PubMed Health⌕ Search

Biomedical subjects

T J Dresing

Publications and source records attributed to T J Dresing.

5 recordsLinked to original sources

Congestive heart failure treatment: the pacing approach.

Early reports of physiologic pacing for congestive heart failure (CHF) yielded conflicting results, and little enthusiasm was generated for pacing as a mode of therapy for CHF. Small, uncontrolled studies, which had little or no follow-up demonstrated that pacing from the left ventricle could synchronize contraction of the ventricles and improve overall ventricular performance. These encouraging reports led to a number of larger, multicenter trials, which have been recently reported. These trials have consistently shown improvements in such objective measurements as peak exercise oxygen consumption, ejection fraction, heart rate variability, 6-minute walk test distance and anaerobic threshold, as well as subjective improvements such as quality of life assessment. A number of large, multicenter double-blinded trials are ongoing which will seek to further assess the benefits of biventricular or multisite pacing. Among the important issues, which will be addressed by ongoing trials, are the possibility of pacing induced arrhythmias, the benefit of adding defibrillator capability to these pacing systems, and the development of novel delivery systems, which will make implantation of these systems more accessible to clinicians. Studies to date have largely excluded patients with traditional indications for pacing, and have been confined chiefly to patients with PR interval prolongation, and left bundle branch block with a QRS duration greater than 120 milliseconds, with New York Heart Association class II or III CHF. Whether this therapy will offer benefit to other patients who do not meet these criteria is also unknown at present. Another novel mode of pacing therapy, which may be clinically appropriate for a broader range of CHF patients, is contractility modulation, which involves subthreshold pacing to increase intracellular calcium and enhance inotropy. Early data suggests that the benefits of these two forms of pacing therapy may be additive.

Cardiac Pacing, Artificial↗

Usefulness of impaired chronotropic response to exercise as a predictor of mortality, independent of the severity of coronary artery disease.

Chronotropic incompetence, or an attenuated heart rate response to exercise, has been shown to be associated with an adverse outcome. It is not known whether chronotropic incompetence predicts all-cause mortality independent of angiographic severity of coronary artery disease (CAD). Study subjects included consecutive patients who underwent first-time, symptom-limited exercise treadmill testing and coronary angiography within 90 days; no patient was taking beta blockers or had a history of heart failure, valve disease, or prior revascularization. Chronotropic response was measured in 2 ways: (1) failure to reach 85% of the age-predicted maximum heart rate, and (2) a low chronotropic index, a measure of exercise heart rate response that accounts for effects of age, physical fitness, and resting heart rate. Angiographic severity of CAD was assessed using the Duke Prognostic Weight Score, with a score > or = 42 considered to be indicative of severe CAD. Among 384 eligible patients, failure to reach 85% of the age-predicted maximum heart rate occurred in 61 (16%) and a low chronotropic index was noted in 133 (35%). Severe CAD was present in 63 (16%). During 6 years of follow-up there were 56 deaths. Mortality was predicted by failure to reach target heart rate (RR 1.85, 95% confidence interval [CI] 1.01 to 3.39, chi-square = 4, p = 0.05), by severe CAD (RR 2.21, 95% CI 1.24 to 3.95, chi-square = 8, p = 0.007), and, most strongly, by a low chronotropic index (RR 2.72, 95% CI 1.60 to 4.61, chi-square = 15, p = 0.0002). In a multivariable model, low chronotropic index remained predictive of death (adjusted RR 2.22, 95% CI 1.29 to 3.82, p = 0.004), whereas severe CAD no longer predicted death (adjusted RR 1.27, 95% CI 0.70 to 2.31, p > 0.4). Thus, chronotropic incompetence is a strong and independent predictor of death, even after accounting for the angiographic severity of CAD.

Confidence Intervals↗

Direct effects of smooth muscle relaxation and contraction on in vivo human brachial artery elastic properties.

The direct effect of smooth muscle relaxation on arterial elastic properties is controversial. Studies in animals show both a decrease and an increase in elastic modulus. In human subjects, the contribution of smooth muscle to arterial elastic mechanics has been limited by difficulty in separating the direct effects of a vasodilator drug on the arterial wall from the indirect effects due to reduced blood pressure. The purpose of the present study was to assess the direct contribution of vascular smooth muscle to brachial artery elastic mechanics in normal human subjects in vivo. We measured brachial artery compliance and incremental elastic modulus (Einc) in eight normal subjects (age, 22 to 51 years) by using intravascular ultrasound. A 3.5F 30-MHz intravascular ultrasound catheter was placed through a sheath into the brachial artery, and intraarterial pressure, cross-sectional area, and wall thickness were measured simultaneously under baseline conditions and after the administration of intra-arterial nitroglycerin (100 micrograms) and norepinephrine (1.2 micrograms). A pressurized cuff surrounding the brachial artery was inflated to reduce transmural brachial artery pressure. Using this technique, we were able to measure the following arterial characteristics for the first time in human subjects in vivo: (1) the effective unstressed arterial radius and (2) the pressure-area, stress-strain, and pressure-Einc relations over a wide pressure range (0 to 100 mm Hg). Intra-arterial nitroglycerin increased brachial artery area by 22% and intraarterial norepinephrine decreased brachial artery area by 17% at 100 mm Hg transmural pressure (P < .001 versus baseline).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Quantum yields for the cyclization and configurational isomerization of 4E,15Z-bilirubin.

Extraction of a solution of bilirubin configurational isomers in chloroform with an aqueous solution of human serum albumin was found to remove selectively the 4Z,15E-isomer. This phenomenon was used to develop a method for the purification of the 4E,15Z-isomer of bilirubin. The quantum yield for the cyclization and configurational isomerization of the 4E,15Z-isomer bound to a molar excess of human serum albumin was measured at 450 and 510 nm. The quantum yield for cyclization to form lumirubin was 0.12 and 0.19 at 450 and 510 nm, respectively. The quantum yield for configurational isomerization to form 4Z,15Z-bilirubin was 0.03 and 0.05 at 450 and 510 nm. An analysis of previously published data on the quantum yield for the formation of lumirubin from 4Z, 15Z-bilirubin bound to human serum albumin suggests that all of the formation of lumirubin may occur via consecutive photochemical processes with the 4E,15Z-isomer as an intermediate.

Bilirubin↗