Juice powder concentrate and systemic blood pressure, progression of coronary artery calcium and antioxidant status in hypertensive subjects: a pilot study.

Because micronutrients from plants may have beneficial cardiovascular effects, the hypothesis that an encapsulated juice powder concentrate might affect several measures of vascular health was tested in free living adults at low cardiovascular risk. Blood pressure, vascular compliance, lipid and antioxidant markers, and serial electron beam tomography (to calculate a coronary artery calcium score as a measure of atherosclerosis burden), were monitored in 51 pre-hypertensive and hypertensive subjects over 2 years. By the end of follow-up, systolic and diastolic blood pressure decreased significantly (-2.4 +/- 1.0 mmHg, P < 0.05 and -2.2 +/- 0.6 mmHg, P < 0.001), and large artery compliance improved significantly (1.9 +/- 0.6 ml mmHg(-1) x 100, P < 0.01). The progression of coronary artery calcium score was smaller than expected compared with a historical database (P < 0.001). Laboratory testing showed a significant decrease in homocysteine (P = 0.05), HDL cholesterol (P = 0.025) and Apo A (P = 0.004), as well as a significant increase in beta-carotene, folate, Co-Q10 and alpha-tocopherol (all P < 0.001). The phytonutrient concentrate we utilized induced several favorable modifications of markers of vascular health in the subjects. This study supports the notion that plant nutrients are important components of a heart healthy diet.

Postoperative morbidity in the morbidly obese parturient woman: supraumbilical and low transverse abdominal approaches.

OBJECTIVE: Our purpose was to determine the differences in postoperative morbidity in obese women who had a supraumbilical or a Pfannenstiel incision at cesarean delivery. STUDY DESIGN: A case-control retrospective review was conducted of all patients who were at >150% ideal body weight when undergoing cesarean delivery between 1989 and 1995 by means of either a supraumbilical or a Pfannenstiel incision. Patients were excluded if medical records were unavailable. A total of 15 women who had a supraumbilical incision and 54 who had a low transverse incision were included in the analysis. Antenatal complications were examined, as were age, weight, and training level of the surgeon. Postoperative complications were then compared. RESULTS: The groups were similar in age and antepartum complications. However, mean weight and percentage of ideal body weight in the supraumbilical group were both higher (P <.00001 and P <.0001, respectively), with the supraumbilical group 83 lb heavier on average. No significant differences were seen in any postoperative complication. CONCLUSION: Postoperative morbidity in morbidly obese women undergoing cesarean delivery does not differ between a supraumbilical approach and the low transverse abdominal incision.

Alpha 1-blocker combination therapy for hypertension.

Combination therapy is a cost-effective and rational approach to treatment of severe hypertension and of mild to moderate hypertension that is refractory to monotherapy. The method has several advantages, most notably improved tolerability and enhanced antihypertensive efficacy. Long-term prospective studies are needed to confirm that such agents as calcium channel blockers, ACE inhibitors, and alpha 1 blockers reduce end-organ damage more effectively than do older antihypertensive drugs. However, scientific evidence strongly suggests that reducing risk factors for end-organ damage reduces heart, brain, kidney, and large-artery injury. Alpha 1 blockers appear to be a particularly suitable choice for use in combination regimens. The only class of agents that should be avoided in combination with alpha 1 blockers is central alpha agonists; all other agents act in an additive or synergistic fashion. Unlike diuretics and beta blockers, alpha 1 blockers do not adversely affect serum lipid, glucose, or insulin levels. In fact, alpha 1 blockers may improve these measurements and also counteract the adverse effects of other antihypertensive agents on them. Alpha1-blocker therapy may bring about regression of LVH, and it does not have deleterious effects on disorders that often coexist with hypertension (e.g., gout, chronic obstructive lung disease, peripheral ischemia).

The effects of nonsteroidal anti-inflammatory drugs on blood pressures of patients with hypertension controlled by verapamil.

