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

Myocardial oxidative and glycolytic reserves were evaluated in four harbor seals, Phoca vitulina richardsi, and six domestic pigs, Sus scrofa (hematocrits: 58 +/- 5 and 34 +/- 1%., respectively). Progressive hypoxia was induced by lowering arterial hemoglobin-oxygen saturation in 10% decrements, each maintained for 10-min periods, until the onset of heart failure. Myocardial oxygen consumption rate (VO2), lactate release/uptake rate (L), and triple product, an index of myocardial energetic demand, were determined at each saturation level. Onset of L began in pigs at Sao2 = 57 +/- 5% and in seals at Sao2 = 35 +/- 4%. Cumulative oxygen consumption (VO2) during hypoxia, determined from the onset of cardiac lactate release, was 435 ml O2/100 g in seals and 172 ml O2/100 g in pigs. Cumulative lactate release during the same period was 14 mM/100 g in seals and 4.6 mM/100 g in pigs. The pigs' left ventricular contractile response (dP/dtmax) was greater than that of seals throughout the time of lactate release. Total myocardial energetic sources were higher in seals than in pigs, and seals were better able to tolerate myocardial hypoxia than were pigs. In a separate experiment, two seals and six pigs were made acutely hypoxic until cessation of cardiac output (seals, 17.5 min; pigs, 7.4 min) and were then reoxygenated. Both seals recovered promptly to control levels of cardiac mechanical function, whereas none of the pigs recovered. Additionally, five pigs were beta-blocked with 0.10 mg/kg of propranolol and were subjected to acute hypoxia. Tolerance to cardiac hypoxia in beta-blocked pigs was significantly increased compared with that of control animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses of harbor seal and pig heart to progressive and acute hypoxia. 222 Nov 53

Fetal and neonatal biophysical and biochemical changes were studied in four preterm infants who developed cardiogenic shock as a result of severe perinatal asphyxia. Fetal distress was documented by the presence of severe late and variable decelerations associated with decreased fetal heart rate variability. Severity of fetal acidosis was decumented by scalp and umbilical cord blood pH. Apgar scores at 1, 5, and 10 minutes were all equal to or less than 5. Although the clinical findings shortly after birth resembled respiratory distress syndrome, it was possible to make a primary diagnosis of cardiac failure with the recognition of cardiomegaly, hepatomegaly, electrocardiographic changes of myocardial hypoxia, decreased myocardial contractility, elevated central venous pressure, and severe lactic acidosis. The treatment of heart failure, including use of inotropic agents, resulted in rapid improvement in the clinical condition, with reversal of the abnormal findings within 24 to 36 hours. Concomitant with this improvement, the increase in arterial blood pressure was paralleled by increase in peripheral (toe) temperature.
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PMID:Cardiogenic shock associated with perinatal asphyxia in preterm infants. 718 61

In virgin, male Sprague-Dawley rats, subcutaneous injections of 2.5 mg/kg or 250 mg/kg isoproterenol increased heart rate and aortic dF/dt and decreased total peripheral resistance. The net systemic response was an arterial hypotension. The larger dose of isoproterenol initially produced a greater hypotension; reflex compensatory responses followed. Cardiac failure occurred by 24 hours post-isoproterenol. The extent of cardiac failure was isoproterenol dose dependent. By gross inspection of the epicardial surface of the hearts of the isoproterenol-treated rats, anatomical injury also appeared to be isoproterenol dose dependent. The data presented in this study support the existing theory that isoproterenol-induced myocardial damage is due to a relative myocardial hypoxia produced by artereial hypotension and myocardial hyperactivity. The data also indicate that reflex responses to arterial hypotension occur and may be detrimental. Cardiac failure is produced by massive quantities of isoproterenol, and the degree of cardiac failure is dose dependent.
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PMID:The hemodynamics of isoproterenol-induced cardiac failure in the rat. 722 40

