Myocardial infarction (MI) is a leading cause of heart failure and ventricular arrhythmias, driven by excessive inflammation and adverse cardiac remodeling. The purinergic P2X7 receptor (P2X7R) plays a critical role in acute MI, however, the long-term effect of P2X7R on chronic MI and arrhythmia remains unknown. This study investigated the effects of long-term modulation of P2X7R on inflammation, fibrosis, and arrhythmias in a rat model of MI. Male Sprague–Dawley rats underwent left anterior descending coronary artery ligation and were assigned to sham, MI, MI + Brilliant Blue G (BBG, P2X7R antagonist), or MI + BzATP (P2X7R agonist) groups for 28 days. BBG treatment significantly reduced ventricular tachycardia induction rates, shortened QT, QTc, and Tpeak-Tend intervals, and improved cardiac function, as evidenced by increased ejection fraction, fractional shortening, and cardiac output. Histological analyses revealed reduced inflammatory cell infiltration, necrosis, and collagen deposition in the MI + BBG group compared to MI groups. ELISA confirmed that BBG lowered pro-inflammatory cytokines TNF-α, IL-1β and TGF-β1 levels. P2X7 mRNA expression was attenuated by BBG, but not significantly altered. These findings demonstrate that BBG mitigates post-MI inflammation, fibrosis, and arrhythmias while enhancing cardiac function.

BACKGROUND:Acupuncture at different traditional acupuncture point locations activates different autonomic pathways and modulates systemic inflammation. Electroacupuncture preconditioning (EAP) at PC6 or ST36 has been demonstrated to be cardioprotective during acute myocardial ischemia (MI) injury, but the mechanism remains unclear. As inflammation is crucial for repair post-MI, we aimed to investigate whether the protective effect of EAP at PC6 or ST36 is related to the suppression of inflammation and whether autonomic pathways are involved. METHODS:Mice underwent ligation of the left anterior descending (LAD) coronary artery to generate model MI after 3 days of EAP at PC6 or ST36. Echocardiography and triphenyltetrazolium chloride (TTC) staining were used to evaluate cardiac function and myocardial infarction area. Cardiac troponin (cTn)I and norepinephrine (NE) were measured by enzyme-linked immunosorbent assay (ELISA). Flow cytometry was employed to determine macrophage M1/M2 phenotypic polarization, and the levels of pro- and anti-inflammatory cytokines in cardiac tissue were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). In addition, unilateral cervical vagotomy and chemical sympathetic blockade were employed to clarify specific autonomic pathways. RESULTS:EAP at PC6 or ST36 preserved cardiac function, reduced myocardial infarct size, decreased serum cTnI levels, promoted M2 macrophage polarization and decreased the cardiac pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-18 and nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3). Compared to EAP at ST36, EAP at PC6 yielded a better cardioprotective effect and regulated the anti-inflammatory cytokine transforming growth factor (TGF)-β. Moreover, sympathetic nerves were involved in the protective effect of EAP at PC6, while the vagus nerve was necessary for EAP at ST36. CONCLUSION:Our findings suggest that EAP at PC6 or ST36 activates different autonomic pathways and modulates M2 macrophage polarization, resulting in the suppression of myocardial inflammation.

OBJECTIVES:The purpose of this study is to assess the effects of acupuncture on glucose control, lipid metabolism, myocardial fibrosis, and the development of diabetic cardiomyopathy (DCM) in mice with type 2 diabetes. METHODS:After modelling, mice were divided into three groups: the control, model (DCM), and PC6+ST36 group. Acupuncture was applied at PC6 and ST36 acupoints for 15 min every other day, three times a week for 8 weeks during the development of diabetic cardiomyopathy. Heart function was assessed by echocardiography and electrocardiogram. Serum glucose, lipid metabolism and ANP were assessed via ELISA. The myocardium was assessed by histology, immunoblotting, RNA-seq and CUT&Tag on the day after all the treatments were finished. RESULTS:Acupuncture at Neiguan and Zusanli reduced abnormal glucose (mean difference of fed glucose decrease from 19.63 mmol/L to 12.62 mmol/L, P=0.008) and improved lipid metabolism (mean difference of TC decrease from 23.70 mmol/L to 17.81 mmol/L, P value is 0.038, TG from 27.14 mmol/L to 18.70 mmol/L, P value is 0.006, LDL from 19.36 mmol/L to 14.35 mmol/L, P value is 0.015, FFA from 578.96 mmol/L to 328.98 mmol/L, P value is 0.0001) in mice with diabetic cardiomyopathy. Both impaired systolic function (mean difference of EF increase from 52.84% to 71.10%, P value is 0.004, FS increase from 26.39% to 39.38%, P value is 0.008) and damaged diastolic function (mean difference of IVRT decrease from 26.50 ms to 16.33 ms, P value is 0.025, E/A ratio increase from 0.91 to 1.22, P value is 0.07) were observed in the DCM group, whereas acupuncture enhanced cardiac function in mice with DCM. Cardiac fibrosis was alleviated in the PC6+ST36 group, accompanied by reduced expression of fibrosis-related genes (Col1a1 family). Moreover, acupuncture inhibited cardiac apoptosis in mice with DCM to some extent. CONCLUSIONS:Acupuncture at Neiguan and Zusanli can improve heart function and myocardial hypertrophy by inhibiting cardiac apoptosis and fibrosis in mice with DCM.

