The goal of the China chest pain center (CPC) is to optimize the diagnosis and treatment processes for patients with acute chest pain by establishing a regional cooperative rescue system. This article introduces the developing history, accreditation criteria, current status, efficiencies of accreditation, and prospects of the China CPC.

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Percutaneous coronary intervention (PCI) has become the mainstay in the treatment of coronary heart disease (CHD). In the past 10 years, the number of PCI procedures for CHD has maintained an annual growth of 15%–20% on average in China. As a consequence, in-stent restenosis (ISR) has become an increasingly serious problem with the wide application of coronary stents. Certainly, current treatment regimens for ISR are unsatisfactory in some aspects. Coronary artery bypass surgery has many risk factors and contradictions and a second stent implantation is associated with the risk for recurrent ISR and additional stent implantations; the rate of recurrent ISR in lesions after plain old balloon angioplasty is high (up to 27%). Therefore, all these regimens are suboptimal for the treatment of ISR. In recent years, drug-coated balloon (DCB), a novel interventional technique, has been increasingly used in coronary and peripheral artery interventions in Europe and Asia. In China, several DCB products have been or will be marketed for clinical application. The introduction of DCB provides a new choice for the treatment of coronary artery diseases in China. Based on several national and international clinical trials, >20 experienced experts in the PCI field from China have proposed the China expert consensus on clinical application of the DCB with evidence-based validation and session discussion in order to promote the standardized application of the DCB in the treatment of coronary artery diseases in China.

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The benefits of atherosclerotic cardiovascular disease prevention/treatment and lipid-lowering therapy come from the reduction of cholesterol itself. However, based on safety considerations, all guidelines note that high-intensity statin therapy is not suitable for the Asian/Chinese population. Therefore, moderate-intensity statin therapy is more beneficial for the Chinese population. However, for some very high-risk patients when moderate-intensity statin cannot satisfy the lipid-lowering needs, statin combination with ezetimibe is an ideal choice.

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Objective: This study aims to evaluate the effects of exercise training on heart function of mice with diabetic cardiomyopathy. Materials and Methods: Twenty-four healthy C57 mice were randomly divided into three groups high-fat exercise group (n = 8), high-fat control group (n = 8), and low-fat control group (n = 8). High-fat groups were fed with a high-fat diet for 16 weeks, and the high-fat exercise group was subjected to aerobic treadmill exercise and resistance exercise for 8 weeks. After 24 weeks, the cardiac structure and function of the three groups were detected, and the indexes of the mouse heart were analyzed and compared. Results: The high-fat control group maintained hyperglycemia. The results of echocardiography showed that left ventricular eject fraction in the high-fat exercise group and the low-fat control group was significantly higher than that of the high-fat control group (68.99% ± 2.04% vs. 60.41% ± 2.31%, 66.16% ± 2.12% vs. 60.41% ± 2.31%, P < 0.01). In the diastolic function of the heart, blood flow peak velocities of the early peak at the mitral valve in the high-fat exercise group and the low-fat control group were significantly higher than that in the high-fat control group (709.73 ± 45.48 mm/s vs. 441.51 ± 44.83 mm/s, 632.92 ± 27.22 mm/s vs. 441.51 ± 44.83 mm/s, P < 0.01), the peak velocities of the atrial peak at the mitral valve were significantly lower than that of the high-fat control group (443.77 ± 18.09 mm/s vs. 523.67 ± 57.87 mm/s, 460.36 ± 18.24 mm/s vs. 523.67 ± 57.87 mm/s, P < 0.05), and the ratio of E/A was significantly higher than that of the high-fat control group (1.63 ± 0.06 vs. 0.85 ± 0.045, 1.38 ± 0.072 vs. 0.85 ± 0.045, P < 0.01). Myocardial performance index decreased (0.86 ± 0.095 vs. 0.97 ± 0.091, 0.88 ± 0.073 vs. 0.97 ± 0.091, P > 0.05), but there was no significant difference. Conclusion: The above data indicated that 8 weeks of exercise training can improve the heart function of mice with diabetic cardiomyopathy, especially diastolic heart function. Left ventricular systolic function had some trend to improve, but there is no statistical difference. Exercise intervention may promote the rehabilitation of diabetic cardiomyopathy.

