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Biomedical subjects

T Giles

Publications and source records attributed to T Giles.

At least 19 recordsLinked to original sources
PubMed2006

Ultrasound-guided fine needle aspiration cytology in the diagnosis and management of thyroid nodules.

OBJECTIVE: To examine the accuracy of fine needle aspiration cytology (FNAC) in the diagnosis of thyroid nodules and compare the inadequacy rates for ultrasound-guided and freehand FNAC. METHODS: A retrospective study of 434 patients with thyroid nodules who underwent diagnostic FNAC over a 2-year period. Cytological diagnoses have been compared with the histological assessment of resection specimens in 69 cases. RESULTS: The inadequacy rate was significantly lower from ultrasound guided FNAC (24/373 cases, 6.4%) than from freehand FNAC (8/61 cases, 13.1%) (P = 0.043). Seventy-six percentage of patients had a non-neoplastic cytological diagnosis and, after multidisciplinary review, the patients were reassured and assigned to clinical follow-up. Sixty-seven patients had a resection for cytological appearances consistent with non-neoplastic disease (n = 34), suspicious of follicular neoplasia (n = 23), or suspicious of malignancy (n = 10), and two patients had resections following inadequate cytology with ultrasound appearances suspicious of a neoplasm. The overall accuracy of FNAC analysis for malignancy was 97.0%, with sensitivity 83.3%, specificity 98.0%, positive predictive value 71.4% and negative predictive value 98.4%. The overall accuracy of FNAC analysis for the prediction of neoplasia was 97.5%, with sensitivity 80.5%, specificity 97.8%, positive predictive value 89.2% and negative predictive value 95.9%. Difficulties in cytological diagnosis were associated with lymphoid infiltrates and with degenerative changes in follicular adenomas. CONCLUSION: Ultrasound-guided FNAC has a significantly lower yield of inadequate aspirates than palpable FNAC. The ability of FNAC to predict neoplasia in 89% patients and to exclude neoplasia in 95.9% patients makes an important contribution to the multidisciplinary assessment of patients.

Adolescent↗
PubMed2005

Impairment of cardiac function in hypertensive patients with Type 2 diabetes: a LIFE study.

AIMS: Type 2 diabetic patients with hypertension have an increased left ventricular (LV) mass and impaired cardiac function compared to hypertensive patients without diabetes. However, it is unknown if the impaired cardiac function can be explained solely by LV hypertrophy, or is independently related to diabetes. The aim of the present study was to compare LV function between diabetic and non-diabetic hypertensive patients with electrocardiographic LV hypertrophy. METHODS: In 937 patients participating in the LIFE echocardiographic substudy, all echocardiograms were centrally evaluated by a core reading centre measuring LV mass, systolic and diastolic LV function. Known diabetes was present in 105 patients. RESULTS: Left ventricular mass was similar in diabetic and non-diabetic patients. Endocardial systolic LV function, estimated by LV ejection fraction, was reduced and indices of midwall systolic LV function were impaired in the diabetic patients. Diastolic LV filling pattern was impaired and arterial stiffness, measured by pulse pressure/stroke index, was increased in diabetic patients. CONCLUSIONS: Systolic and diastolic LV function in hypertensive patients with electrocardiographic LV hypertrophy and diabetes are impaired independent of LV mass, most likely reflecting the adverse effects of diabetes per se.

Aged↗
PubMed2001

Angiotensin receptor blockers: evidence for preserving target organs.

Hypertension is a major problem throughout the developed world. Although current antihypertensive treatment regimens reduce morbidity and mortality, patients are often noncompliant, and medications may not completely normalize blood pressure. As a result, current therapy frequently does not prevent or reverse the cardiovascular remodeling that often occurs when blood pressure is chronically elevated. Blockade of the renin-angiotensin system (RAS) is effective in controlling hypertension and treating congestive heart failure. Both angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) inhibit the activity of the RAS, but these two classes of antihypertensive medications have different mechanisms of action and different pharmacologic profiles. Angiotensin-converting enzyme inhibitors block a single pathway in the production of angiotensin II (Ang II). In addition, angiotensin I is not the only substrate for ACE. The ACE inhibitors also block the degradation of bradykinin that may have potential benefits in cardiovascular disease. Bradykinin is, however, the presumed cause of cough associated with ACE inhibitor therapy. Data from clinical trials on ACE inhibitors serve to support the involvement of the RAS in the development of cardiovascular disease. Angiotensin receptor blockers act distally in the RAS to block the Ang II type 1 (AT1) receptor selectively. Thus, ARBs are more specific agents and avoid many side effects. Experimental and clinical trials have documented the efficacy of ARBs in preserving target-organ function and reversing cardiovascular remodeling. In some instances, maximal benefit may be obtained with Ang II blockade using both ARBs and ACE inhibitors. This review describes clinical trials that document the efficacy of ARBs in protecting the myocardium, blood vessels, and renal vasculature.

