Aims Heart rate reduction therapy using ivabradine, a selective inhibitor of the funny current of the sinoatrial node, is widely used in the systolic heart failure cohort. However, the optimal target of heart rate remains controversial. The association between heart rate and 'overlap' between E-wave and A-wave in the pulse wave transmitral flow Doppler echocardiography might be a key to find the ideal heart rate in each individual. Methods and results We performed transthoracic echocardiography in patients with systolic heart failure, and the association between heart rate, deceleration time, and overlap length between E-wave and A-wave was assessed. In total, 368 patients with systolic heart failure (median 76 years old, 190 men, median ejection fraction 40%) were included. The measured overlap length was 35 (À72, 115) ms. Given the results of multiple linear regression analyses, we constructed a formula: estimated overlap length (ms) = À589 + 6.2 × heart rate (bpm) + 0.81 × deceleration time (ms), which had a good agreement with actually measured one (r = 0.62). The ideal heart rate, at which the overlap length is 'zero' and probably cardiac output is maximized, is calculated as follows: ideal heart rate (bpm) = 93-0.13 × deceleration time (ms). Conclusions We proposed a novel formula using deceleration time to estimate ideal heart rate that achieves a zero overlap between E-wave and A-wave in patients with systolic heart failure. Prognostic impact of the formula-guided heart rate optimization should be studied.
Small dense low-density lipoprotein cholesterol (sdLDL-C) and remnant-like particle cholesterol (RLP-C) are the novel atherosclerotic risk factors and might be strongly associated with inflammation. The basic evidence supports that sdLDL and RLP have some different mechanisms inducing an inflammatory response. Many studies have focused on the mechanism of inflammation of sdLDL-C or RLP-C per se, with limited data on the association between sdLDL-C and RLP-C in the real-world, population-based setting. Thus, the aim of this study was to investigate the association between sdLDL-C and RLP-C with inflammation. Methods: We examined the baseline cross-sectional data of participants from the Jichi Medical School-II Cohort Study. In total, 5,305 participants (2,439 men and 2,866 women) were included in this study. Results: Of all quartiles of sdLDL-C, the fourth had the highest high-sensitivity C-reactive protein (hs-CRP) level. Once adjusted for age, sex, smoking status, homeostasis model assessment of insulin resistance, antidyslipidemic and antihyperglycemic medication use, and RLP-C, sdLDL-C was significantly and positively associated with hs-CRP (geometric mean, 95% confidence interval (CI), 0.36 mg/L (0.34-0.38 mg/L), 0.37 mg/L (0.35-0.39 mg/L), 0.40 mg/L (0.37-0.42 mg/L) versus 0.44 mg/L (0.42-0.47 mg/L), P<0.001 for trend). After stratifying the participants into four sdLDL-C×four RLP-C categories, the group in the fourth sdLDL-C quartile and the forth RLP-C quartile had the highest hs-CRP level (geometric mean, 95% CI, 0.52 mg/L, 0.48-0.57 mg/L, interaction P = 0.75). Conclusions: SdLDL-C and RLP-C had different associations with inflammation. Our results support sdLDL-C as the potential novel factor of cardiovascular disease, independently of RLP-C.mended levels, cardiovascular events continue to occur. Therefore, we need to manage the novel target as the primary management, or the residual risk of CVD beyond lowering LDL-C 6) .Small dense low-density lipoprotein cholesterol (sdLDL-C) associated with triglyceride-rich lipoprotein (TRL) metabolism, and TRL-cholesterol, which is also known as remnant cholesterol, might be the better factors for the prediction of CVD than total LDL-C 5,[7][8][9][10][11] . In fact, elevated sdLDL-C and remnant Copyright©2020 Japan Atherosclerosis Society This article is distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License.
This study aimed to investigate the associations of body mass index (BMI) and metabolically unhealthy weight with all-cause mortality, cardiovascular disease (CVD) mortality, and cancer mortality as well as the effect of age on the associations. This prospective study enrolled Japanese individuals in the general population. Participants were divided into eight phenotypes according to the BMI classification and metabolic status. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using a Cox regression hazard model. In total, 10,824 individuals with a mean age of 55.3 years were evaluated. During a mean follow-up of 18.4 years (198,776 person-years), 2,274 participants died. Among the metabolically unhealthy, the association between BMI and mortality was J-shaped after adjustment for various confounders (multivariable HR [95% CI] for all-cause mortality: underweight, 2.0 [1.5–2.7]; obesity 2.8 [2.1–3.6]). The association remained the same in metabolically unhealthy participants aged <65 years and ≥65 years. The results were compatible in the analyses restricted to subjects who never smoked. Regardless of age, metabolically unhealthy underweight (MUHU) have approximately a 3-fold higher risk of CVD mortality, compared with metabolically healthy normal weight. Not only metabolically unhealthy obesity, but also MUHU was strongly associated with an increased risk of mortality. More attention should be given to the health issues of metabolically unhealthy participants without obesity, particularly those with MUHU.
Hyperprogressive disease (HPD) is a paradoxical phenomenon involving the acceleration of tumor progression after treatment with immune checkpoint inhibitors (ICIs). A 66-year-old male smoker with advanced lung adenocarcinoma started pembrolizumab for progressive disease following first-line chemotherapy. He developed HPD after two cycles, and a re-biopsy revealed transformation to small-cell carcinoma. He subsequently underwent two lines of chemotherapy for small-cell carcinoma until progression and ultimately died. Transformation to small-cell carcinoma may be a cause of HPD during ICI therapy. The possibility of pathological transformation should be considered in cases of HPD with resistance to ICI therapy.
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