The morphology of the contractile myocardium was studied experimentally in fibrillation and defibrillation of the ventricles on 30 rabbits. Morphology of the contractile myocardium appears as vacuolated dystrophy of the cardiomyocytes, destruction of mitochondria and contracture lesions of the myofibrils. The latter with progressing fibrillation become irreversible. Myocardial changes are related both to the mechanical lesions of cardiomyocytes and the haemodynamic disorders, developing as a result of ventricular fibrillation, which leads to marked myocardial hypoxia. The changes in the microcirculatory bed contribute to the development of the latter. Hyperfunction of the intracellular structures, especially of mitochondria and myofibrils, taking place under unfavourable conditions leads to a rapid energy depletion, which is one of the main causes of development of the acute cardiac insufficiency in this type of arrhythmias. Studies of cardiac defibrillation enabled one to elicit the dynamics of morphological changes, appearing in the myocardium as related to the duration of ventricular fibrillation.
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PMID:[Myocardial morphology in fibrillation and defibrillation of the heart ventricles]. 730 Jan 1

Positive inotropic agents that increase the sensitivity of myofilaments to calcium have recently been described (Kitada et al., 1987; Cottney et al., 1990; Ferroni et al., 1991; Lee and Allen, 1991; Beier et al., 1992). These drugs appear to augment contractility independently of cAMP or calcium, and thus may have fewer of the adverse side effects seen with other currently available agents (Katz, 1986; Packer 1989). The clinical utility of "calcium-sensitizers" has been questioned on the theoretical grounds that such agents may interfere with relaxation and impair diastolic function (Hajjar and Gwathmey, 1991). Previous studies have shown a small but significant negative lusitropic effect of the calcium sensitizer EMD 53998 in ferret papillary muscle, although this effect was considered to be outweighed by powerful augmentation of contractility. Modelling studies have suggested that the impairment of relaxation by calcium-sensitizers may be even more severe when myocardial calcium is abnormally elevated, such as in hypoxia (Allen and Orchard, 1987; Lodge and Gelband, 1988) and end-stage heart failure (Hajjar and Gwathmey, 1991). We have examined the effects of EMD 53998 and milrinone on contractility and calcium flux in a cell culture model of myocardial hypoxia. The results indicate that increased calcium sensitivity results in marked impairment of relaxation under hypoxic conditions, possibly due to the impaired calcium sequestration and increased calcium availability exhibited by hypoxic myocytes. These studies show that the effects of calcium sensitizers can be strongly influenced by the prevailing status of intracellular calcium handling, and may be deleterious in the diseased or ischemic myocardium.
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PMID:Negative lusitropy and abnormal calcium handling in hypoxic cardiac myocytes exposed to the calcium-sensitizer EMD 53998. 823 Feb 39

A 59-year-old man with obesity was admitted with nocturnal dyspnea and nocturnal precordial oppression. Catheter data disclosed no cardiac failure. Polysomnography was performed for a total of 3 nights. The diagnosis of obstructive sleep apnea syndrome was made because apnea index was 50 times/hour in average, the max apnea time was about 80 seconds and disappearance of airflow during decrease of endoesophageal pressure was observed. At the max apnea time, ST-T change in leads V2-5 was observed with severe desaturation (arterial oxygen saturation: 49%). It was considered that myocardial hypoxia following sleep apnea might be the cause of nocturnal precordial oppression.
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PMID:[ST-T changes associated with severe hypoxia in a case of obstructive sleep apnea syndrome]. 848 59

Neonatal asphyxia is a major topic of neonatal research. However, no clear-cut physiologic parameters exist which enable an early identification of neonatal infants who are either at risk to develop brain damage or posthypoxic heart failure. Parameters indicating dysfunction of the heart and kidneys as creatinine and creatinine kinase have been evaluated. In our study, 47 asphyxiated infants (umbilical artery pH < 7.18 and either a 1-min Apgar score < 4 or a 5-min Apgar score < 7) were compared to 27 nonasphyxiated controls regarding significant differences in creatinine, creatinine kinase, its MB fraction, and a newly introduced myocardial hypoxia indicator -- troponin T -- to establish the value of these parameters in the retrospective diagnosis of asphyxia. Further we evaluated two subsets of these 47 asphyxiated infants with either subsequent signs of encephalopathy (seizures) or heart failure. Creatinine, creatinine kinase and troponin T were significantly elevated in asphyxiated infants compared with controls; no differences were found in creatinine kinase and its MB fraction. In asphyxiated infants with heart failure, troponin T was significantly higher than in the other asphyxiated infants. However, none of the parameters studied was significantly different in patients with brain damage compared with asphyxiated infants without neurological sequelae. Troponin T has a high positive predictive value in the postnatal diagnosis of asphyxia. The diagnostic power of troponin T equals that of creatinine. However, troponin T is more sensitive in the identification of infants with asphyxia and cardiocirculatory failure than creatinine. Creatinine kinase and its MB fraction have no diagnostic value.
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PMID:Value of myocardial hypoxia markers (creatine kinase and its MB-fraction, troponin-T, QT-intervals) and serum creatinine for the retrospective diagnosis of perinatal asphyxia. 961 54