High-output heart failure (HF) occurs with sustained volume overload. Hence, clarifying how compensated high-output states transition to maladaptive HF is essential for developing interventions that preserve cardiac function. Therefore, this study investigated the mechanism by which volume overload induced by aortocaval shunt (AVS) and aldosterone (Ald) affects the progression of myocardial function and structural remodeling. AVS was surgically induced in rats, and osmotic mini-pumps delivering Ald (1.0 μg·h-1) for 4 weeks were intraperitoneally implanted. Cardiac function and structure were serially assessed using echocardiography before surgery and at 4, 12, and 24 weeks under isoflurane. At 23 weeks, atrial natriuretic peptide was analyzed, and at 24 weeks, comprehensive electrophysiological, hemodynamic, morphometric, and histological examinations were performed to characterize cardiopathy. Early diastolic mitral annular velocity (E') remained relatively unchanged after 24 weeks, whereas early diastolic filling wave (E) velocity, atrial contraction wave velocity, and E/E' ratio increased. However, AVS did not markedly reduce systolic function; it was associated with progressive elevation of cardiac output, left ventricular hypertrophy, and dilation. Histological and morphometric analyses confirmed concentric hypertrophy, eccentric remodeling, and focal fibrosis. Ald induced similar diastolic changes and structural remodeling but caused an earlier decline in systolic function at 8 weeks. These findings demonstrate a 2-phase trajectory of high-output stress: an early compensated stage with elevated filling pressure, followed by a decompensated stage with progressive systolic decline. Moreover, Ald accelerates this systolic decline. Therefore, targeting Ald receptors in the early compensation phase may protect against systolic impairment caused by volume overload.

Calcium/calmodulin-dependent protein kinase II (CAMKII) is a critical regulator of cardiac electrophysiology. However, the role of the four bases deletion polymorphism in Camk2d which codes delta subunit of CAMKII, particularly those involving intron sequences, remains poorly understood. This study aimed to investigate the impact of Camk2d c.1044+125_128delGTTT missing polymorphism on cardiac morphology and arrhythmogenesis in normal adult Sprague-Dawley (SD) rats. A total of 85 SD rats were genotyped by Sanger sequencing, revealing a distribution of 25.9% wild-type (WT), 48.2% heterozygous, and 25.9% homozygous variants. Echocardiography, Hematoxylin-Eosin staining, Masson's trichrome staining and transmission electron microscopy indicated no significant differences in cardiac structure or baseline function among the three groups. In freely moving rats, premature atrial arrhythmias were detected in 2 of 9 WT rats, 1 of 9 heterozygous rats, and 1 of 9 homozygous rats. Premature ventricular contractions (PVCs) were observed in none of 9 WT or homozygous rats, 3 of 9 heterozygous rats, with one heterozygous rat exhibiting frequent PVCs. Electrical programmed stimulation revealed a higher incidence of inducible atrial fibrillation in homozygous rats compared to WT rats and a higher incidence of inducible ventricular tachycardia in heterozygous rats compared to WT rats. These findings suggest that deletion polymorphism in the intron sequences of Camk2d are unexpectedly common in normal SD rat populations and that such polymorphism predispose to ventricular arrhythmias without overt structural heart disease. Our study highlights the potential arrhythmogenic risk associated with non-coding DNA sequence alterations in Camk2d and underscores the importance of genetic screening in experimental animal models.

