UMLS:C0018801 - FACTA Search

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

When treating severe cardiac failure with dynamic cardiomyoplasty, knowledge about the optimal way of stimulating the latissimus dorsi (LD) muscle is of obvious importance. We evaluated a new stimulation protocol in four goats using in situ electrical stimulation of the left LD muscle. Stimulation was started using a burst of two pulses with an interpulse interval of 100 msec for 50 bursts/min. The number of pulses was increased every 2 weeks concomitant with a decrease in interpulse interval. This resulted after 12 weeks in 60 bursts/min using bursts of six pulses with an interpulse interval of 20 msec after 12 weeks. Force measurements, which were done every 2 weeks, showed an early decrease in contraction and relaxation speed as reflected in the ripple (= interstimulus amplitude/peak force amplitude measured at 10 Hz). Fatigue resistance increased significantly within 4 weeks of conditioning as indicated by preservation of force, positive dF/dt, and negative dF/dt. Full preservation of these variables was seen even during a 1-hour fatigue test at the end of the conditioning period. Skeletal muscle enzyme activity as an indicator of muscle damage showed a significant rise in creatine kinase enzyme activity only on the first day following the start of LD stimulation. LD muscle biopsies revealed almost complete transformation to type I muscle fibers with a significant increase in capillary/fiber ratio when compared to the nonstimulated LD muscle. However, some biopsies, in particular near the electrodes, did show some signs of skeletal muscle damage. Contraction characteristics of the fully transformed LD muscles were tested by increasing the number of bursts of six pulses from 50/min to 100/min. Interpulse intervals of 20 and 33 msec were used. These tests revealed that maximal force, positive dF/dt, and negative dF/dt was reached with 50 bursts/min using a six pulse burst with interpulse intervals of 20 msec.
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PMID:A new stimulation protocol for cardiac assist using the latissimus dorsi muscle. 769 48

The contraction-relaxation cycle of the heart is dependent on a cycle of ATP production and utilization and a cycle of Ca uptake and Ca release by the sarcoplasmic reticulum (SR). Heart failure (HF) is associated with abnormalities of myocardial Ca and ATP cycling, but the time course of their development is unknown. This study tested the hypothesis that, compared with ATP-utilizing and Ca-uptake activities, decreases in ATP-synthesis and Ca-release activities occurred earlier in the development of HF and persisted longer during recovery from HF. HF was induced by right ventricular pacing of dogs at 250 beats/min. Dogs were studied after 1 week of pacing (n = 8, early HF), at HF (n = 11, severe HF), and 4 weeks after cessation of pacing (n = 9) and were compared with dogs not subjected to pacing. At early HF, there were decreased activities (p < 0.05) of the SR Ca-release channel (rate constant from 199 +/- 36 x 10(-4) to 90 +/- 16 x 10(-4) s-1), mitochondrial ATP synthesis (from 11.2 +/- 2.4 to 7.0 +/- 2.2 international units (IU)/g), and creatine kinase (CK) from 2028 +/- 266 to 1811 +/- 79 IU/g). The decreased Ca-channel activity was due to a 32% decrease in maximal activity (rate constant from 249 +/- 50 x 10(-4) to 170 +/- 29 x 10(-4) s-1) and to a 2-fold increase (from 19.1 +/- 12.4 to 42.0 +/- 14.2%) in inhibition of maximal channel activity (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sarcoplasmic reticulum Ca-release channel and ATP-synthesis activities are early myocardial markers of heart failure produced by rapid ventricular pacing in dogs. 784 99