It is well established that cardiac failure increases cardiac B-type natriuretic peptide (BNP) expression due to myocardial stretching. However, patients with ischemic heart disease also display increased plasma BNP and proBNP concentrations despite preserved cardiac function. In this study, we examined whether acute myocardial hypoxia increases cardiac BNP expression. Surgical reduction of the blood flow to an area of the anterior ventricular wall in pigs reduced the myocardial oxygen tension from 46 +/- 4 to 13 +/- 5 mmHg. The tissue contents of VEGF and BNP mRNA increased 1.8-fold and 3.5-fold, respectively (n=10, P<0.005) in hypoxic compared with normoxic ventricular myocardium after 2.2 +/- 0.2 h; the magnitude of the increase in BNP mRNA expression was positively correlated with that of VEGF in hypoxic myocardium (r=0.66, P<0.05). In support of a hypoxia-induced increase of BNP gene transcription, the content of a premature BNP mRNA was increased in hypoxic myocardium (4.8-fold, P<0.005) and in freshly harvested ventricular myocytes when kept in culture flasks and oxygen-deprived for 3 h (2.2-fold, P=0.002). ProBNP peptide accumulated in the medium of freshly harvested ventricular myocyte cultures but was undetectable in ventricular myocardium, indicating rapid release of the newly synthesized proBNP peptide. Accordingly, the plasma proBNP concentration increased after 2 h of myocardial hypoxia (P=0.028). Cumulatively, the data suggest that acute hypoxia stimulates cardiac BNP expression.
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PMID:Acute myocardial hypoxia increases BNP gene expression. 1557 92

Although many animal studies indicate insulin has cardioprotective effects, clinical studies suggest a link between insulin resistance (hyperinsulinemia) and heart failure (HF). Here we have demonstrated that excessive cardiac insulin signaling exacerbates systolic dysfunction induced by pressure overload in rodents. Chronic pressure overload induced hepatic insulin resistance and plasma insulin level elevation. In contrast, cardiac insulin signaling was upregulated by chronic pressure overload because of mechanical stretch-induced activation of cardiomyocyte insulin receptors and upregulation of insulin receptor and Irs1 expression. Chronic pressure overload increased the mismatch between cardiomyocyte size and vascularity, thereby inducing myocardial hypoxia and cardiomyocyte death. Inhibition of hyperinsulinemia substantially improved pressure overload-induced cardiac dysfunction, improving myocardial hypoxia and decreasing cardiomyocyte death. Likewise, the cardiomyocyte-specific reduction of insulin receptor expression prevented cardiac ischemia and hypertrophy and attenuated systolic dysfunction due to pressure overload. Conversely, treatment of type 1 diabetic mice with insulin improved hyperglycemia during pressure overload, but increased myocardial ischemia and cardiomyocyte death, thereby inducing HF. Promoting angiogenesis restored the cardiac dysfunction induced by insulin treatment. We therefore suggest that the use of insulin to control hyperglycemia could be harmful in the setting of pressure overload and that modulation of insulin signaling is crucial for the treatment of HF.
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PMID:Excessive cardiac insulin signaling exacerbates systolic dysfunction induced by pressure overload in rodents. 2040 9

Myocardial ischemia and heart failure are accompanied by well characterized changes in myocardial substrate metabolism. While the normal heart in the fasting state mostly relies on oxidation of fatty acids for energy production, acute myocardial ischaemia is accompanied by increased exogenous myocardial glucose uptake and suppressed utilization of fatty acids. This metabolic shift can be detected using metabolic imaging using labeled glucose and fatty acid analogs. Recently, also specific tracers for the detection of myocardial hypoxia have been tested. In the assessment of myocardial viability metabolic imaging has an established role. Metabolic imaging has also greatly improved our understanding about metabolic derangements in the failing heart and currently metabolic modulation as a therapy of heart failure is studied. While experimental and clinical results are promising, larger clinical trials are warranted to better understand the value of metabolic imaging in the detection and prognosis of ischemic heart disease.
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PMID:Metabolic imaging in myocardial ischemia and heart failure. 2058 13


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