Encyclopedias as Topic
Myocardial Infarction
Heart Defects, Congenital
Myocardium
Heart Ventricles
Heart Valve Diseases
Postpoliomyelitis Syndrome
Hypertrophy, Left Ventricular
Click Chemistry
Gene Deletion
Ventricular Remodeling
Myocardial oxygenation during high work states in hearts with postinfarction remodeling. (1/2864)
BACKGROUND: Postinfarction left ventricular remodeling (LVR) is associated with reductions in myocardial high-energy phosphate (HEP) levels, which are more severe in animals that develop overt congestive heart failure (CHF). During high work states, further HEP loss occurs, which suggests demand-induced ischemia. This study tested the hypothesis that inadequate myocyte oxygen availability is the basis for these HEP abnormalities. METHODS AND RESULTS: Myocardial infarction was produced by left circumflex coronary artery ligation in swine. Studies were performed in 20 normal animals, 14 animals with compensated LVR, and 9 animals with CHF. Phosphocreatine (PCr)/ATP was determined with 31P NMR and deoxymyoglobin (Mb-delta) with 1H NMR in myocardium remote from the infarct. Basal PCr/ATP tended to be decreased in postinfarct hearts, and this was significant in animals with CHF. Infusion of dobutamine (20 microg x kg-1 x min-1 IV) caused doubling of the rate-pressure product in both normal and LVR hearts and resulted in comparable significant decreases of PCr/ATP in both groups. This decrease in PCr/ATP was not associated with detectable Mb-delta. In CHF hearts, rate-pressure product increased only 40% in response to dobutamine; this attenuated response also was not associated with detectable Mb-delta. CONCLUSIONS: Thus, the decrease of PCr/ATP during dobutamine infusion is not the result of insufficient myocardial oxygen availability. Furthermore, in CHF hearts, the low basal PCr/ATP and the attenuated response to dobutamine occurred in the absence of myocardial hypoxia, indicating that the HEP and contractile abnormalities were not the result of insufficient oxygen availability. (+info)Myocardial creatine kinase kinetics in hearts with postinfarction left ventricular remodeling. (2/2864)
This study examined whether alterations in myocardial creatine kinase (CK) kinetics and high-energy phosphate (HEP) levels occur in postinfarction left ventricular remodeling (LVR). Myocardial HEP and CK kinetics were examined in 19 pigs 6 wk after myocardial infarction was produced by left circumflex coronary artery ligation, and the results were compared with those from 9 normal pigs. Blood flow (microspheres), oxygen consumption (MVO2), HEP levels [31P magnetic resonance spectroscopy (MRS)], and CK kinetics (31P MRS) were measured in myocardium remote from the infarct under basal conditions and during dobutamine infusion (20 micrograms. kg-1. min-1 iv). Six of the pigs with LVR had overt congestive heart failure (CHF) at the time of study. Under basal conditions, creatine phosphate (CrP)-to-ATP ratios were lower in all transmural layers of hearts with CHF and in the subendocardium of LVR hearts than in normal hearts (P < 0.05). Myocardial ATP (biopsy) was significantly decreased in hearts with CHF. The CK forward rate constant was lower (P < 0.05) in the CHF group (0.21 +/- 0.03 s-1) than in LVR (0.38 +/- 0.04 s-1) or normal groups (0.41 +/- 0.03 s-1); CK forward flux rates in CHF, LVR, and normal groups were 6.4 +/- 2.3, 14.3 +/- 2.1, and 20.3 +/- 2.4 micromol. g-1. s-1, respectively (P < 0.05, CHF vs. LVR and LVR vs. normal). Dobutamine caused doubling of the rate-pressure product in the LVR and normal groups, whereas CHF hearts failed to respond to dobutamine. CK flux rates did not change during dobutamine in any group. The ratios of CK flux to ATP synthesis (from MVO2) under baseline conditions were 10.9 +/- 1.2, 8. 03 +/- 0.9, and 3.86 +/- 0.5 for normal, LVR, and CHF hearts, respectively (each P < 0.05); during dobutamine, this ratio decreased to 3.73 +/- 0.5, 2.58 +/- 0.4, and 2.78 +/- 0.5, respectively (P = not significant among groups). These data demonstrate that CK flux rates are decreased in hearts with postinfarction LVR, but this change does not limit the response to dobutamine. In hearts with end-stage CHF, the changes in HEP and CK flux are more marked. These changes could contribute to the decreased responsiveness of these hearts to dobutamine. (+info)Nicotine-modified postinfarction left ventricular remodeling. (3/2864)