Selective and specific changes in gene expression characterize the end-stage failing heart. However, the pattern and relation of these changes to evolving systolic and diastolic dysfunction during development of heart failure remains undefined. In the present study, we assessed steady-state levels of mRNAs encoding a group of cardiac proteins during the early development of left ventricular dysfunction in dogs with pacing-induced cardiomyopathy. Corresponding hemodynamic assessments were made in the conscious state in the same animals and at the same time points at baseline, after 1 week of ventricular pacing, and at the onset of clinical heart failure. Systolic dysfunction dominated after 1 week of pacing, whereas diastolic dysfunction was far more pronounced with the onset of heart failure. Atrial natriuretic factor mRNA was undetectable in 7 of 12 hearts at baseline but was expressed in all hearts at 1 week (P < .01 by chi 2 test), and it increased markedly with progression to failure (P = .05). Creatine kinase-B mRNA also rose markedly with heart failure (P < .01). Levels of mRNA encoding beta-myosin heavy chain, mitochondrial creatine kinase, phospholamban, and sarcoplasmic reticulum Ca(2+)-ATPase did not significantly change from baseline, despite development of heart failure. Additional analysis to determine if these mRNA changes were related to the severity of diastolic or systolic dysfunction revealed that phospholamban mRNA decreased in hearts with larger net increases in end-diastolic pressure (+19.2 +/- 1.9 mm Hg) compared with those hearts in which it did not change (+4.0 +/- 4.9, P < .02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endomyocardial gene expression during development of pacing tachycardia-induced heart failure in the dog. 792 7

We report a 46-year-old man with bacterial endocarditis and cardiac failure, who developed status epileptics. The patient was apparently well until July of 1991 when there was a gradual onset of fever and general fatigue. He was hospitalized to the cardiology service of our hospital where diagnosis of bacterial endocarditis and aortic insufficiency was made. On October 9, 1991, he suddenly developed cardiogenic shock, and emergency replacement of the aortic valve was made; at the operation, the main trunk of the left coronary artery showed embolic occlusion, and the myocardial movement was markedly diminished; serum creatine kinase was 3.150 IU/l. His cardiac failure did not resolve, and renal failure developed in December 1991, for which peritoneal dialysis was necessary. On February 2, 1992, he suddenly developed a clonic seizure which started from his face with a transient post-ictal left hemiparesis; a cranial CT scan was unremarkable. He was treated with phenytoin and glycerol, however, he developed status epileptics on February 3; he developed cardiac arrest after the injection of phenytoin 750 mg. He was resuscitated, however, his status did not resolve. Neurological consultation was asked on February 4. On physical examination, his blood pressure was 80/40 mmHg heart rate 77/min and regular, and body temperature 39.1 degrees C. The palpebral conjunctiva were slightly anemic, however, the bulbar conjunctiva were not icteric. No cervical adenopathy was noted. Glade II systolic murmur was heard in the apex; the lungs were clear. The abdomen was flat and soft without organomegaly. No edema was present in the legs. On neurologic examination, he was comatose without response to painful stimuli. He repeatedly had convulsion lasting for 30 seconds every 2 to 3 minutes; his convulsions started with the conjugate deviation of the eyes to the left followed by turning of the head toward left, and then clonic convulsions started in this left upper limb extending to other extremities. The optic fundi were unable to visualize because of corneal clouding; light reflex was sluggish on the right side; no oculocephalic response was elicited; corneal reflex was also lost bilaterally. Extremities were hypotonic, and no automatic movement was seen. The triceps brachii reflex was diminished, but all the other deep reflexes were lost; no plantar response was elicited. Meningeal sign was absent. He was treated with intravenous diazepam; the interval of convulsions prolonged, however, blood pressure dropped to 40 to 40 mmHg. On February 4, intravenous thiopental anesthesia was instituted, and assisted respiration was started.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 46-year-old man with cardiac failure and statues epileptics]. 794 26

NMR spectroscopy is a powerful and non-invasive technique with which to study cardiac energy metabolism in vivo. This method makes use of the "spin" properties of certain atomic nuclei. The naturally occurring phosphorus nucleus (P-31) is visible by NMR and phosphorus-31 NMR spectra contain signals from the major components of energy metabolism. In vivo, the phosphocreatine to ATP ratio (PCr/ATP) is used as an index of the energy status and viability of the myocardium. However, it is the response of this metabolic index to differing physiological and pharmacological stresses that has helped to elucidate the mechanisms that regulate cellular respiration and to highlight abnormalities in heart failure. As there are many technical difficulties involved with cardiac NMR, 31-phosphorus studies of skeletal muscle have provided an indirect way of studying abnormalities in myocardial metabolism in vivo. One of the unique features of NMR is that it permits in vivo measurements of fluxes through key enzymes in energy metabolism using magnetization transfer. Determination of the rates of energy transfer through the creatine kinase reaction and energy turnover in vivo will provide new insights into the control of energy metabolism in health and disease. Alternatively, carbon-13 NMR can be used to measure fluxes through the different metabolic pathways of synthesis and catabolism following administration of selectively labelled carbon-13 substrates. In conclusion, the non-invasive and versatile nature of NMR spectroscopy makes it an ideal method to assess and evaluate energy metabolism in vivo.
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PMID:Evaluation of myocardial energy status in vivo by NMR spectroscopy. 811 45