Despite optimal standard therapy, residual inflammation continues to increase major adverse cardiovascular events (MACE) in patients with coronary heart disease (CHD). New immunomodulatory drugs targeting specific immune pathways have shown mixed efficacy across trials, warranting comprehensive evaluation of their role in secondary prevention. We performed a systematic review and meta-analysis of 25 randomized controlled trials (RCTs) from January 1, 2014, to October 1, 2024, identified from eight databases: the cochrane library, (public medicine) pubmed, embase, web of science, china national knowledge infrastructure (CNKI), wanfang data knowledge service platform(WanFang), Weipu information database(VIP), and china biomedical literature database (SinoMed). Eligible studies assessed the efficacy of immunomodulatory agents, including colchicine, and canakinumab on MACE. Primary outcome was MACE incidence; secondary outcomes included, angina, and inflammatory biomarkers. Risk ratios (RR) with 95 https://www.crd.york.ac.uk/PROSPERO/view/CRD42024597008PROSPERO : CRD42024597008.

P2X7 receptor (P2X7R) plays an important role in modulating inflammation and fibrosis, but information is limited whether Zusanli (ST36) can inhibit inflammation and fibrosis by regulating P2X7R. Isoprenaline at 5 mg/kg was subcutaneously injected to wild-type and P2X7R knockout mice for 7 days, while treatment groups received electroacupuncture (EA) stimulation at ST36 for 7 sessions. Following 7-session treatment, Masson’s trichrome staining was performed to assess the fibrosis. Morphology, electrocardiogram, and echocardiography were carried out to evaluate the cardiac function and structure. Western blotting, hematoxylin and eosin staining, immunohistochemistry, and biochemical analysis of inflammatory cytokine and transmission electron microscopy were carried out to characterize the effect of ST36 on inflammation. P2X7R was overexpressed in ISO-treated mice. EA at ST36, but not at non-points, reduced ISO-induced cardiac fibrosis, increases in HW/BW, R+S wave relative to mice in ISO groups. In addition, EA at ST36 downregulated ISO-upregulated P2X7R and NLRP3 in ventricle. Moreover, EA reduced cytokines of IL-1β, IL-6, and IL-18 in serum, and inhibited foam cell gathering, inflammatory cell infiltration, and autophagy. However, EA at ST36 failed to attenuate the cardiac fibrosis and hypertrophy in P2X7R knockout mice. In conclusion, EA at ST36 attenuated ISO-induced fibrosis possibly via P2X7R.

Electroacupuncture (EA) at the Neiguan acupoint (PC6) has shown significant cardioprotective effects. Sympathetic nerves play an important role in maintaining cardiac function after myocardial infarction (MI). Previous studies have found that EA treatment may improve cardiac function by modulating sympathetic remodeling after MI. However, the mechanism in how EA affects sympathetic remodeling and improves cardiac function remains unclear. The aim of this study is to investigate the cardioprotective mechanism of EA after myocardial ischemic injury by improving sympathetic remodeling and promoting macrophage M2 polarization. We established a mouse model of MI by occluding coronary arteries in male C57/BL6 mice. EA treatment was performed at the PC6 with current intensity (1 mA) and frequency (2/15 Hz). Cardiac function was evaluated using echocardiography. Heart rate variability in mice was assessed via standard electrocardiography. Myocardial fibrosis was evaluated by Sirius red staining. Levels of inflammatory factors were assessed using RT‐qPCR. Sympathetic nerve remodeling was assessed through ELISA, western blotting, immunohistochemistry, and immunofluorescence staining. Macrophage polarization was evaluated using flow cytometry. Our results indicated that cardiac systolic function improved significantly after EA treatment, with an increase in fractional shortening and ejection fraction. Myocardial fibrosis was significantly mitigated in the EA group. The sympathetic nerve marker tyrosine hydroxylase and the nerve sprouting marker growth‐associated Protein 43 were significantly reduced in the EA group, indicating that sympathetic remodeling was significantly reduced. EA treatment also promoted macrophage M2 polarization, reduced levels of inflammatory factors TNF‐α, IL‐1β, and IL‐6, and decreased macrophage‐associated nerve growth factor in myocardial tissue. To sum up, our results suggest that EA at PC6 attenuates sympathetic remodeling after MI to promote macrophage M2 polarization and improve cardiac function.

