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At least 1,225 records · Page 68Linked to original sources
PubMed1989

Relationship between the coronary diameter and occurrence of vasospastic angina in patients with normal coronary arteries.

Coronary artery diameters were measured after various interventions in 30 patients without angina pectoris (group 1) and in 15 with angina pectoris (group 2: rest, or rest and effort angina) who had normal coronary arteries. The coronary artery diameters were significantly smaller in many coronary segments in group 2 than in group 1 during a control state, after exercise and ergonovine, but became nearly identical after isosorbide dinitrate in both groups. Patients in group 1 had diffuse narrowing but no focal vasoconstriction after ergonovine and all the segments had a diameter of more than 50% of that after isosorbide dinitrate. The change of coronary artery diameter in group 2 patients who had no vasospasm by ergonovine was the same as that in group 1. Patients in whom vasospastic angina was induced had local vasoconstriction or severe diffuse narrowing (less than 45%). These results indicate that angina pectoris patients with normal coronary arteries had an acceleration of coronary arterial basal tone, but vasospastic angina pectoris was not induced just by the general response of the coronary artery to various interventions in addition to the accentuated basal tone. For vasospastic angina to occur, local abnormal response to various interventions must be present.

Adult↗
PubMed1993

Echocardiographic variables as prognostic indicators and therapeutic monitors in chronic congestive heart failure. Veterans Affairs cooperative studies V-HeFT I and II. V-HeFT VA Cooperative Studies Group.

BACKGROUND: Echocardiographic indexes of ventricular function have become indispensable in clinical cardiology but have not been tested as prognostic markers or therapeutic monitors in clinical trials. In two Veterans Administration trials on heart failure (Vasodilator-Heart Failure Trials I and II, V-HeFT I and II), echocardiographic variables were analyzed as predictors and monitors and were compared with other indicators of cardiac performance. METHODS AND RESULTS: Echocardiograms were recorded before randomization and at follow-up intervals. Baseline measurements of left ventricular internal diameters (LVIDd, LVIDs), wall thickness (THd, THs), radius to thickness ratios (Rd/THd, Rs/THs), and mitral E-point septal separation (EPSS) were evaluated as predictors of mortality individually, in multivariate regression models with each other, and with nonechocardiographic predictors. Within-subject changes were compared between treatment groups. Cumulative survival curves were compared between strata formed by cut-points of EPSS and Rs/THs data. In Cox regression analyses, EPSS, LVIDs, and Rs/THs were significant predictors of mortality. In V-HeFT I, Rd/THd was a predictor in the presence of ejection fraction and peak oxygen uptake. In patients with EPSS > or = 21, there was an 83% increase in mortality in the subgroup of patients with Rs/THs > or = 2.5 compared with Rs/THs < 2.5 (p = 0.003), whereas there was no statistical difference for EPSS < 21. EPSS showed improvement in patients treated with hydralazine-isosorbide dinitrate compared with placebo at 2 and 18 months and a trend toward deterioration between 36 and 66 months. In V-HeFT II, there were no differences between enalapril and hydralazine-isosorbide dinitrate groups at follow-up. CONCLUSIONS: Echocardiographic variables, EPSS, LVIDs, and Rs/THs were shown to be predictors of mortality and monitors of treatment for heart failure in clinical trials.

Drug Therapy, Combination↗
PubMed2000

A clinical investigation on tong xin luo capsule in treatment of coronary heart disease with silent myocardial ischemia.

36 cases of coronary heart disease with silent myocardial ischemia (SMI) were treated sequentially with Tong Xin Luo (TXL) capsule and isosorbide dinitrate in random order. The results showed that both drugs were effective in decreasing episodes of SMI and shortening the duration of asymptomatic myocardial ischemia. TXL, however, was found with a better action and was superior to isosorbide dinitrate. It was also found that TXL could improve diastolic function of the left ventricle as well.

Adult↗
PubMed1987

Nitrate tolerance.

The organic nitrates are the most widely used agents in the management of patients with angina pectoris. When initially administered by the oral route, the nitrates produce profound changes in systemic hemodynamics and significant and prolonged improvement in exercise duration. It has been shown that during short periods of regular oral nitrate administration, the hemodynamic, antiischemic and antianginal effects of the nitrates are greatly reduced. Thus, when initially administered, oral isosorbide dinitrate prolongs exercise duration for a period of several hours, but during sustained 4-times-daily therapy, exercise tolerance is improved for only 2 hours after administration. Studies with transdermal preparations of isosorbide dinitrate and nitroglycerin also show improvement during short-term administration for up to 8 hours, but after several days of once-daily therapy, the effects of these agents are similar to placebo. It is apparent that nitrate tolerance is a clinically relevant problem. Although tolerance develops rapidly during nitrate therapy, it is reversed promptly during nitrate-free periods. Oral nitrates maintain their antianginal effects when given 2 or 3 times daily with provision of a nitrate-free period. Studies are currently underway to investigate the effects of intermittent administration schedules with transdermal nitrate preparations.

