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Thomas D Giles

Publications and source records attributed to Thomas D Giles.

At least 37 records · Page 2Linked to original sources
PubMed2005

ACE inhibitors: over two decades of use.

During the meeting of the American Society of Hypertension, Inc. in San Francisco, CA, on May 16, 2005, a roundtable was convened to discuss angiotensin-converting enzyme inhibition as it relates to both blood pressure control and issues of end-organ protection. Dr. Domenic A. Sica of Virginia Commonwealth University, Richmond, VA, moderated the panel discussion. Participants included Dr. Thomas D. Giles of the Louisiana State University Health Sciences Center, New Orleans, LA, and President of The American Society of Hypertension, Inc.; Dr. Henry R. Black of Rush University Medical Center, Chicago, IL; and Dr. Vito M. Campese of the University of Southern California, Los Angeles, CA.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

Pathophysiologic, diagnostic, and therapeutic aspects of the metabolic syndrome.

The metabolic syndrome, characterized by increases in waist circumference, blood pressure, and triglyceride concentrations combined with reduced high-density lipoprotein and evidence of glucose intolerance, results from the interaction of visceral or central obesity with insulin resistance. This syndrome presents a clinical situation of systemic inflammation and increased cardiovascular risk. Blood pressure, even if only in the "prehypertensive" range, plays an important role in increasing the risk of cardiovascular disease. Recognition and treatment of each individual component of the metabolic syndrome is critical in reducing cardiovascular risk. Treatment should begin with lifestyle changes, including diet, exercise, and weight reduction. Antihypertensive therapy should be directed toward reduction of blood pressure to levels as close to optimal (<120/80 mm Hg) as feasible, and treatment protocols that do not cause worsening of glucose intolerance should be selected. Therapy for dyslipidemia should be directed at reducing triglycerides and increasing high-density lipoprotein. Glucose-lowering agents may be indicated, and drugs such as metformin and thiazolidinediones, which reduce insulin resistance, should form the basis of therapy. Carefully chosen therapy will effectively improve cardiovascular outcomes.

Antihypertensive Agents↗
PubMed2005

Expanding the definition and classification of hypertension.

Cardiovascular abnormalities are frequently the cause, as well as the effect, of elevated blood pressure. As such, early cardiovascular disease (CVD) may be established before identifiable blood pressure thresholds are crossed. To identify individuals at risk for CVD at an earlier point in the disease process, as well as to avoid labeling persons as hypertensive who are at low risk for CVD, the Hypertension Writing Group proposes incorporating the presence or absence of cardiovascular risk factors, early disease markers, and target organ damage into the definition and classification scheme of hypertension. To describe both the complexity and progressive nature of hypertension, the following definition is proposed: "Hypertension is a progressive cardiovascular syndrome arising from complex and interrelated etiologies. Early markers of the syndrome are often present before blood pressure elevation is observed; therefore, hypertension cannot be classified solely by discrete blood pressure thresholds. Progression is strongly associated with functional and structural cardiac and vascular abnormalities that damage the heart, kidneys, brain, vasculature, and other organs and lead to premature morbidity and death." Classification of hypertension must involve assessing global cardiovascular risk to situate an individual's risk for CVD and events along a continuum. As knowledge of early CVD continues to evolve, the approach to classifying individuals along that continuum can be expected to evolve accordingly. The four categories currently used to classify hypertension are normal, prehypertension, and stages 1 and 2 hypertension. The population identified with prehypertension includes a subgroup with early CVD. We believe it would be preferable to classify all individuals as either normal or hypertensive, based on their cardiovascular evaluation, using the four categories of normal and stages 1, 2, and 3 hypertension.

Antihypertensive Agents↗
PubMed2005

Roundtable discussion: hypertension in children and adolescents.

Following a hypertension symposium held in Philadelphia, PA, on June 8, 2004, a roundtable discussion was held to discuss the treatment of hypertension in adolescents and children. The participants included Thomas D. Giles, MD, of Louisiana State College of Medicine, New Orleans, LA; Bonita Falkner, MD, of the Department of Medicine and Pediatrics, Thomas Jefferson University, Philadelphia, PA; Allan B. Schwartz, MD, of the Division of Nephrology and Hypertension, Drexel University College of Medicine, Philadelphia, PA; Raymond R. Townsend, MD, of the Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA; and Marvin Moser, MD, of the Department of Medicine/Cardiology, Yale University School of Medicine, New Haven, CT.

Adolescent↗
PubMed2004

Effects of olmesartan medoxomil on systolic blood pressure and pulse pressure in the management of hypertension.

