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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our earlier work showed that stress had progressively more serious consequences in a hamster model of congestive heart failure as the magnitude of heart failure worsened. Based on that study, we hypothesized that the intensity of the stressor used might play an important part in determining this outcome as well as in influencing coronary reactivity to arginine vasopressin (AVP). Cardiomyopathic (2.5, 6.5, and 10 months) hamsters (CMHs) were stressed with a 2-hr period of supine immobilization for five consecutive days. Stressor intensity was increased by exposing the hamsters to progressively longer periods at 4 degrees C: the low stress group was never put in the cold; the moderate stress group was exposed to cold for 1 hr, and the high stress group for 2 hr. CMHs were anesthetized and sacrificed 5 days after stress, and their hearts were perfused using a modified Langendorff system. Maximum +/- dP/dt, developed pressure, ventricular relaxation time, (T), and coronary vascular resistance (CVR) were recorded, and CVR was also measured following coronary infusion of AVP. Stressor intensity had no effect on cardiac mechanics in 2.5-month CMHs. In 6.5-month CMHs, only the high-intensity stressor impaired ventricular mechanics (decreased maximum +/- dP/dt and developed pressure, increased T; P < 0.05), while low and moderate stress produced no effects. In 10-month CMHs, stress at all intensities exacerbated ventricular dysfunction (decreased maximum +/- dP/dt and developed pressure; P < 0.05). These results support our first hypothesis that stressor intensity interacts multiplicatively with severity of the underlying disease to influence the course of heart failure. However, our second hypothesis was not supported, because stress-regardless of intensity-affected reactivity of the coronary vasculature to AVP only in 2.5-month CMHs. A further test of the relation of stressor intensity and coronary vascular reactivity requires study of additional groups of CMHs during the period of their disease characterized by coronary vasospasm.
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PMID:The role of stressor intensity in influencing the course of heart disease in cardiomyopathic hamsters. 867 70

A 50-year-old man experienced acute heart failure four years after initial mitral valve replacement (MVR) for left atrial thrombosis using a CarboMedics prosthesis, despite satisfactory coagulation control with warfarin. After initial MVR, late cardiac tamponade occurred twice and left circumflex branch stenosis was treated with percutaneous transluminal coronary angioplasty (PTCA). Re-MVR with an Edwards-TEKNA valve was performed after echocardiography and cineradiography showed mitral valve thrombosis, with thrombi on both mitral valve leaflets and covering most of the left atrial wall. Post-surgery progress was favorable with warfarin and dipyridamole therapy. After six weeks cardiac catheter revealed complete right external iliac artery occlusion. Cardiac dysfunction and atrial flutter apparently accelerated thrombosis after a common cold activated coagulation. Cardiac tamponade, circumflex branch stenosis, and right external iliac artery occlusion occurred despite satisfactory coagulation control by warfarin. Warfarin suppresses some coagulation factors but cannot always correct hypercoagulability. Two months after re-MVR, coagulation tests showed normal TT, F1 + 2, and D-Dimer but an increase in TAT, suggesting involvement of additional coagulation factors. After artificial valve replacement, therapy should achieve a PT-INR level of 3.0-4.5, with close follow-up using other indices of fibrinolysis and coagulation activity in addition to TT.
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PMID:[A case of valve thrombosis of CarboMedics prosthesis four years after mitral valve replacement: relationship of anticoagulant therapy to coagulation and fibrinolysis activating factors]. 891 69

The cold stress leads to increased levels of catecholamines, of their precursors and metabolites, with increased oxygen consumption by the myocardium. Atrial cardiomyocytes of amiodarone-treated rats, previously stressed by cold, showed a marked decrease of the morphological alterations observed in the animals submitted to cold stress without amiodarone protection. Such results indicate, at the subcellular level, that amiodarone could improve cardiac function by a propranolol-like action when there is heart failure, a condition in which there is a high level of catecholamine.
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PMID:Propranolol-like action of amiodarone. An electronmicroscopic study in rats under cold stress. 916 19

