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Hypertension in adolescents has attracted increasing attention. However, large, well-designed studies accurately demonstrating epidemiological characteristics of adolescent hypertension remain insufficient. We, therefore, conducted a population-based multicenter study with repeated blood pressure visits to offer precise prevalence of it. We randomly recruited 42 025 adolescents aged 12 to 17 years in 6 centers throughout China from 2018 to 2019. The initial hypertension was estimated in all centers through one blood pressure measurement visit. Confirmed hypertension was evaluated in 3 blood pressure visits in 2 of 6 centers including 16 220 subjects. Hypertension was defined using American and Chinese guidelines and standardized by sex and age using 2010 China population census data. Standardized prevalence of initial and confirmed hypertension were 18.6% (95% CI, 17.3%–20.0%) and 5.9% (95% CI, 4.7%–7.2%) using 2017 American Association Pediatrics hypertension guidelines, respectively and which were 24.5% (95% CI, 23.0%–25.9%) and 8.8% (95% CI, 7.3%–10.3%) using 2018 Chinese hypertension guidelines. Male (odds ratio [OR], 1.275 [95% CI, 1.070–1.520]), parental hypertension history (OR, 1.387 [95% CI, 1.159–1.660]), higher heart rate (OR, 1.043 [95% CI, 1.037–1.049]), higher waist circumference (OR, 1.036 [95% CI, 1.027–1.046]), and adiposity indexes including overweight (OR, 2.211 [95% CI, 1.781–2.745]), and obesity (OR, 3.085 [95% CI, 2.330–4.084]) were identified as risk factors. In conclusion, the prevalence of hypertension was quite high evaluated by both guidelines with several risk factors, and a single blood pressure measurement visit leads to an overestimation of hypertension prevalence among adolescents.

ObjectiveElevated levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) are associated with heart failure-related death in hypertrophic cardiomyopathy (HCM), but the relationship between NT-proBNP level and sudden cardiac death (SCD) in HCM remains undefined.MethodsThe study prospectively enrolled 977 unrelated patients with HCM with available NT-proBNP results who were prospectively enrolled and followed for 3.0±2.1 years. The Harrell’s C-statistic under the receiver operating characteristic curve was calculated to evaluate discrimination performance. A combination model was constructed by adding NT-proBNP tertiles to the HCM Risk-SCD model. The correlation between log NT-proBNP level and cardiac fibrosis as measured by late gadolinium enhancement (LGE) or Masson’s staining was analysed.ResultsDuring follow-up, 29 patients had SCD. Increased log NT-proBNP levels were associated with an increased risk of SCD events (adjusted HR 22.27, 95% CI 10.93 to 65.63, pConclusionNT-proBNP is an independent predictor of SCD in patients with HCM and may help with risk stratification of this disease.

Risk stratification of young patients with hypertension remains challenging. Generally, machine learning (ML) is considered a promising alternative to traditional methods for clinical predictions because it is capable of processing large amounts of complex data. We, therefore, explored the feasibility of an ML approach for predicting outcomes in young patients with hypertension and compared its performance with that of approaches now commonly used in clinical practice. Baseline clinical data and a composite end point—comprising all-cause death, acute myocardial infarction, coronary artery revascularization, new-onset heart failure, new-onset atrial fibrillation/atrial flutter, sustained ventricular tachycardia/ventricular fibrillation, peripheral artery revascularization, new-onset stroke, end-stage renal disease—were evaluated in 508 young patients with hypertension (30.83±6.17 years) who had been treated at a tertiary hospital. Construction of the ML model, which consisted of recursive feature elimination, extreme gradient boosting, and 10-fold cross-validation, was performed at the 33-month follow-up evaluation, and the model’s performance was compared with that of the Cox regression and recalibrated Framingham Risk Score models. An 11-variable combination was considered most valuable for predicting outcomes using the ML approach. The C statistic for identifying patients with composite end points was 0.757 (95% CI, 0.660–0.854) for the ML model, whereas for Cox regression model and the recalibrated Framingham Risk Score model it was 0.723 (95% CI, 0.636–0.810) and 0.529 (95% CI, 0.403–0.655). The ML approach was comparable with Cox regression for determining the clinical prognosis of young patients with hypertension and was better than that of the recalibrated Framingham Risk Score model.

