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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:New insights and approaches to reduce end-organ damage in the treatment of hypertension: subsets of hypertension approach. 157 52

Hypertension is a major risk factor for cardiovascular diseases, including coronary artery disease (CAD), stroke, left ventricular hypertrophy (LVH), congestive heart failure, peripheral vascular disease, renal failure, and aortic aneurysms. It is also a potent promoter of atherosclerosis. Observational studies have shown a linear relationship between a wide range of blood pressures and the risk for CAD and stroke. Clinical trials have indicated that hypertension reduction leads to the predicted reduction in stroke incidence, but that CAD incidence is affected to a lesser extent than predicted. The modest effect of traditional antihypertensive drugs on CAD may be due to several factors, including failure to reverse well-established coronary atherosclerosis, particularly if multiple risk factors are not reduced as well. Metabolic side effects of antihypertensive drugs or excessive lowering of blood pressure leading to inadequate myocardial perfusion, especially in patients with increased left ventricular (LV) mass, also may play important roles. Hypertension is a major cause of renal failure, particularly in black males, but control of the hypertension does not necessarily prevent deterioration of renal function. Increased glomerular pressure is thought to play a causative role in the development of renal failure in hypertensive and diabetic patients. Antihypertensive drugs may have a direct effect on the arterial wall, which may be independent of their antihypertensive action. Beta-adrenergic blockers, calcium antagonists, and angiotensin-converting enzyme (ACE) inhibitors inhibit the development of vascular lesions in response to hypercholesterolemia or to iatrogenic balloon injury, but the clinical importance of these observations remains to be determined.
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PMID:Vascular effects of systemic hypertension. 157 75

Mexiletine is thought to exert minimal negative inotropic actions, but its effects have not been evaluated in patients with severe congestive heart failure. The haemodynamic response to an oral loading dose of mexiletine (400 mg) was assessed in 20 patients with severe chronic heart failure. Mexiletine caused marked haemodynamic deterioration, with stroke work index decreasing in 18 of the patients. Two hours after mexiletine, mean cardiac and stroke work indexes decreased by 15% and 25%, respectively (both P less than 0.001), while heart rate and systemic vascular resistance increased by 10% and 20%, respectively (both P less than 0.05). Simultaneously, left ventricular filling pressure and right atrial pressure increased by 37% and 36%, respectively (both P less than 0.001), but mean arterial pressure did not change. Furthermore, clinical deterioration, with onset of dyspnoea at rest, developed in five patients at the time of peak haemodynamic effect. Plasma mexiletine concentrations were within the accepted therapeutic range of 0.5 to 2.0 micrograms.ml-1 in all but two of the patients. Nevertheless, the plasma concentration was an important determinant of haemodynamic effect. The stroke work index decreased by 38% in the patients with a mexiletine level above the median value of 1.3 micrograms.ml-1 (range 25 to 56%), but only 13% (range 15 to 43) in patients with lower plasma concentrations. In conclusion, although mexiletine may cause cardiodepressant effects in any patient with severe left ventricular dysfunction, dosing which results in a high (but still therapeutic) plasma level is more likely to cause haemodynamic deterioration.
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PMID:Cardiodepressant effects of mexiletine in patients with severe left ventricular dysfunction. 157 27

Milrinone is known to have beneficial haemodynamic and clinical effects in patients with congestive heart failure. An investigation into the safety and efficacy of milrinone in patients following heart surgery was undertaken by the European Milrinone Multicentre Trial Group. This paper reports the efficacy, the effects on left heart function, and the adverse events in the study. Ninety-nine adult patients, 61 coronary artery bypass grafting (CABG), 33 valve surgery (VS), and five CABG+VS were studied. Three dosage regimens were investigated sequentially. All patients received a loading dose of intravenous milrinone 50 micrograms kg-1 over 10 min, followed by an infusion of either 0.375 micrograms kg-1 min-1, 0.5 microgram kg-1 min-1, or 0.75 microgram kg-1 min-1 over 12 h. The groups were comparable for age, weight, and surface area; however, in the group receiving 0.5 microgram kg-1 min-1 there were more females and patients undergoing mitral valve surgery. Efficacy criteria of an increase in cardiac index of 30% and/or a decrease in mean pulmonary capillary wedge pressure of 25% were fulfilled by 77 patients at the 60-min measurement. Of the remaining 22 patients, 17 were clinically satisfactory and fulfilled efficacy criteria at some time during the study. At 15 min and 60 min there was a dose-related decrease in systolic and diastolic arterial pressure; however, there was no significant difference in the mean arterial pressure measurements. In all groups there was an improvement in cardiac index at 15 min following the start of milrinone, which was sustained during and up to 4 h after the infusion. This was closely associated with changes in stroke volume index and systemic vascular resistance, and not solely due to a change in heart rate.
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PMID:Milrinone in the treatment of low output states following cardiac surgery. 160 Sep 64

