UMLS:C0018801 - FACTA Search

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Query: UMLS:C0018801 (heart failure)
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Hypothermia is commonly found in accidents on land and at sea, yet its pulmonary circulatory effects have not been studied before. To study the effects of hypothermia on the right heart function and pulmonary circulation, cardiac catheterization was carried out on nine anaesthetized beagle dogs. The dogs were cooled between ice bags until the temperature in the pulmonary artery was 25 degrees C and then rewarmed using a heating box especially constructed for this purpose. Heart rate decreased significantly (P < 0.01) during cooling. Cardiac output also diminished mainly because of decreased heart rate. Total pulmonary resistance increased in the cold (P < 0.05) and returned to the initial level during rewarming. The peak rate of increase in pressure (dP/dtmax) of the right ventricular pressure curve did not show any significant change. Retardation in relaxation in hypothermia was indicated by an increase (P < 0.01) in the peak negative dP/dt of the right ventricular pressure curve. According to our results, the contraction rate did not change, but the relaxation rate decreased significantly during cooling. No signs of heart failure were observed and all parameters returned to normal during rewarming. In conclusion, right ventricular function was not compromised even during deep hypothermia.
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PMID:Effects on dogs of surface-induced hypothermia and rewarming on the right heart function and pulmonary circulation. 1075 Nov

The symptoms and severity of anemia depend on various factors, including the degree of anemia, the rapidity of its onset, and the age and physiologic status of the patient. Although the human body tries to counterbalance the effects of anemia by various mechanisms, almost every organ system of the human body is eventually affected. The symptoms experienced by patients vary from cold skin, dizziness, and palpitations to pulmonary edema, heart failure, depression, and severe impairment of cognitive function. Anemia substantially impacts patients' quality of life, a fact that has been shown in several clinical trials in patients with renal disease as well as in patients suffering from various malignancies undergoing chemotherapy. These studies evaluated the administration of recombinant human erythropoietin (r-HuEPO, epoetin alfa) to anemic patients, and it was shown that raising hemoglobin levels with epoetin alfa ameliorated the symptoms of anemia and significantly improved the functional status and overall quality of life in cancer patients. Furthermore, preliminary data indicate that the correction of anemia in cancer patients may in addition improve treatment efficacy and possibly overall survival.
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PMID:Symptomatology of anemia. 1139 46

Cardiac transplantation is the most successful therapy for refractory heart failure, but clinical transplantation is still confronted with the problems of acute rejection and acute pump failure. The limiting factor in achieving prolonged survival remains cardiac allograft vasculopathy. In recent years it has become apparent that from brain death onward, the cardiac endothelium plays a key role in these acute and chronic events. Brain death is associated with an inflammatory response that primes the endothelium for cumulative injury during the subsequent stages of ischemic cold storage, reperfusion and allorecognition. As a structural and functional interface, the endothelium is the site at which inflammatory cells move from the bloodstream through the vessel wall into the parenchyma. The endothelium interacts with the complement system, the coagulation and inflammatory cascades, circulating leukocytes, the immune system, the smooth muscle in the vessel wall, and the surrounding matrix and cardiomyocytes. A better understanding of its many roles may lead to expansion of our therapeutic possibilities and better outcomes overall. This article reviews the possible roles of the endothelium in relation to cardiac transplantation, and discusses the diagnostic and therapeutic modalities that are available to date.
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PMID:The endothelium in clinical cardiac transplantation. 1189 59

Heart failure during the immediate period of an acute myocardial infarction constitutes a major insult to this pathology; since, once installed, it is associate to ventricular dysfunction and expansion of the left ventricle. It can appear either early or delayed. Subsequent to the acute insult, the myocardium is subjected to diverse changes in its anatomical conformation and to diastolic and systolic alterations, which will affect the hemodynamic constants of the patient. Changes in the parietal ventricular architecture as well as at the neurohumoral level will also occur. The clinical signs of heart failure are: dyspnea, pallor, tachycardia, diaphoresis, cold skin, oliguria, somnolence, and gallop, which can be observed at the very beginning of the coronary occlusion. Its clinical identification, through in-hospital studies supported by adequate hemodynamic monitoring, is of utter relevance since it will lead to appropriate and fast treatment. The groups of patients with acute myocardial infarction with high risk for the development of cardiac failure are: patients with extensive Q wave infarction, diabetic, patients over 65 years of age, and those with a history of previous myocardial infarction(s). The cornerstone of treatment must be focused on reducing the myocardial ischemia, which can be achieved through the use of modern therapeutics and, given the case, pharmacological agents, coronary intervention procedures, or cardiac surgery must be taken into account. At present it is known that angiotensin converting enzyme inhibitors, betablockers, inotropics, are useful to improve ventricular function in patients with acute myocardial infarction.
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PMID:[Heart failure in acute myocardial infarction]. 1200 71

