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1.
BMJ Open ; 13(11): e073528, 2023 11 29.
Article En | MEDLINE | ID: mdl-38030250

OBJECTIVE: This study aimed to determine the potential influence of ambient temperature on the incidence of acute myocardial infarction (AMI). DESIGN: A retrospective observational cohort study. SETTING: Changchun, a northeastern city in China, has a temperate continental humid climate. PARTICIPANTS: 1933 AMI patients admitted to the outpatient department of the First Hospital of Jilin University were included in the study from 1 January 2017 to 31 December 2019. OUTCOME MEASURE: We explored the effect of daily minimum and maximum temperatures, as well as temperature changes on two adjacent days, on the incidence of daily AMI from 1 to 5 days later in Changchun. RESULTS: We found that the average daily number of AMI cases was higher from October to April in cold season compared with the period between May and September in warm season. When the daily maximum temperature is ≤-6°C on the -2nd day, the incidence of AMI>3 persons more than doubled (from 8.51% and 10.88% to 20.23%) in the next 2 days (p=0.027); and more than 65% of the days had a maximum temperature fluctuation on |(-2nd day) - (-3rd day)| ≥2°C in these days, the OR of the daily incidence of AMI>3 persons is 3.107 (p=0.018); and in these days with enhanced temperature fluctuations, the proportion of AMI patients with hypertension had increased significantly from 20.83% to 45.39% (p=0.023). CONCLUSION: Ambient temperature as environmental factor has a seasonal effect on the incidence of AMI in temperate continental humid climate regions, with a 2-3 days lag. Furthermore, the key factor contributing to the increase in the daily incidence of AMI during the cold season is temperature fluctuations, and maintaining a constant temperature may aid in preventing the occurrence of AMI. TRIAL REGISTRATION NUMBER: ChiCTR2300068294.


Hospitalization , Myocardial Infarction , Humans , Seasons , Temperature , Retrospective Studies , Cold Temperature , China/epidemiology , Myocardial Infarction/epidemiology , Myocardial Infarction/etiology
2.
Biochim Biophys Acta Gen Subj ; 1866(1): 130010, 2022 01.
Article En | MEDLINE | ID: mdl-34525397

BACKGROUND: Humanin is an endogenous mitochondria-derived peptide that plays critical roles in oxidative stress, inflammation and CAD. In this study, we measured the levels of circulating humanin, markers of oxidative stress and inflammation in patients with unstable angina and MI and studied the relationship between these parameters and major adverse cardiac events (MACE). METHODS: A total of 327 subjects were recruited from the inpatient department at First Hospital of Jilin University and divided into 3 groups [control, angina and myocardial infarction (MI)] based on the clinical data and the results of the angiography. Serum humanin and thiobarbituric acid reactive substances (TBARS) were measured at the time of initial admission. The hospitalization data and MACE of all patients were collected. RESULTS: Circulating humanin levels were lower in the angina group compared to controls [124.22 ±â€¯63.02 vs. 157.77 ±â€¯99.93 pg/ml, p < 0.05] and even lower in MI patients [67.17 ±â€¯24.35 pg/ml, p < 0.05 vs controls] and oxidative stress marker were higher in MI patients compared to the control and angina groups [12.94 ±â€¯4.55 vs. 8.26 ±â€¯1.66 vs. 9.06 ±â€¯2.47 umol/ml, p < 0.05]. Lower circulating humanin levels was an independent risk factor of MI patients. Circulating humanin levels could be used to predict MACE in angina group. CONCLUSIONS: Lower circulating humanin levels was an independent risk factor for CAD, and a potential prognostic marker for mild CAD. GENERAL SIGNIFICANCE: Humanin may become a new index for the diagnosis and treatment of CAD.


Coronary Artery Disease/metabolism , Intracellular Signaling Peptides and Proteins/analysis , Adult , Angina Pectoris/metabolism , Angina Pectoris/physiopathology , Biomarkers/blood , Coronary Artery Disease/blood , Female , Heart , Humans , Inflammation/metabolism , Intracellular Signaling Peptides and Proteins/blood , Intracellular Signaling Peptides and Proteins/metabolism , Male , Middle Aged , Mitochondria , Myocardial Infarction/metabolism , Oxidative Stress/physiology , Prognosis , Risk Factors
3.
BMC Sports Sci Med Rehabil ; 13(1): 139, 2021 Oct 30.
Article En | MEDLINE | ID: mdl-34717743

OBJECTIVE: The purpose of this retrospective study is to evaluate the effectiveness of early cardiac rehabilitation on patients with heart failure following acute myocardial infarction. METHODS: Two hundred and thirty-two patients who developed heart failure following acute myocardial infarction were enrolled in this study. Patients were divided into heart failure with reduced ejection fraction group (n = 54) and heart failure with mid-range ejection fraction group (n = 178). Seventy-eight patients who accepted a two-week cardiac rehabilitation were further divided into two subgroups based on major adverse cardiovascular events. Key cardio-pulmonary exercise testing indicators that may affect the prognosis were identified among the cardiac rehabilitation patients. RESULTS: Early cardiac rehabilitation significantly reduced cardiac death and re-hospitalization in patients. There was more incidence of diabetes, hyperkalemia and low PETCO2 in the cardiac rehabilitation group who developed re-hospitalization. Low PETCO2 at anaerobic threshold (≤ 33.5 mmHg) was an independent risk factor for re-hospitalization. CONCLUSIONS: Early cardiac rehabilitation reduced major cardiac events in patients with heart failure following acute myocardial infarction. The lower PETCO2 at anaerobic threshold is an independent risk factor for re-hospitalization, and could be used as a evaluating hallmark for early cardiac rehabilitation.