Cigarette smoking has been noted to impair wound healing in tissues such as skin, bone, and gut. This study was designed to examine whether nicotine adversely affects postinfarction cardiac wound healing and remodeling in an experimental model of myocardial infarction. For this purpose, two groups of rats were studied. The control group received a simple bandage, and the nicotine group had a section (1.75 mg/day) of a nicotine patch attached on their backs. After a 7-day treatment period, an anterior wall infarction was induced. A bandage-free 7-day healing period followed, after which hearts were isolated for mechanical tests. Nicotine-treated rats developed significantly enlarged left ventricles with thin, infarcted walls and a rightward shift in the passive pressure-volume relationship. Pressure-strain analysis also indicated possible changes in the material properties of the wound for nicotine-treated rats. In conclusion, nicotine has significant adverse effects on postinfarction healing and left ventricular remodeling. These observations have important clinical implications because of the enhanced risk for development of heart failure. (+info)Endothelin system-dependent cardiac remodeling in renovascular hypertension. (4/2864)
The aim of the present study was to analyze whether the cardiac endothelin system contributes to cardiac remodeling in rats with 2-kidney, 1 clip (2K1C) renovascular hypertension. The endothelin system seems to be a promising candidate for cardiac remodeling because endothelin (ET)-1 promotes growth of cardiomyocytes in vitro and induces cardiac collagen synthesis. The activity of the cardiac endothelin system was analyzed by measuring cardiac tissue big ET-1 and ET-1 concentrations as well as by estimating the cardiac expression of the ETA and ETB receptors 10 days, 4 weeks, and 12 weeks after the renal artery was clipped. The effects of long-term treatment with ETA, ETB, and combined ETA/ETB receptor antagonists on cardiac hypertrophy, media/lumen ratio of intracardiac arteries, and left ventricular fibrosis were also analyzed. This study demonstrated that the overall left ventricular cardiac endothelin system has a similar activity in the early, middle, and late stages of 2K1C renovascular hypertension compared with sham-operated controls. Fibrosis of the left ventricle and hypertrophy of intracardiac arteries, however, were markedly altered after long-term treatment with endothelin receptor antagonists in a blood pressure-independent manner. These 2 effects are mediated by different subtypes of endothelin receptors. ETA receptor blockade completely normalized the hypertrophy of intracardiac arteries (P<0. 01 compared with 2K1C without treatment) in renovascular hypertension, whereas the ETB antagonist reduced cardiac fibrosis of the left ventricle (P<0.001 compared with 2K1C without treatment) to baseline values. This study demonstrates that the cardiac endothelin system plays an important role in the development of cardiac fibrosis as well as in hypertrophy of intracardiac arteries in 2K1C renovascular hypertensive rats. (+info)Decreased left ventricular filling pressure 8 months after corrective surgery in a 55-year-old man with tetralogy of Fallot: adaptation for increased preload. (5/2864)
A 55-year-old man with tetralogy of Fallot underwent corrective surgery. Left ventricular filling pressure increased markedly with increased left ventricular volume one month after surgery, then decreased over the next 7 months, presumably due to increased left ventricular compliance. (+info)Beneficial effect of myocardial angiogenesis on cardiac remodeling process by amlodipine and MCI-154. (6/2864)
The present study examined the effect of long-term treatment with amlodipine and MCI-154 (a Ca2+ sensitizer) on progressive cardiac dysfunction and microvasculature in the dilated cardiomyopathic (DCM) hamster heart. After treatment of DCM hamsters (Bio 53.58) with amlodipine or MCI-154 for 15 wk from the age of 5 wk, amlodipine and MCI-154 were found to cause an increase in left ventricular percent fractional shortening and decreases in left ventricular diastolic dimension and isovolumic relaxation time in echocardiograms (P < 0.01). A hemodynamic study showed that the diastolic time constant decreased in the amlodipine-treatment group (P < 0.05). In a morphometric study employing a double-staining method that discriminated arteriolar and venular capillaries, amlodipine and MCI-154 caused increases in total capillary density (P < 0.05) and the proportion of venular capillaries (P < 0.05). Moreover, Northern blot analysis showed that the expression of mRNA for vascular endothelial growth factor was significantly increased by amlodipine and MCI-154. They preserve coronary microvasculature in the DCM hamster and might induce angiogenesis of small vessels, thereby contributing to preservation of cardiac systolic and diastolic function. (+info)Effects of AT1-receptor blockade on progression of left ventricular dysfunction in dogs with heart failure. (7/2864)