Takotsubo cardiomyopathy (TCM) has been reported to occur after subarachnoid hemorrhage, and the involvement of a critical activity of catecholamines has been mentioned, but the details of its onset have not been fully clarified. Recently, proper arterial stiffness could be measured with cardio-ankle vascular index. Therefore, we aimed to clarify the role of arterial stiffness in onset of TCM using rabbits under infusion of noradrenaline and injection of blood into brain ventricle. Rabbits were divided into three groups: infusion of noradrenaline (group A), infusion of noradrenaline + injection of saline into the brain ventricle (group B), infusion of noradrenaline + injection of blood in the brain ventricle (group C). Aortic arterial stiffness beta ( A β) and femoral arterial stiffness beta ( F β) were defined according to definition of the cardio-ankle vascular index. Blood pressure (BP), A β, F β, and femoral vessel resistance (FVR) were measured. Left ventricular movement were monitored with echocardiography. BP increased uniformly in all three groups. F β in the group A, B and C increased from 3.6 ± 3.2, 3.6 ± 3.6 and 3.9_ ± 4.2 to 15 ± 2, 17.9 ± 2.4, 34.8 ± 9.1 due to the ICP enhancements in addition to noradrenaline administration, respectively. F β in groups B and C was significantly larger than that in group A. On echocardiography, a much higher akinesic area of the apex was observed in group C compared with group A and B. Cardiac movements similar to TCM were observed slightly in group B and definitely in group C. Noradrenaline administration infusion and blood injection into the brain ventricle induced TCM accompanying with enhanced femoral arterial stiffness. These results suggested that elevated arterial stiffness might be involved in the formation of TCM in addition to a critical activity of catecholamines and an increase in intracranial pressure with blood injection.

Rapid occlusion is the culprit leading to implantation failure of biological blood vessels. Although adenosine is a clinical-proven drug to overcome the problem, its short half-life and turbulent burst-release limit its direct application. Thus, a pH/temperature dual-responsive blood vessel possessed controllable long-term adenosine secretion was constructed based on acellular matrix via compact crosslinking by oxidized chondroitin sulfate (OCSA) and functionalized with apyrase and acid phosphatase. These enzymes, as adenosine micro-generators, controlled the adenosine release amount by "real-time-responding" to acidity and temperature of vascular inflammation sites. Additionally, the macrophage phenotype was switched from M1 to M2, and related factors expression proved that adenosine release was effectively regulated with the severity of inflammation. What's more, the ultra-structure for degradation resisting and endothelialization accelerating was also preserved by their "double-crosslinking". Therefore, this work suggested a new feasible strategy providing a bright future of long-term patency for transplanted blood vessels.

Hypertension is the leading cause of morbidity and mortality globally among all cardiovascular diseases. Purinergic signalling plays a crucial role in hypertension through the sympathetic nerve system, neurons in the brain stem, carotid body, endothelium, immune system, renin-angiotensin system, sodium excretion, epithelial sodium channel activity (ENaC), and renal autoregulation. Under hypertension, adenosine triphosphate (ATP) is released as a cotransmitter from the sympathetic nerve. It mediates vascular tone mainly through P2X1R activation on smooth muscle cells and activation of P2X4R and P2YR on endothelial cells and also via interaction with other purinoceptors, showing dual effects. P2Y1R is linked to neurogenic hypertension. P2X7R and P2Y11R are potential targets for immune-related hypertension. P2X3R located on the carotid body is the most promising novel therapeutic target for hypertension. A 1 R, A 2A R, A 2B R, and P2X7R are all related to renal autoregulation, which contribute to both renal damage and hypertension. The main focus is on the evidence addressing the involvement of purinoceptors in hypertension and therapeutic interventions.

射血分数保留的心力衰竭(HFpEF)是危害人们生活质量的心血管疾病之一,占心力衰竭患者的一半,其发生发展与性别、年龄、慢性肾病、糖尿病、高血压以及肥胖等联系紧密[1-4].HFpEF的关键特点是左心室舒张功能受损,包含主动舒张延长和被动充盈受限.心肌肌浆网Ca2+-ATP酶(SERCA2a)由跨膜螺旋蛋白(M1～10)、核苷酸结合结构域、磷酸化结构域、致动器结构域和管腔环组成,通过调控舒张期细胞质内的Ca2+浓度,进而在心室舒张功能中扮演着重要作用.翻译后修饰影响SERCA2a的功能和活性.本综述总结了 SERCA2a的翻译后修饰在心室舒张功能中的病理生理功能,以及其调控机制和潜在的靶点药物.