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Left atrial appendage closure (LAAC) technology has been developing over 10 years from its research and development to routine clinical application and has acquired solid evidence-based support through the Protection in Patients with Atrial Fibrillation, PREVAIL, and other registered studies. However, this technology still faces misinterpretation and confusion over its concept and acceptance as a universal clinical application. In this review, we try to provide an in-depth analysis of current perceptions and arguments focused on LAAC from its concept, operation, and other important issues.

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As a serious and terminal stage of multiple cardiovascular diseases, heart failure (HF) is one of the most critical components of the current global strategies for the prevention and management of chronic diseases. With aging and the increased incidence of various cardiovascular diseases and related risk factors in the population, HF has also become a main reason for hospitalization and death of the elderly in China, which has resulted in a heavy burden on public health system and the economy. A 2003 report suggested that the prevalence of HF in China was 0.9%, higher in women than in men, and is increasing in proportion with aging. Although the mortality rate of HF seen in hospitals has declined, the long-term prognosis of HF in China is discouraging as demonstrated by a 3-year mortality rate of approximately 30%. HF diagnosis by brain natriuretic peptide, N-terminal pro-B-type natriuretic peptide, and echocardiography in China is unsatisfactory. Room for improvement is needed in drug and nondrug HF treatment in China. Intensive efforts are also needed to promote a real-world use of the current guidelines for recommended drugs that could improve HF patients' prognosis, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and β-blockers. Much work is also needed to embrace the concept of HF management and systems in China. In the future, more attention should also be given to domestic epidemiological and clinical study of HF, focusing on transformation of experimental results to a clinic setting, and ongoing recognition of and attention to HF preserved ejection fraction. An efficient HF management system in China should also highlight the importance of establishing the most cost-effective prevention and therapy strategies.

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Background: Antiplatelet drugs are widely used in the prevention and treatment of arterial thrombotic diseases but are associated with increased risk of bleeding. Alginate oligosaccharide (AOS), a biodegradable polymer extracted from macroalgae, has been shown to inhibit phosphorylation of mitogen-activated protein kinases, which, in turn, are critical for platelet activation. The present study aimed to examine whether AOS possesses antiplatelet and antithrombotic activity, and if so, the underlying mechanisms. Methods: We detected the effects of AOS on human platelet aggregation and adenosine triphosphate (ATP) release induced by thrombin and collagen, as well as platelet clot retraction and spreading. FeCl₃-injured mouse mesenteric arteriole thrombosis was evaluated in adult C57BL/6 mice pretreated with either AOS (200 mg/kg/d through gavage for 7 consecutive days) or clopidogrel (30 mg/kg/d for 2 days). The impact of AOS on bleeding time in comparison to clopidogrel was also analyzed. Results: At a range of 0.1–1.0 mg/mL, AOS concentration dependently inhibited human platelet aggregation and ATP release induced by thrombin and collagen, as well as platelet clot retraction and spreading. The final occlusion time injured by FeCl₃in mice pretreated with AOS was significantly increased (from 11.9 ± 0.9 min in vehicle control to 17.6 ± 1.0 min, P < 0.01), as well as the first occlusion time (from 4.4 ± 0.5 min in vehicle control to 7.6 ± 0.7 min, P < 0.01). Bleeding time on tail snip was 534 ± 62 s in vehicle control, 581 ± 60 s in mice with AOS pretreatment (P = 0.59 vs. control), and 1260 ± 83 s in mice receiving clopidogrel pretreatment (P < 0.01 vs. control). Preliminary mechanistic investigation using human platelets showed a decreased level of phosphorylated MAP kinases (i.e., p38, Erk1/2, and JNK) by AOS. Conclusions: AOS has antiplatelet and antithrombotic activity, with minimal impact on bleeding time.

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Objective: The aim of this study is to observe the maintenance of stem cell properties of purified CD34-positive cells in vessel walls during in vitro expansion. Materials and Methods: Cells that migrated from the adventitial tissues of rat were collected and purified by microbead selection method to obtain CD34+ vascular wall-resident stem (VRS)/progenitor cell (PC). Those purified CD34+ VRS/PCs were evaluated by flow cytometry and immunofluorescent staining. The CD34+ VRS/PCs were continuously cultured until passage P3. Each passaged cell was evaluated by flow cytometry with anti-CD34. Results: After microbead selection, the CD34+ cells reached 88.07% ± 4.36% and these cells expressed neither endothelial (CD31) nor mature smooth muscle cell (smooth muscle-myosin heavy chain and SM22α) markers. Incubation of the purified CD34+ VRS/PCs at a density of 1.5 × 10⁵ cells/100-mm dish, resulted in a gradual reduction of CD34-positive traits when passaged in vitro, starting at P1. Interestingly, the purified primary CD34+ VRS/PCs at a density of 1.0 × 10⁴ cells per 100-mm dish show the traits of colony form growth, and P1 passaged cells were 79.2% ± 2.15% positive for CD34, then gradually lost the traits of CD34-positive cells when passaged in vitro. Conclusions: High purity CD34+ VRS/PCs can be obtained by magnetic bead screening. In vitro, low cell densities contribute to the maintenance of CD34+ VRS/PC traits.

