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Biomedical subjects

D C Russell

Publications and source records attributed to D C Russell.

At least 19 recordsLinked to original sources
PubMed2001

Myocardial free fatty acid and glucose use after carvedilol treatment in patients with congestive heart failure.

BACKGROUND: Use of beta-adrenoreceptor blockade in the treatment of heart failure has been associated with a reduction in myocardial oxygen consumption and an improvement in myocardial energy efficiency. One potential mechanism for this beneficial effect is a shift in myocardial substrate use from increased free fatty acid (FFA) oxidation to increased glucose oxidation. METHODS AND RESULTS: We studied the effect of carvedilol therapy on myocardial FFA and glucose use in 9 patients with stable New York Heart Association functional class III ischemic cardiomyopathy (left ventricular ejection fraction </=35%) using myocardial positron emission tomography studies and resting echocardiograms before and 3 months after carvedilol treatment. Myocardial uptake of the novel long chain fatty acid metabolic tracer 14(R, S)-[(18)F]fluoro-6-thia-heptadecanoic acid ([(18)F]-FTHA) was used to determine myocardial FFA use, and [(18)F]fluoro-2-deoxy-glucose ([(18)F]-FDG) was used to determine myocardial glucose use. After carvedilol treatment, the mean myocardial uptake rate for [(18)F]-FTHA decreased (from 20.4+/-8.6 to 9.7+/-2.3 mL. 100 g(-1). min(-1); P<0.005), mean fatty acid use decreased (from 19.3+/-7.0 to 8.2+/-1.8 micromoL. 100 g(-1). min(-1); P<0.005), the mean myocardial uptake rate for [(18)F]-FDG was unchanged (from 1.4+/-0.4 to 2.4+/-0.8 mL. 100 g(-1). min(-1); P=0.14), and mean glucose use was unchanged (from 11.1+/-3.1 to 18.7+/-6.0 micromoL. 100 g(-1). min(-1); P=0.12). Serum FFA and glucose concentrations were unchanged, and mean left ventricular ejection fraction improved (from 26+/-2% to 37+/-4%; P<0.05). CONCLUSIONS: Carvedilol treatment in patients with heart failure results in a 57% decrease in myocardial FFA use without a significant change in glucose use. These metabolic changes could contribute to the observed improvements in energy efficiency seen in patients with heart failure.

Adrenergic beta-Antagonists↗
PubMed2001

Early manifestations of "sick euthyroid" syndrome in patients with compensated chronic heart failure.

BACKGROUND: A "sick euthyroid" syndrome occurs in patients with severe decompensated chronic heart failure (CHF) and other chronic illnesses and is related to adverse prognosis, but it has not been described in patients with compensated CHF. The aim of this study was to determine whether manifestations of the sick euthyroid syndrome occur in patients with compensated CHF caused by ischemic heart disease. METHODS AND RESULTS: Thyroid hormonal responses to thyrotropin-releasing hormone (TRH) stimulation were compared in 8 patients with New York Heart Association class I/II CHF considered secondary to ischemic heart disease and 7 control patients after serial 10-minute blood sampling over 3-hour periods. Secretory dynamics of TRH-induced thyroid-stimulating hormone (TSH) release were compared by using deconvolution analysis. Changes in serum thyroxine (T4), triiodothyronine (T3), reverse T3 (rT3), and rT3/T4 concentration ratios were compared. Patients with CHF had lower baseline serum T3 concentrations (P <.001), with lower maximum serum T(3) (P <.01) and higher maximum serum rT(3) (P <.05) concentrations after TRH stimulation but similar estimated TRH-induced TSH secretory burst amplitude, mass, and 3-hour production rates, compared with control patients. CONCLUSIONS: Patients with compensated CHF display the derangements in thyroid hormone metabolism of impaired peripheral conversion of T4 and T3 and increased production of rT(3) in the presence of normal dynamic function of the hypothalamic-pituitary-thyroid axis, which are consistent with early manifestations of a sick euthyroid state.