Acupuncture point specificity has been recognized as a key scientific issue in traditional Chinese medicine (TCM), but there is limited clinical trial or animal study to verify the characteristics of PC6, BL15, and ST36 in the protection from myocardial injury. We aimed to compare the effects among these three acupoints on the acute myocardial infarction mice model and to explore possible mechanisms for the first time. We found that PC6 is the most appropriate acupoint to deliver efficacy and safety to treat acute MI in mice. BL15 stimulation improved the systolic function, but increased the risk of arrhythmia. ST36 only slightly attenuated systolic function and had no effect on arrhythmia during MI. RNA profiles of skin tissue in local acupoints demonstrated that the most altered DEGs and related pathways may partly support its best effects of PC6 treatment on MI injury, and support the observed phenomenon of the acupoint specificity.

Background Atrioventricular nodal reentrant tachycardia (AVNRT) is a common arrhythmia. Growing evidence suggests that family aggregation and genetic factors are involved in AVNRT. However, in families with a history of AVNRT, disease-causing genes have not been reported. Objective To investigate the genetic contribution of familial AVNRT using a whole-exome sequencing (WES) approach. Methods Blood samples were collected from 20 patients from nine families with a history of AVNRT and 100 control participants, and we systematically analyzed mutation profiles using WES. Gene-based burden analysis, integration of previous sporadic AVNRT data, pedigree-based co-segregation, protein-protein interaction network analysis, single-cell RNA sequencing, and confirmation of animal phenotype were performed. Results Among 95 related reference genes, seven candidate pathogenic genes have been identified both in sporadic and familial AVNRT, including CASQ2, AGXT, ANK2, SYNE2, ZFHX3, GJD3, and SCN4A. Among the 37 reference genes from sporadic AVNRT, five candidate pathogenic genes were identified in patients with both familial and sporadic AVNRT: LAMC1, ryanodine receptor 2 (RYR2), COL4A3, NOS1, and ATP2C2. To identify the common pathogenic mechanisms in all AVNRT cases, five pathogenic genes were identified in patients with both familial and sporadic AVNRT: LAMC1, RYR2, COL4A3, NOS1, and ATP2C2. Considering the unique internal candidate pathogenic gene within pedigrees, three genes, TRDN, CASQ2, and WNK1, were likely to be the pathogenic genes in familial AVNRT. Notably, the core calcium-signaling pathway may be closely associated with the occurrence of AVNRT, including CASQ2, RYR2, TRDN, NOS1, ANK2, and ATP2C2. Conclusion Our pedigree-based studies demonstrate that RYR2 and related calcium signaling pathway play a critical role in the pathogenesis of familial AVNRT using the WES approach.

Abstract Background: Atrioventricular nodal reentrant tachycardia (AVNRT) is a common arrhythmia. Growing evidence suggests that family aggregation and genetic factors are involved in AVNRT. However, in families with a history of AVNRT, disease-causing genes have not been reported. Objective: To investigate the genetic contribution of familial AVNRT using a WES approach. Methods: Blood samples were collected from 20 patients from nine families with a history of AVNRT and 100 control participants, and we systematically analyzed mutation profiles using whole-exome sequencing. Gene-based burden analysis, integration of previous sporadic AVNRT data, pedigree-based co-segregation, protein-protein interaction network analysis, single-cell RNA sequencing, and confirmation of animal phenotype were performed. Results: Among 95 reference genes, seven pathogenic genes have been identified both in sporadic and familial AVNRT, including CASQ2, AGXT, ANK2, SYNE2, ZFHX3, GJD3, and SCN4A. Among the 37 reference genes from sporadic AVNRT, five pathogenic genes were identified in patients with both familial and sporadic AVNRT LAMC1, RYR2, COL4A3, NOS1, and ATP2C2. Considering the unique internal pathogenic gene within pedigrees, three genes, TRDN, CASQ2, and WNK1, were likely to be the pathogenic genes in familial AVNRT. Notably, the core calcium-signaling pathway may be closely associated with the occurrence of AVNRT, including CASQ2, RYR2, TRDN, NOS1, ANK2, and ATP2C2. Conclusion: These results revealed the underlying mechanism for familial AVNRT.

