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

Results of earlier experiments suggested that hamsters with inherited heart disease were at a higher risk of succumbing to stress during the vasospastic, lesion-forming period of their lives rather than later when the process of congestive heart failure had begun. To test this hypothesis, we stressed cardiomyopathic hamsters (CMH) whose ages differed by about 3 months; the younger of the two groups of stressed hamsters was in the vasospastic phase of the disease. The stressor was cold immobilization in which stressor intensity was manipulated using two durations of cold exposure. Log rank survival curves revealed no difference in mortality with the more intense stressor. However, significantly fewer of the older hamsters succumbed to the less intense stressor (46% as compared with 85% of the younger CMHs). Examination of the hearts in the experiment where mortality rate was the same for both groups revealed evidence of cardiac dilatation, indicative of heart failure, only in the older hamsters following stress. Since the younger hamsters did not show these changes and since they, but not the older animals, have coronary microvascular spasm and an increased susceptibility to stress, it would appear that the process of coronary vasospasm should be viewed as an independent and additional risk factor in determining the consequences of stress. Because of the effects of stress in the younger cardiomyopathic hamster, we believe that a neural link--which can be activated by stress--may be involved in the pathogenetic process of coronary vasospasm.
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PMID:Hamsters with coronary vasospasm are at increased risk from stress. 188 13

Extracorporeal circulation can be utilized successfully to rewarm accidental hypothermia victims. This paper describes a 51 year-old man who had been immersed in cold sea water for about 45 minutes. At the time of rescue his ECG was isoelectric. The core temperature was 27 degrees C. Cardiopulmonary resuscitation was performed for 190 minutes before extracorporeal circulation was established. Without active surface rewarming the temperature had dropped to 24 degrees C. Biventricular heart failure became evident during rewarming. Sternotomy and pericardiotomy were carried out to exclude cardiac tamponade, which was not found. After two hours of reperfusion the patient could be weaned from bypass supported by high-dose vasopressor infusion. He was extubated the following day. He was discharged after 12 days without any signs of permanent damage to organs.
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PMID:[Deep accidental hypothermia with asystole. A successful treatment with heart-lung machine after prolonged cardiopulmonary resuscitation]. 199 75

A review of the first 52 consecutive coronary artery bypass surgery patients to receive oxygenated blood cardioplegia, with warm reperfusion cardioplegia ('hot shot'), was undertaken to evaluate its effectiveness in myocardial protection. The chosen parameters of ischaemia were: (i) the occurrence of ventricular fibrillation (VF) on release of the aortic cross-clamp (ACC); (ii) the occurrence of bradycardia due to cardiac conduction defects; (iii) the use of inotropes with or without the use of the intra-aortic balloon pump (IABP); (iv) evidence of myocardial infarction (MI) on the postoperative electrocardiograph (ECG); and (v) peri-operative cardiogenic mortality. Warm induction cardioplegia was cooled after cardiac standstill. Repeat cold cardioplegia was given as required at intervals and warm reperfusion cardioplegia was given prior to release of the ACC. Of the 52 patients studied none developed VF after release of the ACC; one patient with pre-operative complete heart block required temporary cardiac pacing; no patient required inotropes or IABP and there was no postoperative MI or mortality. The warm blood cardioplegia technique has not resulted in any detectable evidence of inadequate myocardial protection. A beneficial effect has been demonstrated by the absence of VF, cardiac conduction defects, myocardial failure, MI and mortality.
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PMID:Warm blood cardioplegia as an adjunct to myocardial preservation during coronary artery bypass grafting. 200 Nov 97

