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Aim: To investigate the association between dental health and incident cardiovascular disease (CVD) in secondary prevention setting. Materials and Methods: A total of 888 patients with known CVD hospitalized in the cardiology unit were prospectively enrolled. We assessed the association between missing teeth and three variables of periodontitis and major adverse cardiovascular events (MACE), defined as a composite of cardiac death, acute myocardial infarction, stroke and hospital re‐admission for congestive heart failure. Results: During a median (Q1, Q3) follow‐up of 4.6 (1.4, 6.7) years, an additional missing tooth was associated with a 3% (95% confidence interval [CI]: 1%–5%) higher hazard of MACE (p =.004). Compared with patients with 0 to ≤4 missing teeth, periods free from MACE (95% CI) by 5 years of follow‐up were, on average, shorter by 0.17 (−0.04 to 0.37) years, 0.26 (0.04–0.49) years and 0.59 (0.34–0.85) years in patients with 5 to ≤7, 8 to ≤13 and >13 missing teeth, respectively. No significant associations were observed between periodontal measures and MACE incidence. Conclusions: In hospitalized patients with existing CVD, the total number of missing teeth was associated with incident MACE. [ABSTRACT FROM AUTHOR]

A 44‐year‐old woman who was quarantined for 5 days after the diagnosis of coronavirus disease of 2019 (COVID‐19) was transferred to our hospital with the complaint of chest pain. The patient was unvaccinated. Electrocardiography revealed ST elevation in the lateral leads. Echocardiographic biventricular dysfunction with oedematous wall thickening was identified. Cardiac enzyme levels were elevated; however, C‐reactive protein (CRP) levels, and the coronary angiogram were normal. The patient required mechanical circulatory support to stabilize haemodynamics and was treated with remdesivir, baricitinib, and intravenous methylprednisolone. She recovered after 13 days of mechanical support. Serial cardiac magnetic resonance imaging revealed acute myocardial oedema and subsequent fibrosis. An endomyocardial biopsy on admission showed mild interstitial inflammatory infiltrates with endomyocardial fibrous thickening and mild interstitial fibrosis of the myocardium. Normal CRP levels suggested minor involvement of interleukin (IL)‐6, supporting the efficacy of baricitinib. [ABSTRACT FROM AUTHOR]

We report on a 52‐year‐old Brazilian immigrant woman with past histories of chronic kidney disease and uveitis, presenting with symptomatic atrioventricular block. Her country of origin being endemic for Trypanosoma cruzi infection, we suspected Chagas disease as the aetiology, diagnosis of which was confirmed by serological tests. Further systemic workup identified an emerging nodular lesion in the lung, which turned out to be a sarcoid epithelioid granuloma on biopsy. Involvement of the kidneys and eyes was suggestive of systemic extension of the lung sarcoidosis. Although imaging modalities did not detect inflammatory foci in the myocardium, the rare coexistence of histologically proven sarcoidosis raised the intriguing concept of cardiac manifestation having arisen from two possibly overlapping aetiologies: Chagas disease and cardiac sarcoidosis. The case highlights a treatment dilemma increasingly likely to be encountered in this globalized world, and also raises the potential, but intriguing, association of these two diseases. [ABSTRACT FROM AUTHOR]

Purpose: A multicenter, randomized, double‐blind, placebo‐controlled trial was conducted to evaluate the efficacy, safety, and appropriate dose of ulipristal acetate (UPA) in Japanese women with symptomatic uterine fibroids (UFs). Methods: A total of 121 premenopausal women with UFs were enrolled to receive either placebo, UPA‐2.5 mg, UPA‐5 mg, UPA‐10 mg, or leuprorelin acetate (LEU), a reference drug, for 12 weeks. The primary end point was the rate of patients having achieved amenorrhea for 35 days at Week 12. Results: The rates for amenorrhea were 4.5%, 60.0%, 72.7%, 88.0%, and 76.2% in the placebo, UPA‐2.5 mg, UPA‐5 mg, UPA‐10 mg, and LEU groups, respectively. The median times to amenorrhea were 20.0, 5.0, 5.0, and 23.0 days for treatment with UPA‐2.5 mg, UPA‐5 mg, UPA‐10 mg, and LEU, respectively. A significant dose‐response of UPA for the rate of amenorrhea was observed. The overall incidence rates of adverse events were 45.8% in the placebo group, 56.5%‐80.0% in the UPA groups, and 100.0% in the LEU group. There were no notable safety issues with UPA. Conclusions: Ulipristal acetate was effective and well tolerated in Japanese women with UFs. The recommended dose of UPA is considered to be 10 mg. [ABSTRACT FROM AUTHOR]