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Objectives: Pulmonary arterial hypertension (PAH) is a syndrome resulting from a restricted flow through the pulmonary arterial circulation, giving rise to increased pulmonary vascular resistance (PVR) and ultimately right heart failure. Previous reports have suggested that Galectin-3 (Gal-3) induced endothelial cell morphogenesis and regulated myofibroblast activation. The aim of this study was to determine the diagnostic utility of circulating Gal-3 as a potential biomarker of disease severity in PAH. Methods: Gal-3 was measured in plasma from 31 patients with PAH, diagnosed from the right heart catheterization as well as 18 healthy controls by ELISA. Chronic hypoxia-induced pulmonary hypertension models were established in Sprague-Dawley rats. Lung tissues were collected for histological analysis including Gal-3 lung qualitative localization by immunohistochemistry. Total mRNA was extracted from pulmonary arteries in rats and quantitative polymerase chain reaction was performed with total cellular mRNA to measure Gal-3 expression. Results: Plasma level of Gal-3 was significantly decreased in PAH patients compared with healthy controls (P < 0.001). Within the subgroups, only by idiopathic PAH (IPAH) patients expressed the lower level of Gal-3 (n = 16, P < 0.001). Gal-3 levels were inversely correlated with mean pulmonary arterial pressure (mPAP) (r = − 0.570, P = 0.021) and PVR (r = − 0.550, P = 0.027), and correlated with cardiac output (r = 0.530, P = 0.035) in IPAH patients. A Gal-3 cutoff value <1.765 ng/ml yielded 93% sensitivity and 88% specificity for IPAH patients. Immunohistochemistry identified Gal-3 distribution throughout the adventitia of the pulmonary arterioles. The expression of Gal-3 mRNA was significantly downregulated in the pulmonary arteries from lung tissue samples in pulmonary hypertension rats. Conclusions: Gal-3 might be involved in the pathogenesis of PAH and plasma Gal-3 could serve as a promising new biomarker of diagnosis and disease severity in IPAH.

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Background: Myocardial fibrosis is closely associated with cardiac dysfunction, arrhythmia, and sudden cardiac death. A model of myocardial fibrosis induced by isoprenaline was used to determine the influence of exogenous adiponectin on myocardial fibrosis. Materials and Methods: A total of 30 mice were equally and randomly divided into three groups as follows: isoproterenol (ISO, n = 10), adiponectin and isoproterenol (APN + ISO, n = 10), and sham (n = 10). ISO (7.5 mg/kg/day) was injected intraperitoneally (i. p.) in the ISO group and APN + ISO group for three consecutive days to establish a model of myocardial fibrosis; normal saline was injected in the sham group. From day 4, adiponectin was injected (10 μg/kg/day; i. p.) in the APN + ISO group for 32 days; normal saline was injected in ISO and sham groups for 32 days. Five weeks later, mice were sacrificed, and myocardial tissue was dyed by Sirius Red to observe the collagen morphology. The collagen volume fraction was calculated. Protein and messenger RNA (mRNA) expression of type-I and type-III collagen in the myocardium was detected by reverse transcription-polymerase chain reaction and western blotting, respectively. Results: Type-I collagen in myocardial interstitial tissue was significantly increased in the ISO group. Collagen in myocardial interstitial tissue in the ISO + APN group was decreased significantly compared with the ISO group. Expression of type-I collagen mRNA in ISO and ISO + APN groups was significantly higher than that in the sham group (3.01 ± 0.78, 2.32 ± 0.82 vs. 1, respectively; P < 0.01). Expression of type-I collagen mRNA in the ISO + APN group was significantly lower than that in the ISO group (2.32 ± 0.82 vs. 3.01 ± 0.78, respectively; P < 0.01). Expression of type-III collagen mRNA in the ISO group, and ISO + APN group was significantly higher than that in the sham group (2.39 ± 0.70, 1.62 ± 0.57 vs. 1, respectively; P < 0.01). Expression of type-III collagen mRNA in the ISO + APN group was significantly lower than that in the ISO group (1.62 ± 0.57 vs. 2.39 ± 0.70, respectively; P < 0.01). Expression of type-I collagen protein in the myocardium in the ISO + APN group was significantly higher than that in the sham group (0.73 ± 0.19 vs. 0.28 ± 0.15, respectively; P < 0.001), but it was significantly lower than the expression of type-I collagen protein in the ISO group (0.53 ± 0.17 vs. 0.73 ± 0.19, respectively; P < 0.001). Conclusions: Supplementation with exogenous adiponectin can inhibit myocardial fibrosis induced by ISO.