Iron catalysis is involved in the generation of the highly cytotoxic hydroxyl radical and in the chain reactions of subsequent lipid peroxidation that lead to irreversible membrane damage. Assuming that ischemically stored heart transplants may incur free radical injury at the time of reoxygenation, we assessed the effects of the iron chelator deferoxamine in 70 isolated isovolumic buffer-perfused rat hearts subjected to the following protocol: cardioplegic arrest; cold (2 degrees C) storage for 5 hours; global ischemia at 15 degrees C for 1 hour, intended to simulate the implantation procedure; and normothermic reperfusion for 1 additional hour. During poststorage ischemic arrest, the following techniques of myocardial protection were evaluated: hypothermia alone; high-pressure (60 cm H2O) cardioplegia given at 0, 30, and 55 minutes of arrest; low-pressure (30 cm H2O) cardioplegia given at 0 and 55 minutes of arrest; and low-pressure (30 cm H2O) cardioplegia only given at 55 minutes of arrest. Treated hearts had deferoxamine (6 mumol) added to the cardioplegic solution used throughout the experimental time course. Further, in the treated group subjected to the protocol of single cardioplegic delivery at end ischemia, deferoxamine was given both in the cardioplegic reperfusate and in the Krebs buffer over the 15 initial minutes of reflow. Based on comparisons of postreperfusion ventricular pressure development, maximal rate of rise of ventricular pressure, left ventricular compliance, and coronary flow, the best myocardial protection was afforded by deferoxamine given as an additive to single-dose cardioplegic solution at the end of arrest and to the reperfusate during the initial phase of reoxygenation. As the drug has no inotropic effect, its protective action is most likely related to a decrease in catalytic iron available for free radical production and lipid peroxidation. These results support the hypothesis that oxidative damage may contribute to donor heart failure and demonstrate that this form of damage can be efficiently acted upon by iron chelation. The clinical relevance of these data stems from the fact that deferoxamine is available for human use and might become an effective means of improving donor heart preservation in the setting of clinical heart transplantation.
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PMID:A promising approach for improving the recovery of heart transplants. Prevention of free radical injury through iron chelation by deferoxamine. 236 51

Progress in chemotherapy and cardiosurgery has remarkably decreased the mortality due to infective endocarditis (IE) in recent years. In chemotherapy for IE, parental administration of antibiotics has been used routinely, the patients suffer from the psychological and physiological burden due to frequent injections and long period of therapy, even though the therapy for IE is successful. In this report, we present a case of IE caused by S. mitis, which was remarkably improved by oral administration of AMPC. A case, 69. y.o. female. She felt like a common cold and visited a G.P. Cardiomegaly was pointed out and positive inflammatory findings in serological examination were found. A low grade fever continued, and she was admitted to the hospital. Blood cultures were positive for S. mitis. For further examination, she was transferred to the university hospital. Based on the extensive blood cultures and cardioechogram, she was diagnosed IE caused by S. mitis. Because there were no symptoms of heart failure, we decided to try oral administration of AMPC, 4 g/day or 6 g/day at an interval of 6 hours. On the second day of therapy, the blood culture turned to be negative for pathogens, and on the fourth day body temperature became normal. On about the 60th day, the CRP finding became negative. Concentrations in the serum of AMPC were more than 10 folds of AMPC-MIC (0.5 microgram/ml) for S. mitis. The patient, however, suffer from complications of lung embolism and was operated for exchange of heart valves. After surgery, she has been well without any symptoms from IE.
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PMID:[A case of infective endocarditis (IE) improving with orally administered amoxicillin (AMPC)]. 250 99

Eighty consecutive patients receiving maximum inotropic and intraaortic balloon support underwent emergency coronary artery bypass grafting 3.4 +/- 1 days (mean +/- standard error) after infarction for severe left ventricular power failure (stroke work index less than 25 gm-m, left atrial pressure greater than 20 mm Hg). All underwent induction of cardioplegia with a 37 degrees C glutamate/aspartate blood cardioplegic solution, multidose cold (4 degrees C) replenishment, and warm reperfusate. Viable areas were grafted first to ensure cardioplegic distribution. Left ventricular power failure was reversed in 94% of patients; 75 of 80 patients had discontinuation of inotropic drugs and intraaortic balloon support. The early mortality rate (less than 30 days) was only 7% (3/45) with early operation (less than 18 hours) and rose to 31% (11/35, p less than 0.05) if operation was delayed more than 18 hours. Six of 14 early deaths were due to progression of preoperative organ failure despite reversal of shock. Eighteen of 66 early survivors died of end-stage heart failure (21/80), a 26% late mortality rate. Nonsurvivors (early and late) had a higher incidence of extending versus evolving infarction (33/64 versus 2/16, p less than 0.05), a longer delay from shock to operation (11/45 versus 24/35, p less than 0.05), more preoperative organ failure (9/9 versus 26/71, p less than 0.05), and a greater incidence of previous infarction (22/43 versus 13/37, p greater than 0.05). Thirty of 45 late survivors (67%) remain physically active. We conclude that left ventricular power failure should be considered a medical/surgical emergency that necessitates prompt angiography and can be reversed in selected patients. Postoperative mortality (early and late) is due principally to delay of operation leading to progression of preoperative organ failure or progression of underlying cardiac disease if infarction becomes established.
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PMID:Studies on prolonged acute regional ischemia. VI. Myocardial infarction with left ventricular power failure: a medical/surgical emergency requiring urgent revascularization with maximal protection of remote muscle. 281 6

