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Biomedical subjects

D G Vidt

Publications and source records attributed to D G Vidt.

At least 19 recordsLinked to original sources
PubMed2003

Pathogenesis and treatment of resistant hypertension.

Current prevalence estimates suggest that approximately 25% of the world's population has arterial hypertension making this one of the most common conditions for which individuals seek health care. Currently, hypertension is considered resistant if blood pressure (BP) cannot be reduced to <140/90 mmHg with an appropriate triple-drug regimen, including an oral diuretic with all agents administered at or near maximal dosages. This definition has evolved with the development of new therapies and evidence-based data supporting treatment to lower BP goals. With current poor hypertension control rates worldwide, more individuals are being referred for resistant or refractory hypertension. Causes for refractory hypertension are multi-factorial and a systematic approach to evaluation can be most beneficial in identifying the causative factors. This review focuses initially on those causes of resistance to treatment that can be evaluated cost-effectively in the outpatient setting. These include a search for nonadherence, assessing the adequacy of the treatment regimen, ruling out drug interactions and associated conditions. Pseudoresistance and evidence of volume expansion can also often be identified in the office setting. In the absence of the above factors, assessment for secondary causes of hypertension, not yet identified, is appropriate, and further hemodynamic and/or neurohumoral assessment may be indicated to facilitate more targeted and individualized therapy. This careful step-wise evaluation is not only cost-effective and office-based, but also largely noninvasive, and capable of identifying the causative factors in the vast majority of patients with apparently resistant hypertension.

Antihypertensive Agents↗
PubMed2002

Ischaemic nephropathy: can we preserve renal function?

Atherosclerotic occlusive disease of the renal arteries or ischaemic nephropathy represents a frequent cause of progressive renal failure and is often amenable to therapy. Newer, non-invasive diagnostic studies are now available to identify patients with potentially correctable renovascular disease and avoid the risks of aortic cannulation or contrast nephrotoxicity. Before preceding with an intervention, careful assessment of the risks vs benefits of revascularisation are mandatory and intervention should be considered primarily for management of refractory hypertension or progressive renal dysfunction.

Aged↗
PubMed2002

New strategies for blood pressure control.

EDUCATIONAL OBJECTIVES: (1) understand the evidence-based data regarding blood pressure (BP) control; (2) review the current short-fall in hypertension control efforts; (3) appreciate physicians' attitudes toward aggressive BP therapy; (4) review the newer clinical trial evidence in support of treatment to lower BP goals.

Antihypertensive Agents↗
PubMed2001

A forced titration study of antihypertensive efficacy of candesartan cilexetil in comparison to losartan: CLAIM Study II.

An 8-week, multicentre (72 sites in the US), double-blind, randomised, parallel group, forced titration study compared the antihypertensive efficacy of candesartan cilexetil and losartan. A total of 611 patients with essential hypertension (diastolic blood pressure 95 to 114 mm Hg) were randomised initially to candesartan cilexetil 16 mg once daily or losartan 50 mg once daily. After 2 weeks of randomised treatment, the doses of candesartan cilexetil and losartan were doubled to 32 mg and 100 mg once daily and continued respectively for 6 weeks. At week 8, candesartan cilexetil lowered the blood pressure (BP) at 24 h (trough), 6 h (peak) and 48 h post dose to a significantly greater extent (P < 0.05) than losartan: candesartan cilexetil lowered trough BP by 13.4/10.5 mm Hg, peak BP by 15.5/12.9 mm Hg and 48-h BP by 10.5/9.9 mm Hg compared to a reduction of trough BP by 10.1/9.1 mm Hg, peak BP by 12.0/9.5 mm Hg, and 48-h BP by 5.9/7.0 mm Hg by losartan. The responder and control rates were numerically higher in the candesartan cilexetil group, but the differences did not reach statistical significance; the responder rates were 58.8% for the candesartan cilexetil group and 52.1% for the losartan group and control rates were 49.0% for the candesartan cilexetil group and 44.6% for the losartan group. Overall, both treatment regimens were well tolerated. A total of 15 of the 611 (2.5%) patients withdrew from the study due to an adverse event, including nine (2.9%) in the candesartan cilexetil group and six (2.0%) in the losartan group. In conclusion, this forced titration study confirms that candesartan cilexetil is more effective in lowering BP than losartan when compared at once daily maximum doses.