The objective of the present study was to determine the effects of early long-term monotherapy with the angiotensin II AT1-receptor antagonist valsartan on the progression of left ventricular (LV) dysfunction and remodeling in dogs with moderate heart failure (HF). Studies were performed in 30 dogs with moderate HF produced by multiple sequential intracoronary microembolizations. Embolizations were discontinued when LV ejection fraction was 30-40%. Two weeks after the last embolization, dogs were randomized to 3 mo of oral therapy with low-dose valsartan (400 mg twice daily, n = 10), to high-dose valsartan (800 mg twice daily, n = 10), or to no treatment at all (control, n = 10). Treatment with valsartan significantly reduced mean aortic pressure and LV end-diastolic pressure compared with control. In untreated dogs, LV ejection fraction decreased (37 +/- 1 vs. 29 +/- 1%, P = 0.001) and end-systolic volume (ESV) and end-diastolic volume (EDV) increased (81 +/- 5 vs. 92 +/- 5 ml, P < 0.001; 51 +/- 3 vs. 65 +/- 3 ml, P = 0.001, respectively) after 3 mo of follow-up compared with those levels before follow-up. In dogs treated for 3 mo with low-dose valsartan, ejection fraction was preserved (37 +/- 1 vs. 38 +/- 2%, pretreatment vs. posttreatment) as was ESV but not EDV. In dogs treated for 3 mo with high-dose valsartan, ejection fraction decreased (35 +/- 1 vs. 31 +/- 2%, P = 0.02) and ESV and EDV increased in a manner comparable to those levels in controls. Valsartan had no significant effects on cardiomyocyte hypertrophy or on the extent of interstitial fibrosis. We conclude that, for dogs with moderate HF, early long-term therapy with the AT1-receptor blocker valsartan decreases preload and afterload but has only limited benefits in attenuating the progression of LV dysfunction and chamber remodeling. (+info)Ventricular dilatation in the absence of ACE inhibitors: influence of haemodynamic and neurohormonal variables following myocardial infarction. (8/2864)
OBJECTIVE: To examine the relation between patterns of ventricular remodelling and haemodynamic and neurohormonal variables, at rest and during symptom limited exercise, in the year following acute myocardial infarction in patients not receiving angiotensin converting enzyme (ACE) inhibitors. DESIGN: A prospective observational study. PATIENTS: 65 patients recruited following hospital admission with a transmural anterior myocardial infarction. METHODS: Central haemodynamics and neurohormonal activation at rest and during symptom limited treadmill exercise were measured at baseline before hospital discharge, one month later, and at three monthly intervals thereafter. PATIENTS were classified according to individual patterns of change in left ventricular end diastolic volumes at rest, assessed at each visit using transthoracic echocardiography. RESULTS: In most patients (n = 43, 66%) ventricular volumes were unchanged or reduced. Mean (SEM) treadmill exercise capacity and peak exercise cardiac index increased at month 12 by 200 (24) seconds (p < 0.001 v baseline) and by 0.8 (0.4) l/min/m2 (p<0.05 v baseline), respectively, in this group. In patients with limited ventricular dilatation (n = 11, 17%) exercise capacity increased by 259 (52) seconds (p < 0.001 v baseline) and peak exercise cardiac index improved by 0.8 (0.7) l/min/m2 (NS). In the remaining 11 patients with progressive left ventricular dilatation, exercise capacity increased by 308 (53) seconds (p< 0. 001 v baseline) and peak exercise cardiac index similarly improved by 1.3 (0.7) l/min/m2 (NS). There were trends towards increased atrial natriuretic factor (ANF) secretion at rest and at peak exercise in this group. CONCLUSIONS: Ventricular dilatation after acute myocardial infarction is a heterogeneous process that is progressive in only a minority of patients. Compensatory mechanisms, including ANF release, appear capable of maintaining and improving exercise capacity in most patients for at least 12 months, even in those with a progressive increase in ventricular size. (+info)An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
Myocardial infarction (MI), also known as a heart attack, is a medical condition characterized by the death of a segment of heart muscle (myocardium) due to the interruption of its blood supply. This interruption is most commonly caused by the blockage of a coronary artery by a blood clot formed on the top of an atherosclerotic plaque, which is a buildup of cholesterol and other substances in the inner lining of the artery.
The lack of oxygen and nutrients supply to the heart muscle tissue results in damage or death of the cardiac cells, causing the affected area to become necrotic. The extent and severity of the MI depend on the size of the affected area, the duration of the occlusion, and the presence of collateral circulation.
Symptoms of a myocardial infarction may include chest pain or discomfort, shortness of breath, nausea, lightheadedness, and sweating. Immediate medical attention is necessary to restore blood flow to the affected area and prevent further damage to the heart muscle. Treatment options for MI include medications, such as thrombolytics, antiplatelet agents, and pain relievers, as well as procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).