ACTIONS OF THE SYMPATHETIC NERVOUS SYSTEM: The sympathetic nervous system is an important cardiovascular regulator, particularly during stress and exercise; its sympathetic nervous activity is regulated in centers in the brain stem and transmitted to organs and blood vessels that are innervated by sympathetic nerve endings. In the heart, the sympathetic nervous system increases heart rate and contractility. The effect of the sympathetic nervous system in different vascular beds depends on the degree of innervation, the distribution of postjunctional receptors and the effect of local mediators. Overactivation of the sympathetic nervous system may lead to hypertension and is involved in heart failure. The degree of sympathetic activation determines prognosis in heart failure. Hence, vasodilators ideally should also blunt sympathetic activity, or at least avoid activating it. DIFFERENCES AMONG CALCIUM ANTAGONISTS: Calcium antagonists are widely used for the treatment of hypertension and coronary artery disease. Their main mechanism of action is inhibition of L-type Ca2+ channels. Short-acting nifedipine leads to a marked increase in heart rate, sympathetic nerve activity and plasma catecholamines, similar to those induced by a cold pressor test. With long-acting nifedipine heart rate does not increase, but sympathetic nerve activity does increase. Other calcium antagonists have been less thoroughly investigated, but indirect evidence suggests differences between the different classes. Verapamil and diltiazem lower heart rate. Plasma noradrenalin measurements suggest that verapamil does not stimulate the sympathetic nervous system, but tends to suppress it. Second-generation dihydropyridines with longer duration of action do not increase heart rate; their effects on peripheral sympathetic nerve activity are not clear. Thus, in summary, the different classes of calcium antagonists differ with regard to their effects on sympathetic nerve activation. A decrease in heart rate and nerve activity might be beneficial for long-term prognosis, particularly in hypertension and heart failure.
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PMID:Calcium antagonists and sympathetic nerve activation: are there differences between classes? 953 92

Metabolic differences between cardiomyopathic hamsters (CMHs), as they progress through various physiologic phases before reaching end-stage heart failure (HF), and healthy hamsters (HHs) are often difficult to demonstrate. We suggest that metabolic differences, magnified by application of chronic stress (S: cold immobilization 2 hr/day for 5 days) followed by acute stress (AS: 55 min global ischemia /30 min reperfusion), can be used to characterize different stages in this cardiomyopathic process. High performance liquid chromatography (HPLC) and 31P NMR methods were used to monitor the effects of acute stress applied to nonstressed (NS) and previously stressed CMHs (NS-2.5-month NS-5-month; S-2.5-month, S-5-month) and HHs (NS-HH, S-HH). Cardiac tissue extracts from nonstressed and stressed hamsters were analyzed for ATP and PCr at baseline and after completion of ischemia/reperfusion (AS) using HPLC. In nonstressed hamsters, ATP and PCr were 12% lower in CMHs (both NS-2.5- and NS-5-month) than in NS-HHs. After exposure to stress, ATP was 26% lower in CMHs (S-2.5- and S-5-month) compared to S-HHs, whereas there were minimal differences in PCr between the groups. 31P NMR monitoring of metabolism in the perfused beating heart during application of acute stress produced similar changes (%) in ATP and PCr in all groups (NS and S), whereas Pi increase was less in NS-5-month (118%) compared to NS-2.5-month (179%) and NS-HHs (306.8%), P < 0.05; and in S-5-month (148%) compared to S-2.5-month (216%) and S-HHs (222%). The changes in myocardial pH were inversely related to changes in Pi: NS-5-month (-13.5%); NS-2.5-month (-9.7%); NS-HH (-17.7%). pH changes in stressed cardiomyopathic hamsters were similar to those of S-HHs. The postischemic recovery of ATP and Pi return closer to baseline values in cardiomyopathic hamsters (both NS and S) compared to healthy hamsters. The data suggest that cardiomyopathic hamsters have baseline metabolic abnormalities, and their responses to chronic cold immobilization stress, acute ischemia, and chronic cold immobilization stress plus acute ischemia are different from those in HHs. These responses may help to characterize specific stages of disease.
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PMID:Metabolic abnormalities and differential responses to stress associated with hamster cardiomyopathy. 975 Dec 22