Myocardial blood flow (MBF) reserve is impaired in patients with symptomatic chronic heart failure. Whether this is already present in asymptomatic left ventricular (LV) dysfunction, and whether it is affected by angiotensin converting enzyme (ACE) inhibition, is unknown. We examined MBF in 20 patients with asymptomatic LV dysfunction and compared them to healthy volunteers. MBF (reserve) was assessed with positron emission tomography (PET) and N-13 ammonia at rest, during dipyridamole stress test (DST) and during cold pressor test (CPT). Further, in the LV-dysfunction group, we studied the effects of 3 months treatment with ACE inhibition with a second PET study. Patients were randomized double-blind to perindopril 4 mg daily or placebo. MBF at rest was similar in controls and patients. DST-induced MBF reserve, however, was decreased in patients vs. controls (1.71+/-0.2 vs. 2.62+/-0.5, respectively p < 0.05). Also CPT-induced MBF was lower in patients (1.14+/-0.06 vs. 1.23+/-0.03, p < 0.05). After 3 months double-blind treatment, CPT-induced MBF decreased in the placebo group (from 1.12+/-0.02 to 0.93+/-0.06), but was preserved in the perindopril group (from 1.16+/-0.08 to 1.14+/-0.08 shifts from baseline: -0.19+/-0.05 vs. -0.02+/-0.07 respectively p = 0.07). This was compatible with a trend to a smaller increase in coronary vascular resistance during CPT (1.23+/-0.08 vs. 1.03+/-0.06, placebo vs. perindopril, p = 0.06). In patients with asymptomatic LV dysfunction, MBF, both after vasodilation and after CPT, is already impaired. ACE inhibition with perindopril during this short-term treatment had no significant effects.
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PMID:Impairment of myocardial blood flow reserve in patients with asymptomatic left ventricular dysfunction: effects of ACE-inhibition with perindopril. 1202 49

The purpose of the work presented here was to investigate the responses mediated by alpha-adrenoceptors and also contractility of vascular smooth muscle in large peripheral vessels following doxorubicin (DXR)-induced heart failure. Cardiac failure was induced by DXR injection. Thirty saline-treated (normal group) and 30 DXR-treated rabbits (1 mg/kg administered intravenously twice weekly for 8 weeks) were studied. Chronic heart failure was confirmed by echocardiography and later also by histopathology. The DXR-treated hearts were subdivided by ejection fraction >40 or <40 into non-failing (control) and failing (test) groups. Animals were sacrificed by overdose with pentobarbitone sodium (i.v. injection). Arteries and veins were carefully removed with as little connective tissue as possible and placed in cold physiological salt solution. The arterial and venous rings were mounted in 10 ml isolated organ baths, maintained at 37 degrees C and gassed with 95% O(2) plus 5% CO(2). The rings were then placed under different resting tensions. After initial application of tension tissues were left to equilibrate for a 60-min period. Then all preparations were contracted with KCl (Krebs solution, Na free and high KCl, 125 mM) and allowed to contract for 5-10 min. Following complete washout with normal Krebs, an additional 30 min equilibration period was allowed. Then cumulative concentration-response curves to noradrenaline (NA) obtained by increasing the concentration of the agonist in half-log increments. In contraction responses to NA the renal artery and aorta were the most sensitive preparations (pD(2) values: 5.75 and 5.36, respectively). Compared with control, in DXR-treated rabbits, maximum response (E(max)) of NA was not modified in the aorta; renal and saphenous arteries, renal and saphenous veins, whereas it was significantly lower in the vena cava. Compared with control rabbits, in DXR-treated rabbits the pD(2) of NA was significantly increased in the thoracic aorta whereas there was no significant difference between groups in the other studied vessels. Contraction to KCl showed no significant difference between two groups. These results suggest that the sympathetic regulation of vascular contraction is impaired by DXR-induced heart failure through reduction in the alpha-adrenoceptors.
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PMID:Effects of noradrenaline and KCl on peripheral vessels in doxorubicin induced model of heart failure. 1210 Sep 71