In medical terms, the heart is a muscular organ located in the thoracic cavity that functions as a pump to circulate blood throughout the body. It's responsible for delivering oxygen and nutrients to the tissues and removing carbon dioxide and other wastes. The human heart is divided into four chambers: two atria on the top and two ventricles on the bottom. The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs, while the left side receives oxygenated blood from the lungs and pumps it out to the rest of the body. The heart's rhythmic contractions and relaxations are regulated by a complex electrical conduction system.
Congenital heart defects (CHDs) are structural abnormalities in the heart that are present at birth. They can affect any part of the heart's structure, including the walls of the heart, the valves inside the heart, and the major blood vessels that lead to and from the heart.
Congenital heart defects can range from mild to severe and can cause various symptoms depending on the type and severity of the defect. Some common symptoms of CHDs include cyanosis (a bluish tint to the skin, lips, and fingernails), shortness of breath, fatigue, poor feeding, and slow growth in infants and children.
There are many different types of congenital heart defects, including:
1. Septal defects: These are holes in the walls that separate the four chambers of the heart. The two most common septal defects are atrial septal defect (ASD) and ventricular septal defect (VSD).
2. Valve abnormalities: These include narrowed or leaky valves, which can affect blood flow through the heart.
3. Obstruction defects: These occur when blood flow is blocked or restricted due to narrowing or absence of a part of the heart's structure. Examples include pulmonary stenosis and coarctation of the aorta.
4. Cyanotic heart defects: These cause a lack of oxygen in the blood, leading to cyanosis. Examples include tetralogy of Fallot and transposition of the great arteries.
The causes of congenital heart defects are not fully understood, but genetic factors and environmental influences during pregnancy may play a role. Some CHDs can be detected before birth through prenatal testing, while others may not be diagnosed until after birth or later in childhood. Treatment for CHDs may include medication, surgery, or other interventions to improve blood flow and oxygenation of the body's tissues.
The myocardium is the middle layer of the heart wall, composed of specialized cardiac muscle cells that are responsible for pumping blood throughout the body. It forms the thickest part of the heart wall and is divided into two sections: the left ventricle, which pumps oxygenated blood to the rest of the body, and the right ventricle, which pumps deoxygenated blood to the lungs.
The myocardium contains several types of cells, including cardiac muscle fibers, connective tissue, nerves, and blood vessels. The muscle fibers are arranged in a highly organized pattern that allows them to contract in a coordinated manner, generating the force necessary to pump blood through the heart and circulatory system.
Damage to the myocardium can occur due to various factors such as ischemia (reduced blood flow), infection, inflammation, or genetic disorders. This damage can lead to several cardiac conditions, including heart failure, arrhythmias, and cardiomyopathy.
The heart ventricles are the two lower chambers of the heart that receive blood from the atria and pump it to the lungs or the rest of the body. The right ventricle pumps deoxygenated blood to the lungs, while the left ventricle pumps oxygenated blood to the rest of the body. Both ventricles have thick, muscular walls to generate the pressure necessary to pump blood through the circulatory system.
Heart valve diseases are a group of conditions that affect the function of one or more of the heart's four valves (tricuspid, pulmonic, mitral, and aortic). These valves are responsible for controlling the direction and flow of blood through the heart. Heart valve diseases can cause the valves to become narrowed (stenosis), leaky (regurgitation or insufficiency), or improperly closed (prolapse), leading to disrupted blood flow within the heart and potentially causing symptoms such as shortness of breath, fatigue, chest pain, and irregular heart rhythms. The causes of heart valve diseases can include congenital defects, age-related degenerative changes, infections, rheumatic heart disease, and high blood pressure. Treatment options may include medications, surgical repair or replacement of the affected valve(s), or transcatheter procedures.
Post-poliomyelitis syndrome (PPS) is a condition that affects polio survivors years after recovery from the initial acute poliomyelitis infection. The symptoms of PPS include new onset weakness, fatigue, and pain in the muscles that were previously affected by the poliovirus. These symptoms can occur gradually or suddenly, and they may be worsened by exercise or other physical stressors.
PPS is thought to be caused by ongoing degeneration of the enlarged motor neurons that survived the initial polio infection. It is estimated that up to 50% of polio survivors may experience symptoms of PPS. While there is no cure for PPS, treatment typically focuses on managing symptoms and maintaining function through physical therapy, assistive devices, and pain management strategies.
Left ventricular hypertrophy (LVH) is a medical condition in which the left ventricle of the heart undergoes an enlargement or thickening of its muscle wall. The left ventricle is the main pumping chamber of the heart that supplies oxygenated blood to the rest of the body.