During 10 years of clinical use involving almost 3 million patient-years, acebutolol has become established as a remarkably safe and well-tolerated beta-blocking agent, effective in treating essential hypertension and cardiac arrhythmias. The existence of a long-lived active metabolite (diacetolol) confers a 24-hour duration of action, which permits effective use of a once-daily regimen, particularly for hypertension. Acebutolol has low lipid solubility and low protein binding; the former property reduces the risk of central side effects, and the latter means that displacement interactions with other drugs are unlikely. Because acebutolol and its metabolite normally have both renal and hepatic excretion pathways, an alternative pathway is available should either be compromised through disease. Acebutolol is cardioselective, and clinical use has borne out the low incidence of bronchospasm in patients with impaired lung function. The possession of intrinsic sympathomimetic activity (ISA) leads to only modest reductions in cardiac output, which in turn reduces the chance of excessive bradycardia and the likelihood of precipitating heart failure. A combination of selectivity and ISA may be responsible for the low incidence of tiredness and cold extremities observed with acebutolol compared with other beta blockers. The unique pharmacologic and pharmacokinetic profile of acebutolol confers several therapeutic advantages and may be responsible for the generally low level of side effects experienced in clinical use.
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PMID:Acebutolol: ten years of experience. 285 85

The informative value of various functional and laboratory diagnostic methods was reviewed in 150 patients with unstable angina (UA). High informativeness (92%) and sensitivity (83%) of isometric hand grip under computerized electrocardiographic monitoring was demonstrated for the diagnosis and control of treatment in these patients. Isometric loading brought out a dramatically reduced coronary reserve, latent heart failure and electrical instability of the myocardium. The cold test with a small area of skin exposure is of low diagnostic value in UA cases and cannot be recommended for clinical use. Serial myoglobin assays add to the accuracy of diagnosis and have high predictive value.
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PMID:[Methods of diagnosing unstable stenocardia and monitoring its treatment]. 286 42

Since 1975 mitomycin C (MMC) has been suggested to be cardiotoxic, especially when combined with or given following doxorubicin. Data on dose dependency or incidence concerning this side effect were not known. We have initiated a prospective study to obtain some more data on these subjects. Forty-four MMC-treated patients were studied, 37 of them could be evaluated. All patients were studied by repeated physical examinations, chest X-rays, electro- and echocardiography and radionuclide left ventricular ejection fraction (EF) determinations. The results were evaluated per cumulative dose level. One of the patients developed cardiac failure after 30 mg m-2 MMC and only 150 mg m-2 doxorubicin. The cardiac failure was predicted by a drop in EF determined during a cold pressor test. None of the other patients developed clinical cardiotoxicity, nor did the studied parameters change. The literature on this subject was also reviewed. Based on the combined data from the present study and the literature, we suggest that MMC-related cardiotoxicity is dose dependent, occurring at cumulative dose levels of 30 mg m-2 or more, mainly in patients also (previously or simultaneously) treated with doxorubicin. The incidence is likely to be less than 10% even for this risk group.
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PMID:A prospective study on the dose dependency of cardiotoxicity induced by mitomycin C. 313 99

Fourteen patients with advanced breast cancer were treated with a combination of vincristine, mitozantrone and prednisolone. Before, during and after cessation of treatment radionuclide assessment of ventricular performance was obtained at rest, in response to cold pressor-induced stress and on recovery from stress. Six of 14 patients (46%) developed abnormalities of left ventricular ejection fraction (LVEF). One patient developed clinical signs of cardiac failure. Mitozantrone is an active agent in the treatment of advanced breast cancer but it can produce cardiotoxicity. In this particular middle-aged population, changes in LVEF occurred over a wide range of cumulative doses. Further investigation is required to determine the nature and prognosis of this iatrogenic toxicity.
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PMID:Cardiotoxicity of mitozantrone assessed by stress and resting nuclear ventriculography. 316 98


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