Aged↗
PubMed2001

An evaluation of myocardial fatty acid and glucose uptake using PET with [18F]fluoro-6-thia-heptadecanoic acid and [18F]FDG in Patients with Congestive Heart Failure.

UNLABELLED: Understanding the metabolic consequences of heart failure is important in evaluating potential mechanisms for disease progression and assessing targets for therapies designed to improve myocardial metabolism in patients with heart failure. PET is uniquely suited to noninvasively evaluate myocardial metabolism. In this study, we investigated the kinetics of 14(R,S)-[18F]fluoro-6-thia-heptadecanoic acid (FTHA) and [18F]FDG in patients with stable New York Heart Association functional class III congestive heart failure and a left ventricular ejection fraction of no more than 35%. METHODS: Twelve fasting patients underwent dynamic PET studies using [18F]FTHA and FDG. From the dynamic image data, the fractional uptake rates (Ki) were determined for [18F]FTHA and FDG. Subsequently, serum free fatty acid and glucose concentrations were used to calculate the myocardial free fatty acid and glucose uptake rates, respectively. Uptake rates were compared with reported values for [18F]FTHA and FDG in subjects with normal left ventricular function. RESULTS: The average Ki for [18F]FTHA was 19.7 +/- 9.3 mL/100 g/min (range, 7.2-36.0 ml/100 g/min). The average myocardial fatty acid use was 19.3 +/- 2.3 mmol/100 g/min. The average Ki for FDG was 1.5 +/- 0.37 mL/100 g/min (range, 0.1-3.3 mL/100 g/min), and the average myocardial glucose use was 12.3 +/- 2.3 mmol/100 g/min. CONCLUSION: Myocardial free fatty acid and glucose use in heart failure can be quantitatively assessed using PET with [18F]FTHA and FDG. Myocardial fatty acid uptake rates in heart failure are higher than expected for the normal heart, whereas myocardial glucose uptake rates are lower. This shift in myocardial substrate use may be an indication of impaired energy efficiency in the failing heart, providing a target for therapies directed at improving myocardial energy efficiency.

Cardiomyopathy, Dilated↗
PubMed1999

Increased prevalence of patent foramen ovale in patients with severe chronic obstructive pulmonary disease.

This study was designed to assess the prevalence of patent foramen ovale (PFO) in patients with severe chronic obstructive pulmonary disease (COPD) and the magnitude of any effects of right-to-left interatrial PFO shunting on systemic arterial oxygen desaturation after the Valsalva maneuver. The prevalence of PFO was compared between a group of 20 patients with severe chronic obstructive pulmonary disease (FEV1% <50%; FEV1/FVC <50%) and 20 control subjects (FEV1% >70%; FEV1/FVC >70%) by contrast transesophageal echocardiography during the Valsalva maneuver with simultaneous measurement of systemic arterial oxygen saturation (SaO2) by pulse oximetry. Patients with severe COPD (FEV1 = 27.2% +/- 8.4%; FEV1 /FVC = 44.3% +/- 11.0%) had a significantly higher pulmonary artery systolic pressure (38.3 +/- 7.3 vs 21.0 +/- 2.4 mm Hg; P <.005), higher prevalence of PFO (14/20 = 70% vs 7/20 = 35%; P <.05), and greater systemic arterial desaturation after Valsalva (Sao2 change: -2.6% +/- 1.4% vs -1.1% +/- 0.9%; P <.005) than control subjects. In the severe COPD group, the degree of systemic arterial desaturation after Valsalva in patients with PFO was significantly greater than in patients without PFO (Sao2 change: -3.1% +/- 1.4% vs -1.5% +/- 0. 5%; P <.05). Significant systemic arterial oxygen desaturation was observed after Valsalva in 45% of patients with interatrial PFO shunting and severe COPD. This significantly correlated with the degree of pulmonary hypertension (r = 0.6; P <.05). We conclude (1) that patients with severe COPD have an increased prevalence of PFO and (2) that approximately one half of subjects with severe COPD and PFO demonstrate statistically significant systemic arterial oxygen desaturation after the Valsalva maneuver.