Angiotensin Receptor Antagonists↗
PubMed2000

First On-line beta-NMR on oriented nuclei: magnetic dipole moments of the (nup(1/2))(-1) 1/2(-) ground state in 67Ni and (pip(3/2))(+1) 3/2(-) ground state in 69Cu

The first fully on-line use of the angular distribution of beta emission in detection of NMR of nuclei oriented at low temperatures is reported. The magnetic moments of the single valence particle, intermediate mass, isotopes 67Ni(nup(-1)(1/2);1/2(-)) and 69Cu(pip(1)(3/2);3/2(-)) are measured to be +0.601(5) &mgr;(N) and +2.84(1) &mgr;(N), respectively, revealing only a small deviation from the neutron p(1/2) single-particle value in the former and a large deviation from the proton p(3/2) single-particle value in the latter. Quantitative interpretation is given in terms of core polarization and meson-exchange currents.

Journal Article↗
PubMed1997

Patterns of physician use of angiotensin converting enzyme inhibitors in the inpatient treatment of congestive heart failure.

Randomized clinical trails have demonstrated that angiotensin-converting enzyme (ACE) inhibitors reduce mortality, improve symptoms, and decrease hospitalization rates in congestive heart failure (CHF) patients with impaired left ventricular systolic function. Guidelines from the Agency for Healthcare Policy and Research (AHCPR) endorse the use of ACE inhibitors in eligible CHF patients and note their underutilization in practice. Randomly selected records of 1,212 Medicare CHF patients in Louisiana, discharged between July 1993 and October 1993, were reviewed. Abstracted data were used to characterize practice patterns and pertinent clinical factors influencing current ACE inhibitor utilization by practicing physicians in eligible Medicare CHF patients admitted to acute care hospitals. A total of 1,133 patients admitted were discharged alive; mean age was 77.6 years (64% female; 68% white). One third of the patients (34%) were already receiving ACE inhibitors on admission; of these, 85% were discharged on ACE inhibitors. The remaining 66% of patients were not on an ACE inhibitor on admission; only 35% of these are documented to have been placed on an ACE inhibitor(s) at discharge. Overall, a significantly large number of CHF patient charts (48%) lacked documentation of LV systolic function assessments. On multivariate logistic regression modeling, the following key clinical variables were positively related to the prescription of ACE inhibitors: low ejection fraction, dyspnea and orthopnea, normal creatinine levels, high diastolic blood pressure, cardiomegaly, and increasing age. Among patients with low ejection fraction, factors contributing to not being discharged on ACE inhibitors included: high creatinine levels, history of myocardial infarction or ischemic heart disease, renal failure, and being African American. This study documents the underutilization of ACE inhibitors in patients with impaired left ventricular systolic function. Results suggest the need for increased physician-based educational efforts concerning the use of ACE inhibitors in CHF patients, and also for increasing left ventricular systolic function assessments and documentation of findings in patient charts.

Aged↗
PubMed1996

The cost-effective way forward for the management of the patient with heart failure.

Heart failure is a huge healthcare issue not only for clinicians but for healthcare managers also, with increasing pressure to demonstrate the cost-effectiveness of therapies especially for common chronic conditions. The cost-effectiveness of heart failure treatments relate to their effects on the progression of the disease, the associated quality of life for the patient, and the actual cost of the disease management. Direct costs are usually associated with hospitalization. Indirect costs, such as the loss of production through absence from work, are more difficult to determine. Studies such as CONSENSUS, SOLVD, SAVE and the Munich Heart Failure trial have all shown that angiotensin-converting enzyme inhibitors offer effective therapy in all these aspects. Non-pharmacological strategies that have also been shown to favorably influence both the costs and benefit include the addition of a nurse practitioner to assist in patient management.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Duration of effects of isradipine during twice daily therapy in angina pectoris.

