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Barry J Materson

Publications and source records attributed to Barry J Materson.

15 recordsLinked to original sources
PubMed2006

Elevated platelet P-selectin expression and platelet activation in high risk patients with uncontrolled severe hypertension.

BACKGROUND: Uncontrolled severe hypertension is associated with alarming rates of cardiovascular events but the mechanisms of vascular injury are not well understood. Recent investigative interest has focused on platelet activation and platelet P-selectin (CD62P) as direct mediators of vascular inflammation and injury. We investigated the association of extreme blood pressure (BP) elevation with platelet P-selectin and fibrinolytic markers in high risk patients with severe hypertension. METHODS: Cross-sectional comparison of platelet CD62, tissue plasminogen activator antigen (tPA), and plasminogen activator inhibitor-1 activity (PAI-1) among 3 BP groups: untreated severely hypertensive patients (SHT; n=18), untreated mildly hypertensive patients (MHT; n=19), and normotensive controls (NT; n=16). RESULTS: Platelet CD62 was greatest in SHT (p=0.00008) and showed a strong correlation with both systolic (p=0.0002, r=0.52) and diastolic (p=0.0003, r=0.52) BP. tPA was greater in SHT than MHT or NT (ANOVA; p=0.02) and correlated with diastolic BP but not SBP. PAI-1 did not correlate with either SBP or DBP but was related to body mass index, diabetes, and dyslipidemia. CONCLUSIONS: Platelet CD62 demonstrated a strong and graded association with both systolic and diastolic BP that persisted in the presence of multiple concomitant risk factors. The association of BP with CD62P was stronger than with either PAI-1 or tPA-Ag. Platelet activation and platelet CD62 increase in a BP-dependent manner and this relationship persists at extreme levels of BP. Platelet activation and platelet CD62 may participate in the accelerated target organ injury observed in high risk patients with severe hypertension.

Blood Pressure↗
PubMed2006

Nonpharmacologic therapy for hypertension: does it really work?

Nondrug therapy of hypertension really does work but requires strong motivation by both patient and physician. In addition to global health benefits, prescription of weight loss, exercise, moderation of salt and alcohol intake, Dietary Approach to Stop Hypertension (DASH) eating plan, and tobacco avoidance can decrease the risk for normotensive and prehypertensive patients of developing fixed hypertension. Initiating and maintaining a healthy lifestyle may be sufficient to avoid pharmacologic therapy for some patients and is a valuable adjunct to drug therapy for most. Blood pressure lowering can be achieved by weight reduction (5-20 mm Hg/10 kg), DASH eating plan (8-14 mm Hg), dietary sodium reduction (2-8 mm Hg), increased physical activity (4-9 mm Hg), and moderation of alcohol consumption (2-4 mm Hg). Combination of two or more modalities may have an additive benefit. Cessation of tobacco abuse not only has global health benefits, but may reduce blood pressure.

Alcohol Drinking↗
PubMed2005

David Ayman, MD: an early investigator of clinical hypertension.

Dr. David Ayman (1901-1986) was an astute clinician and observer who challenged medical dogma by performing placebo-controlled studies and by meticulous measurement of blood pressure under standardized conditions. He demonstrated that almost all drugs reported to have an antihypertensive effect in the early 20th century had achieved nothing more than placebo response. He noted the marked variability of blood pressure and devised methods to reduce that variability. These observations led to his publications concerning what is now known as "white coat" or office hypertension. He determined blood pressure personally in 1524 members of 277 families over three generations and made observations on the hereditary nature of hypertension that countered the single-gene thinking of the day. His work is proof that clinical inquisitiveness, hard work, and the courage to challenge conventional wisdom can result in significant contributions to medicine and science.

Biomedical Research↗
PubMed2005

Treating stage 2 hypertension.

The prevalence of hypertension increases with advancing age, due primarily to increases in systolic blood pressure. Systolic hypertension is the most common form of hypertension in individuals over 50 years of age and reflects pathologic decreases in arterial compliance. Systolic blood pressure elevation is a more important risk factor for cardiovascular disease than is diastolic blood pressure elevation. Stage 2 hypertension, defined as blood pressure > or =160/100 mm Hg, is often found in older persons, who are at highest risk for cardiovascular events. In this clinical review, hypertension experts utilize a case study to provide a paradigm for treating older patients with stage 2 hypertension.

Age Factors↗
PubMed2003

Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.

The National High Blood Pressure Education Program presents the complete Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Like its predecessors, the purpose is to provide an evidence-based approach to the prevention and management of hypertension. The key messages of this report are these: in those older than age 50, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease (CVD) risk factor than diastolic BP; beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg; those who are normotensive at 55 years of age will have a 90% lifetime risk of developing hypertension; prehypertensive individuals (systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg) require health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and CVD; for uncomplicated hypertension, thiazide diuretic should be used in drug treatment for most, either alone or combined with drugs from other classes; this report delineates specific high-risk conditions that are compelling indications for the use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); two or more antihypertensive medications will be required to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg) for patients with diabetes and chronic kidney disease; for patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using two agents, one of which usually will be a thiazide diuretic, should be considered; regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan. Positive experiences, trust in the clinician, and empathy improve patient motivation and satisfaction. This report serves as a guide, and the committee continues to recognize that the responsible physician's judgment remains paramount.

