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PubMed1980

[The use of organic nitrates to lower intraocular pressure in outpatient and surgical treatment (author's transl)].

Intravenously administered nitroglycerin lowers intraocular pressure both in glaucoma patients and healthy subjects. The effect is dose-related. The use of the drug in ocular hypotensive therapy before and after surgery is suggested. Nitrates administered orally (isosorbide dinitrate 2 x 40 mg daily, depot form) bring about a comparable lowering of IOP and are suitable for outpatient treatment.

Dose-Response Relationship, Drug↗
PubMed1993

Pilot trial to determine the efficacy of a low dose of fish oil in the treatment of angina pectoris in the geriatric patient.

23 geriatric patients completed a single-blind placebo controlled, crossover trial using fish oil as adjunctive therapy for stable angina pectoris. The results indicated a significant reduction in the number of anginal attacks, as well as a significant reduction in the consumption of sublingual isosorbide dinitrate tablets. A possible prolonged carry over effect of fish oil was noted after crossover from the active substance to placebo.

Aged↗
PubMed1994

Cost-effectiveness study of nitrate therapy using a decision analysis methodology.

The cost-assessment technology of decision analysis was applied to isosorbide dinitrate (ISDN), the standard therapy for angina; isosorbide mononitrate (ISMO), approved mid-1992; and nitroglycerin patches to measure the effect of economics on clinical practice and administrative choices. The evaluation was conducted to illustrate the utility of this method for decision makers in various sectors of the health care system, including physicians, pharmacy benefit administrators, formulary committees, and manufacturers. Findings indicate that despite a higher unit cost for ISMO, total anticipated treatment costs with this new long-acting nitrate are lower than those associated with ISDN (28%) and nitroglycerin patch (16%) therapy in patients with stable angina, and ISMO requires less dosing titration and is associated with fewer tolerance effects.

Angina Pectoris↗
PubMed1986

Some issues concerning transdermal nitroglycerin patches.

There is sufficient evidence to suggest that the duration of action of transdermal nitroglycerin patches is between 20 and 26 hours, as measured by exercise testing. At 24 hours there may be some patient variability, particularly with lower doses; however, the majority of patients show an increase in exercise time at 24 hours. In studies of the same patients, higher doses of transdermal nitroglycerin resulted in greater increases in exercise time, suggesting that higher doses may be more effective and that titration to higher doses is desirable. However, there is insufficient information from the chronic studies reported in the literature to draw any definitive conclusions. In the only crossover comparative studies reported in the literature to date, transdermal nitroglycerin appears to be as effective as isosorbide dinitrate and nifedipine. While transdermal nitroglycerin patches appear to be an effective mode of therapy, further studies are needed to confirm these findings.

Administration, Topical↗
PubMed1984

Isosorbide 5-mononitrate and isosorbide 2-mononitrate kinetics after intravenous and oral dosing.

Isosorbide 5-mononitrate (IS-5-MN) and isosorbide 2-mononitrate (IS-2-MN) kinetics were studied in two groups of young healthy subjects after intravenous injection of 5 mg of both and after oral doses of 20 mg of IS-2-MN and 10, 15, and 20 mg of IS-5-MN. Mononitrate plasma levels were measured by GLC with capillary columns. After intravenous injection, IS-5-MN and IS-2-MN plasma levels declined biexponentially and could be described by an open two-compartment body model. Distribution t 1/2 was rapid; 8.6 min for IS-5-MN and 12.5 min for IS-2-MN. Substances were distributed throughout body water; volume of distribution at steady state (Vd ss) was 48 l for IS-5-MN and 55 l for IS-2-MN and elimination t 1/2 was 4.15 hr for IS-5-MN and 1.9 hr for IS-2-MN. Total plasma clearance was 8.5 l/hr for IS-5-MN and 23.2 l/hr for IS-2-MN. After oral doses the mononitrates were rapidly and completely absorbed (absorption t 1/2 ranged from 2.5 to 5 min) from the gastrointestinal tract without first-pass metabolism, i.e., absolute systemic availability was 100%. In the dose range studied, kinetics of the two mononitrates were linear. Compared with isosorbide dinitrate, mononitrate kinetics are different because of greater systemic availability, slower clearance, and smaller Vd ss.

Absorption↗
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↗
PubMed1993

Effect of vasodilator therapy on mortality in chronic congestive heart failure.