Candida species can cause clinical manifestations in various organs of the cardiovascular system, i.e., the pericardium, myocardium, and endocardium, with endocarditis being the best-known clinical entity. Endocarditis is seen primarily in intravenous drug users and in individuals with damaged native valves, especially in congenital heart disease or rheumatic valvular diseases, and in prosthetic heart valves. The authors present a case of Pichia ohmeri endocarditis in an intravenous drug user, with an unusual presentation form. This is a case of a 42-year-old man, an intravenous heroin user, who was admitted to our Vascular Surgery Department because of fever and acute serious ischemia of the left inferior limb. He presented with fever (39 degrees C), a pale and cold left limb, absence of the left popliteal pulse, and a pansystolic murmur at the cardiac apex. The transthoracic echocardiogram showed a large vegetation on the anterior leaflet of the mitral valve and severe mitral regurgitation with good left ventricular systolic function. Empirical antibiotic therapy was started. Six days after admission, embolectomy was performed with partial clinical recovery. Three blood cultures and the embolus showed a teleomorphic form of Candida guilliermondii - Pichia ohmeri. Therapy with intravenous liposomal amphotericin B, fluocitosin, imipenem, and aztreonam was started. Two weeks later, his clinical condition deteriorated with acute heart failure refractory to medical therapy, mandating mechanical ventilation and high-dose vasopressor and inotropic amine support. He underwent urgent mitral valve replacement with a biologic prosthetic valve. Rapid stabilization of the cardiac status occurred, but ischemic limb lesions required further vascular interventions.
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PMID:Native valve endocarditis due to Pichia ohmeri. 1238 36

Prostaglandins released from blood vessels modulate vascular tone, and inhibition of their production during exogenous infusions of catecholamines causes increased venoconstriction. To determine the influence of prostaglandin production on venoconstriction during physiological stimuli known to cause sympathetic activation, and to assess its importance in chronic heart failure (CHF), we studied 11 normal subjects (62 +/- 4 yr) and 14 patients with CHF (64 +/- 2 yr, left ventricular ejection fraction 23 +/- 1%, New York Heart Association classes II and III) (means +/- SE). Dorsal hand vein distension was measured during mental arithmetic (MA), cold pressor test (CPT), and lower body negative pressure (LBNP; -10 and -40 mmHg), with saline infusion in one hand and local indomethacin (cyclooxygenase inhibitor) infusion (3 microg/min) in the other. Acetylcholine (0.01-1 nmol/min) dilated veins preconstricted with PGF(2alpha) in normals but, consistent with endothelial dysfunction, barely did so in CHF patients (P = 0.001). Nonendothelial venodilation to sodium nitroprusside (0.3-10 nmol/min) was not different between normals and CHF patients. Resting venous norepinephrine levels were higher in CHF patients (2,812 +/- 420 pmol/l) than normals (1,418 +/- 145 pmol/l, P = 0.007). In normals, indomethacin caused increased venoconstriction to MA (from 4.9 +/- 1.5 to 19.2 +/- 4.5%, P = 0.022) and CPT (from 2.9 +/- 3.8 to 17.6 +/- 4.2%, P = 0.007). In CHF, indomethacin caused increased venoconstriction to MA (from 6.6 +/- 3.9% to 19.0 +/- 4.5%, P = 0.014), CPT (from 9.6 +/- 2.1% to 20.1 +/- 3.7%, P = 0.001), and -40 mmHg LBNP (from 10.7 +/- 3.0% to 23.2 +/- 3.8%, P = 0.041). Control responses for all tests were not different between normals and CHF patients. The effects of indomethacin on venoconstriction to MA and CPT were not different between normals and CHF patients, but venoconstriction to -40 mmHg LBNP was accentuated in CHF patients (P = 0.036). Inhibition of prostaglandins by indomethacin significantly enhances hand vein constriction to physiological stimuli in both normals and CHF patients, although a differential effect exists for LBNP.
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PMID:Prostaglandin modulation of venoconstriction to physiological stress in normals and heart failure patients. 1257 11

