Biomedical subjects

S H Taylor

Publications and source records attributed to S H Taylor.

At least 37 records · Page 2Linked to original sources

PubMed1993

Side effects of dihydropyridine therapy: comparison of amlodipine and nifedipine retard.

The efficacy and tolerability of amlodipine (5 mg, once daily), nifedipine retard (20 mg, twice daily), and placebo were compared in a multicenter, three-way, crossover study involving 97 patients with mild-to-moderate hypertension. Each patient underwent three, 2-week treatment periods separated by 2-week washout periods without therapy. Comparable and significant (p < 0.05) blood pressure reductions were observed after amlodipine and nifedipine retard when compared with placebo, except in the case of supine systolic blood pressure with nifedipine retard. A significantly greater incidence of treatment-related side effects was observed with nifedipine retard (41%) compared with amlodipine (27%, p < 0.05) or placebo (16%, p < 0.01). Amlodipine treatment was associated with significantly fewer reports of headache and flushing than nifedipine retard (p < 0.05). The lower incidence and reduced severity of vasodilator side effects associated with amlodipine resulted in fewer withdrawals and a better overall tolerability profile.

Adult↗

PubMed1993

Captopril versus digoxin in patients with coronary artery disease and mild heart failure. A prospective, double-blind, placebo-controlled multicenter study. The CADS Study Group.

We conducted a prospective, double-blind, placebo-controlled multicenter trial in order to evaluate the long-term effects of captopril (50 mg/day), digoxin (0.25 mg/day) and placebo on quality of life, cardiovascular events, clinical symptoms and exercise tolerance in patients with documented myocardial infarction, resulting in regional wall motion abnormalities, and with mild heart failure (NYHA class II to III without treatment) and exercise not limited by angina. 222 patients were studied, 63 were randomized to captopril, 66 to digoxin, 67 to placebo. Follow-up was conducted for two years. Base line characteristics in the three treatment groups were similar. After one year of therapy, digoxin had significantly improved general well-being (p < 0.01 vs captopril), symptom score (p < 0.05 vs captopril and placebo), and vitality (p < 0.05 vs captopril). Digoxin improved NYHA class in 45% as compared to placebo (28%, p < 0.05). Worsening of angina was more frequent with captopril as compared to digoxin (p < 0.05). However, cardiovascular events during follow-up were lower in the captopril group as compared to placebo and digoxin (p < 0.01 captopril vs placebo). No differences between groups were observed in baseline and follow-up exercise tolerance between the three groups. Dizziness during upright tilt and cough were more frequent with captopril as compared to digoxin or placebo. After two years of follow-up (captopril n = 32, digoxin n = 29, placebo n = 27) general well-being was improved with both digoxin and captopril (p < 0.004 and p < 0.03 vs placebo).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Early side-effects of antihypertensive therapy: comparison of amlodipine and nifedipine retard.

In a multicentre crossover study of 97 patients with mild hypertension, the incidence and severity of adverse effects were observed during the first 14 days of treatment with amlodipine, nifedipine retard or placebo. Amlodipine (5 mg) once daily was equipotent to nifedipine retard (20 mg) twice daily. At these doses, the incidence of adverse effects was significantly greater during treatment with nifedipine retard (41%) than with amlodipine (27%, P < 0.05) or placebo (16%, P < 0.01). In particular, headache and flushing occurred significantly less frequently during the first 14 days of treatment with amlodipine than with nifedipine retard. The lower incidence and reduced severity of vasodilatory side-effects associated with amlodipine resulted in fewer withdrawals during initiation of therapy (2 on amlodipine compared with 7 on nifedipine retard).

Adult↗

PubMed1992

Modulation of inotropic therapy by venodilation in acute heart failure: a randomised comparison of four inotropic agents, alone and combined with isosorbide dinitrate.

The effects of four inotropic agents with differing ancillary properties [a cardiac glycoside (digoxin), a combined alpha- and beta-adrenergic agonist (dobutamine), a beta-adrenergic agonist (prenalterol), and a phosphodiesterase inhibitor (amrinone)] alone and with subsequent addition of isosorbide dinitrate were compared in 48 consecutive acute myocardial infarction patients with radiographic and haemodynamic (pulmonary artery occluded pressure greater than 18 mm Hg) left ventricular failure. All agents with the exception of dobutamine reduced the elevated left heart filling pressure; only digoxin and dobutamine augmented the cardiac stroke volume index. All drugs except digoxin reduced the SVRI; an arteriolar constrictor response was evident 60 min after digoxin and a tachycardia resulted after combined alpha- and beta- and beta-adrenergic stimulations (dobutamine and prenalterol, respectively). The addition of isosorbide dinitrate reversed the inotrope-induced elevations of systemic arterial pressure and resulted in additional reductions in left heart filling pressure. These data suggest that, in the absence of substantial venodilator properties in an inotropic compound, reduction in elevated left heart filling pressure is not achieved with inotropic therapy alone in acute left ventricular failure and combining a venodilator may be haemodynamically advantageous.