Dosage Forms↗
PubMed1986

[Left ventricular function in dilated cardiomyopathy. Noninvasive determination of end-systolic stress-diameter and shortening fraction-stress relations].

The ejection fraction and fractional shortening are parameters of left ventricular function dependent on the conditions of load. They are not perfect indices of myocardial contractility. The study of the relationships between stress and diameter and fractional shortening and stress in end-systole provides a better means of assessing the contractile state of the myocardium. The relationships between end-systolic stress-diameter and end-systolic stress-fractional shortening were studied non-invasively in 10 normal subjects (Group I) and 7 patients with severe dilated cardiomyopathy (Group II). End-systolic longitudinal stress of the left ventricle was calculated from Grossman's formula by coupling automatic measurement of blood pressure (cuff method) with simultaneous M mode recordings guided by 2D echocardiography. The line of regression of end-systolic stress-end-systolic diameter was determined in all cases from a series of 14 points obtained after sublingual administration of 10 mg of isosorbide dinitrate. The line of regression of fractional shortening-end-systolic stress was established in both groups by using the values observed under basal conditions and at the peak of action of the isosorbide dinitrate. The following results obtained: Under basal conditions, patients in Group II had greater end-diastolic diameters (69 +/- 8 vs 49 +/- 4 cm, p less than 0.01), greater end-systolic diameters (61 +/- 8 vs 33 +/- 4 mm, p less than 0.001) and higher end-systolic stress (140 +/- 54 vs 67 +/- 13 10(3) dyn/cm2, p less than 0.001). Fractional shortening was lower in Group II than in Group I (12 +/- 5 vs 33 +/- 5%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

Behavioural effects of glutamate receptor agonists in morphine-dependent rats.

Glutamate receptors are implicated in the development and expression of drug dependence. Substantial experimental evidence suggests that antagonists acting at the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors attenuate the severity of opioid withdrawal. However, it is less clear whether opioid withdrawal can be potentiated by agonists of glutamate receptors. The present study evaluated the behavioural effects of various agonists of glutamate receptors, as well as a nitric oxide (NO) donor, in morphine-dependent rats trained to discriminate 0.1 mg/kg of naloxone from saline. None of the following drugs produced appreciable levels of naloxone-like responding (substitution tests) or potentiated the discriminative stimulus effects of naloxone: NMDA (3-56 mg/kg), glycine (100-1000 mg/kg), glutamate (1000-3000 mg/kg), kainate (0.3-3 mg/kg), isosorbide dinitrate (30-300 mg/kg). Nevertheless, expression of some morphine withdrawal-like somatic and behavioural signs ('wet-dog'-like shaking, scream on touch, ptosis, tremor, chewing, weight loss) was facilitated by NMDA, glycine, and isosorbide dinitrate. These results suggest that, compared to somatic symptoms, subjective effects of opioid withdrawal (as reflected by discriminative stimulus effects) are not mimicked by direct activation of glutamate receptors.

Animals↗
PubMedDate not supplied

Erythrocyte aldehyde dehydrogenase and disulfiram-like side effects of hypoglycemics and antianginals.

Disulfiram-like responses to various drug therapies are caused by elevated ethnol-derived blood acetaldehyde concentrations resulting from drug-induced inhibition of aldehyde dehydrogenase enzymes. We have found that the nitrate ester antianginal drugs, isosorbide dinitrate and nitroglycerin, are potent inhibitors of human erythrocyte aldehyde dehydrogenase. To further characterize this drug-induced enzyme inhibition, erythrocyte aldehyde dehydrogenase activities were measured in patients undergoing therapy with nitrate ester antianginals (isosorbide dinitrate and nitroglycerin) and sulfonylurea hypoglycemics (chlorpropamide and tolazamide). The erythrocyte enzyme was decreased by approximately 25% in sulfonylurea-treated patients, whereas in the nitrate ester-treated patients, an 88% inhibition was observed. The minimal enzyme inhibition in the sulfonylurea-treated group was unexpected because these therapies have well-documented disulfiram-like side effects. This weak inhibition contrasted with the severe inhibition observed in the nitrate ester-treated group where the disulfiram-like side effects are not considered a serious clinical problem. This apparent anomaly was attributed to differences in inhibition of the erythrocyte and liver aldehyde dehydrogenase by the parent drugs and their hepatic metabolites.