Autonomic functions, such as increased sympathetic and parasympathetic activity and the brain's suprachiasmatic nucleus, higher nervous centres, depression, hostility and aggression appear to be important determinants of heart rate variability (HRV), which is, itself, an important risk factor of myocardial infarction, arrhythmias, sudden death, heart failure and atherosclerosis. The circadian rhythm of these complications with an increased occurrence in the second quarter of the day may be due to autonomic dysfunction as well as to the presence of excitatory brain and heart tissues. While increased sympathetic activity is associated with increased levels of cortisol, catecholamines, serotonin, renin, aldosterone, angiotensin and free radicals; increased parasympathetic activity may be associated with greater levels of acetylecholine, dopamine, nitric oxide, endorphins, coenzyme Q10, antioxidants and other protective factors. Recent studies indicate that hyperglycemia, diabetes, hyperlipidemia, ambient pollution, insulin resistance and mental stress can increase the risk of low HRV. These risk factors, which are known to favour cardiovascular disease, seem to act by decreasing HRV. There is evidence that regular fasting may modulate HRV and other risk factors of heart attack. While exercise is known to decrease HRV, exercise training may not have any adverse effect on HRV. In a recent study among 202 patients with acute myocardial infarction (AMI), the incidence of onset of chest pain was highest in the second quarter of the day (41.0%), mainly between 4.0-8.0 AM, followed by the fourth quarter, usually after large meals (28.2%). Emotion was the second most common trigger (43.5%). Cold weather was a predisposing factor in 29.2% and hot temperature (> 40 degrees celsius) was common in 24.7% of the patients. Dietary n-3 fatty acids and coenzyme Q10 have been found to prevent the increased circadian occurrence of cardiac events in our randomized controlled trials, possibly by increasing HRV. We have also found that n-3 fatty acids plus CoQ can decrease TNF-alpha and IL-6 in AMI which are pro-inflammatory agents. There is evidence that dietary n-3 fatty acids canenhance hippocampal acetylecholine levels, which may be protective. Similarly, the stimulation of the vagus nerve may inhibit TNF synthesis in the liver and acetylecholine, the principal vagal neurotransmitter, significantly attenuates the release of pro-inflammatory cytokines TNF-alpha, interleukin 1,6 and 18, but not the anti-inflammatory cytokine IL-10 in experiments. Therefore, any agent which can enhance brain acetylecholine levels, may be used as a therapeutic agent in protecting the suprachiasmatic nucleus, higher nervous centres, vagal activity and sympathetic nerve activity which are known to regulate the body clock and HRV and the risk of SCD and heart attack.
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PMID:Brain-heart connection and the risk of heart attack. 1265 78

We have demonstrated that Cre-loxP-mediated gene-switch transgenesis is an effective approach to achieve targeted and temporally regulated gene manipulation in the heart. Using this approach, we have established animal models with targeted activation of different MAPK pathways. From these animal models, we identified distinct features of cardiac pathology associated with individual MAPK branches (summarized in Fig. 8). Specifically, Ras activation appears to promote cardiac hypertrophy, whereas p38 and JNK activation does not. Whereas Ras activation leads to depressed diastolic function associated with suppressed calcium transients and SR calcium uptake, p38 activity seems to modulate cellular contractility without affecting intracellular calcium cycling. Although all three models displayed extensive remodeling in the myocardium, the extent and the composition of interstitial fibrosis are different among them, with Ras- and p38-activated hearts promoting collagen-based fibrosis, and JNK activation leading to induction in fibronectin-based reticular fiber. In addition, JNK activation leads to loss of Cx43 expression and abnormal cell-cell communication. Therefore, ERK, p38, and JNK are three distinct intracellular signaling pathways that contribute to different aspects of cardiac pathology during heart failure. Combining sophisticated genetic manipulation with comprehensive analysis at physiological, molecular, and genomic levels, the transgenic animals established in these studies should serve as valuable model systems to identify and dissect the underlying mechanisms for different aspects of cardiac pathology such as hypertrophy, contractile dysfunction, and abnormal cell-cell communication. The insights learned from these investigations may help to develop novel therapeutic approaches to confront this devastating disease.
Cold Spring Harb Symp Quant Biol 2002
PMID:Using a gene-switch transgenic approach to dissect distinct roles of MAP kinases in heart failure. 1285 68

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