Adult↗

PubMed1992

Treatment of ischemic heart disease in the 1990s: key issues for the physician.

During recent years, understanding of the basic pathology, pathophysiology, and morbid risk of ischemic heart disease has increased immensely, but a wide gulf still exists between such knowledge and its practical application to the individual patient. Although the treatment of ischemic heart disease continues to pose many dilemmas for the physician in the 1990s, the key issues are easy to define, particularly with regard to pharmacotherapy. The basic pathologic processes and their rate of development and progression, their pathophysiologic consequences, and their morbidity and mortality risks are becoming increasingly clear. Until methods are developed to reconstitute the obstructed coronary arteries, clinical attention must be directed primarily to alleviating symptoms and ECG signs of myocardial ischemia and improving the deranged hemodynamic disorder. These primary objectives are now achievable with modern anti-ischemic drugs such as nicorandil. With the availability of efficacious drugs against clinical symptoms, ECG signs, and hemodynamic associates of ischemic heart disease, clinical attention must be redirected to retardation or even regression of the primary myocardial ischemic syndrome. This therapeutic goal can be achieved only by correction of the secondary risk factors that are present in many patients with ischemic heart disease. Only by such a comprehensive approach, namely, that of treatment allied to prevention, can the gap between knowledge and its practical application to the individual patient be narrowed.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiography↗

PubMed1992

Amlodipine in post-infarction angina.

Once-daily administration of amlodipine is a highly effective treatment for patients with angina pectoris. This study has confirmed its benefit in a relatively large subgroup of patients with post-myocardial infarction angina. Amlodipine reduced the number of angina attacks and nitroglycerin consumption and substantially improved the ability of the patient to perform physical exercise. The circadian pattern of angina attacks was markedly attenuated by amlodipine with patients reporting fewer attacks during the mid-morning peak that was clearly evident at baseline. The advantage of once-daily dosing, together with the excellent control of angina achieved in post-infarction patients, make amlodipine a good choice for therapy.

Amlodipine↗

PubMed1992

Comparison of early side effects with amlodipine and nifedipine retard in hypertension.

The frequency and severity of adverse effects during the first 14 days of treatment with amlodipine (5 mg once daily), nifedipine retard (20 mg twice daily) or placebo were compared in a multicentre, three-way, cross-over study involving 97 patients with mild-to-moderate hypertension. All three groups of patients were well matched for age, sex and baseline blood pressure. Amlodipine and nifedipine retard produced highly significant and comparable reductions in blood pressure, indicating that the doses were therapeutically equivalent. The incidence of adverse effects considered to be definitely or probably related to nifedipine retard treatment (41%) was significantly higher than for placebo (16%, p less than 0.01) or amlodipine (27%, p less than 0.05). There were no significant differences in the incidence of vasodilator-related adverse effects between amlodipine and placebo. In contrast, headache, flushing and dizziness were reported more frequently by patients while on nifedipine retard than on placebo or amlodipine. The convenience of once-daily dosing, together with a lower incidence of adverse effects, with consequently fewer withdrawals from therapy, suggests that amlodipine has clinical advantages over nifedipine retard in the treatment of hypertension.

Adolescent↗

PubMed1992

Therapeutic targets in ischaemic heart disease.

The adequate treatment of a disease syndrome is dependent upon a clear definition of the symptomatic, pathological, physiological and prognostic targets against which therapy is to be deployed. The syndromes of ischaemic heart disease, including angina pectoris, are complex in origin, pathology, pathophysiology and natural history, and a complete clinical profile is difficult, if not impossible, to achieve in individual patients. The prime goals of pharmacotherapy in ischaemic heart disease are easy to define, but difficult to accomplish in practice. Relief of pain, breathlessness and fatigue are the prime clinical targets for pharmacotherapy. In view of their sinister significance, the electrophysiological indications of myocardial ischaemia, whether symptomatic or silent, are also crucial targets towards which therapy must be directed. Ischaemic heart disease is accompanied by a wide variety of regional and global abnormalities of myocardial contractile function associated with widespread reflex stimulation of the peripheral vascular system and neuroendocrine systems. Primarily, drug therapy must be directed at correction of these pathophysiological components of the syndrome. Longer term but no less essential goals in the treatment of ischaemic heart disease are the prevention of the clinical sequelae of the syndrome and its progression. A natural sequel of coronary artery obstructive disease is successive thrombotic events and loss of myocardium. Calcium antagonists, by preventing the increase in myocardial cytosolic calcium during acute ischaemic episodes, defer cell necrosis; in this respect, they are unique among currently available antianginal drugs. With regard to progression, the prime pathological cause of ischaemic heart disease is coronary atheroma.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed1992