Aldehyde Dehydrogenase↗
PubMed1998

Two cases of hypertrophic cardiomyopathy with coronary vasospasm.

Chest pain in patients with hypertrophic cardiomyopathy seems to be caused by relative myocardial ischemia due to the left ventricular outflow pressure gradient and myocardial hypertrophy. However, in 2 cases of hypertrophic cardiomyopathy chest pain was associated with coronary vasospasm. Thus, chest pain in these cases was decreased not by a beta-blocker but by isosorbide dinitrate and a calcium antagonist. Because beta-blockers are commonly used for hypertrophic obstructive cardiomyopathy and chest pain may be aggravated by beta-blockers in patients with coronary vasospasm, a combination of beta-blocker, isosorbide dinitrate and calcium antagonist was necessary for this hypertrophic cardiomyopathy with variant angina.

Adrenergic beta-Antagonists↗
PubMed1996

[The emergence of silent myocardial ischemia as the manifestation of the nitrate withdrawal syndrome in patients with ischemic heart disease].

The aim of the study was to evaluate feasibility of emergence of nitrate withdrawal syndrome consequently to discontinuation of short-term nitrate administration for coronary heart disease. 12 males with stable effort angina functional class III were subjected to 24-h Holter ECG monitoring. In a randomized cross-over trial each patient received for 3 days isosorbide dinitrate (10-30 mg 4 times a day) followed by 3-day course of placebo. The monitoring was performed on day 3 of the drug or placebo administration and on the first day of their withdrawal. Isosorbide dinitrate discontinuation had no negative effects on the patients' condition though significantly increased the number and duration of episodes of asymptomatic myocardial ischemia. 4 patients developed episodes of asymptomatic myocardial ischemia at rest which were not observed in placebo application. It is believed that much caution should be used in planning interrupted regimes of nitrates therapy in patients with severe angina pectoris.

Aged↗
PubMed1986

Hemodynamic factors limiting the response to transdermal nitroglycerin in severe chronic congestive heart failure.

To clarify the continuing controversy concerning the use of transdermal nitroglycerin (TDN), the shortterm hemodynamic responses to sublingual, oral and transcutaneous nitrates were evaluated and compared in 22 patients with severe chronic congestive heart failure. Sixteen patients showed favorable hemodynamic effects with TDN, but the doses needed to achieve this response varied greatly: 10 mg/24 hours in 6 patients, 20 mg/24 hours in 5 patients, 40 mg/24 hours in 3 patients and 60 mg/24 hours in 2 patients. Of the 6 remaining patients, 3 did not respond to high-dose TDN even though they showed marked effects after sublingual and oral nitrate administration; 3 others did not respond to any nitrate formulation by any route. TDN produced immediate increases in cardiac index and decreases in right and left ventricular filling pressure, mean arterial pressure and systemic vascular resistance (p less than 0.01). These effects, however, became rapidly attenuated within 3 to 6 hours; after 18 to 24 hours, only modest decreases in right and left ventricular filling pressures were observed. After removal of TDN treatment, rebound decreases in cardiac index and rebound increases in mean arterial pressure and systemic vascular resistance occurred, but right and left ventricular filling pressures returned to pretreatment values without rebound changes. Isosorbide dinitrate, 40 mg orally, produced hemodynamic effects that were greater in magnitude than effects seen after administration of TDN (p less than 0.05 to 0.01), but 4 patients in whom tolerance to TDN developed showed reversible cross tolerance to oral isosorbide dinitrate.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed2001

Left ventricular diastolic heart failure with normal left ventricular systolic function in older persons.

Underlying causes and precipitating causes of congestive heart failure (CHF) should be treated when possible. Older persons with CHF and normal left ventricular (LV) ejection fraction should have maintenance of sinus rhythm, treatment of hypertension and myocardial ischemia, slowing of the ventricular rate below 90 beats/minute, and reduction of salt overload. First-line drug treatment in the management of these persons is the use of loop diuretics combined with beta blockers as tolerated. Angiotensin-converting enzyme (ACE) inhibitors should be administered if CHF persists despite diuretics and beta blockers. If persons are unable to tolerate ACE inhibitors because of cough, rash, or altered taste sensation, angiotensin II type 1 receptor antagonists should be given. If CHF persists despite diuretics, beta blockers, and ACE inhibitors or the person is unable to tolerate beta blockers, ACE inhibitors, and angiotensin II type 1 receptor antagonists, isosorbide dinitrate plus hydralazine should be administered. Calcium channel blockers should be used if CHF persists despite administration of diuretics and the person is unable to tolerate beta blockers, ACE inhibitors, angiotensin II type 1 receptor antagonists, and isosorbide dinitrate plus hydralazine. Digoxin, beta blockers, verapamil, and diltiazem may be used to slow a rapid ventricular rate in persons with supraventricular tachyarrhythmias. Digoxin should not be used in persons with CHF in sinus rhythm with normal LV ejection fraction.