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Background: Our study sought to assess the effect of atorvastatin (ATV) and trimetazidine (TMZ) combination treatment in patients with non-ST elevation acute coronary syndromes (NSTE-ACS) undergoing percutaneous coronary intervention (PCI). Materials and Methods: Two hundred and fifty patients with NSTE-ACS who were undergoing PCI were enrolled in this study. Standard secondary prevention of coronary heart disease drug treatment was administered to both the groups (the ATV + TMZ group and the ATV group). In the ATV + TMZ group, patients were given 80mg of the combination medical orally 12h before PCI, 60mg 30min before PCI, and a further 20mg every day for 30t days after PCI, and. In the ATV group, patients were given only 80mg orally 12h before PCI, with a further 20mg every day for 30t days after PCI. Echocardiography was executed and plasma N-terminal pro brain natriuretic peptide (NT-pro-BNP) levels were measured just prior to the PCI and at 30 days after PCI. The major cardiovascular events (MACE) were also evaluated in both groups 30 days after PCI. Results: MACE occurred in 14.17% of patients in the ATV group and 6.50% of those in the ATV + TMZ group (P = 0.047). NT-pro-BNP levels were decreased 30 days after PCI for both groups; however, NT-pro-BNP levels in the ATV + TMZ group were significantly lower than those in the ATV group (P < .05). Cardiac function in NSTE-ACS patients, as reflected by the increased left ventricular ejection fraction, fractional shortening as well as decreased left ventricular end-diastolic dimension (P < .05) increased in all groups at 30 days after intervention, but cardiac function parameters were more significantly improved in the group administered with ATV + TMZ (P < .05). Conclusions: Our study suggests that short-term pretreatment with the combination of ATV and TMZ administration before PCI could reduce the incidence of MACE, further decrease NT-pro-BNP levels and improve cardiac function compared to a single administration of the ATV.

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Background: Nuanxin capsule is a standardized Chinese herbal medication that is commonly used alongside conventional treatment for chronic heart failure (CHF) in China. However, whether or not it improves outcomes is unknown due to the lack of high-quality randomized controlled trials (RCTs). Methods: We did a patient-level pooled-analysis of 14 RCTs in which 1112 CHF patients from nine medical centers in China were enrolled. These patients were randomly assigned to treatment with Nuanxin capsule in addition to conventional treatment, conventional treatment with placebo, or conventional treatment alone. Our primary outcomes were mortality and rehospitalization rate. Secondary outcomes included New York Heart Association (NYHA) functional classification, plasma brain natriuretic peptide, 6-min walking distance, echocardiographic parameters, and noninvasive hemodynamic parameters. Results: Treatment with Nuanxin capsule significantly decreased mortality (risk ratio [RR] = 0.30, 95% confidence interval [CI] 0.15–0.58, P = 0.0003, I² = 0%) and rehospitalization rate (RR = 0.47, 95% CI 0.36–0.62, P < 0.00001, I² = 0%). Nuanxin capsule therapy also had favorable effects on secondary outcomes. Fail-safe = 0.05 value for NYHA functional classification showed negligible publication bias, with a very low probability that future studies can change the current conclusion. Conclusion: We provided conclusive evidence for the beneficial effects of Nuanxin capsule in patients with CHF.