MicroRNAs are key molecules involved in the regulation of endothelial function. They are important risk factors and biomarkers for the development of hypertension related to endothelial dysfunction. However, the gene expression patterns associated with hypertension development related to endothelial dysfunction have not been fully elucidated. We conducted a case-control study of 65 patients with essential hypertension (EH) and 61 controls without EH. Plasma levels of miR-122 and its target protein high-affinity cationic amino acid transporter 1 (CAT-1) were measured by qRT-PCR and ELISA, respectively. miR-122 expression in plasma of patients with EH was significantly higher than that of the control group (p = 0.001), while CAT-1 expression in patients with EH was significantly lower than that in the control group (p = 0.018). miR-122 expression in plasma of young patients with EH was significantly higher than that in young people without EH (p = 0.0004), and CAT-1 expression in plasma of young patients with EH was also significantly lower than that of the control group (p = 0.002). CAT-1 expression in the plasma of young participants was significantly higher than that of individuals aged ≥40 years (p = 0.003), whereas miR-122 expression was significantly lower (p = 0.001). We showed that among patients with EH, the high expression of miR-122 contributed to endothelial dysfunction by suppressing the expression of the CAT-1 protein, which led to a decrease in CAT-1 expression in plasma. Therefore, high expression of miR-122 appears to be a risk factor for endothelial dysfunction in EH, especially in younger patients.

Patients with hypertrophic cardiomyopathy (HC) caused by compound variants have severe clinical manifestations, but significant clinical heterogeneity remains. Clinical diversity in these patients may result from different combinations of variants. We analyzed the role of cis-compound variants in a Chinese HC pedigree. Exome sequencing was performed in the proband. Identified variants were detected with bi-directional Sanger sequencing in a pedigree that comprised 3 generations and 28 family members. Follow-up was performed for 16 years. Two missense variants (c.2465TC, p.Met822Thr; c.4258CT, p.Arg1420Trp) were identified in the MYH7 gene. These variants were absent in our 761 in-house people without HC and predicted to be pathogenic.Both variants were detected in 11 family members, thus they were believed to inherit cis. In the 11 members, only 5 developed HC, the other 6 were asymptomatic variant carriers with an abnormal electrocardiogram. The HC members had mild hypertrophy with a maximum left ventricular wall thickness of 13 to 21 mm and showed a low incidence of cardiovascular events. In conclusion, the cis-compound variants of Met822Thr and Arg1420Trp in MYH7 are causal but relatively benign, variants associated with familial HC. This finding suggests that different types of compound variants might need to be analyzed for a genotype-phenotype study.

MicroRNAs have emerged as crucial regulators of cardiac homeostasis and remodeling in various cardiovascular diseases. We previously demonstrated that miR-221 regulated cardiac hypertrophy in vitro. In the present study, we demonstrated that the cardiac-specific overexpression of miR-221 in mice evoked cardiac dysfunction and heart failure. The lipidated form of microtubule-associated protein 1 light chain 3 was significantly decreased and sequestosome 1 was accumulated in cardiac tissues of transgenic (TG) mice, indicating that autophagy was impaired. Overexpression of miR-221 in vitro reduced autophagic flux through inhibiting autophagic vesicle formation. Furthermore, mammalian target of rapamycin (mTOR) was activated by miR-221, both in vivo and in vitro. The inactivation of mTOR abolished the miR-221-induced inhibition of autophagy and cardiac remodeling. Our previous study has demonstrated that cyclin-dependent kinase (CDK) inhibitor p27 was a direct target of miR-221 in cardiomyocytes. Consistently, the expression of p27 was markedly suppressed in the myocardia of TG mice. Knockdown of p27 by siRNAs was sufficient to mimic the effects of miR-221 overexpression on mTOR activation and autophagy inhibition, whereas overexpression of p27 rescued miR-221-induced autophagic flux impairment. Inhibition of CDK2 restored the impaired autophagic flux and rescued the cardiac remodeling induced by either p27 knockdown or miR-221 overexpression. These findings reveal that miR-221 is an important regulator of autophagy balance and cardiac remodeling by modulating the p27/CDK2/mTOR axis, and implicate miR-221 as a therapeutic target in heart failure.

Purpose: To evaluate the safety and efficacy of endovascular treatment for iliac artery stenosis caused by Takayasu arteritis (TA). Methods: Twenty-three consecutive TA patients (mean age 28.6±9.5 years; 17 women) with 30 iliac artery stenoses underwent percutaneous transluminal angioplasty (PTA) and selective stent implantation between January 2007 and December 2016. All had claudication (Rutherford category 2 or 3). The changes in the Rutherford category, ankle-brachial index (ABI), 6-minute walking capacity, and adverse events were assessed. Results: The success rate of endovascular therapy for iliac artery lesions was 93.3% (28/30). Guidewires could not cross either lesion in a patient with bilateral stenoses. Twenty-four lesions were treated by PTA alone and the other 4 lesions with provisional stents. One patient had a puncture site hematoma. Over an average of 4.8±3.3 years, 18 patients remained asymptomatic or had mild intermittent claudication. The other 4 patients developed moderate to severe intermittent claudication due to progression of a previously existing iliac lesion (n=1) or restenosis (n=3); all 4 underwent PTA. At the last follow-up, improvements were seen in the ABI (0.95±0.12 vs 0.51±0.22, p

