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PubMed2001

Isosorbide dinitrate in the treatment of anal fissure: a randomised, prospective, double blind, placebo-controlled trial.

OBJECTIVE: To assess the efficacy of isosorbide dinitrate in healing anal fissures. DESIGN: Randomised, prospective, double blind, placebo controlled trial. SETTING: Teaching hospital, The Netherlands. SUBJECTS: 37 consecutive subjects with anal fissure diagnosed in the surgical outpatient department. INTERVENTIONS: After randomisation, 20 patients were given isosorbide dinitrate, and 17 patients placebo. MAIN OUTCOME MEASURES: Healing of anal fissure, recurrence, and tolerance. RESULTS: Both groups were treated for a median (range) of 5 weeks (range 1-10). After this period, 17 in the isosorbide group had healed compared with 6 controls (p < 0.003). The fissure recurred in 2 patients who had had an initial good response to isosorbide, and in 2 in the control group. Side effects (particularly headache) were more common after isosorbide dinitrate, but not significantly so (9/20 compared with 3/17). CONCLUSIONS: Isosorbide dinitrate is an effective treatment for anal fissure, and is significantly better than placebo.

Adult↗
PubMed2000

[Comparative study of isosorbide dinitrates and mononitrates in patients with ischemic heart disease and stable angina pectoris caused by stenosing coronary atherosclerosis].

In an open clinical trial 19 patients with angina pectoris (functional class II-III) received in turn either non-retard tablets of isosorbide dinitrate (nitrosorbid, cardiket) in a mean dose 80 mg/day or isosorbide 5-mononitrate (mono mac) in a mean dose 51.5 mg/day. Each drug was given for a month. The effect was assessed by changes in frequency of anginal attacks and exercise tolerance. Non-retard isosorbide dinitrate and isosorbide 5-mononitrate demonstrate a good antiischemic effect, are safe and well tolerated. Isosorbide dinitrate and mononitrates do not differ significantly in reduction of the anginal attacks and by an increase in exercise tolerance but the effective dose of mono mac was 1.5-2 times less than that of nitrosorbide or cardiket, thus it is more cost-effective.

Aged↗
PubMed1996

Abrupt cessation of short-term continuous treatment with isosorbide dinitrate may cause a rebound increase in silent myocardial ischaemia in patients with stable angina pectoris.

OBJECTIVE: To examine by Holter electrocardiographic monitoring the effect of abruptly stopping nitrate treatment in patients with stable angina pectoris. PATIENTS: 12 men with confirmed ischaemic heart disease and stable exertional class 3 angina (Canadian). All had episodes of horizontal or down sloping ST segment depression during 24 hour electrocardiographic monitoring. All were nitrate responders. DESIGN: Each patient was given isosorbide dinitrate (10-30 mg four times a day) and placebo (four times a day) for three days in a randomised crossover trial. There was a washout period of 3-5 days between the two treatment periods. Holter monitoring was performed on the third day of isosorbide dinitrate and placebo administration and on the first day of their withdrawal. RESULTS: When treatment with isosorbide dinitrate was stopped there was a significant increase in the total number and duration of painless episodes of myocardial ischaemia. During placebo and isosorbide dinitrate administration 8 patients had episodes of painless myocardial ischaemia whereas after isosorbide dinitrate cessation they were recorded in all 12 patients. Episodes of silent myocardial ischaemia at rest appeared in 4 patients after isosorbide dinitrate withdrawal. CONCLUSION: Abrupt cessation of short-term continuous nitrate treatment in patients with severe angina may cause a rebound increase in myocardial ischaemia which is predominantly silent.

Aged↗
PubMed1988

Changes in myocardial ischaemia during isosorbide dinitrate or indoramin therapy in patients with stable angina using relations between the ST segment and heart rate.

The effect of isosorbide dinitrate or indoramin on myocardial ischaemia was examined in patients with stable angina pectoris. In a prospective trial, randomization resulted in 8 and 9 patients, respectively, given isosorbide dinitrate in a dose of 30-90 mg daily, and indoramin in a dose of 75-225 mg daily; 2 of these patients were serially examined during the two types of therapy. Changes in myocardial ischaemia were assessed by exercise testing using 12 standard electrocardiographic leads and a bipolar lead CM5. Individual and group comparisons showed that isosorbide dinitrate resulted in an increase in ST segment depression, the maximal ST/heart rate slope and the ratio of net ST segment depression to increases in heart rate (at least P less than 0.01). In contrast, with indoramin therapy there were no significant changes in these indices. The results in these patients suggest that isosorbide dinitrate leads more consistently to increases in the severity of myocardial ischaemia than indoramin, although this effect on ischaemia is apparently less than the benefit of these agents on exercise performance.

