Penatalaksanaan Fisioterapi Komprehensif Pada Kasus Pasca Coronary Artery By Pass Grafting Et Causa Coronary Artery Disease Involving 3 Vessels (CAD3VD): Case Report

Coronary heart disease is a malfunctioning of the heart caused by stenosis of the heart blood vessels which can affect one or more arteries. In these cases the patient had Triple Vessels Disease (3-VD), where there was ≥50-70% stenosis in most of the main branches of the heart blood vessels, then the patient underwent a revascularization operation Coronary Artery Bypass Grafting (CABG) with a postoperative condition, namely pain. in the sternum and lower right leg, accumulation of pulmonary sputum, decreased thoracic expansion, shortness of breath, decreased activity and functional ability. The management of physiotherapy that is given is chest physiotherapy and active and passive exercises in extremity. After 3 times of therapy, the results obtained from the degree of shortness of T0: 5 to T3: 3, the decrease in pain T0: 6 to T3: 3, then tenderness T0: 6 to T3: 3 and silent pain T0: 4 to T3: 3 increased the difference in thoracic expansion in the axilla T0: 1 cm becomes T3: 2 cm, at ICS T0: 1 cm changes to T3: 2 cm and there has been no increase in the xypoideus process, by 2 cm at T0 and T3. Activity and functional abilities were calculated using the Barthel index on T0 of the total dependency category, changing to T3: weight dependence. Chest physiotherapy and active-passive exercises in extremity can alleviate problems in post-CABG surgery.Keywords: Coronary Artery Bypass Grafting, Chest Physiotherapy, active and pasive exercise in extremity

Nursing Skill and Responsibility in Administration of Injection Actilyse

Actilyse can break blood clots that form in the heart, blood arteries, or lungs during a heart attack. This medication is also given to stroke patients to improve recovery and reduce the likelihood of impairment. Recombinant DNA technology was used to create Activase, a tissue plasminogen activator. It is a sterile, purified glycoprotein of 527 amino acids. It is made by combining complementary DNA (cDNA) from a human melanoma cell line with the natural human tissue-type plasminogen activator. After reconstitution with Sterile Water for Injection, USP, Activase is a sterile, white to off-white lyophilized powder for intravenous injection.

Organoprotective properties of combination therapy with ramipril and indapamide in hypertensive patients with non-alcoholic fatty liver disease

Objective. To assess the effect of combined antihypertensive therapy with ramipril and indapamide on the structural and functional state of the heart, blood vessels, kidneys, autonomic nervous system and liver in hypertensive patients with non-alcoholic fatty liver disease (NAFLD). Design and methods. We performed a prospective controlled study including 30 patients with hypertension (HTN) stages I–II, 1–2 degrees with NAFLD (fatty liver index (FLI) > 60) aged 45 to 65 years. Five-seven days before the initial examination, patients discontinued antihypertensive drugs, after the washout period one of the fixed combinations of ramipril (2,5/5 mg/day) and indapamide (0,625/1,25 mg) was prescribed depending on the required dosage and recommendations on lifestyle changes and weight loss were given. Clinical examination, measurement of “office” blood pressure (BP), ambulatory BP monitoring (ABPM), central aortic pressure (CAP), pulse wave velocity (PWV), echocardiography and heart rate variability assessment were performed. The functional state of the kidneys and the structural and functional state of the liver were also assessed before and after treatment. Results. After 24-week therapy with a fixed combination of ramipril and indapamide (an average dosage 4,04 ± 1,24 and 1,01 ± 0,31 mg, respectively) target BP levels was achieved. According to ABPM, both daytime and nocturnal systolic BP (SBP) and diastolic BP (DBP) decreased. In addition, CAP (SBPao, DBPa) and augmentation index decreased. There was also a decrease in the stiffness of the arterial wall in muscle-type vessels (PWVm) (p = 0,0166) and in the number of patients with paradoxical test (p = 0,0320). There was a significant increase in creatinine clearance (Cockroft–Gault) after treatment (p = 0,0439) with no increase in glomerular filtration rate (CKD-EPI) (p = 0,1617). There was a significant change in the structural and functional indicators of the heart: increased left ventricular (LV) ejection fraction (p = 0,0398), decreased LV posterior wall thickness (p = 0,0457), LV end-systolic diameter (p = 0,0286), relative wall thickness (p = 0,0419) and LV myocardial mass index (p = 0,0002). There was a decrease in SDNN < 50 (p < 0,0001) and increase in RMSSD (p < 0,0001), which indicates a decrease in the sympathetic activity and an increase in parasympathetic regulation. Also the number of patients with normotonic type of autonomic reactivity in the orthostatic test increased after treatment (12 (24,0%) vs 19 (63,3%), p = 0,0456). The liver function and structure also improved showing decrease in total bilirubin (p = 0,0038) and gamma-glutamyltransferase (p = 0,0498), as well as the indices of liver steatosis (p = 0,0278) and fibrosis (p = 0,0166). Conclusions. Thus, combined antihypertensive therapy with ramipril and indapamide is well tolerated by patients, highly effective and demonstrates organoprotective properties regarding the heart, blood vessels, kidneys, autonomic nervous system and liver.