Isradipine, a 1,4 dihydropyridine calcium channel antagonist, is a potent coronary artery dilator that increases coronary blood flow with little effect on cardiac contractility. Isradipine is an approved antihypertensive agent, but its antianginal effects have not been well documented. In this placebo-controlled, double-blind, parallel-group design study we evaluated the duration of effects and safety of isradipine 10 mg bid in male patients with chronic stable angina pectoris. Seventy-two patients experiencing moderately severe angina between 3 and 7.5 minutes during a standard Bruce exercise test received placebo in a single-blind manner for 8-14 days. Sixty-one of these patients had reproducible treadmill exercise test results on three consecutive occasions and underwent further exercise tests at 3, 8, and 12 hours after a placebo period. Patients were then randomized (double blind) to either placebo or isradipine 10 mg bid for 2 weeks. Symptom-limited exercise tests were repeated predose and at 3, 8, and 12 hours after the 0800 hour dose dosing. Exercise duration increased significantly from baseline (last qualifying test during the single-blind placebo therapy, i.e., 0800 hours predose at visit 4) in the isradipine group compared to the placebo group prior to the administration of the 0800 hour dose (i.e., 12 hours after the 2000 hour dose) by 51 vs. 18 seconds, p = 0.04; and after the administration of the 0800 hour dose at 3 hours by 78 vs. 29 seconds, p = 0.005; and at 8 hours by 54 vs. 18 seconds, p = 0.04. Similarly, statistical significance was achieved when exercise data were analyzed using visit 4 (single-blind placebo therapy) corresponding time points as baseline. At 12 hours after the 0800 hour dose, exercise tolerance did not increase significantly after isradipine compared to placebo. Time to 1-mm ST-segment depression increased significantly after isradipine at 3 hours post 0800 hour dose compared to placebo (87 vs. 7 seconds, p < 0.01) but not at the 0, 8, or 12-hour postdose time points, regardless of which baseline was used. Isradipine therapy did not affect the rate-pressure double product. A significant correlation between the mean increase in total exercise time and mean plasma isradipine concentration was also present (p = 0.0295). During double-blind treatment, drug-related adverse events were experienced by four patients in the isradipine group and two patients in the placebo group. None of the patients experienced ischemic complications during the study.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

Enalapril in the treatment of congestive heart failure.

Congestive heart failure (CHF) is a complex clinical syndrome affecting 1% of the U.S. population. The basic dysfunction, a lack of sufficient blood flow to the periphery, triggers reflex neurohumoral mechanisms that cause systemic vasoconstriction and sodium and water retention as the body attempts to protect vital organs. This, in turn, results in additional work for the failing heart and further deterioration. Vasodilators, in general, and angiotensin converting enzyme (ACE) inhibitors, in particular, interrupt this pathophysiology and improve hemodynamics. Enalapril, a long-acting ACE inhibitor, has been demonstrated to improve New York Heart Association (NYHA) functional class, pulmonary capillary wedge pressure, cardiac index, maximum oxygen uptake, and exercise tolerance in CHF patients. Data from a recent trial provide evidence that a group of patients with severe CHF who were treated with enalapril showed reduced heart size, reduced need for other heart-failure medication, and reduced mortality.

Captopril↗
PubMed1989

Usefulness of nicardipine as monotherapy for chronic, stable angina.

Using a double-blind, Latin square protocol designed to detect dose response, nicardipine hydrochloride, a new calcium antagonist, was studied as monotherapy for stable exertional angina. Eighty-one patients were enrolled in the trial and 62 patients were included in greater than or equal to 1 primary efficacy analyses. Patients received 1 to 2 weeks of placebo run-in, then 5 weeks of treatment with placebo and with 10, 20 and 30 mg of nicardipine given 3 times daily. Patients completed symptom diaries, were monitored with 24-hour electrocardiographic Holter monitors and underwent serial exercise treadmill tests. By 1 hour, 10, 20 and 30 mg of nicardipine administered 3 times daily produced statistically significant, dose-related improvements in all key exercise parameters, which persisted at the 4-hour evaluation. The systolic blood pressure at rest and during exercise decreased, but the pulse slightly increased. The peak rate-pressure product was unchanged. The side effects were not severe. Nicardipine hydrochloride is an effective, well-tolerated medication for the treatment of stable exertional angina, and is a good alternative to currently available calcium antagonists.

Adult↗
PubMed1989

Sustained high-dose nitroglycerin transcutaneous patch therapy in angina pectoris: evidence for attenuation of effect over time.

The safety and efficacy of using continuous high-dose transcutaneous nitroglycerin in doses up to 100 mg/24 hours in chronic stable angina was assessed in 20 patients using serial treadmill testing. Patients had first to show a response to sublingual nitroglycerin with a 20% improvement in exercise time. All patients were then titrated with 20 mg (40 cm2), 60 mg (120 cm2), 80 mg (160 cm2) or 100 mg (200 cm2) patches, until intolerable headache in association with a 10 mmHg reduction in blood pressure and a ten-beat increment in heart rate. Drug was then discontinued for 2 days and patients underwent three repeat stress tests to reestablish a consistent drug-free baseline. Patients were then randomized in double-blind fashion to receive either active patch (N = 11) in previous titration dose or placebo patch (N = 9), with treadmill tests performed at 0 (1 hour after previous patch removal), 4, and 24 hours after patch application at baseline and at weeks 1 and 2. Venous blood was obtained for measurement of plasma nitroglycerin levels. After the first 24 hours of active patch therapy, there was a significant reduction in systolic blood pressure (P = .05), a significant increase in heart rate (P = .01), and a minor increase in exercise tolerance (P = .06) compared to placebo. At weeks 1 and 2, there was an attenuation of drug effect in all of these parameters. Plasma nitroglycerin levels demonstrated consistently high plasma levels over each 24-hour dosing interval, on day 1, week 1, and week 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗
PubMed1983

Quaternary opiate antagonists lower blood pressure and inhibit leucine-enkephalin responses.