The genetic factors related to early-onset hypertension are largely unknown. This study aimed to determine the spectrum of steroid metabolism gene variants and the clinical relationships of these variants to phenotypes in Chinese patients with early-onset hypertension. A total of 306 consecutive early-onset hypertensive patients were recruited. All coding exons and flanking intronic regions of KCNJ5, CYP11B1, and CYP17A1 were sequenced. Long-distance polymerase chain reaction was used to search for a CYP11B1/CYP11B2 chimeric gene. Pedigree investigations and genotype-phenotype analyses were performed for patients with rare variants. Nine rare variants were detected in eight patients (2.6%), but no CYP11B1/CYP11B2 chimeric gene was identified. One patient and two of her siblings were found to carry compound heterozygous mutations (C183Y and T390R) in CYP17A1 and were eventually diagnosed with atypical congenital adrenal hyperplasia. Patients with rare variants had younger ages of onset [17 (16, 20) vs. 30 (23, 35) years old, p = 0.010] and higher systolic blood pressure (148.5 ± 9.6 vs. 137.9 ± 17.8 mmHg, p = 0.021) than those without rare variants. Additionally, the patients and their relatives carrying rare variants exhibited increased serum free corticosterone [230.4 (7.4, 533.0) vs. 1.9 (0.9, 6.7)ng/ml, p = 0.001] and 11-deoxycorticosterone [16.16 (0.59, 33.23) vs. 0.77 (0.41, 0.96)ng/ml, p = 0.038] levels. Genetic testing is useful for the etiologic diagnosis of early-onset hypertension. Rare variants in steroid metabolism genes were associated with more severe clinical expression and abnormal circulating steroid metabolites in patients with early-onset hypertension.

Background The FHOD3 (formin homology 2 domain‐containing 3) gene has recently been identified as a causative gene of hypertrophic cardiomyopathy (HCM). However, the pathogenicity of FHOD3 variants remains to be evaluated. This study analyzed the spectrum of FHOD3 variants in a large HCM and control cohort, and explored its correlation with the disease. Methods and Results The genetic analysis of FHOD3 was performed using the whole exome sequencing data from 1000 patients with HCM and 761 controls without HCM. A total of 37 FHOD3 candidate variants were identified, including 25 missense variants and 2 truncating variants. In detail, there were 27 candidate variants detected in 33 (3.3%) patients with HCM, which was significantly higher than in the 12 controls (3.3% versus 1.6%; odds ratio, 2.13; P FHOD3 candidate variant experienced significantly more risk of cardiovascular death and all‐cause death (adjusted hazard ratio [HR], 3.71; 95%, 1.32–8.59; P =0.016; and adjusted HR, 3.02; 95% CI, 1.09–6.85; P= 0.035, respectively). Conclusions Our study suggests that FHOD3 is a causal gene for HCM, and that the presence of FHOD3 candidate variants is an independent risk for cardiovascular death and all‐cause death in HCM.

OBJECTIVES This study aimed to assess the safety, blood pressure changes, and biochemical responses of superselective adrenal artery embolization (SAAE) in hypertensive patients with idiopathic hyperaldosteronism (IHA). BACKGROUND SAAE is a minimally invasive procedure that has been used to successfully treat aldosterone-producing adenoma. However, its effect for patients with IHA is unevaluated. METHODS A total of 41 hypertensive patients who were diagnosed with IHA and underwent SAAE at the Fuwai Hospital between December 2010 and June 2016 were prospectively enrolled. The blood pressure, antihypertensive medications, plasma aldosterone and potassium levels, and adverse events were assessed. The primary endpoint was the change in home blood pressure at 12 months, compared with baseline. RESULTS SAAE was technically successful in 39 patients. Postoperatively, home and 24-hr mean blood pressures were reduced by 14/9 and 10/7 mmHg at 1 month, respectively, and by 13/7 and 11/7 mmHg at 12 months, respectively. The number of antihypertensive agents used reduced by 1.0 and 1.1 at 1 month and 12 months, respectively (all p