Adult↗
PubMed1987

The acute effects of intravenous isosorbide dinitrate during cardiac surgery.

The acute effects of intravenous isosorbide dinitrate during open heart surgery were studied in 15 adult patients. Consistent and significant (p less than 0.001) reductions in pulmonary vascular resistance (25% before, 23% after, cardiopulmonary bypass) and mean pulmonary artery pressure (14% before, 13% after, cardiopulmonary bypass) were observed in the absence of significant changes in cardiac index, mean systemic arterial pressures or right or left atrial filling pressures. These findings indicate that after cardiopulmonary bypass, when right ventricular dysfunction with raised pulmonary vascular resistance may occur, selective reduction of right ventricular afterload with isosorbide dinitrate may prove beneficial.

Blood Pressure↗
PubMed1991

Comparison of the effect of isosorbide-5-mononitrate and isosorbide dinitrate in a slow-release form on exercise-induced myocardial ischemia.

A randomized, double blind, placebo-controlled crossover study on 20 patients with exercise-induced angina pectoris and reproducible ST-segment depression during exercise-stress test was performed to compare the effect of a single dose of 120 mg of isosorbide dinitrate in a slow-release form with that of a twice-daily application of 20 mg of isosorbide-5-mononitrate. Symptom-limited exercise tests were done, and nitrate plasma levels were measured in the subjects 6, 10, and 24 hours after the first administration of the drug. Both drugs produced a highly significant reduction in the size of exercise-induced ST-depressions (P less than .001) 6 and 10 hours after the first administration of isosorbide dinitrate as well as 6 hours after the first and 4 hours after the second dose of isosorbide-5-mononitrate. The effect was still significant (P less than .05) 24 hours after the administration of isosorbide dinitrate in a slow-release form and 18 hours after the second dose of isosorbide-5-mononitrate. In the case of the drug isosorbide dinitrate, nitrate plasma levels for its metabolite, isosorbide-5-mononitrate, were highest 10 hours after first application. In the case of the drug isosorbide-5-mononitrate, nitrate plasma levels were highest 4 hours after the second dose. Two 20 mg doses of isosorbide-5-mononitrate and a single dose of 120 mg isosorbide dinitrate in a slow release form have a comparable effect on the reduction of exercise-induced ST-segment depressions.

Adult↗
PubMed1978

A patient with repeated syncopal attacks after using isosorbide dinitrate.

The case of a patient with repeated attacks of collapse induced by sublingual isosorbide dinitrate is reported. The patient was an 81 year-old female who was admitted to Yura Hospital because of attacks of precordial pain. Several minutes after the sublingual administration of isosorbide dinitrate (10 mg) for an anginal attack, she developed a sensation of general weakness, and thereafter because unconscious. Arterial blood pressure fell and became unmeasurable. Electrocardiograms recorded during the syncopal attack showed sinus tachycardia and significant elevation of ST-segment in right precordial leads. In response to a drip infusion of noradrenaline, arterial blood pressure returned to normal with recovery of consciousness. Two similar syncopal attacks induced by sublingual isosorbide dinitrate occurred in the next three days. These attacks were not due to augmentation of the vagal reflex. Decrease of venous return probably was the primary etiological factor.

Aged↗
PubMed1977

Plasma concentrations of isosorbide dinitrate after oral administration of a sustained-release formulation to human subjects.

1. A peak of mean plasma concentrations of isosorbide dinitrate of 5.8 ng/ml was reached at 0.5 h after a single oral dose of 5 mg in a standard tablet formulation. Thereafter mean concentrations declined with a half-life of about 48 min. 2. A peak of mean concentrations of isosorbide dinitrate of 3.2 ng/ml was reached at 2--4 h after a single oral dose of 20mg in a sustained-realease capsule formulation (Iso Mack Retard). Thereafter mean concentrations declined by about twofold during 6 h and were still detectable at 12 h after dosing. 3. When corrected by dose/bodyweight variations, the mean area under the isosorbide dinitrate plasma concentration curve from the sustained-release capule was 76% of that from the standard tablet and this formulation-related difference in bioavailability was statistically significant (p less than 0.05). 4. The results showed that sustained-release formulation is a useful way to maintain plasma concentrations of isosorbide dinitrate for several hours.