BACKGROUND: Nonsteroidal anti-inflammatory drugs may attenuate the antihypertensive effects of diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, central alpha-agonists, and other vasodilators. Their effects on the antihypertensive efficacy of calcium channel blockers are inadequately studied in small numbers of patients but appear to be minimal. METHODS: A three-phase, randomized, double-blind, placebo-controlled multicenter study included 162 patients aged 18 to 75 years with essential hypertension. After diastolic blood pressure was controlled to 90 mm Hg or less with once-daily verapamil hydrochloride, patients received ibuprofen, naproxen, or placebo matching capsules for 3 weeks, and blood pressure, heart rate, weight, and adverse effects were evaluated. A general linear model with 95% confidence intervals was used to compare each nonsteroidal anti-inflammatory drug treatment group with the placebo group. RESULTS: No significant differences in sitting, standing, or supine blood pressure were noted with naproxen or ibuprofen compared with placebo. The percentages of patients in each treatment group with increases of 10 mm Hg or more in either systolic or diastolic blood pressure were similar. Statistically significant increases in weight were seen with both nonsteroidal anti-inflammatory drug therapies. Changes in pulse rate were not significant. The incidence of adverse effects was similar across all three treatment groups. CONCLUSIONS: The addition of naproxen or ibuprofen to the treatment of hypertensive patients in whom blood pressure is controlled by once-daily verapamil does not cause an increase in blood pressure. Verapamil may therefore offer considerable advantages in maintaining control of blood pressure in patients who regularly receive nonsteroidal anti-inflammatory drug therapy.

Hypertension and coronary heart disease risk factor management.

The primary goal in the treatment of essential hypertension is to reduce all end organ damage, not simply to reduce blood pressure. Hypertension is associated with an increased risk of cerebrovascular, cardiovascular and renal morbidity and mortality. Pharmacologic therapy has reduced some, but not all, of these complications. To achieve maximal decrease in morbidity and mortality rates in hypertensive related diseases the overall impact of antihypertensive drug therapy on the pathogenesis of damage to each end organ must be considered.

Hypertension and coronary heart disease risk factor management.

The primary goal in the treatment of essential hypertension is to reduce all end organ damage, not simply to reduce blood pressure. Hypertension is associated with an increased risk of cerebrovascular, cardiovascular and renal morbidity and mortality. Pharmacological therapy has reduced some, but not all, of these complications. In order to achieve maximal decrease in morbidity and mortality in hypertensive related diseases the overall impact of antihypertensive drug therapy on the pathogenesis of damage to each end organ must be considered. The pharmacological therapy of mild hypertension has reduced complications of most pressure related (arteriolar) damage such as cerebrovascular accidents, congestive heart failure, and some cases of chronic renal failure, but atherosclerotic complications, coronary heart disease, angina, myocardial infarction and sudden death have not been convincingly reduced. A more pathophysiologic and individualized approach to the treatment of hypertension is recommended in place of the traditional stepped care approach which has primarily emphasized diuretics and beta blockers as initial therapy. This new approach in the subsets of hypertension, which is based on eight parameters: (1) Pathophysiology; (2) Haemodynamics; (3) End organ damage; (4) Concomitant medical diseases and problems; (5) Demographics; (6) Adverse effects of drugs and quality of life; (7) Compliance with medication regimen; (8) Total health care costs: direct and indirect costs. Hypertension is not just a disorder of increased intraarterial pressure, but in fact, a syndrome of commonly associated genetic and/or acquired abnormalities including dyslipidaemia, insulin resistance, impaired glucose tolerance, central obesity, renal abnormalities, structural abnormalities of smooth muscle, and abnormal cellular cation transport or membranopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Transdermal clonidine as an adjunct to nifedipine-GITS therapy in patients with mild-to-moderate hypertension.

Calcium channel blockers and central alpha-agonists are among the classes of antihypertensive drugs that yield the most favorable overall effects on risk factors for hypertension-related end-organ damage. An open-label prospective trial in 42 patients with a mean baseline blood pressure of 144/102 mm Hg sought to assess the usefulness of adjunctive treatment with transdermal clonidine (0.1 to 0.3 mg/day) in patients responding inadequately to nifedipine--gastrointestinal therapeutic system (GITS) (30 to 60 mg/day) monotherapy. Thirty-nine patients who failed to reach the goal of a seated mean diastolic blood pressure of < 90 mm Hg when treated only with once-a-day nifedipine-GITS entered a transdermal clonidine (once a week) titration phase followed by an 8-week maintenance course of the two drugs combined. The 35 patients completing this last phase responded with a mean seated diastolic blood pressure of 127/87 mm Hg. Only six patients required the highest dose of clonidine for control. A 97% compliance rate with the transdermal medication contrasted with a compliance rate of only 73% for the oral nifedipine. Two of three patients who had contact dermatitis after wearing a transdermal clonidine patch withdrew from the trial prematurely; other minor side effects required no interruption of therapy. The nifedipine-clonidine combination not only achieved blood pressure control in these patients but may prove advantageous in combining the protective effects of the two agents against complications of the hypertensive syndrome.