Adult↗
PubMed2003

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report.

"The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure" provides a new guideline for hypertension prevention and management. The following are the key messages(1) In persons older than 50 years, systolic blood pressure (BP) of more than 140 mm Hg is a much more important cardiovascular disease (CVD) risk factor than diastolic BP; (2) The risk of CVD, beginning at 115/75 mm Hg, doubles with each increment of 20/10 mm Hg; individuals who are normotensive at 55 years of age have a 90% lifetime risk for developing hypertension; (3) Individuals with a systolic BP of 120 to 139 mm Hg or a diastolic BP of 80 to 89 mm Hg should be considered as prehypertensive and require health-promoting lifestyle modifications to prevent CVD; (4) Thiazide-type diuretics should be used in drug treatment for most patients with uncomplicated hypertension, either alone or combined with drugs from other classes. Certain high-risk conditions are compelling indications for the initial use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); (5) Most patients with hypertension will require 2 or more antihypertensive medications to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg for patients with diabetes or chronic kidney disease); (6) If BP is more than 20/10 mm Hg above goal BP, consideration should be given to initiating therapy with 2 agents, 1 of which usually should be a thiazide-type diuretic; and (7) The most effective therapy prescribed by the most careful clinician will control hypertension only if patients are motivated. Motivation improves when patients have positive experiences with and trust in the clinician. Empathy builds trust and is a potent motivator. Finally, in presenting these guidelines, the committee recognizes that the responsible physician's judgment remains paramount.

Adrenergic alpha-Agonists↗
PubMed2002

Blood pressure-independent impact of antihypertensive agents on cardiovascular and renal disease.

Reduction of elevated blood pressure clearly protects against target organ damage, but the different targets do not necessarily benefit to the same degree. There is considerable debate over whether or not there is a drug-specific benefit above and beyond that conferred by blood pressure reduction alone. We performed a Medline search to identify recent randomized clinical trials including 300 or more patients who were followed for at least 2 years. We critically reviewed these papers to find like trials for comparisons. There was too much dissimilarity to perform a meaningful meta-analysis. We found that the literature does not support a definitive conclusion either in favor of or against an overall drug-specific protective effect. However, by grouping like trials, it is possible to support an additional protective effect by angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on reducing the rate of decline in renal function and in reducing proteinuria.

Antihypertensive Agents↗
PubMed2002

Effects of severe, uncontrolled hypertension on endothelial activation: soluble vascular cell adhesion molecule-1, soluble intercellular adhesion molecule-1 and von Willebrand factor.

OBJECTIVES: The molecular mechanisms whereby severe, uncontrolled hypertension (SHT) is translated into acute vascular target organ dysfunction have not been completely defined. We sought to determine whether SHT is associated with pressure-dependent endothelial activation as assessed by soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1) and von Willebrand Factor (vWF). METHODS: We determined sVCAM-1, sICAM-1 and vWF in three groups: (i) untreated patients referred specifically for treatment of SHT [diastolic blood pressure (DBP) > or = 120 mm Hg; n = 24]; (ii) untreated patients with established mild hypertension (MHT; DBP 95-100 mmHg; n = 19); and (iii) normotensive volunteers (DBP < or = 90; n = 16). RESULTS: By analysis of variance, sVCAM-1 (P = 0.002), sICAM-1 (P = 0.02) and vWF (P = 0.009) were greater in SHT and MHT than in normotensives but did not differ between SHT and MHT. We observed a significant positive correlation between blood pressure and soluble activation markers at lower blood pressures (normotensives and MHT considered together) that was not present in SHT. CONCLUSIONS: Even mild elevation of blood pressure may be sufficient to activate the expression of adhesion molecules. Mechanisms other than the endothelial expression of adhesion molecules may be important in mediating the accelerated target organ injury produced by SHT in humans. Concentrations of soluble adhesion molecules and vWF may depend more strongly upon factors in the hypertensive microenvironment other than the absolute level of blood pressure.

Adult↗
PubMedDate not supplied

Response to six classes of antihypertensive medications by body mass index in a randomized controlled trial.

Blood pressure increases with increasing body mass index (BMI) and BMI is linearly related to blood pressure in population studies. Obesity has been said to cause resistance to antihypertensive medications. We compared short-term and 1-year blood pressure response by BMI category and weight change with hydrochlorothiazide, atenolol, diltiazem-SR, captopril, clonidine, prazosin, or placebo in 1292 male veterans. Drug doses were titrated to achieve goal diastolic blood pressure <90 mm Hg over 4-8 weeks. Patients who achieved goal blood pressure were maintained for 1 year. BMI did not predict change in systolic, diastolic or pulse pressures during titration for any drug. At 1 year obese patients (BMI >30) were 2.5 times more likely to have diastolic blood pressure controlled by atenolol than normal weight (BMI <27) patients (p=0.01). Only prazosin patients gained weight: 1.7 lb (end-titration, p<0.0001; 1-year, p=0.02). Obesity does not appear to cause resistance to antihypertensive medications.

Aged↗