Adult↗
PubMed1976

Isosorbide dinitrate and intra-aortic balloon pumping in preinfarctional angina. Effects on central circulatory dynamics.

The dynamics of the central circulation were measured by a radionuclidic technique in 18 men with high-risk preinfarctional angina who received therapy with isosorbide dinitrate (n equals 18), intra-aortic balloon pumping (n equals 8), or both (n equals 8). Administration of 5 mg of isosorbide dinitrate sublinqually was associated with a reduction in stroke volume index (SVI), cardiac index (CI), systemic arterial blood pressure, and left ventricular end-diastolic volume (LVEDV) and with increased left ventricular ejection fraction (LVEF). Intra-aortic balloon pumping did not alter SVI or CI, but decreased systolic blood pressure and LVEDV and increased LVEF and diastolic blood pressure. The combination of therapy with isosorbide dinitrate and intraaortic balloon pumping resulted in decreased SVI, systolic blood pressure, and LVEDV and increased LVEF. Thus, therapy with isosorbide dinitrate reduced left ventricular preload, and intra-aortic balloon pumping reduced blood pressure, which resulted in a decreased LVEDV and an increase in LVEF. Therapy with isosorbide dinitrate and intra-aortic balloon pumping act to alter central circulatory dynamics in favor of reducing myocardial oxygen demand.

Adult↗
PubMed1983

The effects of glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside on haemodynamics, coronary blood flow and myocardial oxygen consumption - an experimental study.

The influences of glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside intravenously on haemodynamics, coronary circulation and myocardial oxygen consumption were investigated in closed chest dogs (n = 8). In an attempt to simulate heart failure the dogs received blood transfusion (15 ml/kg) in the presence of halothane-induced myocardial depression. All three nitrates reduced the loads for the left ventricle. With isosorbide dinitrate and sodium nitroprusside the preload and pulmonary pressure decreased to a greater extent than with glyceryl trinitrate. The haemodynamic results suggest that sodium nitroprusside is the favourable nitrate in left ventricular failure because it produces a balanced reduction in the ratio of pre- and afterload. Four micrograms/kg X min sodium nitroprusside induced marked coronary dilatation; glyceryl trinitrate had only a slight coronary vasodilating effect. With isosorbide dinitrate the myocardial blood flow remained well adapted to oxygen demand, the coronary vascular resistance did not change. Sodium nitroprusside produced a significant change of the transmural myocardial blood distribution-expressed as the epi/endocardial blood flow ratio. The ratio was increased by sodium nitroprusside, much more than by glyceryl trinitrate or isosorbide dinitrate.

Animals↗
PubMed1994

Dose-Related Hepatic Blood Flow Effects Differentiate Nicorandil, Hydralazine, and Isosorbide Dinitrate in Healthy Subjects.

Dose response on hepatic blood flow of nicorandil (2.5, 5, and 10 mg), isosorbide dinitrate (5, 15, and 40 mg), and hydralazine (10, 25, and 50 mg) was assessed in 18 healthy subjects (6 per drug) using a three-period crossover design. Indocyanine green clearance was used to estimate hepatic blood flow before and at two timepoints after dosing. Greater hepatic blood flow changes occurred 90 (than 30) min after nicorandil and isosorbide dinitrate, and 60 (than 150) min after hydralazine. Nicorandil (mixed vasodilator) decreased hepatic blood flow by minus sign13 plus minus 4% (p < 0.05), minus sign15 plus minus 7%, and minus sign21 plus minus 6% (p < 0.05) (mean plus minus standard error of the mean) after 2.5, 5, and 10 mg, respectively; blood pressure was not reduced and heart rate was unchanged. Individual changes correlated poorly with plasma nicorandil concentrations. Isosorbide dinitrate (predominant venodilator) decreased hepatic blood flow by minus sign23 plus minus 9%, minus sign27 plus minus 5% (p < 0.05), and minus sign26 plus minus 7% (p < 0.05) after 5, 15, and 40 mg, respectively; blood pressure decreased (8--12 mm Hg) and heart rate increased (8 beats min(minus sign1)). Hydralazine (arterial dilator) increased hepatic blood flow by 29 plus minus 16%, 32 plus minus 11% (p < 0.05), and 33 plus minus 26% after 10, 25, and 50 mg, respectively; blood pressure was unchanged and heart rate increased (16 beats min(minus sign1)). Hepatic vascular resistance increased after nicorandil and isosorbide dinitrate but decreased after hydralazine. As assessed by hepatic blood flow response, nicorandil behaves more like a predominant venodilator than a direct arterial dilator. Dose and time variables were important to understanding the overall hemodynamic profile of each drug.