Aged↗
PubMed1999

Effect of raised plasma beta endorphin concentrations on peripheral pain and angina thresholds in patients with stable angina.

OBJECTIVE: To determine whether changes in plasma concentrations of beta endorphins alter angina threshold and peripheral pain threshold in patients with stable angina. DESIGN: Latin square design comparison of angina thresholds by exercise treadmill test and peripheral pain thresholds using a radiant heat source in eight patients with stable angina under control conditions, after stimulation of pituitary beta endorphin release by ketoconazole, after suppression of pituitary beta endorphin release by dexamethasone, and after blockade of opioid receptors by intravenous naloxone. RESULTS: An approximately fivefold increase in circulating concentrations of beta endorphins was found after administration of ketoconazole (mean (SEM): 13.9 (1.2) v 73.8 (6.2) pg/ml; p < 0.05), which was associated with an increase in peripheral pain threshold to a radiant heat source (time to onset of pain perception 72 (19) v 123 (40) seconds; p < 0.05), but no significant difference in angina threshold. A reduction in circulating concentrations of beta endorphins after pretreatment with dexamethasone was statistically non-significant (13.9 (1.2) v 9.0 (1.5) pg/ml; NS) and was not associated with any change in either peripheral pain or angina thresholds. No effects were seen after blockade of opioid receptors by previous administration of intravenous naloxone. CONCLUSIONS: Increased plasma concentrations of beta endorphins alter peripheral pain threshold but not angina threshold in patients with stable angina pectoris.

Angina Pectoris↗
PubMed1998

Detection of coronary vasospasm by posthyperventilation technetium-99m sestamibi single-photon emission computed tomography imaging in patients with coronary artery disease.

Forced hyperventilation is simple, safe to perform, and can be used as a provocative test for coronary vasospasm. This study assesses whether a vasospastic component of angina might be detected in patients with angiographically "nonobstructive" coronary artery disease by posthyperventilation technetium-99m (Tc-99m) sestamibi single-photon emission computed tomography (SPECT) cardiac imaging. Eleven patients with angiographically nonobstructive coronary artery disease underwent Tc-99m sestamibi SPECT imaging at rest and after forced hyperventilation. Vessel diameters were measured by quantitative angiography before and after forced hyperventilation, and posthyperventilation SPECT images were compared with dipyridamole Tc-99m sestamibi stress images. Forced hyperventilation resulted in a 15% reduction in coronary artery diameter in stenotic segments (p <0.01), and a 17% reduction in adjacent nonstenotic segments (p <0.001). Myocardial uptake of Tc-99m sestamibi in segments perfused by vessels with angiographically nonobstructive stenoses was reduced by 24% following forced hyperventilation (p <0.001) compared with only 4% following dipyridamole (p <0.02). These findings suggest that posthyperventilation Tc-99m sestamibi SPECT imaging in patients with angina pectoris and nonobstructive coronary artery disease may be useful in identifying a vasospastic component of angina.

Angina Pectoris↗
PubMed1998

Regional differences in cell shape and gap junction expression in rat Achilles tendon: relation to fibrocartilage differentiation.