The human heart secretes both atrial natriuretic peptide and brain natriuretic peptide. This study attempts to clarify the pathophysiological significance of the peptides in cardiovascular diseases. Using immunoradiometric assay, plasma brain natriuretic peptide and atrial natriuretic peptide levels in essential hypertension, various secondary hypertension, chronic renal failure, chronic heart failure during cardiac pacing, and acute myocardial infarction were determined. Mean plasma brain natriuretic peptide and atrial natriuretic peptide levels in healthy subjects were 3.7 +/- 0.3 and 5.7 +/- 0.3 pmol/L, respectively, and increased as a function of age. Plasma brain natriuretic peptide levels showed a larger increase than atrial natriuretic peptide levels in various cardiovascular diseases. In chronic renal failure, whereas plasma atrial natriuretic peptide levels decreased significantly after hemodialysis and were correlated with the changes in body weight, changes in plasma brain natriuretic peptide levels were less prominent and did not show such a correlation. In chronic heart failure, both basal plasma brain natriuretic peptide and atrial natriuretic peptide levels were also significantly elevated. However, in response to acute ventricular or atrial pacing, brain natriuretic peptide levels did not show any increase in contrast to the marked increase of atrial natriuretic peptide levels. In acute myocardial infarction, brain natriuretic peptide levels showed more prominent changes than atrial natriuretic peptide levels and were correlated with serum levels of creatine kinase and cardiac myosin light chain I in most patients. These results suggest that both brain and atrial natriuretic peptides play an important role in the regulation of cardiovascular homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial and brain natriuretic peptides in cardiovascular diseases. 828 65

The prognosis of acute myocardial infarction depends on the development of left-ventricular dilatation and chronic heart failure. Serial echocardiography was performed on admission and on days 2, 4 and 6, to discover the temporal course of any early myocardial adaptation. There were 78 patients (20 women, 58 men; mean age 59 [49-69] years) with acute myocardial infarction and systemic thrombolysis, first studied up to 4 hours after onset of symptoms. The patients were divided into two groups according to infarct size as measured by creatine kinase ("area under the curve"--AUC); group 1: CK AUC < 12 IU/ml.h; group 2: CK AUC > 12 IU/ml.h. While there was no difference between the two groups on admission and on day 2, filling patterns differed significantly at the end of the first postinfarction week in that maximal early diastolic flow velocity (E) in group 1 was 0.65 m/s, but 0.73 m/s in group 2 (P < 0.05); maximal late diastolic flow velocity (A), group 1: 0.71, group 2: 0.58 m/s (P < 0.01); E/A ratio: 0.89 vs 1.22 (P < 0.001); integrated E/A ratio 1.37 vs 1.77 (P < 0.001), and the atrial component of left-ventricular filling 42 vs 36% (P < 0.001). It is concluded that the serial measurement of left-ventricular filling by Doppler echocardiography in the first post-infarction week can identify patients with impaired left-ventricular function through differences in flow pattern. Drug or interventional treatment can then be started early to prevent further left-ventricular dilatation and in this way improve prognosis.
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PMID:[Early diagnosis of left ventricular dysfunction following acute myocardial infarct. Doppler echocardiography in a study of its course]. 831 49