Cardiovascular comorbidity in patients with nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease worldwide. It is characterized by hepatic steatosis and stetohepatitis and in some cases can progress to cirrhosis with or without hepatic failure and hepatocellular carcinoma. At present, NAFLD is deemed a predictor of cardiovascular risk. Besides, it can aggravate pre-existing cardiovascular conditions. Structural and functional changes in the heart, liver and blood vessels are interdependent and mutually aggravating. Metabolic factors (dyslipidemia, hyperglycemia and insulin resistance) contribute to hepatic, cardiac and vascular damage, and NAFLD and comorbid cardiovascular disorders together can activate fibrogenesis in the heart, blood vessels and liver.

Ultra-Performance Liquid Chromatography-Q-Exactive Orbitrap-Mass Spectrometry Analysis for Metabolic Communication between Heart and Kidney in Adriamycin-Induced Nephropathy Rats

<b><i>Background/Aims:</i></b> Although the adriamycin-induced nephropathy model is frequently employed in the study of nephrotic syndrome and focal segmental glomerulosclerosis, the accompanying myocardial damage has always been a cause for concern. Therefore, there is a great need to study cardiorenal communication in this model. <b><i>Methods:</i></b> An adriamycin-induced nephropathy model was established via tail vein injection. The levels of the biochemical indicators serum albumin, serum globulin, serum total protein, serum cholesterol, serum creatinine (SCr), urinary protein, and urinary creatinine (UCr) were measured, and histopathological changes in the heart and kidneys were assessed using hematoxylin-eosin staining. Metabolomic changes in the heart, blood, and kidneys were analyzed using the metabolomics method based on ultra-performance liquid chromatography Q-Exactive Orbitrap mass spectrometry. <b><i>Results:</i></b> Compared with the control group, the model group showed significant decreases in serum protein and total protein levels, albumin/globulin ratio, and creatinine clearance rate as well as significant increases in serum cholesterol, SCr, urinary protein, and UCr levels. Significant pathological changes were observed in the renal pathology sections in the model group, including diffusely merged glomerular epithelial cells, inflammatory infiltration, and vacuolated glomerular cells. Additionally, thickened myocardial fibers, swollen nuclei, inflammatory infiltration, and partial myocardial necrosis could be seen in the cardiac pathology sections in the model group. Based on multivariate statistical analysis, a total of 20 differential metabolites associated with 15 metabolic pathways were identified in the heart, 7 differential metabolites with 7 metabolic pathways were identified in the blood, and 16 differential metabolites with 21 metabolic pathways were identified in the kidney. Moreover, 6 common metabolic pathways shared by the heart and kidney were identified: arginine and proline metabolism; arginine biosynthesis; glutathione metabolism; alanine, aspartate, and glutamate metabolism; beta-alanine metabolism; and histidine metabolism. Among these metabolic pathways, alanine, aspartate, and glutamate metabolism was shared by the heart, blood, and kidney. Succinic acid was found to be the key regulatory metabolite in cardiorenal metabolic communication. <b><i>Conclusion:</i></b> Six metabolic pathways were found to be involved in cardiorenal metabolic communication in an adriamycin-induced nephropathy model, in which alanine, aspartate, and glutamate metabolism may be the metabolic link between the heart and kidney in the development and maintenance of oxidative stress and inflammation. Succinic acid may serve as a key regulatory metabolic switch or marker of cardiac and renal co-injury, as shown in an adriamycin-induced nephropathy model.

Alisma Shugan Decoction Attenuates Hepatic fibrosis and Endoplasmic Reticulum Stress in Mice with Carbon Tetrachloride-Induced fibrosis

Background: Over the years, Alisma Shugan Decoction (ASD), because of its potent anti-inflammation activity, has been used in traditional Chinese medicine (TCM) for treatment of many inflammation-associated disorders including those of the heart, blood vessel and brain. Methods: Herein, we examined the probable therapeutic effect of ASD in carbon tetrachloride (CCI4)-induced liver injury and fibrosis mice models. Results: Our results demonstrate that ASD dose-dependently reduced the fibrosis-related increased collagen deposition secondary to liver tissue exposure to CCI4. Data from our biochemical analyses showed significantly less liver damage biomarkers including ALT, AST and hydroxyproline in the ASD-treated samples, suggesting hepato-protective effect of ASD. Furthermore, we demonstrated that treatment with ASD significantly reversed CCI4-induced elevation of TNF-α, IL-6, IL-1β and MCP-1. Comparative immunohistochemical staining of liver samples revealed that ASD dose-dependently downregulated the expression of pro-apoptotic, Bax while upregulating anti-apoptotic Bcl2 protein. Interestingly, NF-κB signaling, a principal regulator of inflammation was markedly suppressed by ASD treatment. In addition, treatment with ASD deregulated stress signaling pathways by suppressing the expression of markers of unfolded protein response, such as ATF6, IRE and GRP78. Conclusion: In conclusion, the present study provides preclinical evidence for the use of ASD as an efficacious therapeutic option in cases of chemical-induced liver damage and/or fibrosis. Further large-cohort validation of these findings is warranted.