OBJECTIVES This study aimed to evaluate the safety and clinical efficacy of external carotid artery (ECA) stenting in patients with ipsilateral internal carotid artery (ICA) occlusion. BACKGROUND In patients with ICA occlusion, severe ipsilateral ECA stenosis may exacerbate pre-existing cerebral ischemia and cognitive impairment. It remains unclear whether ECA stenting to normalize ECA collaterals to the cerebralis alleviates cerebral ischemia and improves cognitive function. METHODS From January 2008 to June 2019, we retrospectively collected clinical data of 36 consecutive patients with ipsilateral ICA occlusion who had undergone ECA stenting (mean age, 66.7 ± 8.3 years; males, n = 26 [72.2%]). Neurocognitive test results, including Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MOCA) tests, symptom assessment, and adverse events were recorded. RESULTS ECA stenting was successful in all 36 patients. Intra-operatively, six (16.7%) patients experienced hemodynamic depression during balloon dilation and recovered completely within 2 days. Within a 12-month follow-up period, two patients experienced a transient ischemic attack, one patient had a contralateral minor stroke, and 33 patients remained asymptomatic. No other adverse events occurred in the peri-operative or follow-up periods. Compared with baseline, significant MMSE (25.3 ± 1.3 vs. 23.6 ± 1.7; p

Chemokines were seldom investigated in Takayasu arteritis (TA) patients. This study aimed to evaluate the plasma levels of chemokines and their association with disease activity, including C-C chemokine ligand (CCL) 2, CCL3, CCL11, CCL20, C-X-C chemokine ligand (CXCL) 8 and CXCL10.Chemokines were measured in 85 TA patients, and 28 age- and gender-matched healthy controls. The disease activity of these TA patients was assessed according to the National Institute of Health (NIH) criteria. The relationship between the plasma levels of chemokines and disease activity was analyzed.Among the 85 TA patients, 24 (28.2%) patients had active disease according to the NIH criteria. Significantly increased levels of CCL2, CCL3, CCL20, CXCL8 and CXCL10 were observed in TA patients when compared to healthy controls, while increased levels of CCL2, CCL20, CXCL8 and CXCL10 in TA patients with active disease when compared to those with inactive disease (all p 0.05). The plasma cut-off values of CCL2, CCL20, CXCL8 and CXCL10 were 309.6 pg/ml, 131.4 pg/ml, 4.7 pg/ml, and 282.1 pg/ml, which maximized the ability of disease activity assessment and had a sensitivity/specificity of 66.7%/67.2%, 54.2%/77.1%,70.8%/72.1%,83.3%/54.1%, respectively (p 0.05). Among patients with negative erythrocyte sedimentation rate, C-reactive protein or high-sensitivity C-reactive protein, CCL2, CCL20, CXCL8, and CXCL10 still had a high-sensitivity to recognize patients in the active phase.This study showed that the expression level of CCL2, CCL20, CXCL8 and CXCL10 was elevated in active TA patients, indicating that these chemokines might act as potential biomarkers in evaluating the disease activity.

OBJECTIVES To evaluate the safety and feasibility of simultaneous endovascular therapy for supra-arch multivessel stenosis. BACKGROUND Limited data are currently available on simultaneous intervention for supra-arch multivessel stenosis because of concerns regarding the high incidence of procedure-related complications. METHODS From January 2005 to December 2012, the clinical data of 256 consecutive inpatients who underwent simultaneous intervention for supra-arch multivessel stenosis were retrospectively analyzed. The primary end point was a composite of any type of stroke or neurological death within 30 days. RESULTS In total, 535 supra-arch vessels underwent endovascular therapy. In total, 234, 21, and 1 patient underwent simultaneous intervention of 2, 3, and 4 supra-arch vessels, respectively. The lesions involved only the anterior circulation in 40.2% (103/256), only the posterior circulation in 10.5% (27/256), and the combined circulations in 49.2% (126/256) patients. The overall procedural success rate was 99.6% (533/535). The incidence of the primary end point was 3.5%. According to the lesion location, the incidence of the primary end point was 3.9% (4/103), 0% (0/27), and 4.0% (5/126) in the patients who underwent endovascular treatment for the anterior circulation alone, posterior circulation alone, and combined circulations, respectively. According to the number of supra-arch lesions, the incidence of the primary end point was 3.4% (8/234), 4.8% (1/21), and 0% (0/1) in the patients who underwent simultaneous intervention of 2, 3, and 4 vessels, respectively. CONCLUSIONS The study showed that simultaneous intervention for supra-arch multivessel stenosis was safe and technically feasible.

Background Filamin C (FLNC) mutation was reported as a cause of HCM, with a high probability of sudden cardiac death. However, the mutation profile of FLNC, and its relationship with phenotypic expression in HCM, remains to be elucidated. Methods In this study, FLNC gene was sequenced in 540 HCM patients and 307 healthy controls. Results We found that 39 (7.2%) patients carried FLNC mutations, with a similar frequency to that of controls (4.2%, p = 0.101). Pedigree analysis showed that mutations were not well segregated with HCM. The baseline characteristics between HCM patients, with and without mutations, were comparable. FLNC mutations did not increase the risk for either all‐cause mortality (HR 0.746, 95% CI 0.222–2.295, p = 0.575) or cardiac mortality (HR 0.615, 95% CI 0.153–1.947, p = 0.354) in HCM patients during a follow‐up of 4.7 ± 3.2 years. Moreover, there was no significant difference in survival free from sudden cardiac arrest (HR 0.721, 95% CI 0.128–3.667, p = 0.660) and heart failure (HR 0.757, 95% CI 0.318–1.642, p = 0.447). Conclusions FLNC mutations were common in both HCM patients and healthy population. The pathogenicity of FLNC mutations detected in HCM patients and its association with the clinical outcomes should be cautiously interpreted.