Adrenergic beta-Antagonists↗
PubMed1976

[The effects of verapamil on angina threshold during exercise (author's transl)].

The efficacy and duration of the effects of verapamil on angina threshold during exercise were examined in five patients with proved angina pectoris, with the experimental model of a latin square 5 X 5. The effects of verapamil (0,1 mg/kg i.v.) were compared with those of a placebo (20 ml saline i.v.), of isosorbide dinitrate (5 mg, sublingual), of propranolol (0,1 mg/kg i.v.), and of dipyridamol (20 mg i.v.). All the treatments were studied within 20 minutes after administration; the efficacy of the "drugs" was checked against placebo. Verapamil and isosorbide dinitrate significantly prolonged the duration of exercise and total amount of work done before angina and EKG alteration appearance. Similar changes were observed after propranolol, but not significantly different from the effects of placebo. Dipyridamol reduced thw work performance, without significant difference from placebo. The effects of verapamil, though less marked than its peak effects, were still present 70 minutes after administration. The possible mechanism of work performance improvements induced by verapamil in angina pectoris is briefly discussed on the basis of the Triple Product changes observed during exercise.

Adult↗
PubMedDate not supplied

A randomised study of the haemodynamic changes induced by venodilatation and arteriolar dilatation singly and together in left ventricular failure complicating acute myocardial infarction.

A randomised between-group study of the immediate haemodynamic effects of venodilatation by intravenous isosorbide dinitrate infusion (50-200 micrograms/kg/h) and arteriolar dilatation by intravenous hydralazine bolus (0.15 mg/kg) given either in random sequence (Groups 1 and 2; n = 12) or simultaneously (Group 3; n = 6) was undertaken in 18 men with radiographic and haemodynamic evidence (left ventricular [LV] filling pressure greater than 20 mm Hg) of LV failure 6-19 h following acute myocardial infarction. Control measurements (1 h) preceded either two consecutive 90-min treatment periods (Groups 1 and 2) or a single 90-min period (Group 3). Given independently, both drugs reduced systemic arterial pressure and vascular resistance, whereas only isosorbide dinitrate reduced LV filling pressure and only hydralazine increased cardiac output and stroke volume. Isosorbide dinitrate/hydralazine in combination significantly reduced LV filling pressure, systolic and diastolic arterial pressure, and total systemic vascular resistance. Cardiac output, stroke volume, and heart rate were increased. In conclusion, combined arteriolar dilatation and venodilatation appears to be of greater haemodynamic benefit than either alone, if the fall in mean systemic pressure does not compromise peripheral perfusion.

Adult↗
PubMed1987

Antithrombogenic endothelial cell defense. Basal characteristics in cultured endothelial cells and modulation by short-term and long-term exposure to isosorbide nitrates.

The antithrombogenic endothelial cell defense (ATECD) describes the properties that enable the endothelium to prevent circulating blood platelets from adhering to, or aggregating on, the vascular wall. ATECD was investigated in an experimental model in which bovine passage 0 cultured endothelial cells (EC) were incubated with aggregating platelets and autologous plasma in a computer-operated aggregometer-like device. A maximal platelet aggregation required 150 X 10(-6) M adenosine diphosphate (ADP) to be present in ECs. A 5-minute coincubation for ECs and platelets was found to be adequate in evaluating the maximal ATECD value. By increasing the EC number in the aggregation suspension, platelet aggregation was progressively inhibited through a sigmoid curve (50% inhibition of aggregation required 2 X 10(4) EC). Pharmacologic modulations of ATECD by isosorbide dinitrate (ISDN) + 2-isosorbide mononitrate (2-ISMN) + 5-isosorbide mononitrate (5-ISMN) were investigated under experimental conditions reflecting either an acute nitrate effect (platelet + control ECs + drug + ADP) or a chronic effect (platelet + 5-day nitrate-treated ECs + ADP). Under acute circumstances, ISDN antiplatelet activities were profoundly magnified by ECs. Aggregation was fully arrested with 5 X 10(-5) M ISDN and an EC number of 2 X 10(4), whereas the same ISDN concentration alone induced 30% inhibition of control aggregation. In contrast, there were no significant changes in platelet aggregation whether incubation was done in the presence or absence of 2-ISMN or 5-ISMN, ISDN metabolites. Long-term exposure of ECs to isosorbide nitrates (ISN) resulted in increased acquired EC changes in ATECD. 5-ISMN was a poor antiplatelet agent but was capable of counteracting ISDN effects on ATECD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed2000

[Comparative antianginal efficiency of prolonged nitrites in patients treated surgically for ischemic heart disease].