Journal Article↗
PubMed1995

Comparison of efficacy of nisoldipine, metoprolol, and isosorbide dinitrate in patients with stable exertional angina: a randomized, cross-over, placebo-controlled study.

We evaluated the acute antianginal effect of oral nisoldipine (10 mg), metoprolol (40 mg), and long-acting isosorbide dinitrate (20 mg) in 15 patients with stable exertional angina. The patients performed symptom-limited treadmill exercise at 2 h after the administration of placebo (Placebo stages 1 and 2) and each of the active drugs. After Placebo stage 1, the patients were randomized for cross-over evaluation of the acute effect of a single oral dose of placebo (Placebo stage 2), nisoldipine, metoprolol, or long-acting isosorbide dinitrate. All 15 patients developed angina during all of exercise tests and their exercise tests were terminated at the onset of angina. The time until development of 0.1 mV ST segment depression was increased by all three drugs compared to placebo, and it was significantly longer with metoprolol than with isosorbide dinitrate. Similarly, the time to ceasing exercise because of angina was also prolonged by all three drugs. The exercise time was longer with nisoldipine and metoprolol compared to isosorbide dinitrate, but there was no significant difference between nisoldipine and metoprolol. In conclusion, metoprolol and nisoldipine more effectively prolonged exercise compared to long-acting isosorbide dinitrate in patients with stable exertional angina.

Administration, Oral↗
PubMed1988

[Molsidomine and isosorbide dinitrate:/their comparative effectiveness in patients with exertion-induced stenocardia].

The markedness and duration of antianginal effects of 2 mg molsidomine and 10 mg isosorbide dinitrate were compared by means of repeated treadmill tests in 37 coronary patients with stable angina of effort. Peak magnitude of the effect was similar with both drugs, while the duration of the effect of isosorbide dinitrate (4.0 +/- 0.3 hrs) was significantly greater than that of molsidomine (3.4 +/- 0.3 hrs). Molsidomine reached its peak effect significantly earlier, as compared to isosorbide dinitrate. There was a significant correlation between the effectiveness of molsidomine and isosorbide dinitrate in the same patients.

Angina Pectoris↗
PubMed1977

Effect of swallowed isosorbide dinitrate on blood pressure, heart rate and exercise capacity in patients with coronary artery disease.

Blood pressures and heart rates were measured with the patients supine and standing after a placebo and small (5 to 10 mg) and large (10 to 30 mg) doses of isosorbide dinitrate were given orally in double-blind fashion to six patients. Compared to the findings after the placebo, the blood pressure level fell and the heart rate increased after the ingestion of isosorbide dinitrate. The changes were more striking with the patients standing than with them supine, and the larger dose of the drug produced greater changes than the smaller dose. The hemodynamic effects were usually apparent at 15 minutes, peaked between 30 and 120 minutes, and were still present at 240 minutes. Two hours after swallowing a 7.5 to 20 mg dose of isosorbide dinitrate or placebo, administered in random fashion, 10 patients with coronary artery disease and angina pectoris underwent graded, treadmill, exercise testing designed to provoke angina only after 3 minutes or more. Nine of them exercised longer and achieved higher maximal heart rates after taking the isosorbide dinitrate. Thus, in man, swallowed isosorbide dinitrate has a dose-related, "long-acting," pharmacologic effect, and when tested by properly designed protocols, it improves exercise capacity. However, because the problems of nitrate tolerance and dependence have not been resolved, the place of oral nitrates in the management of patients with angina pectoris remains uncertain.

Administration, Oral↗
PubMed1988

Effect of intravenous isosorbide dinitrate versus nitroglycerin on elevated pulmonary arterial wedge pressure during acute myocardial infarction.