Objective This study was performed to explore the effect of the aortic arch type on technical indicators in patients undergoing carotid artery stenting (CAS). Methods The data of 224 consecutive patients who underwent unilateral CAS from January 2011 to December 2012 were retrospectively analyzed. The requirement for placement of the guiding catheter into the common carotid artery with assistance of an angiographic catheter, fluoroscopy time, contrast agent dose, and adverse events were recorded. Results The fluoroscopy time was significantly longer and the contrast agent dose was significantly higher in patients with Type III than Type I and II arches. Significantly more patients with Type III than Type I and II arches required placement of the guiding catheter with assistance of an angiographic catheter (46.2% vs. 15.0%, respectively). The procedural success rate was significantly lower in patients with Type III than Type I and II arches (96.2% vs. 100.0%, respectively). The incidence of death, myocardial infarction, and all types of stroke was significantly higher in patients with Type III than Type I and II arches (7.7% vs. 1.7%, respectively). Conclusions The aortic arch type is an important influential factor in CAS. Type III arches are associated with more difficulties and complications.

The time trends regarding the etiology of renal artery stenosis (RAS) are changing, but few investigations have focused on these issues. This study aimed to analyze the time trends regarding the etiology of RAS in a large patient sample from the China Center for Cardiovascular Disease. Consecutive inpatients with RAS from January 1999 to December 2016 were enrolled in this study. The etiologic diagnosis of RAS was based on established criteria. We retrospectively analyzed the time trends regarding the etiology of RAS during an 18-year period. A total of 2905 patients with RAS were enrolled. There were 2393 (82.4%) patients with atherosclerosis (AS), 345 (11.9%) with Takayasu arteritis (TA), 126 (4.3%) with fibromuscular dysplasia (FMD), and 41 (1.4%) with other causes. Among all patients (n = 2905), patients aged ≤ 40 years (n = 450), patients aged40 years (n = 2455), female patients (n = 1097), male patients (n = 1808), female patients aged40 years (n = 808), and male patients aged40 years (n = 1647), there were a gradual increase in the proportion of atherosclerotic RAS (P 0.05), a gradual decrease in the proportion of RAS caused by TA (P 0.05), and almost no change in the proportion of RAS caused by FMD during the 18-year period (P 0.05). The data show that the primary causes of RAS are AS, TA, and FMD. The proportion of RAS caused by AS and TA gradually increased and decreased, respectively, over time, and the proportion of RAS caused by FMD showed no significant change.

Background Titin-truncating variants (TTNtv) have been detected in a variety of cardiomyopathies and represent the most common cause of dilated cardiomyopathy. However, their significance in hypertrophic cardiomyopathy (HCM) is still unclear. Methods The titin gene ( TTN ) was sequenced for truncating variants in a cohort of 529 Chinese patients with HCM and 307 healthy controls. Baseline and follow-up clinical data (for 4.7 ± 3.2 years) from these patients were obtained. Results We identified 13 and 8 TTNtv in patients with HCM (13 of 529 [2.5%]) and controls (8 of 307 [2.6%]), respectively. The prevalence of TTNtv in patients with HCM and in healthy controls was comparable ( P = 0.895). There were no significant differences in baseline characteristics between patients with and those without TTNtv. However, during follow-up, patients with TTNtv (3 of 13 [23.1%]) were more likely to experience cardiovascular death compared with those without TTNtv (39 of 516 [7.6%]) [adjusted hazard ratio, 6.88; 95% confidence interval, 2.04-23.20; P = 0.002). Conclusions Our study suggests that TTNtv might be a genetic modifier of HCM and confer an increased risk for cardiovascular death.