BACKGROUND: In this analysis, we evaluated the efficacy of the angiotensin II receptor blocker olmesartan medoxomil in reducing systolic blood pressure (SBP) and pulse pressure (PP) in hypertensive patients. METHODS: Data from seven randomized, double blind, placebo controlled, 6- to 12-week efficacy trials of olmesartan 20 mg and 40 mg/day were analyzed to determine changes in trough seated SBP and PP within three cohorts: 1) total cohort (n = 1777); 2) subjects with a wide PP: that is, those with a baseline PP >55 mm Hg (n = 917); and 3) a subpopulation of patients with a wide PP and age > or = 65 years (n = 296). Statistical comparisons used least squares mean values. RESULTS: In the total cohort, olmesartan 20 and 40 mg/day resulted in mean reductions in SBP of 15.1 and 17.6 mm Hg, respectively (P < .001 v placebo). In the wide PP cohort, olmesartan resulted in mean reductions in SBP of 17.7 and 22.0 mm Hg and mean reductions in PP of 7.4 Hg and 8.8 mm Hg for the groups receiving 20 and 40 mg/day, respectively (P < .001 v placebo). In the cohort with wide PP and age > or = 65 years, olmesartan 20 and 40 mg/day produced mean reductions in SBP of 21.8 and 22.5 mm Hg, and PP of 6.7 and 7.6 mm Hg, respectively (P < .05 v placebo). CONCLUSIONS: Olmesartan significantly reduces SBP and PP, and these reductions are more pronounced in patients with a wide baseline PP. In patients with a wide baseline PP and age > or = 65 years, the population at greatest risk for cardiovascular morbidity and mortality, olmesartan reduces PP to an extent similar to that in patients <65 years of age.

Antihypertensive Agents↗
PubMed2004

Diabetes mellitus and heart failure: basic mechanisms, clinical features, and therapeutic considerations.

Diabetic cardiomyopathy encompasses the spectrum from subclinical disease to the full-blown syndrome of congestive heart failure. The prevalence of type 2 diabetes mellitus is increasing at an alarming rate in the western world. and with it, the frequency of diabetes-related heart failure. There is at least early suggestion that target-driven, long-term, intensified intervention that is aimed at multiple risk factors in patients who have type 2 diabetes and microalbuminuria may reduce the risk of macrovascular (cardiovascular) and micro-vascular complications by approximately 50%. Thus, it is imperative that patients, particularly those who are at risk for the cardiovascular dysmetabolic syndrome, be screened aggressively for the presence of glucose intolerance and diabetes. When detected, all metabolic and cardio-vascular parameters should be evaluated and treated aggressively to reach currently recommended clinical targets. Such action will result in great benefit for patients by reducing morbidity and mortality and improving quality of life and will reduce the financial burden that is associated with this epidemic disease.

Cardiomyopathies↗
PubMed2003

The patient with diabetes mellitus and heart failure: at-risk issues.

The risk for cardiovascular disease, particularly congestive heart failure, is significantly higher in patients with type 2 diabetes mellitus than in individuals without diabetes. The presence of hyperglycemia has been associated with changes in the myocardium that are characteristic of diabetic cardiomyopathy and heart failure. Furthermore, insulin resistance may be associated with cardiomyopathy, even in the absence of hyperglycemia, and has been linked with cardiovascular remodeling. The association between heart failure and insulin resistance suggests that agents that improve insulin sensitivity, such as the thiazolidinediones (TZDs), are likely to be of cardiovascular benefit in patients with diabetes and heart failure. Although TZDs have beneficial cardiovascular effects in patients with type 2 diabetes, such as reducing blood pressure, improving endothelial function, and exerting potential antiatherosclerotic effects, one must be aware of the potential of these agents to cause edema or weight gain as a result of fluid retention and fat accumulation. These issues are of particular concern in patients with diabetes who have heart failure. However, the glycemic and cardiovascular benefits of TZDs may outweigh the potential problems of weight gain and fluid retention noted in some patients. Thus the risk-benefit ratio of using TZDs in patients who have diabetes and heart failure must be carefully considered in this patient population with comorbid disorders.

Cardiac Output, Low↗
PubMed2003

Examining therapeutic goals: population versus individual-based approaches.

