% knockdown. Patisiran therapy was typically associated with a reduction in ECV (adjusted mean difference between groups-6.2% [95% confidence interval [CI]-9.5% to-3.0%]; p=0.001) accompanied by a fall in N-terminal pro-B-type natriuretic peptide concentrations (adjusted mean difference between groups-1,342ng/l [95% CI-2,364 to-322]; p=0.012); an increase in 6MWT distances (adjusted mean differences between groups 169m [95%CI 57 to 2,80]; p=0.004) after 12months of therapy; and a median reduction in cardiac uptake by bone scintigraphy of 19.6% (IQR 9.8% to 27.1%).
 
  Reductions in ECV by cardiac magnetic resonance provided evidence for ATTR cardiac amyloid regression in a proportion of patients receiving patisiran.
 Reductions in ECV by cardiac magnetic resonance provided evidence for ATTR cardiac amyloid regression in a proportion of patients receiving patisiran.
  This study sought to determine whether the breast gland adipose tissue is associated with different rates of major adverse cardiac events (MACEs) in pre-menopausal women.
 
  To our knowledge, no study investigated the impact of breast adipose tissue infiltration on MACEs in pre-menopausal women.
 
  Prospective multicenter cohort study conducted on pre-menopausal women >40 years of age without cardiovascular disease and breast cancer at enrollment. The study started in January 2000 and ended in January 2009, and the end of the follow-up for the evaluation of MACEs was in January 2019. Participants underwent mammography to evaluate breast density and were divided into 4 groups according to their breast density. The primary endpoint was the probability of a MACE at 10 years of follow-up in patients staged for different breast deposition/adipose tissue deposition.
 
  The propensity score matching divided the baseline population of 16,763 pre-menopausal women, leaving 3,272 women according to the category of bre-Up [BRECARD]; NCT03779217).
 Among pre-menopausal women, a higher evidence of adipose tissue at the level of breast gland (lowest breast density, category A) versus higher breast density shows higher rates of MACEs. Therefore, the screening mammography could be proposed in overweight women to stage breast density and to predict MACEs. (Breast Density in Pre-menopausal Women Is Predictive of Cardiovascular Outcomes at 10 Years of Follow-Up [BRECARD]; NCT03779217).
  This study sought to investigate nonculprit plaque characteristics in patients with ST-segment elevation myocardial infarction (STEMI) presenting with plaque erosion (PE) and plaque rupture (PR). Pancoronary vulnerability was considered at nonculprit sites 1) the CLIMA study (NCT02883088) defined high-risk plaques with simultaneous presence of 4 optical coherence tomography (OCT) features (minimum lumen area<3.5mm
  ; fibrous cap thickness [FCT]<75μm; maximum lipid arc >180º; and macrophage accumulation); and 2) the presence of plaque ruptures or thin-cap fibroatheromas (TCFA).
 
  PE is a unique clinical entity associated with better outcomes than PR. There is limited evidence regarding pancoronary plaque characteristics of patients with culprit PE versus culprit PR.
 
  Between October 2016 and September 2018, 523 patients treated by 3-vessel OCT at the time of primary percutaneous intervention were included with 152 patients excluded from final analysis.
 
  Overall, 458 nonculprit plaques were identify explain better outcomes in these patients than in STEMI patients with culprit PR.
 STEMI patients with culprit PE have a limited pancoronary vulnerability that may explain better outcomes in these patients than in STEMI patients with culprit PR.
  This study sought to quantify and model conversion of a normal coronary artery calcium (CAC) scan to an abnormal CAC scan.
 
  Although the absence of CAC is associated with excellent prognosis, progression to CAC >0 confers increased risk. The time interval for repeated scanning remains poorly defined.
 
  This study included 3,116 participants from the MESA (Multi-Ethnic Study of Atherosclerosis) with baseline CAC=0 and follow-up scans over 10 years after baseline. Prevalence of incident CAC, defined by thresholds of CAC >0, CAC >10, or CAC >100, was calculated and time to progression was derived from a Weibull parametric survival model. Warranty periods were modeled as a function of sex, race/ethnicity, cardiovascular risk, and desired yield of repeated CAC testing. Further analysis was performed of the proportion of coronary events occurring in participants with baseline CAC=0 that preceded and followed repeated CAC testing at different time intervals.
 
  Mean participants' age was 58 ± 9 years, , and CAC >100 and its impact on missed versus detectable10-year coronary heart disease events. Beyond age, sex, race/ethnicity, diabetes also has a significant impact on the warranty period. The study suggests that evidence-based guidance would be to consider rescanning in 3 to 7 years depending on individual demographics and risk profile.
 100 and its impact on missed versus detectable 10-year coronary heart disease events. Beyond age, sex, race/ethnicity, diabetes also has a significant impact on the warranty period. The study suggests that evidence-based guidance would be to consider rescanning in 3 to 7 years depending on individual demographics and risk profile.