Epidemiological studies confirm that hypertension, particularly systolic hypertension, is a major cardiovascular and cerebrovascular risk factor in the elderly. Clinical trials convincingly demonstrate the benefits of treating both diastolic hypertension in persons up to age 80 years, and isolated systolic hypertension in persons over age 60. The European Working Party on Hypertension in the Elderly (EWPHE) trial showed that reducing elevated blood pressure resulted in a 27% reduction in overall cardiovascular mortality, as well as significant reductions in severe congestive heart failure, strokes and deaths from myocardial infarction. The Systolic Hypertension in the Elderly Program (SHEP) also reported a 36% reduction in the incidence of stroke and decreases in cardiovascular events, including myocardial infarctions, when hypertension was treated. Additional EWPHE data suggest that the optimal level of systolic blood pressure control is between 146 and 158mm Hg, while patients in the SHEP trial with isolated systolic hypertension derived benefits at an average treated systolic blood pressure of 143mm Hg. Elderly study populations comply well with antihypertensive treatment, and blood pressure can be safely lowered with simple drug regimens. Nonpharmacological treatment is recommended for initial treatment of mild diastolic hypertension and isolated systolic hypertension, and as adjuvant treatment with medication. Since all antihypertensive agents can lower blood pressure in the elderly, therapy should be chosen based on its potential for side effects, drug interactions and effects on concomitant disease states.
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PMID:Epidemiology of hypertension in the elderly. 160 54

Hypertension should be detected and treated early in diabetic patients. It markedly affects the morbidity and mortality of diabetic individuals as a result of both atherosclerosis and microvascular disease. Antihypertensive treatment is an effective tool in slowing the progression of early and advanced diabetic nephropathy. No prospective studies have addressed the effects of antihypertensive regimens on the incidence of congestive heart failure, stroke, and coronary artery disease in large groups of diabetic patients. Such studies are urgently needed. Special consideration should be given to the effects of antihypertensive drugs on glycemic control and the lipid profile of the diabetic patient. Because hyperinsulinemia (and insulin resistance) have been advocated as hypertensive and atherosclerotic risk factors, the effects of antihypertensive drugs on insulin action and plasma insulin levels may become an important element in the selection an antihypertensive agent. More information, however, is needed in these areas. ACE inhibitors, calcium channel blockers, and alpha-adrenergic blockers probably offer a more favorable metabolic profile as compared with diuretics and beta-blockers. The former agents should be used as initial drugs in most clinical settings.
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PMID:Management of hypertension in diabetes. 161 71

To examine the effects of beta-adrenergic blockade on neurohormonal activation in patients with congestive heart failure, 15 men had assessments of hemodynamics and supine peripheral renin and norepinephrine levels before and after 3 months of oral therapy with bucindolol, a nonselective beta antagonist. At baseline, plasma renin activity did not correlate with any hemodynamic parameter. However, norepinephrine levels had a weak correlation with left ventricular end-diastolic pressure (r = 0.74, p less than 0.01), stroke volume index (r = 0.61, p less than 0.02) and pulmonary vascular resistance (r = 0.54, p less than 0.05). Plasma renin decreased with bucindolol therapy, from 11.6 +/- 13.4 to 4.3 +/- 4.1 ng/ml/hour (mean +/- standard deviation; p less than 0.05), whereas plasma norepinephrine was unchanged, from 403 +/- 231 to 408 +/- 217 pg/ml. A wide diversity of the norepinephrine response to bucindolol was observed with reduction of levels in some patients and elevation in others. Although plasma norepinephrine did not decrease, heart rate tended to decrease (from 82 +/- 20 vs 73 +/- 11 min-1, p = 0.059) with beta-adrenergic blockade, suggesting neurohormonal antagonism at the receptor level. No changes in I-123 metaiodobenzylguanidine uptake occurred after bucindolol therapy, suggesting unchanged adrenergic uptake of norepinephrine with beta-blocker therapy. Despite reductions in plasma renin activity and the presence of beta blockade, the response of renin or norepinephrine levels to long-term bucindolol therapy did not predict which patients had improved in hemodynamic status (chi-square = 0.37 for renin, 0.82 for norepinephrine).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of bucindolol on neurohormonal activation in congestive heart failure. 167 Sep 2