In response to increased workload, such as hypertension (high blood pressure), aortic valve stenosis, or athletic training, the left ventricular muscle may thicken and enlarge. This process is called "hypertrophy." While some degree of hypertrophy can be adaptive in athletes, significant or excessive hypertrophy can lead to impaired relaxation and filling of the left ventricle during diastole, reduced pumping capacity, and decreased compliance of the chamber.
Left ventricular hypertrophy is often asymptomatic initially but can increase the risk of various cardiovascular complications such as heart failure, arrhythmias, myocardial infarction (heart attack), and sudden cardiac death over time. It is typically diagnosed through imaging techniques like echocardiography or cardiac MRI and confirmed by measuring the thickness of the left ventricular wall.
Click chemistry is a term used to describe a group of chemical reactions that are fast, high-yielding, and highly selective. These reactions typically involve the formation of covalent bonds between two molecules in a simple and efficient manner, often through the use of a catalyst. The concept of click chemistry was first introduced by K. B. Sharpless, who won the Nobel Prize in Chemistry in 2001 for his work on chiral catalysis.
In the context of medical research and drug development, click chemistry has emerged as a valuable tool for rapidly synthesizing and optimizing small molecule compounds with therapeutic potential. By using click chemistry reactions to quickly and efficiently link different chemical building blocks together, researchers can rapidly generate large libraries of potential drug candidates and then screen them for biological activity. This approach has been used to discover new drugs for a variety of diseases, including cancer, infectious diseases, and neurological disorders.
One common type of click chemistry reaction is the copper-catalyzed azide-alkyne cycloaddition (CuAAC) reaction, which involves the reaction between an azide and an alkyne to form a triazole ring. This reaction is highly selective and can be carried out under mild conditions, making it a popular choice for chemical synthesis in the life sciences. Other types of click chemistry reactions include the Diels-Alder cycloaddition, the thiol-ene reaction, and the Staudinger ligation.
Overall, click chemistry has had a significant impact on medical research and drug development by enabling the rapid and efficient synthesis of complex small molecule compounds with therapeutic potential. Its versatility and selectivity make it a powerful tool for researchers seeking to discover new drugs and better understand the molecular mechanisms underlying human disease.
Gene deletion is a type of mutation where a segment of DNA, containing one or more genes, is permanently lost or removed from a chromosome. This can occur due to various genetic mechanisms such as homologous recombination, non-homologous end joining, or other types of genomic rearrangements.
The deletion of a gene can have varying effects on the organism, depending on the function of the deleted gene and its importance for normal physiological processes. If the deleted gene is essential for survival, the deletion may result in embryonic lethality or developmental abnormalities. However, if the gene is non-essential or has redundant functions, the deletion may not have any noticeable effects on the organism's phenotype.
Gene deletions can also be used as a tool in genetic research to study the function of specific genes and their role in various biological processes. For example, researchers may use gene deletion techniques to create genetically modified animal models to investigate the impact of gene deletion on disease progression or development.
Ventricular remodeling is a structural adaptation process of the heart in response to stress or injury, such as myocardial infarction (heart attack) or pressure overload. This process involves changes in size, shape, and function of the ventricles (the lower chambers of the heart).
In ventricular remodeling, the heart muscle may thicken, enlarge, or become more stiff, leading to alterations in the pumping ability of the heart. These changes can ultimately result in cardiac dysfunction, heart failure, and an increased risk of arrhythmias (irregular heart rhythms).
Ventricular remodeling is often classified into two types:
1. Concentric remodeling: This occurs when the ventricular wall thickens (hypertrophy) without a significant increase in chamber size, leading to a decrease in the cavity volume and an increase in the thickness of the ventricular wall.
2. Eccentric remodeling: This involves an increase in both the ventricular chamber size and wall thickness due to the addition of new muscle cells (hyperplasia) or enlargement of existing muscle cells (hypertrophy). As a result, the overall shape of the ventricle becomes more spherical and less elliptical.
Both types of remodeling can negatively impact heart function and contribute to the development of heart failure. Close monitoring and appropriate treatment are essential for managing ventricular remodeling and preventing further complications.
In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.
For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.
Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.
Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.
'Fagopyrum' is the genus name for buckwheat plants, which belong to the family Polygonaceae. There are several species within this genus, including Fagopyrum esculentum (common buckwheat) and Fagopyrum tataricum (Tartary buckwheat). These plants are not related to wheat or grasses, despite their name. They are important crops in some parts of the world, particularly in Asia, and their seeds are used as a source of food and flour. Buckwheat is also valued for its high protein content and unique nutritional profile.