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Aims: Stratification of the risk of malignant arrhythmias in patients with coronary artery disease remains a challenge. This study evaluated the potential of high voltage J-waves in patients with acute ST-segment elevated myocardial infarction (STEMI) to predict the risk of malignant arrhythmias during hospitalization. Methods: A total of 128 consecutive STEMI patients with J-waves were enrolled within 48 h after the onset of the STEMI in this prospective study. The mean age was 62.97 ± 12.1 years, and 108 patients were male. Both 12-lead electrocardiograms (ECGs) and right-sided chest lead ECGs were recorded simultaneously within 10 min of admission to the hospital. Continuous ECG monitoring was administered from admission until discharge. Clinical characteristics and ECG parameters were compared between patients who survived and those who died during hospitalization. Results: Malignant ventricular arrhythmias (MVAs) were seen with J-waves more frequently in STEMI patients who subsequently died (P < 0.05). J-wave voltage, QTDc, Tp-e, and the Tp-e/QT ratio increased significantly in patients who died (P < 0.05). Multivariate logistic regression analysis revealed that J-wave voltage (odds ratio [OR], 89.09; 95% confidence interval [CI], 2.606-3045.108; P < 0.05) and MVAs (OR, 4.296; 95% CI, 1.348–13.693; P < 0.05) were associated with the occurrence of sudden death in patients with STEMI during hospitalization. Conclusions: High voltage J-waves are a potential ECG parameter for predicting sudden death in patients with STEMI during hospitalization.

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Background: Angiotensin-converting enzyme 2 (ACE2) is an ACE homolog that converts angiotensin II into angiotensin-(1–7) (Ang-[1–7]). Tumor necrosis factor α (TNF-α), interleukin-1 β, and interleukin-6 are plasma inflammatory cytokines that play a role in the development of hypertension and chronic heart failure (CHF). However, the relationship between soluble ACE2 (sACE2), Anti-ACE2, Ang-(1–7), and the plasma inflammatory cytokines during the development of CHF remains unclear. Methods and Results: A total of 135 patients with CHF were enrolled in this study (63 males and 72 females), with left ventricular ejection fraction (LVEF) <50%. The height and body weight of each patient was measured to calculate the body mass index. The plasma concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured using immunofluorescence. The patients were divided into four groups according to the quartiles of NT-proBNP levels. The plasma concentrations of sACE2, anti-ACE2, Ang-(1–7), and TNF-α were measured by enzyme-linked immunosorbent assay. The plasma ACE2, anti-ACE2, Ang-(1–7), and TNF-α levels in CHF patients increased with increasing NT-proBNP levels (P < 0.01). The plasma sACE2, anti-ACE2, Ang-(1–7), and TNF-α levels were positively correlated with NT-proBNP levels (r = 0.587, r = 0.949, r = 0.614, and r = 0.711, respectively; P < 0.01). Multiple linear regression analysis showed that TNF-α, Ang-(1–7), and LVEF are independent predictors for NT-proBNP in patients with CHF. Conclusions: The plasma sACE2, anti-ACE2, Ang-(1–7), and TNF-α levels increased in CHF patients with increasing NT-proBNP levels. The simultaneous detection of these markers is significant for diagnosing patients with CHF.

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Angiogenesis, the fundamental process that generates new blood vessels from parental vessels, is essential for embryogenesis and pathogenesis. A variety of underlying molecular and cellular mechanisms control angiogenesis. In this review, we focus on a unique mechanism of action – cholesterol-regulated angiogenesis. We will discuss lipoproteins, including low-density lipoprotein and high-density lipoprotein, cholesterol-rich lipid rafts/caveolae, apoA-I-binding protein (AIBP, also known as NAXE)-regulated cholesterol efflux, the effect of the hydroxycholesterol-activated nuclear receptor liver X receptor α/β on the proangiogenic vascular endothelial growth factor receptor 2 and antiangiogenic Notch signaling, and cholesterol-modified sonic hedgehog signaling. These pathways can be exploited, either alone or in conjunction with the currently available regimen for angiogenesis treatment, to control neovascularization in dyslipidemia. A treatment protocol for angiogenesis that takes into consideration cholesterol management might constitute an important component in precision and personalized medicine.

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Hutchinson–Gilford Progeria syndrome (HGPS) is characterized by accelerated aging leading to death in the teen years, usually due to severe coronary and/or carotid disease. The clinical presentation includes stunted growth, alopecia, loss of subcutaneous fat, osteoporosis, and cardiovascular disorders occurring in late childhood and the teen years including hypertension and accelerated vascular aging that precipitates myocardial infarction and cerebrovascular attacks. The disease is a nuclear laminopathy, due to a Lmna gene mutation. The aberrant protein (Progerin) accumulates in and distorts the nuclear envelope. We review the genetic and biochemical mechanism of HGPS; the clinical presentation with special attention to the cardiovascular pathology and complications; current therapeutic developments to address the disease; and the results of the clinical trials attempting to translate basic research insights into therapeutic benefit. An understanding of HGPS may lead to better treatment of other age-related disorders, particularly cardiovascular diseases.