Quinidine causes vasodilation directly and by inhibition of adrenergic vasoconstriction, but it also exerts negative inotropic activity. Although this drug is often administered to patients with severe congestive heart failure, the net consequences of these opposing actions have not been evaluated in such patients. The hemodynamic and neurohormonal response to oral quinidine (600 mg) in 19 patients with severe chronic heart failure was therefore determined. Vasodilation was the predominant effect of quinidine, with reductions in mean arterial, left ventricular filling and right atrial pressures of -9% (confidence interval [CI] -5 to -13), -8% (CI -19 to 3), -15% (CI -26 to -4), respectively. The quinidine-induced vasodilation increased plasma norepinephrine and epinephrine concentrations by 44% (CI +17 to +72) and 47% (CI +2 to +91), respectively. No change in cardiac performance was noted, with the cardiac index slightly increased (+10%, CI +2 to +17) and stroke work index unchanged (0%, CI -11 to +11) after quinidine. Although the mean serum quinidine concentration was within the therapeutic range or lower in all patients, the serum quinidine concentration and the change in mean arterial pressure did correlate (r2 = 0.64). In conclusion, vasodilation is the predominant hemodynamic effect of oral quinidine in patients with congestive heart failure. However, potential adverse effects may be caused by consequent neurohormonal activation.
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PMID:Hemodynamic and neurohormonal effects of quinidine in patients with severe left ventricular dysfunction secondary to coronary artery disease or idiopathic dilated cardiomyopathy. 167 82

Ibopamine is an orally active derivative of dopamine (DA) which metabolizes to its active form, epinine. Epinine is one of the few catecholamines that possess dopaminergic--DA1 and DA2--activity, alpha 1, alpha 2, beta 1, and beta 2 activity, with indirect sympathomimetic action of dopamine. Ibopamine increased positive dP/dt, stroke volume, aortic blood flow, renal blood flow, and diuresis in animals. In healthy volunteers and patients with heart failure, a single oral dose of ibopamine showed primary vasodilating action (postsynaptic DA1 activity and presynaptic DA2 activity). Following a single oral dose of 100 or 200 mg of ibopamine, the plasma concentration of epinine reached its peak within 30 minutes, and declined rapidly so that concentration was not detectable after 1.5-3 hours. Pharmacokinetics and hemodynamic effects in congestive heart failure patients are also discussed.
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PMID:Clinical pharmacology of ibopamine. 167 50

The acute efficacy of rapid loading of oral long-acting enalapril in congestive heart failure remains to be established. We evaluated the efficacy of this treatment modality in 22 patients with chronic congestive heart failure N.Y.H.A. functional class ranging from II-IV with Creatinine level less than 2 mg/dl. Following hemodynamic evaluation, there was significant favorable change in the left ventricular functional curve. Moreover, acute hemodynamic assessment showed a significant reduction in pulmonary capillary wedge pressure from 19.2 +/- 4.8 to 17.2 +/- 4.7 mmHg (p less than 0.005) and an increases in stroke volume index from 28.3 +/- 9.2 to 33.1 +/- 7.5 ml/m (p less than 0.005). After rapid enalaprilization, blood pressure fell from 127 +/- 21/78 +/- 15 to 108 +/- 21/68 +/- 15 mmHg (p less than 0.005), systemic vascular resistance from 1725 +/- 602 to 1370 +/- 376 dyne.sec.cm-5 (p less than 0.05) and pulmonary vascular resistance from 262 +/- 19 to 218 +/- 65 dyne.sec.cm-5 (p less than 0.05). Cardiac index rose significantly from 2.43 +/- 0.62 to 2.60 +/- 0.50 l/min/m2 (p less than 0.05). In terms of neurohumoral assessments, there was a significant inhibition of the renin-angiotensin-aldosterone system. Aldosterone fell from 21.3 +/- 13.4 to 9.4 +/- 8.0 ng/dl and plasma renin activity rose from 3.3 +/- 4.6 to 11.3 +/- 11.0 ng/nl/hr (p less than 0.005). Plasma norepinephrine and epinephrine levels were found to have significant reduction in addition to antidiuretic hormone concentration. During short-term trial, left ventricular ejection fraction was significantly elevated from 27.5 +/- 6% to 32.8 +/- 10.8% (p less than 0.005). Thus, this limited study clearly demonstrates the rapid administration of enalapril not only achieves inhibition of renin-angiotensin-aldosterone system but also reduces preload and afterload significantly in the failing heart. We conclude that rapid enalaprilization is an effective methodology which still needs meticulous attention, providing significant hemodynamic and symptomatic benefits in patients with chronic congestive heart failure.
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PMID:Enalapril in congestive heart failure: acute hemodynamic and neurohumoral evaluation and short-term follow-up. 167 72


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