Tendon cells have complex shapes, with many cell processes and an intimate association with collagen fibre bundles in their extracellular matrix. Where cells and their processes contact one another, they form gap junctions. In the present study, we have examined the distribution of gap junction components in phenotypically different regions of rat Achilles tendon. This tendon contains a prominent enthesial fibrocartilage at its calcaneal attachment and a sesamoid fibrocartilage where it is pressed against the calcaneus just proximal to the attachment. Studies using DiI staining demonstrated typical stellate cell shape in transverse sections of pure tendon, with cells withdrawing their cell processes and rounding up in the fibrocartilaginous zones. Coincident with change in shape, cells stopped expressing the gap junction proteins connexins 32 and 43, with connexin 43 disappearing earlier in the transition than connexin 32. Thus, there are major differences in the ability of cells to communicate with one another in the phenotypically distinct regions of tendon. Individual fibrocartilage cells must sense alterations in the extracellular matrix by cell/matrix interactions, but can only coordinate their behaviour via indirect cytokine and growth factor signalling. The tendon cells have additional possibilities--in addition to the above, they have the potential to communicate direct cytoplasmic signals via gap junctions. The formation of fibrocartilage in tendons occurs because of the presence of compressive as well as tensile forces. It may be that different systems are used to sense and respond to such forces in fibrous and cartilaginous tissues.

Achilles Tendon↗
PubMed1998

Influence of prior ACE inhibitor therapy on morbidity and mortality following acute myocardial infarction.

BACKGROUND: Angiotensin-converting enzyme inhibitor (ACE-I) therapy reduces complications of acute myocardial infarction (MI) even when the therapy is started very early after an acute event. This study sought to determine whether administration of ACE-I therapy prior to acute MI is related to subsequent patient morbidity and mortality. METHODS: Chart review of 318 consecutive patients admitted between September 1995 and December 1996 with a diagnosis of acute MI. Outcome data were compared between patient groups receiving ACE-I therapy prior to infarction and those who were not. RESULTS: Sixty-four patients (20%) were receiving prior ACE-I therapy. They experienced smaller MIs, as determined by peak creatine kinase elevation (1066 +/- 134 vs. 1510 +/- 95 IU; p < 0.05), and fewer Q-wave infarctions (p < 0.05) than did patients who were not receiving prior treatment. The severity of coronary artery disease, defined by an angiographic score, was similar for the two groups. Mortality rates, including patients resuscitated from ventricular fibrillation, were similar within the first 72 hours of admission (3% vs. 2%; p = NS), but patients receiving prior ACE-I therapy showed a greater long-term in-hospital mortality rate (14% vs. 5%; p < 0.05) related to more heart failure deaths. Multivariate logistic regression analysis identified age, treatment with digoxin prior to acute MI, and left ventricular ejection fraction after infarction, but not ACE-I therapy taken prior to infarction, as significant independent predictors of mortality and combined morbidity and mortality. CONCLUSIONS: In a group of patients experiencing an acute MI, those receiving prior ACE-I therapy were more likely to sustain fewer transmural MIs and smaller infarcts. Chronic ACE-I therapy may have cardioprotective effects during acute myocardial ischemia.

Acute Disease↗
PubMed1998

Prevalence of patent foramen ovale and its contribution to hypoxemia in patients with obstructive sleep apnea.

STUDY OBJECTIVES: The objectives of this study were (1) to assess the prevalence of patent foramen ovale (PFO) by means of contrast transesophageal echocardiography (TEE) in patients with obstructive sleep apnea, and (2) to determine the potential contribution of right to left interatrial shunting to systemic oxygen desaturation following the performance of Valsalva maneuver. DESIGN: Performance of contrast TEE during Valsalva maneuver with simultaneous measurement of systemic arterial oxygen saturation (SaO2) by means of pulse oximetry in patients with obstructive sleep apnea and a control group. SETTING: Government teaching hospital, university hospital affiliate. PATIENTS: Study group comprised 48 patients with documented obstructive sleep apnea and 24 control subjects. INTERVENTIONS: Sleep studies, contrast TEE, Valsalva maneuver, pulse oximetry. MEASUREMENTS AND RESULTS: Thirty-three of 48 patients with obstructive sleep apnea compared with 4 of 24 control patients had a detectable PFO (69% vs 17%; p < 0.0001). All sleep apnea patients had comparable baseline SaO2 regardless of the presence of a PFO (93.9+/-1.7% vs 95+/-1.2%; p=not significant). After performance of a Valsalva maneuver, however, a significantly greater fall in SaO2 was observed in patients with obstructive sleep apnea and PFO compared with patients with obstructive sleep apnea without PFO (-2.4 +/- 1.5% vs -1.3 +/- 0.6%; p=0.007). A statistically significant fall in SaO2 (defined as > 4 SD of recorded SaO2 values after Valsalva maneuver in patients without PFO) was found in one third of patients with sleep apnea and PFO. CONCLUSION: We conclude that there is an increased prevalence of PFO in patients with obstructive sleep apnea that could contribute to significant hypoxemia after a Valsalva maneuver in approximately one third of these patients.