Antihypertensive Agents↗
PubMed2001

Current treatment of hypertension.

Numerous national hypertension guidelines are available. Major similarities and differences have been reviewed, along with both patient and provider barriers to adequate blood pressure control. The current recommended risk stratification of hypertension for treatment decisions together with principles of drug management have been reviewed. Finally, data from recent clinical trials in hypertension together with the lessons learned from those trials have been addressed. It is apparent that most available classes of antihypertensive agents can be effective in the management of hypertension, if used appropriately by providers, in conjunction with optimal adherence with prescribed medications by patients.

Age Factors↗
PubMed2000

Contributing factors in resistant hypertension. Truly refractory disease is rarely found in a properly conducted workup.

Systematic evaluation of each patient with refractory hypertension is necessary to identify conditions or altered mechanisms of hypertension that are amenable to targeted therapy. Issues that should be carefully investigated are appropriateness of the regimen, possible drug interactions, patient compliance, associated conditions (alcohol or recreational drug use, hyperinsulinemia), pseudohypertension, office hypertension, and volume overload. When these problems are eliminated, causes of secondary hypertension should be sought, the most common being coarctation of the aorta, Cushing's syndrome, primary aldosteronism, pheochromocytoma, renovascular disease, thyroid and parathyroid disease, and renal parenchymal disease. In a few cases, a careful hemodynamic and neurohumoral assessment is needed to direct treatment. When the recommended stepwise workup is followed, hypertension that is truly refractory to treatment is a rare finding.

Algorithms↗
PubMed2000

Screening for renal artery stenosis: which patients? Which test?

If a patient has clinical clues suggestive of renovascular hypertension such as persistently high blood pressure despite a multiple-drug regimen, it may be reasonable to screen him or her using captopril renography, duplex ultrasonography, or magnetic resonance angiography.

Humans↗
PubMed2000

Alpha-blockers and congestive heart failure: early termination of an arm of the ALLHAT trial.

The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) is a large, randomized double-blind study comparing four antihypertensive agents (chlorthalidone, doxazosin, amlodipine, and lisinopril) in hypertensive patients older than 55 years. The doxazosin arm was terminated early, when the trial's safety and monitoring board noted a twofold higher incidence of congestive heart failure in patients receiving doxazosin than in those receiving chlorthalidone (8.13% vs 4.45% at 4 years, P < .001).

Adrenergic alpha-Antagonists↗
PubMed1999

Good news for the older patient with diabetes: added cardiovascular risk reduction.

Both hypertension and diabetes carry an increased risk of cardiovascular and renal disease and are commonly associated conditions. The prevalence of hypertension in the diabetic population is particularly high, approximately 40% in middle-aged patients with type II diabetes mellitus and increases to approximately 60% by age 75. Hypertension increases an already high risk of cardiovascular disease events associated with diabetes mellitus and is also a risk factor for the development of microalbuminuria and retinopathy. Overall mortality from heart disease has declined substantially in the USA in the past 30 years. The extent of this mortality rate decline has been assessed from representative cohorts, the NHANES I survey (1971-1975) and the NHANES I epidemiologic follow-up survey (1982-1984). Both cohorts were followed prospectively for 8 to 9 years. Mortality rates for heart disease and ischemic heart disease in men and women with diabetes have not decreased to the extent that they have for nondiabetic patients. Although these decreases in men with diabetes were smaller than their nondiabetic counterparts, women with diabetes had increases for both total and ischemic heart disease. Three recent clinical trials have addressed the effects of aggressive intervention in diabetes, particularly older patients with type II diabetes mellitus.

Age Factors↗
PubMed1999

Differential effects of morning and evening dosing of nisoldipine ER on circadian blood pressure and heart rate.