We compared the effects of Hydralazine and Isosorbide dinitrate (ISDN) with those of an angiotensin-converting-enzyme inhibitor, captopril on mortality in patients with chronic congestive heart failure (NYHA class III and IV). Patients receiving conventional treatment with digoxin and diuretics were randomly assigned to receive either placebo (n = 51), hydralazine-ISDN. (n = 50) or captopril (n = 52) in a double blind trial. At the end of 6 months there were 14 deaths in the placebo group (27.4%) as compared with 11 deaths in the hydralazine-ISDN group (22%)--a mortality reduction of 20% (P > 0.05) and 10 deaths in the captopril group (19.2%)--a mortality reduction of 30% (p > 0.05). At the end of one year, mortality was 50%, 42% and 30% in the placebo, hydralazine-ISDN and captopril groups respectively with a mortality reduction of 16% in the hydralazine-ISDN group (p > 0.05) and 40% in the captopril group (p < 0.05) compared to the placebo group. The mortality reduction was mainly due to reduction in deaths attributed to progressive heart failure. The data suggests that the addition of captopril to conventional treatment significantly reduces mortality in patients with severe congestive heart failure. Hydralazine-isorobide dinitrate also reduced mortality but statistically this was not significant.

Adult↗
PubMed2006

Pharmacological treatment of chronic heart failure.

Heart failure (HF) is associated with a high morbidity and mortality in the Western World. Our knowledge of the epidemiology, pathophysiology, and therapy has improved dramatically during the last 20 years. Pharmacological treatment, as it stands today, is a combination of preventive and symptomatic strategies. The mainstay life-saving drugs are angiotensin-converting enzyme inhibitors and beta-blockers. Additional benefits are obtained when angiotensin-receptor blockers or aldosterone antagonists are added. Digitalis and/or diuretics are useful for symptom reduction. In addition, combination therapy with hydralazine and isosorbide dinitrate is recommended in African Americans.

Adrenergic beta-Antagonists↗
PubMed1980

Effect of sublingual nitroglycerin and long-acting nitrate preparations on esophageal motility.

The effect of nitroglycerin and long-acting nitrates in normal humans is unknown. Therefore, we studied the effect of commonly used clinical doses of nitrate preparations on the esophagus in normal subjects. Three minutes after administration of sublingual nitroglycerin 0.6 mg, a significant reduction in lower esophogeal sphincter pressure occurred (19.0 +/- 2.6 to 12.7 +/- 2.2 mmHg (P < 0.01). This effect was transient, and no effect was seen on amplitude, duration of esophageal contractions or peristaltic wave velocity measured 6 min after nitroglycerin administration. Neither nitroglycerin ointment, 1.5 in. applied to the forearm, nor 20 mg oral isosorbide dinitrate, resulted in a major change in any measured parameter of esophageal motility. In addition, pretreatment with long-acting nitrates did not alter lower esophageal sphincter response to intravenous pentagastrin.

Adult↗
PubMed1994

Management of heart failure. I. Pharmacologic treatment.

OBJECTIVE: This review of the pharmacologic treatment of heart failure due to left ventricular systolic dysfunction summarizes the recommendations of the expert panel for the Agency for Health Care Policy and Research Heart Failure Guideline. It provides specific advice to help guide practitioners through clinical decision making. DATA SOURCES: Data were obtained from English-language studies and referenced in MEDLINE or EMBASE between 1966 and 1993. We used the search terms heart failure, congestive; congestive heart failure; heart failure; cardiac failure; and dilated cardiomyopathy in conjunction with terms for the specific treatments. Where data were lacking, we relied on opinions of panel members and peer reviewers. STUDY SELECTION: Only large prospective trials were used to estimate treatment efficacy. Smaller trials, case series, and case reports were reviewed for the incidence of adverse effects. DATA EXTRACTION AND SYNTHESIS: Randomized clinical trials were reviewed for inclusion and exclusion criteria, patient outcomes, adverse effects, and eight categories of study quality using a defined list of study flaws. CONCLUSION: Angiotensin-converting enzyme (ACE) inhibitors should be given to all patients unless specific contraindications exist. Diuretics should be used judiciously early in treatment to prevent excessive diuresis that could prevent titration of ACE inhibitors to target doses. Digoxin has not been shown to affect the natural history of heart failure and should be reserved for patients who remain symptomatic after treatment with ACE inhibitors and diuretics. Isosorbide dinitrate and hydralazine hydrochloride should be tried in patients who cannot tolerate ACE inhibitors or who have refractory symptoms.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

The effects of acupuncture in treatment of coronary heart diseases.