Objectives: To evaluate the safety and feasibility of subclavian artery stenting for coronary-subclavian steal syndrome (CSSS). Background: CSSS is a rare cause of myocardial ischemia due to ipsilateral subclavian artery stenosis in patients who have undergone coronary artery bypass graft. However, current knowledge of the optimal therapy for CSSS is limited. Methods: The clinical data of 37 patients (33 male; mean age 65 ± 6 years) with CSSS who had undergone subclavian artery stenting between April 2007 and December 2015 were analyzed. Results: The time elapsed between bypass surgery and the diagnosis of CSSS was 6.3 ± 4.3 years (median 5.2 years, range 1.3 months to 17.8 years). The technical success rate was 97.3% (100% for stenosis, 85.7% for occluded lesions). One patient experienced a transient ischemic attack; a second patient developed flow-limiting dissection involving the ostium of the internal mammary artery; and a third patient had a puncture site hematoma. The mean stenosis of target lesions decreased from 87.6 ± 10.6% to 5.9 ± 5.0% immediately after the procedure. A total of 35 (94.6%) patients were discharged with a complete remission of myocardial ischemia. During a follow-up of 44 ± 32 (range 6–112) months, no patient suffered from stroke or myocardial infarction. Stent-restenosis related unstable angina developing in one patient at 36 months and in another patient at 11 months, both of whom were relieved after balloon angioplasty and remained asymptomatic until the last follow-up. Conclusion: Subclavian artery stenting is feasible and safe in patients with CSSS, with a low incidence of perioperative complications and stent restenosis rate. © 2016 Wiley Periodicals, Inc.

Objectives: The relationship between a fragmented QRS (fQRS) and clinical outcomes in patients with hypertrophic cardiomyopathy (HCM) remains unclear. This study aimed to investigate the prognostic significance of fQRS in patients with HCM. Methods: Between 2000 and 2012, 326 unrelated patients with HCM (72% male with a mean age of 52 years) were included and were divided into 2 groups: those with fQRS and those without fQRS. Results: A total of 105/326(32.2%) patients with HCM presented with fQRS at enrollment. During a follow-up of 5.3 ± 2.4 years, 33 patients died, 30 of cardiovascular disease (CVD). Cox regression analysis revealed that fQRS predicted a higher risk of all-cause mortality (adjusted hazard ratio [HR] 2.24; 95% confidence interval [CI] 1.08-4.64; p = 0.030) and CVD mortality (adjusted HR 2.68; 95% CI 1.22-5.91; p = 0.014). Our study also showed that fQRS increased the risk of heart failure-related death (adjusted HR 3.75; 95% CI 1.24-11.30; p = 0.019). Conclusions: Our results indicate that fQRS is associated with adverse clinical outcomes in patients with HCM.

OBJECTIVES This study aimed to evaluate the safety and efficiency of percutaneous transluminal angioplasty (PTA) with selective stenting treating Chinese patients with renal artery stenosis (RAS) due to fibromuscular dysplasia (FMD). BACKGROUND Endovascular data of patients with RAS caused by FMD are scarce in China. METHODS Clinical data of 105 hypertensive patients with RAS caused by FMD underwent endovascular therapy at a single-site between June 2001 and October 2018 were analyzed retrospectively. Baseline blood pressure, use of antihypertensive medications, renal function, and adverse events at a 1-year follow-up were evaluated. RESULTS The patients were aged between 10 and 64 years (mean age 26.7 ± 8.2 years) and 52 (49.5%) were female. In total, 105 patients undergoing endovascular therapy involving 124 RASs. Thirty (24.2%), sixty-four (51.6%), and thirty (24.2%) RASs were multifocal, unifocal, and tubular types, respectively. Ninety-four (89.5%) and eleven (10.5%) patients underwent PTA alone and PTA plus stenting, respectively. The technical success rate for endovascular therapy was 95.2% (100/105) without severe complications. During 1-year follow-up (n = 100), the mean systolic and diastolic blood pressure decreased from 157.6 ± 17.5 and 102.3 ± 14.2 to 129.6 ± 12.3 and 81.3 ± 11.1 mmHg, respectively, and the number of antihypertensive medications reduced from 2.2 ± 1.2 to 0.8 ± 1.0 (all p

OBJECTIVE This study aimed to evaluate the effect of stenting on blood pressure in hypertensive patients with symptomatic proximal subclavian or vertebral artery stenosis. BACKGROUND Whether posterior circulation revascularization could reduce blood pressure in hypertensive patients with posterior circulation hypoperfusion has not been investigated in humans. METHODS A total of 48 patients with essential hypertension (33 males; mean age 63.0 ± 8.7 years) with symptomatic proximal subclavian or vertebral artery stenosis who underwent stenting successfully at the Fuwai Hospital were prospectively enrolled between January 2014 and December 2015. All 48 patients were followed up at 1, 3, and 6 months after the procedure. Blood pressure, use of antihypertensive agents, and complications were investigated. RESULTS Baseline values included office blood pressure of 132/77 ± 10/8 mmHg, mean 24-hr blood pressure of 127/75 ± 12/9 mmHg, and mean antihypertensive agents used of 1.6 ± 0.8. Stenosis of the subclavian and vertebral arteries decreased from 88.9 ± 9.5% and 85.8 ± 7.4% to 5.5 ± 3.5% and 4.6 ± 3.7%, respectively, immediately after the procedure. Reductions in office blood pressure were - 7/-3 (SD 3/2), -9/-4 (5/3), and - 10/-5 (7/5) mmHg at 1, 3, and 6 months, respectively. While 24-hr blood pressures after the procedure reduced by -5/-3 mmHg at 6 months, the total number of antihypertensive agents used at the aforementioned time points was unchanged. CONCLUSION This first prospective cohort study in humans showed that posterior circulation stenting is apparently effective in reducing blood pressure in hypertensive patients with symptomatic proximal subclavian or vertebral artery stenosis.