Diagnostic difficulties of isolated right ventricular myocardial infarction

The article describes a case of isolated right ventricular myocardial infarction induced by proximal occlusion of the right coronary artery in a patient with the left type of heart blood supply. A specific feature of the case was detection of the McConnell’s sign, which is considered characteristic of pulmonary artery thromboembolism.

Circadian Clock-Controlled Checkpoints in the Pathogenesis of Complex Disease

The circadian clock coordinates physiology, metabolism, and behavior with the 24-h cycles of environmental light. Fundamental mechanisms of how the circadian clock regulates organ physiology and metabolism have been elucidated at a rapid speed in the past two decades. Here we review circadian networks in more than six organ systems associated with complex disease, which cluster around metabolic disorders, and seek to propose critical regulatory molecules controlled by the circadian clock (named clock-controlled checkpoints) in the pathogenesis of complex disease. These include clock-controlled checkpoints such as circadian nuclear receptors in liver and muscle tissues, chemokines and adhesion molecules in the vasculature. Although the progress is encouraging, many gaps in the mechanisms remain unaddressed. Future studies should focus on devising time-dependent strategies for drug delivery and engagement in well-characterized organs such as the liver, and elucidating fundamental circadian biology in so far less characterized organ systems, including the heart, blood, peripheral neurons, and reproductive systems.

Differential Pressure, P_D, Capital Parameter in the Determination of Cardiac Health and Prominent Kinetic Indicator of Drugs in the Blood

Background: this work is a suite of previous articles where it has been demonstrated that if the differential pressure remains constant, it allows when it is multiplied by cardiac frequency to determine the volumic cardiac power (KUNYIMA equation). Also it has afforded to calculate differential enthalpy ( that is exothermic energy in ejection fraction. In KUNYIMA Formula the differential pressure has allowed to assess in satisfactory way one part of total energy from cellular metabolism (Keith-Flack node) which enable the heart blood to circulate in the organism. In KUNYIMA relations, made possible the calculation of cardiac exergetic yield nowadays unrecognized by researchers, different from volumic yield defined by ejection fraction. This cardiac exergetic yield has been assimilated to the heart longevity. Aim and objective: this work gives in detail mathematical useful expressions, rational approaches to be followed when differential pressure substantially changes, for example when the blood contains an injected drug at initial concentration and when the kinetic of this drug should be followed. Methodology: Calculations have been our methodology using compartmental analysis. Results: It is shown hereby the use of differential equations in the determination of kinetic parameters Conclusion: Physical Cardiochemistry is improved with new theory.

Pathogenesis of the initial stages of severe COVID-19

Since SARS-CoV-2 first appeared in humans, the scientific community has tried to gather as much information as possible in order to find effective strategies for the containment and treatment this pandemic coronavirus. We reviewed the current published literature on SARS-CoV-2 with an emphasis on the distribution of SARS-CoV-2 in tissues and body fluids, as well as data on the expression of its input receptors on the cell surface. COVID-19 affects many organ systems in many ways. These varied manifestations are associated with viral tropism and immune responses of the infected person, but the exact mechanisms are not yet fully understood. We emphasize the broad organotropism of SARS-CoV-2, as many studies have identified viral components (RNA, proteins) in many organs, including immune cells, pharynx, trachea, lungs, blood, heart, blood vessels, intestines, brain, kidneys, and male reproductive organs. Viral components are present in various body fluids, such as mucus, saliva, urine, cerebrospinal fluid, semen and breast milk. The main SARS-CoV-2 receptor, ACE2, is expressed at different levels in many tissues throughout the human body, but its expression levels do not always correspond to the detection of SARS-CoV-2, indicating a complex interaction between the virus and humans. We also highlight the role of the renin-angiotensin aldosterone system and its inhibitors in the context of COVID-19. In addition, SARS-CoV-2 has various strategies that are widely used in various tissues to evade innate antiviral immunity. Targeting immune evasion mediators of the virus can block its replication in COVID-19 patients. Together, these data shed light on the current understanding of the pathogenesis of SARS-CoV-2 and lay the groundwork for better diagnosis and treatment of patients with COVID-19.