A clinical study on acupuncture at point Neiguan (PC 6) was conducted on the basis of successful treatment of patients with angina pectoris and acute myocardial infarct. The effective rate (91.3%) was found to be far superior to isosorbide dinitrate and nifedipine (P < 0.01). The experimental studies in animal models demonstrated that electro-acupuncture could decrease the elevated ST segments in ECGs and reduce the infarct areas induced by coronary ligation.

Acupuncture Therapy↗
PubMed1983

[Molsidomine in exertion angina].

Molsidomine (M), a new anti-angina drug, was studied by stress tests in 50 cases of stable angina and clinically in 33 patients not controlled by beta-blockers. One hour after sublingual administration of 2 mg of M. to 10 patients, the work required to cause ST depression of 1 mm (WST1) was increased by 94 per cent (p less than 0.005), the total work was increased by 52 per cent (p less than 0.005) and the maximal ST depression (ST max) was reduced by 45 per cent (p less than 0.01). The resting heart rate was unchanged and the blood pressure dropped mildly. In 4 of the 10 patients with exertional angina even while taking beta-blockers, the synergistic effect of M was remarkable. With a sublingual dose of 1 mg, the WST1 and the ST max are very significantly improved. The effect is even more marked at a dose of 2 mg. With a sublingual or oral of 2 mg, WST1 and ST max are very significantly improved at 1 hour and at 3 hours (p less than 0.005). Data from the literature show a significant anti-ischaemic effect until the 6th hour. In two series of 10 patients, 2 mg of M administered orally were compared to 20 mg of isosorbide dinitrate and to 10 mg of nifedipine at the 2nd hour. The WST1 and ST max were very significantly improved by all three drugs to a similar degree.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1995

[Severe methemoglobinemia following large dose of nitrate medication].

A 49-year-old man with ischemic heart disease attempted to commit suicide by ingesting 300 tablets (6 grams) of isosorbide dinitrate. He was admitted with shortness of breath and cyanosis. Severe methemoglobinemia was diagnosed (blood level 47 mg%). After administration of intravenous methylene blue and fluids, there was immediate improvement and he was discharged 48 hours after admission.

Fluid Therapy↗
PubMed1980

Organic nitrate therapy in glaucoma.

We determined the effect of organic nitrates on normal volunteers and patients with open-angle and narrow-angle glaucoma. Nitroglycerin lowered intraocular pressure in all patients when administered by the perfusion technique. Isosorbide dinitrate given orally (2 x 40 mg per day) has a potent decreasing effect on intraocular pressure, which cannot be explained by the influence on arterial blood pressure.

Administration, Oral↗
PubMed1993

Haemodynamic and clinical effects of an intravenous potassium channel opener--a review.

Intravenous nicorandil (4-12 mg) produced a significant decrease in mean arterial blood pressure (-5 to -15%), systemic vascular resistance (-8 to -27%), pulmonary capillary wedge pressure (-15 to -41%) and left ventricular end-diastolic pressure (-8 to -18%) in patients with coronary artery disease, myocardial infarction or congestive heart failure. Cardiac output was significantly increased (+3 to +19%) in most studies. These haemodynamic effects of intravenous nicorandil (4-8 mg) were comparable to those of nitroglycerin (0.3 mg), although a greater decrease in preload was produced by nitroglycerin. Moreover, no significant haemodynamic tolerance developed over a 12 to 24 h period during continuous infusion of nicorandil (2.4 micrograms.kg-.min-1) in patients with heart failure, in contrast to nitroglycerin infusion (0.65 microgram.kg-1 x min-1). Intravenous nicorandil (4-12 mg) was also shown to produce a slightly smaller increase (8-27%) in the diameter of the large coronary arteries compared to that of sublingual nitroglycerin (0.3 mg) (16-32%) and to cause a significant decrease in coronary vascular resistance (-9 to -53%) and a significant increase in coronary sinus flow (+6 to +81%) in patients with coronary artery disease. The efficacy of intravenous nicorandil (2-6 mg.h-1) in unstable angina pectoris has been compared with that of isosorbide dinitrate (2-5 mg.h-1) in a double-blind, multicentre trial. Over a 3 to 9 day period, nicorandil therapy tended to be more effective in abolishing anginal attacks and decreasing nitroglycerin consumption.