Alpha blockers: an effective extension to your patients' risk reduction program.

This symposium discusses a rapidly changing philosophy in how to manage hypertension. Many committees in the United States and Canada over the years have tried to make the treatment of hypertension simple. And in their goal to do that, they have made it difficult and led many down a primrose path with somewhat narrow vision. One famous British physician in 1931 said, "the greatest danger to man with high blood pressure lies in its discovery since some fool is certain to try to reduce it." There is a lot of credence to that rule.

The management of hypertension and associated risk factors for the prevention of long-term cardiac complications.

The management of essential hypertension can no longer be directed toward an isolated reduction in arterial pressure. Optimal reduction in the risk factors associated with hypertension and cardiovascular disease hopefully will reduce coronary heart disease, angina, fatal and nonfatal myocardial infarction, left ventricular hypertrophy, congestive heart failure, and sudden death. Hypertension is a genetic and acquired syndrome that consists of dyslipidemia, insulin resistance and carbohydrate intolerance, central obesity, renal abnormalities, structural abnormalities of smooth muscle, and ion transport abnormalities (membranopathy). The selection of pharmacologic agents should improve the components of the hypertensive syndrome by utilizing the "subsets of hypertension approach" to treatment.

Exercise and hypertension. Maximizing the benefits in patients receiving drug therapy.

Aerobic exercise may prevent hypertension and reduce blood pressure and mortality in hypertensive patients and those at high risk for coronary artery disease. Supervised aerobic exercise at an intensity of 70% to 80% of maximal aerobic capacity is recommended to achieve cardiovascular conditioning and other health benefits. When antihypertensive drug therapy is required, physicians should choose an agent that has favorable secondary effects, including hemodynamic responses to exercise. The most favorable effects are achieved with calcium channel blockers, angiotensin-converting enzyme inhibitors, alpha blockers, and central alpha agonists. The effects of diuretics are less desirable, and beta blockers should be a last choice for hypertensive patients who are physically active.

New insights and approaches to reduce end-organ damage in the treatment of hypertension: subsets of hypertension approach.

Antihypertensive therapy should be directed toward reduction of all end-organ damage including congestive heart failure, left ventricular hypertrophy, coronary heart disease, myocardial infarction, cerebrovascular accident, and chronic renal failure. The Subsets of hypertension approach is based on pathophysiology, hemodynamics, risk factor reduction for end-organ damage, concomitant diseases and problems, demographics, adverse effects on quality of life, compliance, and total health care costs. This approach provides a more individualized and logical treatment of the hypertensive syndrome and addresses the metabolic and structural abnormalities that are present.

Effects of nifedipine GITS and atenolol monotherapy on serum lipids, blood pressure, heart rate, and weight in mild to moderate hypertension.

Forty-nine patients, with ages ranging from eighteen to seventy years and with mild to moderate primary hypertension (sitting diastolic blood pressure of greater than or equal to 95 mmgH and less than or equal to 115 mmHg) were randomized into a twenty-one-week, double-blind, prospective study to determine the effects of monotherapy of nifedipine GITS (gastrointestinal therapeutic system) versus atenolol on serum lipids, lipid subfractions, apolipoproteins, (apo), and blood pressure (BP). Nifedipine GITS and atenolol significantly reduced blood pressure, but nifedipine GITS reduced sitting and standing systolic BP significantly more than atenolol (p = .001). Sitting and standing heart rate decreased significantly (p = 0.001) during atenolol therapy but did not change significantly during nifedipine GITS therapy. Atenolol increased weight (mean change + 2.2 lb; p = 0.011), but nifedipine GITS decreased weight (mean change - 2.4 lb; p = 0.07). Nifedipine GITS had a more favorable effect on the lipid profile. High density lipoprotein cholesterol (HDL-C) and HDL2 subfractions were increased significantly (p = .001) as were apo A1 (p = 0.037) and apo A2 (p = 0.025). Nifedipine GITS increased HDL3 (NS), reduced triglycerides (TG) (NS), and had no significant effect on total cholesterol (TC) low density lipoprotein cholesterol (LDL-C) and apo B. Atenolol significantly increased serum total cholesterol (p = 0.039) and HDL-C and HDL2 (p = 0.049 and 0.048 respectively). Atenolol increased TG (NS) and apo B (NS) with little change in apo A1 and apo A2. It is concluded that nifedipine GITS had equal or better antihypertensive efficacy than atenolol and had a more favorable effect on the lipid profile. These effects may offer advantages in reducing CHD risk.