Gene diagnosis refers to the use of genetic testing in the diagnosis of inheritable conditions, which has gradually been applied in clinical practice with the completion of the gene sequencing efforts of the Human Genome Project and the advancement of gene detection technology. In the specialty field of cardiology, monogenic cardiovascular diseases are defined as monogenic inherited diseases with cardiovascular damage as the only phenotype, or accompanied by cardiovascular damage. Although the incidence of such diseases is relatively low, in the country of China with its vast population of 1.33 billion, the sheer volume of patients with monogenic cardiovascular diseases is alarming. With early onset, severe symptoms, and poor prognosis, delays in diagnosis and treatment of monogenic cardiovascular diseases often have serious consequences. Gene testing is perfectly suited for early diagnosis of monogenic cardiovascular diseases, especially for “pre-symptomatic” diagnosis. In this article, we generally review the characteristics of common monogenic cardiovascular diseases, summarize the progress of the standardized application of gene testing technology in clinical practice, describe the applicable population and condition of genetic testing for different monogenic cardiovascular diseases, analyze the practicality of genetic diagnosis of these inheritable conditions, and provide guidance on identifying suitable candidates for gene diagnosis. In conclusion, gene diagnosis provides new insights into the way physicians diagnose diseases, and is well-positioned to guide clinical decision making and treatment, especially in cardiology. Keywords: Cardiovascular diseases, Precision medicine, Gene testing, Early diagnosis, Cardiovascular diagnostic techniques

Background Animal studies suggested that blocking the activation of the mammalian target of rapamycin (mTOR) pathway might be effective to treat cardiac hypertrophy in LEOPARD syndrome (LS) caused by PTPN11 mutations. Results In the present study, mTOR pathway activity was examined in human myocardial samples from two patients with LS, four patients with hypertrophic cardiomyopathy (HCM), and four normal controls. The two patients with LS had p.Y279C and p.T468 M mutations of the PTPN11 gene, respectively. Although PTPN11 mutation showed initially positive regulation on phosphoinositide 3-kinase, overall the mTOR complex 1 pathway showed widely attenuated activity in LS. This included mildly hypophosphorylated mTOR and ribosomal protein S6 kinase and significantly hypophosphorylated Akt308 and ribosomal protein S6, which is similar to HCM. Akt473 is a basal molecule of the mTOR complex 2 pathway. Akt473 was less affected and showed hyperactivity in LS compared with HCM and normal controls. Additionally, MAPK/ERK kinase and ERK1/2 were significantly more phosphorylated in both HCM and LS than normal controls. Conclusions In LS, the mTOR signaling pathway shows similar activity to HCM and is attenuated compared with normal controls. Thus, caution should be applied when using rapamycin to treat heart hypertrophy in LS.

To evaluate the efficacy of renal artery stent combined with optimal medical therapy as treatment for renal artery stenosis.A prospective cohort study was conducted. Patients with severe atherosclerotic renal artery stenosis received percutaneous renal artery stent because of poorly controlled hypertension or preservation of renal function. The patients also received optimal medical therapy to achieve the blood pressure, lipid and blood glucose targets.All patients underwent a 12 month follow-up to observe the effect of the procedure on blood pressure control, number of antihypertensive medications and creatinine level.Stents were placed in 185 renal arteries of 149 patients. Mean stenosis was 83.1 ± 7.0%. The success rate of renal artery stent was 99.3%. At 12 months, estimated glomerular filtration rate increased significantly compared with baseline (84.1 ± 28.8 vs. 76.5 ± 22.50 ml/min ×1.73 mRenal artery stent combined with optimal medical therapy as a treatment has a beneficial effect on blood pressure control and estimated glomerular filtration rate in selected patients with atherosclerotic renal artery stenosis. Larger studies with a longer follow-up appear necessary to further confirm these intriguing findings.