Aged↗
PubMed1998

Pay-for-performance compensation: moving beyond capitation.

Although capitation has been instrumental in lowering healthcare costs, it also has generated growing concern about quality of and access to healthcare services. Shifting to pay-for-performance compensation programs, however, allows health plans and physicians to balance economic incentives and operational outcomes, which in turn encourages improved performance and benefits providers, payers, and patients alike. A successful pay-for-performance program requires selection of appropriate performance criteria, accurate assessment of the financial impact, development of an effective means of communication between the health plan and physicians, and gradual implementation of the plan.

Capitation Fee↗
PubMed1996

Anomalous right coronary artery in a patient with Kartagener's syndrome.

We report a case of an anomalous right coronary artery arising from the morphological left sinus of Valsalva in a patient with Kartagener's syndrome. Literature review has revealed only a small number of cases of anomalous coronary arteries in patients with dextrocardia and none previously reported in Kartagener's syndrome.

Adult↗
PubMed1995

Indirect potentiation of synaptic transmission by metabotropic glutamate receptors in the rat hippocampal slice.

The role that the metabotropic glutamate receptor plays in synaptic transmission is complex due to the multiple subtypes involved, which initiate a number of intracellular mechanisms. Here we have investigated the role of the metabotropic glutamate receptor in the induction of long-term potentiation (LTP). We have shown that, providing the CA3 region remains attached to the slice, it is possible to induce potentiation by bath perfusion of the metabotropic receptor agonist (1S,3R) 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) alone. The extent of the potentiation observed showed a strong negative correlation with the age of the animal from which the slices were prepared. Perfusion of ACPD was associated with an increase in the excitability of antidromically activated CA3 neurones, the appearance of spontaneous burst firing within the CA3 region, and an increased fibre volley recorded in the CA1 region. Blockade of N-methyl-D-aspartate (NMDA) receptors prevented all these effects. We suggest that the ACPD-induced potentiation of CA1 fEPSPs is an indirect effect caused by spontaneous burst firing and/or increased excitatory drive from CA3 neurones.

2-Amino-5-phosphonovalerate↗
PubMed1989

Cardiac parasympathetic activity during the early hours of acute myocardial infarction.

Cardiac parasympathetic activity was assessed in 21 patients during the first 24 hours of acute myocardial infarction by measuring abrupt beat by beat changes in RR interval, which are expressed as "RR counts". Eleven patients had inferior wall infarction and 10 had anterior wall myocardial infarction. The whole recording period was analysed in 11 patients (five inferior and six anterior), and intermittent hourly periods were analysed in all 21 subjects. Mean RR counts were significantly lower in patients with anterior than inferior infarction, and below the normal range. Although mean heart rates were faster in the group with anterior infarction, there was a dissociation between RR counts and mean heart rate that was consistent with RR interval variability being an independent measure of parasympathetic activity. This study indicates that cardiac parasympathetic activity during acute myocardial infarction can be simply and reliably assessed from continuous electrocardiographic recordings, and it showed significantly lower cardiac parasympathetic activity in patients with anterior infarction.

Adult↗
PubMed1987

Effect of pindolol on neurosympathetic responsiveness, blood flow variability, and conduction in acutely ischaemic myocardium: the importance of heart rate.