The time of administration of once-daily antihypertensive agents may have a significant impact on blood pressure control during awake and sleep periods. Using 24-h ambulatory monitoring, we compared the effects of morning and evening dosing of the long-acting dihydropyridine calcium channel blocker, nisoldipine extended-release (ER), on circadian blood pressure (BP) and heart rate in patients with mild-to-moderate hypertension. After completing a 3-week placebo run-in period, 85 patients were randomized to morning versus evening nisoldipine ER treatment at a fixed 20-mg dose. Patients were treated for 4 weeks, followed by crossover to the alternate dosing regimen for 4 additional weeks. Twenty-four-hour ambulatory monitoring was performed at baseline and at 4 and 8 weeks after randomization. Awake and sleep times were determined by electronic activity recorders (Actigraphy). Similar least-squares (+/-SE) mean changes from baseline in 24-h BP (systolic BP/diastolic BP: -11.9/-7.4 +/- 0.6/0.5 v -11.6/-6.5 +/- 0.6/0.5 mm Hg) and heart rate (1.0/1.7 +/- 0.4/0.4 beats/min) occurred with morning and evening administration, respectively. A significantly greater effect on awake diastolic BP (systolic BP/diastolic BP: -12.6/-8.1 +/- 0.7/0.4 v -11.3/-6.4 +/- 0.7/0.4 mm Hg; P = .16/.01) was observed with morning dosing compared with evening dosing. In addition, small increases in sleep and early morning heart rate were seen with evening compared with morning administration of nisoldipine (sleep, 3.1 +/- 0.4 v 0.4 +/- 0.4 beats/min; P < .001; early morning, 3.5 +/- 0.7 v 0.5 +/- 0.7 beats/min; P = .002). These differential effects on awake BP and sleep heart rate were also observed in patients who had normal (dippers) and elevated (nondippers) BP values during sleep. Appropriate evaluation of the efficacy and safety of long-acting antihypertensive agents is essential when evening administration is being considered. In the present study, the timing of nisoldipine ER administration had no effect on mean changes in BP and heart rate over a 24-h period. However, nisoldipine ER had some differential effects during sleep and awake periods with morning relative to evening dosing.

Antihypertensive Agents↗
PubMed1999

Lovastatin preserves renal function in experimental diabetes.

Although hyperlipidemia has been associated with the progression of glomerulosclerosis, little attention has been directed toward the use of lipid-lowering agents in altering diabetic nephropathy. We tested the hypothesis that lovastatin and the combination of lovastatin and enalapril would preserve renal function in streptozotocin-induced diabetic Wistar rats. Five groups of animals were studied: group 1, nondiabetic (n = 10); group 2, diabetic, insulin only (n = 12); group 3, lovastatin, (15 mg/kg/day, n = 13); group 4, enalapril, (50 mg/L drinking water, n = 10) and group 5, lovastatin plus enalapril, (n = 14). After 8 weeks of treatment, glomerular filtration rate (GFR, insulin clearance) was measured in anesthetized animals. The diabetic group was characterized by a GFR of 0.18 +/- 0.03 ml/min/g of kidney weight (gKW), a blood glucose level of 441 +/- 36 mg/dL, plasma cholesterol and triglyceride levels of 64 +/- 6.0 and 103 +/- 26.0 mg/dL. Lovastatin preserved GFR, 0.52 +/- 0.06 ml/min/gKW compared with the diabetic control subjects (P < 0.05). Enalapril also maintained GFR (0.42 +/- 0.06 ml/min/gKW, P < 0.05). In the lovastatin plus enalapril group, GFR (0.62 +/- 0.05 ml/min/gKW) was greater than in the enalapril group (P < 0.05), but was not different from the lovastatin group. Plasma lipid levels were not altered in any of the groups. Assessment of the kidneys by histology after treatment showed that the mesangial matrix injury score was better in the lovastatin, enalapril, and lovastatin plus enalapril groups compared with the diabetic group (P < 0.05). Lovastatin, enalapril, and lovastatin plus enalapril abrogated the decline in GFR and glomerular injury in diabetic rats. Lovastatin's direct renal protective effect seems to be independent of its lipid-lowering properties.

Animals↗
PubMed1999

Aggressive blood pressure lowering is safe, but benefit is still hard to prove.

In the Hypertension Optimal Treatment (HOT) study, hypertensive patients who were randomly assigned to undergo antihypertensive treatment to achieve a goal diastolic blood pressure of 80 mm Hg or lower did not experience fewer cardiovascular events than did patients who received treatment with goal pressures of 85 or 90 mm Hg. Such aggressive antihypertensive treatment was safe and well tolerated, and did result in fewer cardiovascular events in the subset of patients with diabetes. All patients were randomly assigned to take aspirin 75 mg/day or placebo, and patients in the aspirin group had a 15% lower rate of major cardiovascular events and myocardial infarctions than did patients who received placebo. This finding establishes the efficacy of aspirin in preventing strokes and myocardial infarctions in hypertensive patients.

Adrenergic beta-Antagonists↗