Administration, Sublingual↗
PubMed1986

Contribution of coronary endothelial cells to cardiac adenosine production.

Experiments were performed in isolated non-working guinea pig hearts perfused according to the Langendorff technique (95% O2, 5% CO2), to evaluate the relative contribution of the coronary endothelium to the formation of cardiac adenosine during hypoxia, hypercapnia, and acetylcholine infusion. For this purpose the adenine-nucleotides of the coronary endothelium were prelabeled by perfusion of isolated hearts with 3H-adenosine (10(-8) M) for 35 min. Changes in the relative specific radioactivity (RSA) of adenosine released into the coronary effluent perfusate were used to assess changes in the relative contribution of the coronary endothelium and cardiomyocytes to total cardiac adenosine release. Hypoxic perfusion (15% O2) doubled coronary flow and increased total adenosine release by about two orders of magnitude and in addition, substantially increased the release of 3H-adenosine. The RSA of adenosine, however, was consistently depressed. During hypercapnic acidosis (9% CO2) the increase in coronary flow was associated with only a small and transient rise in cardiac adenosine release, and did not influence the formation of 3H-adenosine. In the unpaced heart, acetylcholine (10(-7) and 2 X 10(-6) M) dose-dependently increased coronary flow and the release of both adenosine and 3H-adenosine. Within the first minute, the RSA of adenosine was increased, but thereafter was decreased relative to control. In the paced heart, the effects of acetylcholine (2 X 10(-6) M) were greatly attenuated. Increasing coronary flow by bradykinin and isosorbide dinitrate or decreasing heart rate by (-)N6-phenylisopropyl-adenosine did not significantly affect effluent perfusate concentration of adenosine or its RSA.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1989

Spontaneous coronary artery spasm in variant angina is caused by a local hyperreactivity to a generalized constrictor stimulus.

To assess whether spontaneous coronary artery spasm in patients with variant angina results from local coronary hyperreactivity to a generalized constrictor stimulus or from a stimulus generated only at the site of the hyperreactive segment, the behavior of spastic and nonspastic coronary segments was studied in six patients with variant angina in whom focal coronary spasm developed spontaneously during cardiac catheterization. None of the patients had critical (greater than 50% luminal diameter reduction) organic coronary stenoses. Coronary diameters were measured by computerized quantitative arteriography during control, spontaneous spasm and ergonovine-induced spasm and after intracoronary nitrates were given. During spontaneous spasm, the luminal diameter of spastic and both proximal and distal nonspastic coronary segments was significantly reduced from control values, 64.2%, 13.2% and 14.8%, respectively. Average diameter reduction of unrelated arteries was 12.3%. Ergonovine, which was also administered to four patients, provoked focal spasm at the same site as spontaneous spasm. During intravenous ergonovine, luminal diameter of spastic segments was reduced by 91.5%, that of nonspastic proximal segments by 17.8% and that of nonspastic distal segments by 11.5%. Luminal diameter of unrelated arteries during ergonovine-induced spasm was reduced by 17.7%. Constriction of spastic segments was greater during ergonovine-induced spasm (p less than 0.05), whereas the extent of diameter reduction of nonspastic segments was not significantly different during spontaneous spasm and ergonovine-induced spasm. Intracoronary isosorbide dinitrate dilated spastic and nonspastic coronary segments to a similar extent from control (20.7%, 18% and 16.5%, respectively; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Influence of antianginal drugs on Lypressin induced T-wave enhancement in the electrocardiogram of the rat].

Lypressin enhances the T-wave in the ECG of the anesthetized Sprague-Dawley rat and this has been used in screening for antianginal activity. After oral administration the durations of action of the organic nitrates, glyceryl trinitrate, isosorbide dinitrate, glyceryl 1,2-dinitrate, glyceryl 1,3-dinitrate and of SIN-1 (3-morpholinosydnonimine), molsidomine and nicorandil were shorter than those of verapamil and nifedipine. The sequence of the durations of action of the substances examined was the same in the rat as in man.

Administration, Oral↗