In the individual patient, the goal of antihypertensive treatment is to lower the blood pressure (BP) to a level that minimizes the patient's risk of cardiovascular complications. However, most of our knowledge regarding what this level of BP should be is derived from population studies and large clinical trials. Population studies have shown that elevated BP is associated with an increased risk of morbidity and mortality from coronary heart disease, stroke, heart failure, and renal failure. Cardiovascular risk begins to increase when BP exceeds 115/75 mm Hg and doubles with each increment of 20 mm Hg in systolic BP and 10 mm Hg in diastolic BP.The clinical benefit of BP reduction in patients with hypertension is well established. Thus, patients with less severe elevations in BP (high-normal) are at increased risk. Patients with diabetes or proteinuria benefit from even more aggressive reductions in BP. Despite the well-established benefits of BP reduction, hypertension is still not well treated, underscoring the need for more aggressive detection and better management. Although data from large clinical trials have provided valuable information to help guide treatment, application of clinical trial results to individual patients is limited by the heterogeneity of patient populations with respect to patient risk, comorbidities, and differences in genetic and environmental background. Ultimately, the treatment decisions should be tailored to each patient, integrating as much information as possible concerning the patient's history, risk, pathophysiology, and lifestyle.

Antihypertensive Agents↗
PubMed2003

Defining the antihypertensive properties of the angiotensin receptor blocker telmisartan by a practice-based clinical trial.

Traditional randomized controlled clinical trials are designed to define the specific properties of individual antihypertensive drugs but do not provide full information about their use in clinical practice. To carry out a large-scale practice-based open-label trial to evaluate the safety and efficacy of an angiotensin receptor blocker (ARB) in controlling blood pressure (BP) in the community setting, 703 practitioners recruited 2705 hypertensive patients. There were three groups: untreated at the time of study entry with uncontrolled BP (>/=140/90 mm Hg) (N = 1957); treated but uncontrolled on current monotherapy (N = 685); and treated and controlled, but with unacceptable side effects (N = 63). After stopping any previous treatment, patients received telmisartan (40 mg daily) for 2 weeks; the dose was increased to 80 mg if BP remained >/=130/85 mm Hg. Participants were then followed for a further 4 weeks. Blood pressure decreased by 18.9/12.3 mm Hg in the untreated group, by 13.1/7.9 mm Hg in the previously treated but uncontrolled group, and increased slightly by 3.5/1.3 mm Hg in the previously controlled group. Patients not responding adequately to the 40-mg telmisartan dose had an initial BP reduction of 7.3/4.5 mm Hg; titration to 80 mg gave an additional 7.5/5.0 mm Hg reduction and controlled BP (<140/90 mm Hg) in 44% of these titrated patients. Overall, control occurred in 56% of white patients; 52% of black patients (who responded well to dose titration); 60% of patients <65 years; and 46% of patients >/=65 years. Thus, in contrast with the relatively flat dose response effects in controlled parallel group trials, this practice-based trial has demonstrated the value of titrating telmisartan to its maximum dose in patients with inadequate BP responses to the initial dose, and has shown its efficacy across major demographic groups.

Adult↗
PubMed2003

Review of methods for texture analysis of myocardium from echocardiographic images: a means of tissue characterization.

This review discusses the definition of texture and identifies its utility in echocardiography for characterization of tissue. Methods used for quantification of texture in echocardiography and other disciplines are discussed. Several methodologies, particularly the wavelet method of texture quantification, seem to be promising. Image texture analysis appears to be a fertile area for research in echocardiography.

Cardiomyopathies↗
PubMed2003

Diabetes mellitus and heart failure.

The metabolic abnormalities associated with diabetes mellitus result in macrovascular and microvascular complications in multiple organ systems; it is the cardiovascular impact that accounts for the greatest morbidity and mortality associated with this disease. Heart failure, both with reduced and preserved systolic function, is a major complication, arising from the frequent associations with coronary atherosclerosis, hypertension, and a specific heart muscle dysfunction (cardiomyopathy) that occurs independently of coronary artery disease. Hyperglycemia, insulin resistance, and hypertension, together with activation of both the circulating and the tissue renin-angiotensin-aldosterone systems, contribute to structural fibrosis and autonomic neuropathy. Thus, it becomes imperative to identify cardiac abnormalities early in the course of both type 1 and type 2 diabetes to allow early and aggressive intervention to control glucose and blood pressure and to normalize blood lipid profiles. Patients with diabetes should be treated to secondary prevention targets, including blood pressure less than 130/80 mm Hg and low-density lipoprotein cholesterol level less than 100 mg/dL. Angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers,beta blockers, calcium channel-blockers, statins, and aspirin have all been demonstrated to significantly reduce cardiovascular morbidity and mortality in patients with diabetes.