Background: While the evaluation of burr speed was discussed regarding platelet aggregation, the association between platform speed and acute lumen gain of rotational atherectomy remains unknown.Methods: Through the evaluation of the potential of low-speed rotational atherectomy (LSRA) in in-vitro experiments, minimum lumen diameter (MLD) and minimum lumen area (MLA) after conventional high-speed rotational atherectomy (HSRA group) and those after LSRA following HSRA (LSRA+HSRA group) treated by 1.5 mm burrs were measured by optical frequency domain imaging (OFDI) in 30 consecutive human lesions.Results: The in-vitro experiments demonstrated that MLD and MLA after LSRA+HSRA were significantly larger (MLD: LSRA+HSRA=1.50 ±0.05 mm, HSRA= 1.43 ±0.05 mm, p=0.015; MLA: LSRA+HSRA= 1.90 ±0.17 mm2, HSRA= 1.71±0.11 mm2, and p= 0.037), requiring more crossing attempts (LSRA= 134 ±20 times, HSRA= 72 ±11 times, and p< 0.001). In human studies, there was no significance in reference vessel diameter and lesion length before the procedure between two groups. MLDs after LSRA+HSRA were significantly larger than those in HSRA (LSRA+HSRA= 1.22 ±0.16 mm, HSRA= 1.07 ±0.14 mm, and p= 0.0078), while MLAs after LSRA+HSRA tended to be larger (LSRA+HSRA= 1.79 ±0.51 mm2, HSRA= 1.55 ±0.47 mm2, and p= 0.19). There was no significance in the occurrence of in-hospital complication, including slow flow or no reflow, major dissection, and procedural myocardial infarction, between LSRA+HSRA and HSRA.Conclusions: LSRA can achieve larger lumen gain compared, whereas HSRA can pass calcified lesions easily. Combination of LSRA and HSRA is a safe and feasible strategy for severely calcified lesions in clinical practice. [ABSTRACT FROM AUTHOR]

Objectives: To evaluate the effectiveness of the proximal optimization technique (POT) to prevent longitudinal stent elongation.Background: The mechanism of stent elongation, which occurs after post-balloon dilation, is still unclear.Methods: A total of 103 lesions treated with optical coherence tomography guided coronary intervention between May 2013 and November 2017 were retrospectively analyzed. Lesions were divided according to the circumferential degree of malapposition at the stent edge immediately after deployment into well-apposed group (<180°) and malapposed group (≥180°). Post-dilation was performed from distal to proximal within the stent until August 2016 (non-POT cohort), and POT was applied thereafter (POT cohort). In the POT cohort, post-dilation was done at the proximal portion of the stent with sufficiently large balloon to minimize malapposition followed by distal dilatations. Stent elongation length was defined as the change in stent length from stent deployment to after post-dilatation.Results: In the non-POT cohort, 72 lesions, including 54 lesions in the well-apposed group and 18 in the malapposed group were analyzed. Stent elongation length was significantly longer in the malapposed group than in the well-apposed group (1.51 ± 1.34 mm vs 0.13 ± 0.84 mm, P < 0.01). In the POT cohort, 31 lesions including 21 in the well-apposed group and 10 in the malapposed group were analyzed. Stent elongation length was not significantly different between the groups (-0.09 ± 0.91 mm vs 0.30 ± 0.99 mm, P = 0.29).Conclusions: Malapposition of the stent edge is responsible for longitudinal stent elongation caused by post-dilatation. POT appeared to effectively prevent longitudinal stent elongation. [ABSTRACT FROM AUTHOR]

5‐Hydroxy‐3‐methylglutaryl‐CoA reductase inhibitors (statins) have beneficial effects in patients with heart failure (HF), regardless of serum cholesterol levels. However, their synergic effects with angiotensin II receptor blocker (ARB) remain to be established. We assessed the existence and potential underlying mechanisms of the effects of combined ARB [losartan (LOS)] and statin [simvastatin (SIM)] on cardiac function in rats and mice with load‐induced HF. Salt‐loaded Dahl salt‐sensitive (DS) rats were treated with vehicle, LOS, SIM, or LOS + SIM for 8 weeks. To mimic load‐induced HF in vitro, cultured neonatal rat cardiomyocytes (NRCM) were cyclically stretched. We also investigated the effect of LOS + SIM on pressure overload‐induced HF using mice with transverse aortic constriction (TAC). LOS + SIM improved left ventricular (LV) function and reduced LV hypertrophy more than the monotherapies in both salt‐loaded DS rats and TAC‐operated mice. LV‐tissue increases in Rho kinase and matrix metalloproteinase‐9 activity were decreased to a greater extent by LOS + SIM than by LOS and SIM monotherapies. Plasma levels of Exp‐3174, a LOS metabolite, were higher in LOS + SIM‐treated DS rats than in LOS‐treated rats. Stretch‐induced hypertrophy of NRCM pretreated with SIM + Exp‐3174 was significantly attenuated from that with LOS, Exp‐3174, SIM, or LOS + SIM. SIM administration significantly enhanced mitophagy in mouse hearts after TAC. However, LOS + SIM reduced mitophagy, and the salutary effect of SIM in mouse hearts after TAC was abolished in AT1R−/− mice. In conclusion, LOS and SIM have beneficial myocardial effects on load‐induced HF via differential pleiotropic effects. Thus, combination therapy of these drugs thus has potential as a therapeutic strategy for HF. [ABSTRACT FROM AUTHOR]