The quaternary opiate antagonists naloxone methylbromide (MB) and naltrexone MB do not cross the blood-brain barrier, and may be used to differentiate peripheral from central nervous system effects of the opioid peptides. When administered intravenously to the conscious, chronically instrumented dog, naloxone MB transiently reduces mean systemic arterial pressure and increases heart rate in a dose-dependent manner over the concentration range from 0.1 to 1.0 mg/kg. The [Leu5]enkephalin response is completely inhibited at naloxone MB doses as low as 0.25 mg/kg, but this inhibition has terminated by 30 min after dosing. Naltrexone MB displays a similar spectrum of activity. This inhibition of the intravenous [Leu5]enkephalin response by the quaternary opiate antagonists indicates that the [Leu5]enkephalin response occurs by activation of peripheral receptor sites. The decrease in mean pressure induced by these antagonists coupled with the inhibition of the [Leu5]enkephalin response suggests that peripheral enkephalins may play a role in blood pressure regulation.

Animals↗
PubMed1983

Extrarenal contributions to indapamide's antihypertensive mechanism of action.

Autonomic responses in heart rate and blood pressure to Valsalva maneuvers and changes in vascular reactivity to pressor doses of phenylephrine and angiotensin II were studied before and after treatment with indapamide, a new antihypertensive diuretic. Six healthy male volunteers, placed on a daily diet consisting of 100 mEq of sodium, 80 mEq of potassium, and a fluid intake of 2500 ml, participated in this single-blind, placebo-controlled study. During active treatment, 5 mg of indapamide was administered once daily for 14 days. On the mornings of hemodynamic testing, samples of blood, 24-hour urine, and plasma were obtained and analyzed for hematocrit, catecholamines and their metabolites, plasma renin activity, and aldosterone levels. Since each subject served as his own control, the results were analyzed by the paired t-test method. Plasma renin activity and 24-hour urinary aldosterone levels increased (p less than 0.05), and serum potassium and chloride levels decreased (p less than 0.05). No other significant laboratory changes were noted after treatment, including changes in the plasma and urinary catecholamine levels. Following treatment, responses in heart rate and blood pressure to Valsalva maneuvers were unaltered. During the control period the doses of phenylephrine and angiotensin II required to raise the systolic pressure 25 to 35 mm Hg and the diastolic pressure 20 to 30 mm Hg were 5.03 +/- 0.72 micrograms/kg and 16.7 +/- 2.1 ng/kg, respectively. After treatment, the doses of phenylephrine and angiotensin II were significantly (p less than 0.05) greater: 10.72 +/- 1.02 micrograms/kg and 31.7 +/- 4.8 ng/kg, respectively. Dose-response relationships to these pressor agents were shifted in parallel to the right after treatment. A small but significant decrease in body weight, which may have reflected a decrease in plasma volume, was observed. However, no orthostatic changes between the supine and erect mean arterial blood pressures or incremental increases in heart rates were noted between the two periods. An increase in hematocrit and blunting of the diastolic overshoot during the Valsalva maneuvers that were used as indexes of plasma volume contraction were also not observed. In summary, our results indicate that changes in vascular responsiveness occurred by mechanisms independent of changes in the autonomic nervous system, since plasma norepinephrine levels did not change and responsiveness to Valsalva maneuvers was unaltered. Furthermore, it appears that this effect on the vasculature was probably not related to changes in plasma volume.

Adult↗
PubMed1982

Leucine-enkephalin: reversal of intrinsic cardiovascular stimulation by pentobarbital.

In the conscious, chronically instrumented dog, leucine-enkephalin ([Leu5]ENK), 35 micrograms/kg injected intravenously, increased heart rate, respiratory rate, systolic and diastolic systemic arterial pressures, mean pulmonary arterial pressure, and cardiac output. After pentobarbital-induced anesthesia, the same dose of [Leu5]ENK decreased heart rate, systemic and pulmonary arterial pressures, and cardiac output. Responses both before and after pentobarbital were blocked by naloxone. These results indicate that barbiturate anesthesia can reverse the cardiovascular stimulatory activity of intravenously administered [Leu5]ENK.

Anesthesia↗