In this study, insomnia in 80-year-olds was related to medical, psychological and social factors. The data were based on examinations every year in people aged between 80 and 89 years. Of 333 people living in the city of Lund and born in 1908, 67% participated. Increased severity of insomnia was significantly associated with use of diuretics, other cardiovascular drugs, hypnotics and laxatives, and with nervousness, difficulty relaxing, anorexia, nausea, constipation, backache, feeling cold, sweating, loss of weight, dizziness, depression, general fatigue, exhaustion, angina pectoris, cardiac insufficiency, worsened objective and subjective health, presence of negative T-waves on ECG, anxiety, total life satisfaction, neuroticism, disbelief in a just world, feeling lonely and lower survival rates. Thus insomnia has widespread associations with different aspects of life in 80-year-olds.
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PMID:Insomnia in an 80-year-old population: relationship to medical, psychological and social factors. 978 73

Cardiac rehabilitation has become an accepted adjunct treatment for the majority of patients with cardiovascular disease, especially for those who have received cardiac surgery. However, improved survival has not been generally demonstrated in a supervised cardiac rehabilitation programme, while some benefits have been found in functional capacity, psychosocial characteristics and lipoprotein patterns of patients who underwent sustained periods of exercise training. The influence of post-surgical conditions on phase II rehabilitation following cardiac surgery has not yet been well addressed. Many factors may influence the timing of phase II rehabilitation following cardiac surgery, especially the pre-operative condition of the patient, the concomitant morbidity, the incidence of peri-operative complications and the rapidity of recovery, mainly influenced by post-operative cardiac and lung function, pain and wound healing. This article reviews the general and specific medical and surgical problems encountered during early follow-up of cardiac surgery patients, which might affect the timing of postoperative rehabilitation, analyses briefly the impacts of less invasive heart surgery on cardiac rehabilitation as well as that of fast tract protocols after conventional heart surgery. Some patients required service intervention during cardiac rehabilitation while others were withdrawn from cardiac rehabilitation for medical reasons or surgery-related complications. Specific problems in patients following cardiac transplantation are depicted briefly. Cardiac transplant recipients may suffer from pre-operative end-stage heart failure, prolonged cold ischaemia of the donor heart, denervation of the cardiac allograft, immunological allomismatch, and unusual psychological stress. In summary, phase II cardiac rehabilitation on a stationary and more recently on an ambulatory basis is generally recommended two to four weeks following uncomplicated coronary and valvular procedures, while patients following cardiac transplantation may be included in such programmes after approximately four to six weeks. The earliest rehabilitation is possible in patients following less invasive heart surgery and may start one to two weeks postoperatively.
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PMID:Optimal timing of rehabilitation after cardiac surgery: the surgeon's view. 985 49

Stress alone is generally not sufficient to produce serious disease, but stress imposed upon pre-existing disease can contribute to disease progression. To explore this phenomenon, cold-immobilization stress was imposed on young 12.5 month, necrotic phase with small vessel coronary spasm) and older (5 month, quiescent phase, between necrosis and heart failure) cardiomyopathic hamsters. Our hypothesis was that changes in mitochondrial energy processes are involved in stress induced pathology. Polarographic and high performance liquid chromatography (HPLC) techniques were used to measure mitochondrial respiration and oxidative phosphorylation and concentrations of phosphocreatine and adenylates, respectively, in hearts from young and old cardiomyopathic hamsters (stressed and unstressed). No significant differences were found between the young (2.5 month) and old (5 month) age groups in unstressed and stressed healthy hamsters and between young (2.5 month) and old (5 month) unstressed cardiomyopathic hamsters with respect to different parameters of mitochondrial oxidative phosphorylation and with respect to concentration of bioenergetic metabolites, except that ADP concentration was higher in older cardiomyopathic hamsters. Application of stress uncovered differences between young and old cardiomyopathic hamsters: respiration control index was lower and State 4 respiration was higher in young compared to old cardiomyopathic hamsters; whereas the total concentration of ATP was decreased to the same level in both cardiomyopathic groups when compared to control. Mitochondrial oxidative phosphorylation in young cardiomyopathic hamsters was more sensitive to Ca2+, as evidenced by partial uncoupling of respiration and oxidative phosphorylation, than in older cardiomyopathic hamsters and controls. In conclusion, young cardiomyopathic hamsters, i.e. in the necrotic phase of disease, were more susceptible to stress induced changes in mitochondrial oxidative phosphorylation than older cardiomyopathic hamsters and controls.
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PMID:Mitochondrial oxidative phosphorylation in heart from stressed cardiomyopathic hamsters. 1019 86