To compare clinical and cost effects of prolonged nitrates (sustac-forte), isosorbide dinitrate (nitrosorbide) and isosorbide-5-mononitrate (mono mac 40), a retrospective analysis was made of 112 cases of ischemic heart diseases (functional class II-III) treated surgically. During their rehabilitation in sanatorium 30-40 days after coronary artery bypass operation the patients received sustac forte (n = 37), nitrosorbide (n = 36), mono mac 40 (n = 39). By clinico-functional effect mono-mac appeared 1.5-2 times more effective than sustac forte or nitrosorbide. By cost-effect parameters, a course 30-day treatment was the cheapest when made with mono mac (3 times more cost effective than sustac-forte and 2 times more effective than nitrosorbide).

Angina Pectoris↗
PubMedDate not supplied

[Clinico-pharmacologic activity of organic nitrates].

A summary of the published literature is presented together with findings from the author's investigations designed to study clinical-and-pharmacological properties of organic nitrates. The history is written up of discovery of a therapeutic effect of organic nitrates, pharmacokinetics, pharmacodynamics are described, indications for administration thereof are determined, ill effects of glycerol trinitrate (nitroglycerin), isosorbide dinitrate (nitrosorbide) and isosorbide-5-mononitrate (olicard) are described.

Humans↗
PubMed1986

Haemodynamic effects of vasodilating drugs on the common carotid and brachial circulations of patients with essential hypertension.

The haemodynamic pattern of the common carotid artery was studied in men with sustained essential hypertension using pulsed Doppler methods before and after administration of vasodilating drugs. Captopril produced both a fall in vascular resistance and an increase in arterial diameter of the common carotid artery. Isosorbide dinitrate increased markedly the arterial diameter but did not change vascular resistance. Nitrendipine decreased vascular resistance with no change in the arterial diameter. In the common carotid circulation of patients with essential hypertension, vasodilating drugs may either dilate small arteries (nitrendipine), large arteries (isosorbide dinitrate), or both (captopril).

Administration, Oral↗
PubMed1993

N-acetylcysteine inhibits angiotensin converting enzyme in vivo.

Nitrate tolerance has been explained by 1) a direct loss of pharmacological effect due to reduced bioconversion and 2) an indirect effect due to activation of the renin/angiotensin system and counter-regulatory vasoconstriction. The sulfhydryl compound N-acetylcysteine (NAC) has been shown to attenuate and partly counteract tolerance to nitrates, and this effect has been attributed to a nitrate/sulfhydryl interaction and increased production of vasoactive intermediates. The effect of NAC on counter-regulatory mechanisms is, however, unknown. This study examined whether NAC modulates the function of the renin/angiotensin system in normal rats and in nitrate-tolerant healthy volunteers. Animal study: Conscious rats received NAC (5 mmol/kg/hr i.v., n = 8) or placebo (N-acetylserine, n = 8). Two hours of NAC infusion significantly reduced the pressor effect of angiotensin I (ANG I) by 39 +/- 14% (mean +/- SEM) and reduced angiotensin converting enzyme activity by 31% in plasma (N-acetylserine: 74 +/- 9 nmol/min/mg, NAC: 51 +/- 7) and 43% in kidney (N-acetylserine: 0.9 +/- 0.3, NAC: 0.5 +/- 0.1 nmol/min/mg protein) (P < .05). Clinical study: Isosorbide dinitrate (5 mg/hr) was infused into six male volunteers for 48 hr. NAC (2 g i.v. followed by 5 mg/kg/hr) was co-infused from 24 to 48 hr. Plasma angiotensin II (ANG II) increased during the first 24 hr of isosorbide dinitrate infusion and decreased from 28 +/- 4 to 14 +/- 2 ng/l after 2 hr of NAC infusion (P < .05). The results suggest that sulfhydryl supplementation modifies the function of the renin/angiotensin system in vivo, an effect probably mediated by inhibition of angiotensin converting enzyme activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcysteine↗