Hypertension strategies for therapeutic intervention and prevention of end-organ damage.

The goals in the treatment of hypertension have been outlined previously. The antihypertensive drugs should achieve as many of these criteria as possible. 1. Efficacious as monotherapy in more than 50% of all patients (demographics) 2. 24-hour blood pressure control during all activities 3. Once per day dosing 4. Hemodynamically logical and effective: reduces SVR, improves arterial compliance, preserves CO and maintains perfusion to all vital organs 5. Lack of tolerance or pseudotolerance: no reflex volume retention or stimulations of neurohumoral mechanisms 6. Favorable biochemical and metabolic effects 7. Reverses the structural, vascular smooth muscle, cardiac hypertrophy, LVH, and improves systemic and diastolic compliance, LV contractility and function, and reduces ventricular ectopy if present 8. Reduces all end-organ damage: cardiac, cerebrovascular, renal, retinal and large artery 9. Maintains normal hemodynamic response to aerobic and anerobic exercise 10. Low incidence of side effects and good quality of life 11. Good compliance with drug regimen 12. Good profile in concomitant diseases or problems The drugs that come closest to these characteristics include CCB, ACEI, CAA, and alpha blockers. All of these agents are effective as monotherapy and should be given as initial therapy to the maximum dose shown in Table 10 or until the advent of side effects, whichever occurs first. Combination therapy should be the next step, using the principal of go low, go slow, using additive or synergistic drug combinations. Therapy should be individualized using the subsets of hypertension approach: Diuretics in particular, especially high-dose diuretics, and BB to a lesser extent, should be reserved as second- or third-line drugs and used for specific indications and in the lowest dose possible to achieve clinical results. For example, diuretics would be reserved for volume overload states, systolic CHF, and volume-resistant hypertension. Beta blockers would be reserved for patients after a Q-wave myocardial infarction, those with obstructive angina, specific cardiac arrhythmias, and other like conditions. Long-term, prospective, clinical trials will be needed to confirm that CCB, ACEI, CAA, and alpha blockers reduce end-organ damage more effectively than diuretics, BB, direct vasodilators, and older antihypertensive drugs. Until then, one must rely on scientific evidence, discussed here, that strongly suggests that reduction in risk factors for end-organ damage will reduce the end-organ damage in heart, brain, kidney, and large arteries.

Nonsteroidal anti-inflammatory drugs and antihypertensives.

Approximately 60 million people in the United States have hypertension (BP greater than or equal to 140/90 mm Hg), 40 million have arthritis clinically suitable for nonsteroidal anti-inflammatory drug (NSAID) therapy, and millions take NSAIDs for nonarthritic conditions, creating considerable potential for concomitant administration of NSAIDs and antihypertensive agents. It is estimated that more than 20 million people are on concurrent therapy. Most NSAIDs produce mild elevations of normal blood pressure levels and can partially or completely antagonize the effects of many antihypertensive drugs. The effect on blood pressure can vary from no effect to hypertensive crisis. In pooled studies, the average increase in mean arterial pressure was 10 mm Hg, and duration was short-lived or chronic. Significant interactions occur in about 1% of patients per year. The risk is greatest in the elderly, blacks, and patients with low-renin hypertension. NSAIDs may block the antihypertensive effects of thiazide and loop diuretics, beta-adrenergic blockers, alpha-adrenergic blockers, and angiotensin-converting enzyme inhibitors. No interactions have been reported with centrally acting alpha agonists or the calcium channel blockers. The mechanism of the hypertensive effects of NSAIDs seem primarily related to their ability to block the cyclo-oxygenase pathway of arachidonic acid metabolism, with a resultant decrease in prostaglandin formation. The prostaglandins are important in normal modulation of renal and systemic vascular dilatation, glomerular filtration, tubular secretion of salt and water, adrenergic neurotransmission, and the renin-angiotensin-aldosterone system. Blockade of salutary effects of prostaglandins by NSAIDs results in a complex series of events culminating in attenuation of the effects of many antihypertensive agents. High-risk patients treated with NSAIDs should be identified and have blood pressure, renal function, and serum potassium frequently monitored.