Keshan disease is an endemic fatal dilated cardiomyopathy that can cause heart enlargement, heart failure, and cardiogenic death. Selenium deficiency is considered to be the main cause of Keshan disease. However, the molecular mechanism underlying Keshan disease remains unclear. Our whole-exome sequencing from 68 patients with Keshan disease and 100 controls found 199 candidate genes by gene-level burden tests. Interestingly, using multiomics data, the selenium-related gene ALAD (δ-aminolevulinic acid dehydratase) was the only candidate causative gene identified by three different analysis approaches. Based on single-cell transcriptome data, ALAD was highly expressed in cardiomyocytes and double mutations of human ALAD dramatically reduced its enzyme activity in vitro compared to negative control. Functional analysis of ALAD inhibition in mice resulted in a Keshan phenotype with left ventricular enlargement and cardiac dysfunction, whereas administration of sodium selenite markedly reversed the changes caused by ALAD inhibition. In addition, sodium selenite reversed Keshan phenotypes by affecting energy metabolism and mitochondrial function in mice as shown by the transcriptomic and proteomic data and the ultrastructure of cardiac myocytes. Our findings are the first to demonstrate that the selenium-related gene ALAD is essential for cardiac function by maintaining normal mitochondrial activity, providing strong molecular evidence supporting the hypothesis of selenium deficiency in Keshan disease. These results identified ALAD as a novel target for therapeutic intervention in Keshan disease and Keshan disease-related dilated cardiomyopathy.

Background Acupuncture at Neiguan (PC6) has long been used for treating cardiovascular diseases, but its antiarrhythmic effect and the underlying mechanisms have not yet been well investigated, especially regarding premature ventricular complexes (PVCs) that occur post-myocardial infarction (MI). The purpose of this study was to study the antiarrhythmic effect of manual acupuncture applied to PC6 for a relatively long period (28 days) and to elucidate the mechanism in mice . Methods An MI mouse model was generated by ligating the left anterior descending coronary artery in male C57/BL6 mice (n = 31). Manual acupuncture at PC6 was applied seven times weekly for 4 weeks. The state of myocardial injury was characterized by electrocardiography (ECG) and echocardiography. Inflammation was detected by ELISA and immunohistochemical stanning. Fibrosis was evaluated by Masson’s trichrome staining. RNA sequencing was used to explore the differentially expressed genes (DEGs) among the different groups after treatment. Results Acupuncture at PC6 lowered the incidence of spontaneous PVCs after MI injury (1/9, 11%) compared to that in mice without acupuncture treatment (6/9, 67%) and improved the ejection fraction from 31.77% in the MI mice to 44.18% in the MI + PC6 mice. Fibrosis was reduced after PC6 treatment. RNA-seq showed many DEGs involved in the immune system and inflammatory response pathway. Further studies confirmed that inflammation at the circulation level and cardiac tissue was inhibited in MI + PC6 mice, accompanied by suppressed sympathetic activation. Conclusions In conclusion, 28-day treatment of acupuncture at PC6 reduced spontaneous PVCs and improved systolic function, possibly by suppressing inflammatory response-mediated fibrosis and sympathetic hyperactivity.

Although elasticity of the conduit arteries is known to be contribute effective peripheral circulation via Windkessel effects, the relationship between changes in intra-aortic blood volume and conduit artery elasticity remains unknown. Here we assessed the effects of change in intra-aortic blood volume induced by blood removal and subsequent blood transfusion on arterial stiffness and the involvement of autonomic nervous activity using our established rabbit model in the presence or absence of the ganglion blocker hexamethonium (100 mg/kg). Blood removal at a rate of 1 mL/min gradually decreased the blood pressure and blood flow of the common carotid artery but increased a stiffness indicator the cardio-ankle vascular index, which was equally observed in the presence of hexamethonium. These results suggest that arterial stiffness acutely responds to changes in intra-aortic blood volume independent of autonomic nervous system modification.

A 32-year-old female with systemic lupus erythematosus (SLE) for more than 7 years, and long-term treatment with cyclophosphamide, cyclosporine, methotrexate, and tacrolimus, later found to be combined with hypertrophic cardiomyopathy (HCM) for one year. The patient denied a family history of cardiomyopathy and sudden cardiac death (SCD). Echocardiography suggested that uneven thickening of the left ventricle (LV), mainly in the lower middle segment. Cardiac magnetic resonance (CMR) showed that the walls of the left ventricular (LV) were significantly thickened, as about 21 mm, mainly in the middle and lower segments. Genetic tests showed no known or suspected pathogenic variations were found and no significant enhancement in CMR, so secondary HCM was diagnosed clinically. After symptomatic treatment, the patient was discharged, and long-term follow-up was conducted. The diagnosis of HCM, which combined with SLE or second to usage of tacrolimus, was based on symptoms, echocardiography, and CMR; no endomyocardial biopsies were performed.