Objective Takayasu arteritis (TAK) is a systemic vasculitis affecting large arteries and large branches of the aorta. Ulcerative colitis (UC) is a prevalent autoimmune colitis. Since TAK and UC share HLA-B*52:01 and IL12B as genetic determinants, and since there are case reports of the co-occurrence of these diseases, we hypothesized that UC is a common complication of TAK. We undertook this study to perform a large-scale analysis of TAK, both to evaluate the prevalence of concurrent cases of TAK and UC and to identify and estimate susceptibility genes shared between the 2 diseases. Methods We analyzed a total of 470 consecutive patients with TAK from 14 institutions. We characterized patients with TAK and UC by analyzing clinical manifestations and genetic components. Genetic overlapping of TAK and UC was evaluated with the use of UC susceptibility single-nucleotide polymorphisms by comparing risk directions and effect sizes between susceptibility to the 2 diseases. Results Thirty of 470 patients with TAK had UC (6.4% [95% confidence interval 4.3-9.0]). This percentage was strikingly higher than that expected from the prevalence of UC in Japan. Patients with TAK complicated with UC developed TAK at an earlier stage of life ( P = 0.0070) and showed significant enrichment of HLA-B*52:01 compared to TAK patients without UC ( P = 1.0 × 10−5) (odds ratio 12.14 [95% confidence interval 2.96-107.23]). The 110 non-HLA markers of susceptibility to UC significantly displayed common risk directions with susceptibility to TAK ( P = 0.0054) and showed significant departure of permutation P values from expected P values ( P < 1.0 × 10−10). Conclusion UC is a major complication of TAK. These 2 diseases share a significant proportion of their genetic background, and HLA-B*52:01 may play a central role in their co-occurrence. [ABSTRACT FROM AUTHOR]

Cellular senescence is an important phenomenon in decreased cellular function. Recently, it was shown that cellular senescence is induced in proliferating cells within a short period of time by oxidative stresses. This phenomenon is known as premature senescence. However, it is still unknown whether premature senescence can be also induced in cardiomyocytes. The aim of the present study was to investigate whether a senescence-like phenotype can be induced in cardiomyocytes by oxidative stress. In cardiomyocytes obtained from aged rats (24 months of age), the staining for senescence-associated β-galactosidase increased significantly and the protein or RNA levels of cyclin-dependent kinase inhibitors increased compared to those of young rats. Decreased cardiac troponin I phosphorylation and telomerase activity were also observed in aged cardiomyocytes. Treatment of cultured neonatal rat cardiomyocytes with a low concentration of doxorubicin (DOX) (10−7 mol L−1) did not induce apoptosis but did induce oxidative stress, which was confirmed by 2′,7′-dichlorofluorescin diacetate staining. In DOX-treated neonatal cardiomyocytes, increased positive staining for senescence-associated β-galactosidase, cdk-I expression, decreased cardiac troponin I phosphorylation, and decreased telomerase activity were observed, as aged cardiomyocytes. Alterations in mRNA expression typically seen in aged cells were observed in DOX-treated neonatal cardiomyocytes. We also found that promyelocytic leukemia protein and acetylated p53, key proteins involved in stress-induced premature senescence in proliferating cells, were associated with cellular alterations of senescence in DOX-treated cardiomyocytes. In conclusion, cardiomyocytes treated with DOX showed characteristic changes similar to cardiomyocytes of aged rats. promyelocytic leukemia-related p53 acetylation may be an underlying mechanism of senescence-like alterations in cardiomyocytes. These findings indicate a novel mechanism of myocardial dysfunction induced by oxidative stress. [ABSTRACT FROM AUTHOR]