Vasodilator therapy for acute heart failure: haemodynamic comparison of hydralazine/isosorbide, alpha-adrenoceptor blockade, and angiotensin-converting enzyme inhibition.

Haemodynamic comparison of three vasodilation regimens [intravenous (i.v.) hydralazine and isosorbide dinitrate (ISDN) combined, i.v. doxazosin, and i.v. enalaprilat] was undertaken in 36 patients with acute left ventricular (LV) failure due to recent myocardial infarction. Each regimen achieved similar reductions in pulmonary artery occluded pressure (PAOP, preload) and systemic arterial pressures (afterload), with increased cardiac and stroke volume (SV) indexes (p less than 0.01). Only the hydralazine and isosorbide combination induced resting tachycardia. Balanced vasodilatation after selective alpha-adrenoceptor blockade (doxazosin) and angiotensin-converting enzyme (ACE) inhibition (enalaprilat) without increase in heart rate (HR) suggests that these therapies may have definite haemodynamic advantages over the hydralazine/ISDN combination.

Adrenergic alpha-Antagonists↗

PubMed1991

Efficacy of celiprolol in the elderly hypertensive patient.

With the rapidly increasing average age of the population of the Western world, care and treatment of the elderly are becoming increasingly important. Cardiovascular diseases are major causes of death and disability in the elderly; hence, identification of cardiovascular risk factors and effective treatment are essential. Evidence indicates that these risk factors in the elderly are similar to those in the young; namely, high blood pressure, hyperlipidemia, glucose intolerance, hyperfibrinogenemia, obesity, and cigarette smoking. The latter two relate to general patient management, whereas the remainder can be significantly influenced by modern drug therapy such as celiprolol. This drug is a third-generation highly selective beta 1-adrenoceptor antagonist with beta 2-agonist and vasodilatory activity giving a unique and advantageous pharmacologic profile for antihypertensive therapy with particular benefits for the elderly. The impact of therapy with celiprolol on the cardiovascular risk factors in the elderly hypertensive patient is reviewed.

Adrenergic beta-Antagonists↗

PubMed1991

Efficacy of doxazosin in specific hypertensive patient groups.

In practice, some of the major problems for the physician who treats hypertension are patients who are resistant to treatment or who have other complicating risk syndromes. Therefore the overall efficacy of an antihypertensive agent must include an assessment of effect in patients with serious ancillary problems. In this article, doxazosin is reviewed for its efficacy in the treatment of severe essential hypertension and specific complications or conditions of mild or moderate essential hypertension, namely, left ventricular hypertrophy, hyperlipidemia, noninsulin-dependent diabetes mellitus, renal insufficiency, pheochromocytoma, chronic obstructive pulmonary disease, peripheral vascular disease, and smoking. Doxazosin is particularly efficacious in many specific subgroups of patients with hypertension, and the results of relevant studies are discussed.

Adrenal Gland Neoplasms↗

PubMed1991

Efficacy and safety of doxazosin in the treatment of patients with mild or moderate essential hypertension and elevated levels of cholesterol.

In hypertensive patients, elevated serum cholesterol is a frequent and sinister additional coronary risk factor. Selective alpha 1-adrenoreceptor inhibitors appear to have the unique ability to control both risk factors. Forty-two patients, ages 42 to 65 years, including 21 men with sustained hypertension and elevated serum cholesterol levels, were included in a trial of monotherapy with doxazosin administered once daily (range, 1 to 16 mg). The influence of the drug on high blood pressure and elevated serum cholesterol was evaluated over a 28-week period, which consisted of a 4-week, single-blind placebo lead-in period, an open 10-week dose-adjustment period, and finally a 14-week maintenance period. Of the 39 efficacy-evaluable patients, 25 (64%) achieved adequate blood pressure control (diastolic blood pressure less than 90 mm Hg or a decrease in diastolic blood pressure greater than 10 mm Hg) at a mean daily dose of 2 mg of doxazosin. No persistent changes occurred in heart rate. In the 32 patients with evaluable lipid data, there were nonsignificant trends to an increase in high-density lipoprotein cholesterol and a reduction in total cholesterol, together with a significant reduction in serum triglyceride concentration. The combined changes in blood pressure and blood lipid levels resulted in a reduction of 36% in the calculated risk of coronary heart disease. Eleven patients reported side effects and four were withdrawn from therapy. These results confirm the antihypertensive and anticholesterolemic efficacy of once-daily treatment with doxazosin.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗

PubMed1991

A double-blind, placebo-controlled, parallel dose-response study of amlodipine in stable exertional angina pectoris.

A placebo-controlled, double-blind, dose-response study of amlodipine (1.25, 2.5, 5, and 10 mg once daily) was carried out in 136 patients with stable exertional angina pectoris. Improvements in total exercise tolerance, time to onset of angina during exercise, ST-segment deviation at maximum common load, frequency of angina attacks, and nitroglycerin consumption were greater following amlodipine than placebo. The maximum improvement in exercise parameters occurred with the highest dose of amlodipine. All doses produced significant reductions in angina attack frequency and the rate of nitroglycerin consumption. Amlodipine was well tolerated and no patients were withdrawn due to adverse events or laboratory abnormalities.

Adult↗

PubMed1991

Hypertension and coronary artery disease: a therapeutic challenge.

The coexistence of the syndromes of essential hypertension and coronary artery disease (CAD) poses a major but common therapeutic challenge. High blood pressure is one of the most potent risk factors for the early development of CAD. Conversely, the presence of CAD significantly worsens the predictive prognosis associated with high blood pressure. Moreover, metabolic risk factors for the acceleration of both syndromes are similar, particularly with regard to abnormalities of the blood lipid profile, carbohydrate intolerance, and obesity. It is clinically crucial, therefore, to direct drug therapy not only at the immediate alleviation of the symptoms and signs of each syndrome but also to control the cardiac and vascular risk factors common to both syndromes. Carvedilol is a third-generation vasodilating beta-adrenoceptor antagonist with advantageous ancillary pharmacologic properties for the treatment of the patient with high blood pressure complicated by CAD. The immediate advantages of the drug in the treatment of both syndromes are distinct. In the patient with high blood pressure, carvedilol controls the pressure throughout the 24 h of the day and suppresses the increase associated with exercise. In the patient with CAD, the drug is efficacious in relieving anginal pain and electrocardiographic signs of myocardial ischemia. By reducing blood pressure and heart rate and retarding their increases during exercise, the drug exhibits a potent ability to reduce left ventricular work, wall stress, myocardial oxygen consumption, and left ventricular myocardial ischemia. In the patient in whom both syndromes coexist, carvedilol affords a remedy for both.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

A review of amlodipine in myocardial ischaemia.

Amlodipine is a dihydropyridine calcium antagonist with a unique pharmacokinetic profile providing advantages over other therapies of its kind. It has been shown to possess high oral absorption, long elimination half-life, smooth onset of action and long duration of pharmacodynamic activity. These properties result in gradual vasodilation, ensuring a low incidence of vasodilatory side effects and once-daily administration. In randomized, double-blind, placebo-controlled studies a dose of 5-10 mg once daily has been established as the most efficacious dose for the treatment of angina pectoris. Amlodipine was found to increase exercise capacity significantly and reduce electrocardiographic evidence of myocardial ischaemia after treadmill exercise testing 24 h after administration compared with placebo in patients suffering from angina pectoris. Angina attack rate and glyceryl trinitrate consumption were also significantly reduced. Amlodipine was shown to possess comparable anti-anginal efficacy with the calcium antagonist diltiazem and the beta-blocker nadolol. In combination with beta-blockers and/or nitrates the addition of amlodipine was found to produce enhanced anti-anginal efficacy with good tolerability. Amlodipine is also effective in reducing the angina attack rate in patients with vasospastic angina. In conclusion, amlodipine is an effective and well-tolerated therapeutic agent given once daily as monotherapy or in combination with beta-blockers and/or nitrates for the treatment of chronic stable angina pectoris and vasospastic angina.

Amlodipine↗

PubMed1990

An exercise hemodynamic comparison of verapamil, diltiazem, and amlodipine in coronary artery disease.