In a subgroup of 45 patients with acute myocardial infarction (AMI) from the German multicenter trial of anisoylated plasminogen streptokinase activator complex (APSAC) (n = 20) versus heparin (n = 25), simultaneous thallium (TI)-201 technetium (Tc)-99m pyrophosphate (PYP) tomography was initiated to elucidate a possible benefit of APSAC over heparin. Findings in the 2 treatment groups were similar with respect to TI-201 defect score, relative scintigraphic infarct size, and in keeping with the main group coronary artery patency, global ejection fraction and maximal creatine kinase level. However, 2 different TI-201/Tc-99m PYP accumulation patterns within the area of infarction (homogeneous, group A; inhomogeneous, group B) were identified. Both treatment groups were similar with regard to the frequency of the homogeneous and inhomogeneous pattern. In comparing the 2 accumulation patterns, creatine kinase peaked earlier in group A than in group B, and global left ventricular ejection fraction was significantly higher in group A than in group B. In Group A, 30 of 31 patients and in group B 7 of 11 patients had a patent infarct-related vessel (p < 0.025). TI-201 defect score was lower in group A than in group B. Likewise, relative size of the infarction as determined from Tc-99m PYP images was significantly lower in group A than in group B. Fifteen patients experienced cardiogenic shock or severe heart failure. Patients in group B had a higher incidence of these in-hospital complications than patients in group A (92 vs 12%, p < 0.0005). Scintigraphic infarct size and TI-201 defect score were greater in patients with the aforementioned clinical events.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison in acute myocardial infarction of anisoylated plasminogen streptokinase activator complex versus heparin evaluated by simultaneous thallium-201/technetium-99m pyrophosphate tomography. 842 Feb 41

To define coronary angiographic characteristics of patients experiencing early primary ventricular fibrillation (VF) in the acute phase of myocardial infarction we studied 266 consecutive patients without clinical evidence of heart failure. Twenty-six patients (group 1) experienced early (< 12 h from the onset of symptoms of myocardial infarction) primary VF whereas 240 patients (group 2) with the same clinical characteristics served as an appropriately matched cohort. All patients were catheterized before or soon after hospital discharge (1 to 8 weeks after the acute event). There was no significant difference in left ventricular ejection fraction between the two groups of patients (39.6 +/- 6% vs 36.9 +/- 8%, P = ns). Patients with early VF had a significantly greater number of diseased vessels than those without VF (3.38 +/- 1.05 vs 2.03 +/- 1.25, P < 0.001) and a higher coronary arteriographic Gensini score (29.31 +/- 4.80 vs 20.16 +/- 4.14, P < 0.001). The left anterior descending coronary artery was identified as the infarct-related vessel in 53.6% of group 1 vs 44.5% of group 2 patients (P < 0.05). The mean maximal serum creatine kinase values were not significantly different (1897 +/- 1062 vs 1426 +/- 839 IU.l-1, P = ns) between the two groups. These data indicate that patients with early primary VF in the setting of acute myocardial infarction may have more extensive coronary artery disease than similar patients without VF. A worse prognosis could be anticipated for these patients on the basis of worse coronary anatomy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early ventricular fibrillation in patients with acute myocardial infarction: correlation with coronary angiographic findings. 845 56

To test whether insulin is a regulatory factor of myocardial MB creatine kinase content, we investigated the correlation between the ability of insulin secretion and the MB fraction of cumulative CK released in patients with acute myocardial infarction. We analyzed 18 patients who underwent successful direct angioplasty within 10 hours of the onset of their first myocardial infarction. Exclusion criteria were age more than 75 years, heart failure, severe obesity, multivessel disease, and history of diabetes mellitus. Cumulative activity of serum MB CK divided by that of total CK was defined as MB%, which was considered to represent myocardial MB CK content. Two weeks or more after the onset of myocardial infarction, 75 gm oral glucose tolerance test with serial determination of plasma glucose and serum insulin (0, 0.5, 1, 2, 3 hours) was done. Urinary and plasma catecholamines and echocardiographic left ventricular (LV) mass were measured. MB% significantly correlated with insulinogenic index (r = 0.564, p = 0.019), insulin area (r = 0.594, p = 0.012), insulin area/glucose area (r = 0.630, p = 0.007), and urinary adrenaline (r = -0.542, p = 0.025) and tended to correlate with plasma adrenaline (r = -0.431, p = 0.084). Age, body mass index, infarct size, glucose metabolism, and LV mass were not significant univariate predictors of MB%. Multivariate analysis showed that the ability of insulin secretion contributed to MB% more than catecholamines did and that insulin area/glucose area was the strongest independent predictor of MB% (t = 3.01, p = 0.015). Thus MB fraction of cumulative CK released, indicative of Myocardial MB CK distribution, strongly related to the ability of insulin secretion in subjects without overt insulin resistance. Regulation by insulin of myocardial MB CK is suggested.
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PMID:MB fraction of cumulative creatine kinase correlates with insulin secretion in patients with acute myocardial infarction: insulin as a possible determinant of myocardial MB creatine kinase. 855 15

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