Biomedical subjects

Robert McKelvie

Publications and source records attributed to Robert McKelvie.

10 recordsLinked to original sources

PubMed2006

Effect of exercise training on myocardial blood flow in patients with stable coronary artery disease.

BACKGROUND: The mechanisms by which exercise training benefits patients with coronary artery disease (CAD) are unclear but may include improved myocardial circulation. The aim of this study was to investigate the effect of exercise training on myocardial blood flow (MBF) and coronary flow reserve (CFR) in patients with stable CAD. METHODS: Twelve patients with documented CAD and ischemic ST-segment depression during exercise testing were randomized to exercise training (n = 7) or sedentary life style (control; n = 5) and underwent rubidium-82 positron emission tomography pre- and postintervention. Global left ventricle MBF and regional MBF in 17 left ventricular segments were calculated. Segments with <75% uptake (2 SD below normal) on stress uptake images were defined as abnormal. RESULTS: Exercise training increased global CFR by 20.8% +/- 27.9% versus control (10.5 +/- 24.1%, P = .0001). In normal segments (exercise training: n = 91; control: n = 46), exercise training did not change resting MBF (-14.1% +/- 16.3% vs -8.8% +/- 15.6%) and hyperemic MBF (-1.93% +/- 19.1% vs 2.86% +/- 20.5%, P = NS) and increased in CFR compared to control (17.0% +/- 25.5% vs 11.3% +/- 23.5%, P = .01). In abnormal segments, the change in resting MBF was not significantly different (-12.6% +/- 18.5% exercise [28 segments] vs -2.9% +/- 18.0% control [39 segments], P = NS). A significant increase was seen in hyperemic MBF with exercise (12.5% +/- 22.1% vs 2.6% +/- 16.3%, P = .02) and CFR (32.8% +/- 32.3% vs 9.5% +/- 24.8%, P = .001). CONCLUSIONS: Exercise training increased CFR in normal and diseased segments, and increased hyperemic flow in diseased segments. These data provide preliminary evidence in support of a favorable effect of exercise training on blood flow to ischemic myocardium.

Coronary Artery Disease↗

PubMed2006

Heart failure.

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Adrenergic beta-Antagonists↗

PubMed2005

The irbesartan in heart failure with preserved systolic function (I-PRESERVE) trial: rationale and design.

BACKGROUND: Although 40% to 50% of patients with chronic heart failure (HF) have relatively preserved systolic function (PSF), few trials have been conducted in this population and treatment guidelines do not include evidence-based recommendations. METHODS AND RESULTS: The Irbesartan in Heart Failure with Preserved Systolic Function (I-PRESERVE) is enrolling 4100 subjects with HF-PSF to evaluate whether 300 mg irbesartan is superior to placebo in reducing mortality and prespecified categories of cardiovascular hospitalizations. The principal inclusion criteria are age > or =60 years, heart failure symptoms, an ejection fraction > or =45%, and either hospitalization for heart failure within 6 months or corroborative evidence of heart failure or the substrate for diastolic heart failure. Additional secondary end points include cardiovascular mortality, cause-specific mortality and morbidity, change in New York Heart Association functional class, quality of life, and N-terminal pro-BNP measurements. Follow-up will continue until 1440 patients experience a primary end point. Substudies will evaluate changes in echocardiographic measurements and serum collagen markers. CONCLUSION: I-PRESERVE is the largest trial in this understudied area and will provide crucial information on the characteristics and course of the syndrome, as well as the efficacy of the angiotensin receptor blocker irbesartan.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2004

Heart failure.

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Adrenergic beta-Antagonists↗

PubMed2004

Heart failure.

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Adrenergic beta-Antagonists↗

PubMed2003

Heart failure.

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Adrenergic beta-Antagonists↗

PubMed2002

A controlled trial of hospital versus home-based exercise in cardiac patients.

BACKGROUND: Large numbers of patients who stand to benefit from the exercise training component of cardiac rehabilitation are not being served due to access issues. Home-based exercise training may be a potentially useful alternative to training in institutional environments. PURPOSE: The purpose of this study was to examine the benefit of 6 months of hospital-based exercise training versus 6 months of monitored, home-based exercise training with respect to physical, quality of life, and social support outcomes in patients after coronary artery bypass graft (CABG) surgery. METHODS: Randomized controlled trial of "direct-to-home" (Home; = 120) versus "direct-to-hospital" (Hosp; = 122) exercise training, 35-49 d post CABG surgery. The primary outcome was peak exercise capacity, measured by peak oxygen consumption (VO(2)) on a symptom-limited cycle ergometer exercise test. Secondary outcomes were health-related quality of life (measured by the SF-36) and social support (measured by the ISEL). Measurements were taken at baseline and after 3 and 6 months of exercise training. RESULTS: The study groups had similar demographic and health profiles at baseline. Peak VO(2) improved significantly in both groups after 6 months of exercise training; 36% in the Hosp group (1,222.1 +/- 269.0 mL x min(-1) to 1,497.2 +/- 594.3 mL x min(-1); < 0.0001) and 31% in the Home group (1,260.3 +/- 306.5 mL x min(-1) to 1,433.4 +/- 589.7 mL x min(-1); < 0.05). The Home group reported greater total social support than the Hosp group at 3 (36.2 +/- 4.5 vs 34.0 +/- 6.7; < 0.0001) and 6 months (36.0 +/- 4.9 vs 34.6 +/- 6.4; = 0.05). The Home group demonstrated a greater improvement in health-related quality of life (physical) by 6 months in comparison to the Hosp patients (51.2 +/- 6.4 vs 48.6 +/- 7.1; = 0.004). CONCLUSION: This study suggests that low-risk CABG surgery patients may be served as well or better with a monitored, home-based exercise program than with an institution-based program.

Coronary Disease↗

PubMed2002

Heart failure.

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Adrenergic beta-Antagonists↗

PubMed2002

Heart failure.

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Adrenergic beta-Antagonists↗

PubMed2001

Vimentin exposed on activated platelets and platelet microparticles localizes vitronectin and plasminogen activator inhibitor complexes on their surface.

Type 1 plasminogen activator inhibitor (PAI-1), the primary inhibitor of tissue-type plasminogen activator (t-PA), is found in plasma and platelets. PAI-1 circulates in complex with vitronectin (Vn), an interaction that stabilizes PAI-1 in its active conform. In this study, we examined the binding of platelet-derived Vn and PAI-1 to the surface of isolated platelets. Flow cytometry indicate that, like P-selectin, PAI-1, and Vn are found on the surface of thrombin- or calcium ionophore-activated platelets and platelet microparticles. The binding of PAI-1 to the activated platelet surface is Vn-dependent. Vn mediates the binding of PAI-1 to platelet surfaces through a high affinity (K(d) of 80 nm) binding interaction with the NH(2) terminus of vimentin, and this Vn-binding domain is expressed on the surface of activated platelets and platelet microparticles. Immunological and functional assays indicate that only -5% of the total PAI-1 in platelet releasates is functionally active, and it co-precipitates with Vn, and the vimentin-enriched cytoskeleton fraction of activated platelet debris. The remaining platelet PAI-1 is inactive, and does not associate with the cytoskeletal debris of activated platelets. Confocal microscopic analysis of platelet-rich plasma clots confirm the co-localization of PAI-1 with Vn and vimentin on the surface of activated platelets, and platelet microparticles. These findings suggest that platelet vimentin may regulate fibrinolysis in plasma and thrombi by binding platelet-derived Vn.PAI-1 complexes.

Animals↗