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Based on epidemiological, genetic, and clinical trial data, there is a consensus now that low-density lipoproteins (LDL) cholesterol causes atherosclerosis and that lowering LDL cholesterol reduces the risk of atherosclerotic cardiovascular disease. Current guidelines on lipid management, therefore, focus on LDL cholesterol. The absolute benefit derived from lowering LDL cholesterol is greatest with the highest baseline risk; the most intensive treatment, therefore, is appropriate in the patients at the highest risk. Regarding the choice of drugs, statins are the basis of lipid management; if treatment goals are not met with statins alone, ezetimibe and proprotein convertase subtilisin/kexin type 9 inhibitors can be added to further reduce cardiovascular risk. Several questions remain open to debate. For example, the long-term net benefit of statin treatment in young patients with a low 10-year, but a high lifetime risk of cardiovascular events has not been demonstrated; in the absence of robust data, also lipid management in very old patients remains a question of clinical judgment. Further, given the evidence from clinical trials for further risk reduction with lowering LDL cholesterol below currently recommended targets, there is no universal consent on how low to go with LDL cholesterol. Also, with the availability of potent but expensive treatment options, the cost-effectiveness of lipid management remains a field of controversy. Finally, new lipid drugs are under development that yet has to prove their role in lipid management.

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Ischemic preconditioning is a protective phenomenon, by which brief ischemic stimuli in a vascular bed are able to counteract the damage from a longer subsequent ischemia. Preconditioning may also confer protection from ischemia to distal tissues and organs. In this case, ischemic preconditioning is known as remote ischemic preconditioning (RIPC). RIPC can be safely and easily reproduced in clinical settings. Indeed, over the past years, its protective actions have been tested in various clinical settings, including cardiac surgery and elective percutaneous coronary interventions. However, translational studies on RIPC have provided conflicting results on reduction of mortality. Recently, studies in humans have investigated the effects of RIPC on coronary circulation, showing that RIPC could have a protective effect on coronaries. This recent area of research may offer innovative insights for designing translational studies on RIPC, unveiling new mechanisms by which RIPC protects the heart. The aims of the present manuscript are to summarize the available clinical evidence on RIPC efficacy for cardioprotection and to review studies assessing the effects of RIPC on coronary circulation in humans.

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Cardiovascular diseases (CVDs) remain the biggest cause of deaths worldwide. More than 17 million people die from CVDs annually. The HeartRescue Global Program is a five-year international healthcare program, sponsored by Medtronic Philanthropy and its partners, that supports community-based demonstration projects specifically designed to expand access to life saving interventions for acute cardiovascular events. Both global in scope and local in nature, HeartRescue focuses on working with healthcare partners in select communities in China, India, and Russia. The Heart Rescue Global Program will draw upon important lessons learned and expertise from within the on-going Heart Rescue-US Project. HeartRescue China has begun operating in select districts of China. This article focuses on introduces in details of the specific aims of the project, major components and activities, Expected Measurable Outcomes of the HeartRescue Program. This article focuses on and introduces in detail.

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This article discusses and briefly reviews several visual and measured clinical phenotypes, which include height, birth weight or preterm birth body mass index, index finger to ring finger distance ratio (2D: 4D), earlobe creases, hair graying or whitening, and xanthoma. As modifiable risk factors and non-modifiable clinical phenotypes (NMCPs), these factors are potential targets for cardiovascular prevention in the new era of precision medicine. A novel score method based on modifiable risk factors and NMCPs can help for more precise diagnosis and prevention of cardiovascular disease.

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In this paper, the authors introduced a kind of hypertension called “C-type Hypertension (CtH)” which is related to “a new type of stress” caused by unhealthy lifestyles. Unlike H-type hypertension caused by an elevated serum level of Hcy, the clinical feature was found to cause a temporary remarkable increase or continually slow increase in the level of human cortisol, the standard biomarker of CtH. This kind of hypertension often appears among young- or middle-age people and may present as a new killer which may result in acute myocardial infarction, acute or chronic heart failure, stroke, or sudden cardiac death.

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