Background: MicroRNAs play a crucial role in the regulation of pathological cardiac remodeling and heart failure. Previously, we found that overexpression of miR-221 induces heart failure in mice. The miR-222 and miR-221 share the same gene cluster, however, the role of miR-222 in the regulation of cardiac function remained ill-defined. Methods and Results: Transgenic mice with cardiac-specific expression of miR-222 (Tg-miR-222) mice were generated. The Tg-miR-222 mice developed significantly enlarged hearts at 4 weeks of age. Transthoracic echocardiograph data indicated that the hearts of Tg-miR-222 mice exhibited an increased left ventricular end-diastolic internal diameter and decreased fractional shortening. We observed that the LC3-II in Tg-miR-222 mice was decreased accompanied with the upregulation of p62, indicating the autophagy inhibition in the hearts of Tg-miR-222 mice. The mTOR pathway, a negative regulator of autophagy, was activated in the hearts of Tg-miR-222 mice. The expression of p27 was downregulated by miR-222 overexpression. Conclusion: Our data indicate that miR-222 overexpression induces heart failure in mice. The downregulation of p27 and the activation of mTOR pathway may be involved in miR-222-induced heart failure and autophagy inhibition. Thus, targeting miR-222 expression may be a therapeutic strategy against pathological cardiac remodeling.

To examine whether spironolactone could reduce the severity of obstructive sleep apnea (OSA) and lower blood pressure in patients with resistant hypertension.This was a blank-controlled, single-center study. Patients with resistant hypertension and moderate-to-severe OSA (apnea-hypopnea index15 events/h) were enrolled and randomly assigned to the therapy or control group. Patients in the therapy group were administered spironolactone 20 mg once daily (up to 40 mg once daily for 4 weeks, if required) in addition to original antihypertensive medication. Follow-up was 12 weeks.Thirty patients were enrolled (n = 15 per group). After 12 weeks of follow-up, apnea-hypopnea index (21.8 ± 15.7 vs. 1.8 ± 12.8, p0.05), hypopnea index (9.8 ± 11.1 vs. -2.7 ± 16.8, p0.05), oxygen desaturation index (20.8 ± 15.0 vs. 0.3 ± 16.1, p0.05), clinical blood pressure, ambulatory blood pressure, and plasma aldosterone level (9.8 ± 6.3 vs. 2.9 ± 6.7, p0.05) were reduced significantly in the therapy group compared with the control group. No side effects were reported.Spironolactone reduced the severity of OSA and reduced blood pressure in resistant hypertension patients with moderate-to-severe OSA. These findings may assist in the treatment of OSA in patients with resistant hypertension.

Objectives To evaluate the early and long-term outcomes of stent placement for left subclavian artery stenosis (LSAS) in patients scheduled for left internal mammary artery-coronary artery bypass grafting (LIMA-CABG). Background Few studies have demonstrated the safety and effectiveness of endovascular therapy for the treatment of LSAS before LIMA-CABG; therefore, use of this therapy requires further exploration and evaluation. Methods Between February 2000 and April 2014, the clinical data of 167 consecutive patients (mean age 64 ± 9 years, 141 males) scheduled for LIMA-CABG with LSAS who were treated by stenting at the Fuwai Hospital were collected and analyzed retrospectively. Results The technical success rate of the procedure was 97.6% (163/167). The mean stenosis of target lesions decreased from 86.5 ± 9.9% to 7.6 ± 4.6% (P

Purpose: To evaluate clinical outcomes of simultaneous bilateral carotid artery stenting (sbCAS) compared with unilateral CAS (uCAS). Methods: The database in our institution was queried to identify all patients treated with CAS from January 2005 to December 2012. In this time frame, 120 (18.8%) patients (mean age 64.9±7.7 years; 96 men) underwent sbCAS and 517 (81.2%) patients (mean age 65.7±7.7 years; 421 men) received uCAS. The primary endpoint was the composite of stroke, myocardial infarction, or death within 30 days or any ipsilateral stroke within 1 year. Results: There was no significant difference in the rates of the primary endpoint between the sbCAS and uCAS groups (6.7% vs 4.6%, p=0.358). The rates of the primary endpoint among symptomatic patients was 8.0% in the sbCAS group and 5.0% in the uCAS group (p=0.299) and 3.1% and 4.0%, respectively (p=0.821) among asymptomatic patients. During the 30-day periprocedural period, the rates of the primary endpoint did not differ significantly between the sbCAS and uCAS groups among all patients (5.8% vs 4.4%, p=0.479), symptomatic patients (6.8% vs 5.0%, p=0.594), or asymptomatic patients (3.1% vs 3.5%, p>0.999). After this period, the incidences of any ipsilateral stroke were similarly low (0.8% and 0.2%, respectively; p=0.342). Conclusion: The study showed that simultaneous bilateral CAS had no more adverse events than unilateral CAS during the periprocedural period or within 1 year. This 1-stage strategy may become a valuable alternative in the treatment of patients with severe bilateral carotid stenosis.