The effects of clonidine hydrochloride versus atenolol monotherapy on serum lipids, lipid subfractions, and apolipoproteins in mild hypertension.

The study objective was to determine the effects of monotherapy with clonidine and atenolol versus placebo on serum lipids, apolipoproteins, and blood pressure in patients with mild primary hypertension. The protocol comprised a double blind, randomized, placebo-controlled 5-month prospective study carried out in an outpatient general internal medicine clinic in a university medical center. There were 92 patients ages 18 to 70, with mild primary hypertension (sitting diastolic blood pressure of greater than 90 mm Hg and less than 105 mm Hg) without significant cardiac, renal, cerebrovascular, hepatic, neoplastic, or hematologic disorders. Patients with severe hyperlipidemia or peripheral vascular disease were also excluded. All factors known to effect serum lipids were held constant throughout the study (i.e., diet, weight, exercise, caffeine, tobacco). Atenolol and clonidine significantly reduced blood pressure when compared with placebo. Atenolol caused significant increases in serum triglycerides and apolipoprotein B (p less than 0.05) and significant reductions in high-density lipoprotein-cholesterol, apolipoproteins A-I and A-II (p less than 0.05). Atenolol also induced a significant adverse effect on all lipid ratios, increasing total cholesterol/high density lipoprotein-cholesterol, low density lipoprotein-cholesterol/high density lipoprotein-cholesterol, apolipoprotein B/apolipoprotein A-I and apolipoprotein B/apolipoprotein A-II ratios and decreasing low density lipoprotein-cholesterol/apolipoprotein-B ratio (p less than 0.05). Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins. Clonidine did not significantly alter any of the lipid ratios.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathophysiology of shock.

Shock is an acute widespread reduction in effective tissue perfusion that invokes an imbalance of oxygen supply and demand, anaerobic metabolism, lactic acidosis, cellular and organ dysfunction, metabolic abnormalities, and, if prolonged, irreversible damage and death. The pathophysiologic events in the various types of shock are different and complex with hemodynamic and oxygenation changes, alterations in the composition of the fluid compartments, and various mediators. Shock results from a change in one or a combination of the following: intravascular volume, myocardial function, systemic vascular resistance, or distribution of blood flow. The clinical types of shock include hypovolemic, cardiogenic, distributive (septic), and obstructive. An understanding of the pathophysiologic changes, rapid diagnosis, appropriate monitoring, and appropriate therapy can reduce the high morbidity and mortality in shock states.

New insights and new approaches for the treatment of essential hypertension: selection of therapy based on coronary heart disease risk factor analysis, hemodynamic profiles, quality of life, and subsets of hypertension.

The pharmacologic therapy of mild primary hypertension (diastolic blood pressure less than 105 mm Hg) has effectively reduced hypertensive arteriolar end organ disease such as cerebrovascular accidents, congestive heart failure, and nephropathy, but there has been no convincing evidence that coronary heart disease (CHD) or its complications, acute myocardial infarction or angina, have been reduced. The risks of therapy with certain antihypertensive drugs may outweigh their treatment benefits as it relates to CHD. The optimal treatment strategy should be to reduce all CHD risk factors, reverse the hemodynamic abnormalities present by lowering the systemic vascular resistance (SVR), preserving cardiac output (CO) and perfusion, and to select the best antihypertensive drug for concomitant medical diseases or problems while maintaining a good quality of life. Antihypertensive drugs that have favorable or neutral effects on CHD risk factors include alpha blockers, calcium channel blockers, central alpha agonists, and angiotensin-converting enzyme inhibitors. On the other hand, diuretics and beta blockers without intrinsic sympathomimetic activity have unfavorable effects on many CHD risk factors. Baseline and serial evaluation of the effects of these drugs on serum lipids, lipid subfractions, glucose, uric acid, electrolytes, exercise tolerance, left ventricular hypertrophy, blood pressure, SVR, CO, perfusion, concomitant diseases, and side effects is necessary to evaluate overall cardiovascular risk.