Cardiomyopathies↗
PubMed2002

Adenoviral gene transfer of endothelial nitric-oxide synthase (eNOS) partially restores normal pulmonary arterial pressure in eNOS-deficient mice.

It has been shown that mice deficient in the gene coding for endothelial nitric-oxide synthase (eNOS) have increased pulmonary arterial pressure and pulmonary vascular resistance. In the present study, the effect of transfer to the lung of an adenoviral vector encoding the eNOS gene (AdCMVeNOS) on pulmonary arterial pressure and pulmonary vascular resistance was investigated in eNOS-deficient mice. One day after intratracheal administration of AdCMVeNOS to eNOS(-/-) mice, there was an increase in eNOS protein, cGMP levels, and calcium-dependent conversion of l-arginine to l-citrulline in the lung. The increase in eNOS protein and activity in eNOS(-/-) mice was associated with a reduction in mean pulmonary arterial pressure and pulmonary vascular resistance when compared with values in eNOS-deficient mice treated with vehicle or a control adenoviral vector coding for beta-galactosidase, AdCMVbetagal. These data suggest that in vivo gene transfer of eNOS to the lung in eNOS(-/-) mice can increase eNOS staining, eNOS protein, calcium-dependent NOS activity, and cGMP levels and partially restore pulmonary arterial pressure and pulmonary vascular resistance to near levels measured in eNOS(+/+) mice. Thus, the major finding in this study is that in vivo gene transfer of eNOS to the lung in large part corrects a genetic deficiency resulting from eNOS deletion and may be a useful therapeutic intervention for the treatment of pulmonary hypertensive disorders in which eNOS activity is reduced.

Adenoviridae↗
PubMed2002

Correlates of pulse pressure reduction during antihypertensive treatment (losartan or atenolol) in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study).

In hypertensive patients, pulse pressure has been related to hypertension-induced target organ damage and risk of cardiovascular events. However, correlates of pulse pressure reduction during antihypertensive treatment have been less extensively investigated. We related pulse pressure changes to clinical and echocardiographic findings before and after 2 years of antihypertensive treatment in 767 patients aged 55 to 80 years (mean 66) in the Losartan Intervention For End point reduction in hypertension study. Over 2 years, blood pressure and pulse pressure were reduced from 173/98 to 147/84 mm Hg and from 75 to 63 mm Hg, respectively, both p <0.001. In linear multivariate analysis controlling for initial pulse pressure, 2-year reduction in pulse pressure correlated negatively with age and concomitant diabetes mellitus, and positively with body height and 2-year reduction in mean blood pressure (multiple R(2) = 0.42, p <0.01). When dividing the study population into 2 groups using a prognostically validated partition for pulse pressure, patients with pulse pressure > or =63 mm Hg after 2 years of antihypertensive treatment (n = 349) were older and shorter, included more women and patients with isolated systolic hypertension, diabetes mellitus, albuminuria, and echocardiographic left ventricular hypertrophy at baseline, and also had a smaller decrease in mean blood pressure and the urinary albumin/creatinine ratio over 2 years (all p <0.05). Thus, in hypertensive patients with electrocardiographic left ventricular hypertrophy, older age, less reduction in mean blood pressure, concomitant diabetes mellitus, and shorter stature are associated with attenuated pulse pressure reduction during antihypertensive treatment.

Aged↗
PubMed2002

Hypertension and lipids: lipid factors in the hypertension syndrome.

Cardiovascular risk factors are identified as physiologic, biochemical, and behavioral, and include hypertension, lipid abnormalities, and hyperglycemia. These factors constitute the "cardiovascular dysmetabolic syndrome" and damage the vascular endothelium by increasing concentrations of reactive molecular species, ultimately increasing cardiovascular morbidity and mortality. Multiple risk factors, particularly hypertension and hypercholesterolemia, often coexist in the same individual. Low-density lipoprotein cholesterol has been demonstrated to upregulate the AT(1) receptor, leading to increases in blood pressure. Treatment of hypercholesterolemia with medications, such as the hydroxymethylglutaryl coenzyme A reductase inhibitors or statins that decrease AT(1) receptor expression and activation, reduce not only cholesterol but blood pressure as well. Treatment of hypertension with angiotensin-converting enzyme inhibitors may also reduce cholesterol. Recognition and identification of multiple risk factors and appropriate treatment in a manner that minimizes excessive oxidative stress is critical to the maintenance of normal endothelial cell function and cardiovascular risk reduction.

Blood Pressure↗