4.
BMC Cardiovasc Disord ; 19(1): 210, 2019 09 06.
Article En | MEDLINE | ID: mdl-31492095

BACKGROUND: The purpose of this study was to analyze cardiopulmonary fitness in Phase I cardiac rehabilitation on the prognosis of patients with ST-Elevation Myocardial Infarction (STEMI) after percutaneous coronary intervention (PCI). METHODS: The study enrolled a total of 499 STEMI patients treated with PCI between January 2015 and December 2015. Patients were assigned to individualized exercise prescriptions (IEP) group and non-individualized exercise prescriptions (NIEP) group according to whether they accept or refuse individualized exercise prescriptions. We compared the incidence of major cardiovascular events between the two groups. IEP group were further divided into two subgroups based on prognosis status, namely good prognosis (GP) group and poor prognosis (PP) group. Key cardio-pulmonary exercise testing (CPX) variables that may affect the prognosis of patients were identified through comparison of the cardio-respiratory fitness (CRF). RESULTS: There is no significant difference in the incidence of cardio-genetic death, re-hospitalization, heart failure, stroke, or atrial fibrillation between the IEP and the NIEP group. But the incidence of total major adverse cardiac events (MACE) was significantly lower in the IEP group than in the NIEP group (P = 0.039). The oxygen consumption (VO2) at ventilation threshold (VT), minute CO2 ventilation (E-VCO2), margin of minute ventilation carbon dioxide production (△CO2), rest partial pressure of end-tidal carbon dioxide(R-PETCO2), exercise partial pressure of end-tidal carbon dioxide(E-PETCO2) and margin of partial pressure of end-tidal carbon dioxide(△PETCO2) were significantly higher in the GP subgroup than in the PP subgroup; and the slope for minute ventilation/carbon dioxide production (VE/VCO2) was significantly lower in GP subgroup than in PP subgroup (P = 0.010). The VO2 at VT, VE/VCO2 slope, E-VCO2, △CO2, R-PETCO2, E-PETCO2 and margin of partial pressure of end-tidal carbon dioxide CO2 (△PETCO2) were predictive of adverse events. The VO2 at VT was an independent risk factor for cardiovascular disease prognosis. CONCLUSIONS: Individualized exercise prescription of Phase I cardiac rehabilitation reduced the incidence of cardiovascular events in patients with STEMI after PCI. VO2 at VT is an independent risk factor for cardiovascular disease prognosis, and could be used as an important evaluating indicator for Phase I cardiac rehabilitation.


Cardiac Rehabilitation , Cardiorespiratory Fitness , Exercise Therapy , Patient Discharge , Percutaneous Coronary Intervention , ST Elevation Myocardial Infarction/therapy , Cardiac Rehabilitation/adverse effects , Cardiac Rehabilitation/mortality , Exercise Therapy/adverse effects , Exercise Therapy/mortality , Female , Health Status , Humans , Male , Middle Aged , Percutaneous Coronary Intervention/adverse effects , Percutaneous Coronary Intervention/mortality , Retrospective Studies , ST Elevation Myocardial Infarction/diagnosis , ST Elevation Myocardial Infarction/mortality , ST Elevation Myocardial Infarction/physiopathology , Time Factors , Treatment Outcome
5.
Pak J Pharm Sci ; 32(1(Special)): 371-375, 2019 Jan.
Article En | MEDLINE | ID: mdl-30852472

The present study designed to investigate the effect of monoamine oxidase inhibitor in the rat model of Coronary heart disease (cardiac hypertrophy). A total of 40 male adult Wistar rats having body weight 300-400 gram were equally distributed in two groups (Test group: Rats with Angiotensin II + monoamine oxidase inhibitor (Befloxatone); Reference group: Rats with cardiac hypertrophy induced by Angiotensin II). Rat model of cardiac hypertrophy were induced by Angiotensin II. Effect of Befloxatone on cardiac hypertrophy was evaluated by electrocardiography, hemodynamic and histological assessment. Vital signs such as pulse rate, and blood pressure were measured. Echocardiographic related variable including ejection fraction were also assessed in both the groups. Also, expression of monoamine oxidase was analyzed using by real-time-PCR and Western blot analysis. In results, we found following 1) monoamine oxidase inhibitor treatment prevents Angiotensin II induced increase in level of ANP and ßeta-myosin, which are responsible for inducing cardiac hypertrophic responses; 2) monoamine oxidase inhibitor ameliorates Angiotensin II induced cell enlargement by reducing the surface area of cells; 3) monoamine oxidase inhibitor attenuates the hypertrophic response triggered by Angiotensin II; 4) monoamine oxidase inhibitor ameliorates increased heart rate and average arterial pressure induced by angiotensin II; 5) Overall finding suggested that monoamine oxidase inhibitor improves left ventricle hypertrophy and ejection fraction by inhibiting monoamine oxidase enzyme in heart. The finding of this study gives the new vision to cardiovascular researchers to develop anti- hypertrophy therapy based on monoamine oxidase inhibition.


Cardiomegaly/drug therapy , Monoamine Oxidase Inhibitors/therapeutic use , Oxazoles/therapeutic use , Angiotensin II , Animals , Cardiomegaly/pathology , Cardiomegaly/physiopathology , Disease Models, Animal , Hemodynamics/drug effects , Male , Monoamine Oxidase Inhibitors/administration & dosage , Myocardium/pathology , Oxazoles/administration & dosage , Rats, Wistar
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