In several studies, investigators have reported associations among air pollution, weather, and daily deaths, usually from all causes. In the current study, we focused on the difference in lag time between exposure to total suspended particulates or extreme weather and cause-specific mortality in an effort to understand the potential underlying mechanism. We used a robust Poisson regression in a generalized additive model to investigate the association between air pollution and daily mortality. We used a loess smooth function to model season, weather, and humidity; indicator variables for hot days were also used. To examine the relationship in a currently meaningful range, we excluded all days with a total suspended particulate concentration higher than 200 microg/m3. We found a significant association on the concurrent day, both for respiratory infection deaths (11% increase/100 microg/m3 increase in total suspended particulate; 95% confidence interval = 5, 17) and for heart-failure deaths (7% increase; 95% confidence interval = 3, 11). The associations with myocardial infarction (i.e., 10% increase; 95% confidence interval = 3, 18) and chronic obstructive pulmonary disease (12% increase, 95% confidence interval = 6, 17) were found for the means of 3 and 4 d prior to death. We observed an effect of cold weather at lag 1 for respiratory infections and an effect of hot weather at lag 0 for heart failure and myocardial infarctions. The association for all causes and cause-specific deaths was almost identical to that noted previously in Philadelphia, Pennsylvania. Smoothed functions of total suspended particulates suggested a higher slope at lower concentrations, and this finding may account for differences noted between European and U.S. studies. Given that both the dependence between weather and daily mortality and the lag between exposure and death varies by cause of death, analyses by specific causes of death would be very useful in the future.
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PMID:Air pollution and cause-specific mortality in Milan, Italy, 1980-1989. 1044 36

We evaluate the acute hemodynamic and neurohormonal effects of losartan in 15 patients with symptomatic chronic heart failure (CHF), mean age 72+/-8 years, which were classified in two subgroups: (A) Patients with left ventricular ejection fraction (LVEF)< or =0.35 (n = 7); (B) subjects with LVEF>0.35 (n = 8). Sympathetic reactivity (blood pressure, heart rate and plasma norepinephrine) and plasma endothelin-1 (ET-1) were evaluated by a cold pressor test (CPT). Single doses of losartan (50 mg p.o.) lowered delta DBP in both subgroups (A, 8+/-9 to 0+/-5 mm Hg, P<0.05; B, 10+/-6 to 3+/-4 mm Hg, P<0.05) and attenuated the rise of HR in patients with mild (4+/-6 to -1+/-2 bpm, P<0.05) but not with severe (4+/-5 to 2+/-5 bpm, n.s.) impairment of left ventricular function. Losartan blunted the response (delta) of PNE during CPT (A, 142+/-131 to 10+/-74 pg/ml, P<0.05; B, 129+/-72 to 1+/-144 pg/ml, P<0.01). A significant rise in plasma ET-1 was observed during CPT in patients from subgroup B (0.64+/-0.40 to 0.81+/-0.40 fmol/ml, P<0.05) but not in patients with LVEF< or =0.35 (1.79+/-0.44 to 1.51+/-0.66 fmol/ml, n.s.). Losartan attenuated the rise in ET-1 during CPT in patients with LVEF>0.35 (delta ET-1 0.17+/-0.86 to 0.03+/-0.11 fmol/ml, P<0.05), with no significant changes in subgroup A. Acute effects of losartan were characterized by a more favorable hemodynamic and neurohumoral response in patients with chronic heart failure and preserved systolic ventricular function related to subjects with lower ejection fractions.
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PMID:Effects of the angiotensin II antagonist losartan on endothelin-1 and norepinephrine plasma levels during cold pressor test in patients with chronic heart failure. 1050 44


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