The effects of a beta-adrenoceptor antagonist with partial agonist activity (pindolol) were assessed in the open-chest anaesthetised dog during 12-minute periods of left anterior descending coronary artery (LAD) occlusion and reperfusion before and after sympathetic stimulation. Regional myocardial catecholamine efflux, blood flow, and epicardial activation abnormalities were assessed in three groups. In a control group (n = 8), two periods of ischaemia resulted in reproducible intraexperimental changes in catecholamine responses, blood flow, conduction abnormalities, and arrhythmias. Intravenous (i.v.) pindolol (0.45 mg/kg before the second occlusion) reduced nerve-stimulated norepinephrine (NE) overflow from nonischaemic (NI) myocardium but did not modify overflow from ischaemic (I) myocardium either during ischaemia or reperfusion. At constant heart rate (atrial pacing, n = 8), pindolol reduced absolute blood flow to I and NI but had no effect on the ratio of endocardial/epicardial blood flow, arrhythmias, or activation abnormalities during occlusion. Following a reduction in heart rate of 32 +/- 6 beats/min (no pacing, n = 8), pindolol resulted in similar reduction in blood flow to I and NI but also increased the ratio of endocardial/epicardial flow and reduced both spontaneous arrhythmias and activation delay during occlusion. The acute effects of pindolol on conduction abnormalities, arrhythmias, and blood flow distribution in I are thus dependent on reduction in heart rate.

Animals↗
PubMed1985

Control of myocardial catecholamine release during acute ischemia.

Regional myocardial catecholamine release during graded stimulation of the left ansa subclavia has been assessed in open-chest anaesthetised dogs during left anterior descending coronary artery (LAD) occlusion and reperfusion. Frequency-dependent release of noradrenaline (NA) in response to stimulation of the ansa was maintained across the ischaemic area during the two early phases of enhanced vulnerability to arrhythmias at 5 and 17 min, but was selectively inhibited after 30 min. Spontaneous NA release from the ischaemic heart did not occur with either alpha 2-adrenoceptor (yohimbine) or neuronal reuptake (desmethylimipramine) blockade alone, but was unmasked by the drug combination. Intracoronary potassium infusions, designed to mimic the concentration range seen in ischaemia, exerted biphasic effects on stimulation-induced NA release, being inhibitory at low dose and stimulatory at high dose. High-dose intracoronary adenosine inhibited NA release in response to high-frequency ansa stimulation but basal release was slightly increased. Thus, catecholamine release from ischaemic myocardium has multifactorial determinants and may be limited by enhanced reuptake, adrenoceptor-mediated negative feedback, and metabolite accumulation. Lack of nerve-terminal response to sympathetic stimulation coincides with the later period of myocardial electrical stability.

Adenosine↗
PubMed1984

Mechanisms of phase 1a and 1b early ventricular arrhythmias during acute myocardial ischemia in the dog.

Two phases of ventricular arrhythmia occur within the first 30 minutes of experimental myocardial ischemia. Possible differences in their mechanisms of pathogenesis were investigated in anesthetized dogs by detailed mapping of patterns of epicardial activation and regional myocardial blood flow during phase 1a and phase 1b early ventricular arrhythmias induced by high ligation of the left anterior descending coronary artery. Data were derived from 80 sites in a 4 by 5 cm area of left ventricular anterior free wall and displayed using computer graphics. Regional myocardial blood flow and the relation of regional flow to epicardial delay did not differ significantly during the 2 phases of arrhythmia in central ischemic or nonischemic areas, although epicardial flow in border region segments was increased during phase 1b. Significantly greater mean epicardial delays and spatial heterogeneity of epicardial delay (assessed by intersite variance within the ischemic area) occurred during phase 1a arrhythmias. Serial studies show striking increases in spatial heterogeneity of delays during phase 1a, but not during phase 1b, relating to temporal dispersion of a phenomenon of transient prolongation of activation delay at individual electrode sites. These data are consistent with the concept that phase 1a and 1b arrhythmias arise through different electrophysiologic mechanisms independent of flow-dependent effects.

Acute Disease↗