A prospective, randomized study compared the effects of equivalent intravenous doses of three slow calcium-channel blockers (verapamil, diltiazem, and amlodipine) on rest and exercise haemodynamics in 30 ischemic heart disease patients. Following a stable control period during which rest and exercise (supine bicycle) hemodynamics were assessed, equivalent hypotensive doses of each compound were administered over 20 minutes and rest/exercise parameters were assessed 10 minutes later. At rest all agents similarly reduced systemic blood pressure; the fall in systemic vascular resistance and the increase in cardiac indices was ranked: amlodipine greater than diltiazem greater than verapamil. The heart rate increase for amlodopine differed from verapamil and diltiazem (+19.4% vs. +1.5% vs. -7%; p less than 0.01). On exercise, similarly greater falls in the systemic vascular resistance index followed amlodipine, compared with verapamil and diltiazem (p less than 0.05). Only amlodipine significantly reduced the exercise pulmonary artery occlusion pressure (PAOP). Exercise cardiac stroke volume improved after diltiazem and amlodipine. In terms of cardiac performance, both amlodipine and diltiazem produced an improvement, whereas verapamil depressed cardiac pumping activity. Thus, hemodynamic differences between slow-calcium-channel blocking drugs may be demonstrated in humans. These differences would be compatible with a predominant peripheral vascular site of action for amlodipine, in contrast with mixed cardiac and peripheral sites for diltiazem and verapamil.

Amlodipine↗

PubMed1990

Efficacy of ibopamine in the treatment of heart failure.

Loss of myocardial contractility, reflexly enhanced vasoconstriction, and neuroendocrine excitation are the pathophysiologic hallmarks of low-output heart failure. Drugs that counter both consequences afford considerable therapeutic potential in retarding and perhaps even in staying the consequences of the syndrome. Ibopamine possesses such potential through its unique ability to stimulate both dopaminergic- and beta-adrenoreceptors in the heart and circulatory system. Stimulation of dopaminergic- receptors and beta 2-adrenoreceptors results in vasodilatation in all regional vascular territories. beta 2-Adrenoreceptor agonist activity also affords mild positive inotropic activity in the heart, whereas stimulation of presynaptic dopaminergic- receptors (DA2) attenuates the increased sympathetic neural outflow. The drug also suppresses the renin-angiotensin-aldosterone system in addition to having a direct natriuretic activity. The pharmacodynamic effects of ibopamine, exerted through its metabolite epinine, are translated into measurable therapeutic benefits in patients with chronic heart failure. The increase in peripheral blood flow induced in all regional vascular territories, including the kidneys, is associated with increased cardiac output and stroke volume and reduction in left ventricular pressure work, wall stress, and myocardial oxygen consumption. Plasma norepinephrine, angiotensin, and aldosterone are also reduced, and renal sodium excretion is enhanced. These hemodynamic and neuroendocrine activities, which are not subject to tolerance during sustained administration of the drug, are accompanied by clinically significant improvement in symptoms, exercise tolerance, and the New York Heart Association classification of disability. More important, no proarrhythmic effects have been observed during sustained treatment, and the minimal side effects observed during long-term treatment enhance the safety profile of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiotonic Agents↗

PubMed1990

The treatment of mild to moderate hypertension with ACE inhibitors.

The efficacy and safety of quinapril were evaluated in patients with mild to moderate hypertension [sitting diastolic blood pressure (DBP) of 95-115 mm Hg] in seven large, multicenter studies and in one large, single-center study. In double-blind trials, 1,367 patients were treated with quinapril and 820 patients were treated with comparative therapies (enalapril, captopril, chlorthalidone, or placebo). The usual effective dosage of quinapril was 10-40 mg/day, with some patients receiving up to 80 mg/day. Diuretics were added optionally for nonresponders in some studies. Quinapril was equally safe and effective administered either once daily (o.d.) or twice daily and was significantly more effective in lowering blood pressure than was placebo. Quinapril and enalapril administered o.d. were similarly effective in producing clinically and statistically significant reductions in resting blood pressure 24 h after dosing. Quinapril in o.d. doses was as effective as captopril administered two or three times daily. Quinapril was well tolerated; the incidence of adverse events was similar to that for placebo and was comparable to or less than that reported for captopril or enalapril. Quinapril in o.d. doses (10-40 mg/day) is safe and effective as first-line therapy for the treatment of mild to moderate hypertension. Diuretics can be safely added for patients who are not controlled by quinapril alone.

Angiotensin-Converting Enzyme Inhibitors↗