To compare the acute and sustained effect of intravenous isosorbide dinitrate to intravenous nitroglycerin in patients with acute myocardial infarction and elevated pulmonary artery wedge pressure, 111 patients were randomized and studied within 96 hours of admission to the coronary care unit. All patients had a pulmonary artery wedge pressure greater than or equal to 10 mm Hg and received either isosorbide dinitrate (74 patients) or nitroglycerin (37 patients) for 24 to 48 hours. Blood pressure, heart rate, pulmonary artery wedge pressure, cardiac output, medication dose in micrograms per minute and retitration episodes were compared at baseline and at 6, 12, 18 and 24 hours. Both drugs significantly (p less than 0.05) lowered pulmonary artery wedge pressure and blood pressure and increased cardiac output. Isosorbide dinitrate required fewer retitration episodes and less increases in dosage than nitroglycerin at 24 hours. In the patient with acute myocardial infarction complicated by high pulmonary artery wedge pressure who requires intravenous nitrates for 24 hours, isosorbide dinitrate may offer the benefit of a more stable hemodynamic effect.

Aged↗
PubMed1988

Influence of exercise on plasma concentrations of isosorbide dinitrate.

As the fall in hepatic blood flow caused by exercise is expected to decrease the elimination of high extraction drugs, the influence of exercise on the fate of the anti-anginal drug isosorbide dinitrate has been assessed. Isosorbide dinitrate 10 mg was given orally, after an overnight fast, on 2 different days to 7 healthy volunteers and the plasma concentrations of the parent compound and its mononitrate metabolites were measured. Heavy bicycle exercise from the 45th to the 105th min after intake of the drug on one of the experimental days did not change the plasma isosorbide dinitrate concentrations as compared to those on the rest day. The concentrations of both mononitrates were lower on the exercise day, but the difference was already present before the exercise started.

Administration, Oral↗
PubMed1975

Effectiveness of isosorbide dinitrate and nitroglycerin in relieving angina pectoris during uninterrupted exercise.

Twenty patients with ischemic heart disease documented by coronary angiograms or ST segment depression in the ECG during treadmill walking, were administered sublingual nitroglycerin 0.3 to 0.6 mg on one occasion and a chewable form of isosorbide dinitrate 5 mg on another occasion during treadmill walking when anginal discomfort was definitely present at a mild degree of intensity. Despite continued walking at a constant speed and grade, angina was relieved in all patients, completely in most patients, partially in a few. The average time from administration of the medication to onset to relief was 74.7 seconds for nitroglycerin and 107.6 seconds for chewable isosorbide dinitrate. Average time to complete relief or maximal incomplete relief was 190.3 seconds for nitroglycerin and 315.1 seconds for chewable isosorbide dinitrate. Ischemic electrocardiographic changes were reverted toward normal by nitroglycerin in 13 subjects and by isosorbide dinitrate in 15. The differences in onset to complete relief were all statistically significant indicating that nitroglycerin is more rapid in its action than is chewable isosorbide dinitrate.

Administration, Oral↗
PubMed1977

Orally administered isosorbide dinitrate in patients with and without left ventricular failure due to acute myocardial infarction.

The oral effectiveness of 10 mg followed by 20 mg of isosorbide dinitrate in 21 patients with acute mycardial infarction was studied over a period of 13 hours. The patients were grouped according to initial left ventricular filling pressure: group I, pressure less than 20 mm Hg, and group II, pressure more than 20 mm Hg. Patients in group II had left ventricular failure. In both groups isosorbide dinitrate resulted in a significant decrease in pulmonary arterial pressure. The left ventricular filling pressure decreased in group I from 13.6 +/- 4.0 to 7.1 +/- 2.6 mm Hg (mean +/- 1 standard deviation) and in group II from 26.9 +/- 4.6 to 19.0 +/- 3.6 mm Hg (P less than 0.001). Cardiac output decreased in group I from 5.1 +/- 1.0 to 4.5 +/- 0.9 liters/min, whereas in group II it increased significantly from 3.5 +/- 0.8 to 4.1 to 0.9 liters/min (P less than 0.001). In both groups, peripheral arterial blood pressure decreased (P less than 0.60). Heart rate remained constant. Whether cardiac output increased or decreased was found to be dependent on the initial left ventricular filling pressure. In patients with an initially high value (above 20 mm Hg), the increase in cardiac output is probably due to the reduction of afterload. An additional factor may be the decrease in left ventricular filling pressure, which leads to an improved blood supply in the affected mural segments as a result of the decrease in the extravascular component of the coronary resistance. Significant changes in cardiac output and left ventricular filling pressure were achieved 3 to 5 hours after oral administration of isosorbide dinitrate. Clinical signs of failure were less pronounced. Isosorbide dinitrate is, therefore, a therapeutic agent in the treatment of left ventricular failure due to acute myocardial infarction.

Administration, Oral↗