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PubMedDate not supplied

[The effect of sodium nitroprusside and nitro-containing vasodilators on rat liver microsomal mono-oxygenases].

It has been shown in vitro that sodium nitroprusside (SN) causes a concentration-dependent suppression of the enzymatic activity of aminopyridine demethylase-APDM(IC50 = 1.86 x 10(-4) M) and ethoxycoumarin O-deethylase-ECOD(IC50 = 1.46 x 10(-4) M) in hepatic microsomes of Wistar rats, which is related to different isoforms of cytochrome P-450. The inhibiting effect of other nitro compounds (nitroglycerin and isosorbide dinitrate) in relation to APDM is less marked than that of SN. These compounds have practically no effect on ECOD activity. It is assumed that the degree of the inhibiting effect of SN, nitroglycerin, and isosorbide dinitrate is connected with the mechanism of NO release.

Animals↗
PubMed2001

The human G-protein beta3 subunit C825T polymorphism is associated with coronary artery vasoconstriction.

AIMS: Abnormal coronary vasomotion plays a role in the clinical expression of coronary artery disease. We hypothesized that the functional C825T polymorphism located in the ubiquitous G-protein beta3 subunit, implicated in the cellular signal transduction of many receptors, could modify artery coronary vasomotion. We assessed the potential association of the pertussis toxin-sensitive G protein beta3 subunit (GNB3) gene C825T polymorphism on coronary vasomotion in humans. METHODS AND RESULTS: We examined the response of angiographically normal human coronary arteries (n=131) after intravenous injection of methylergonovine maleate, a vasoconstrictor, followed by injection of isosorbide dinitrate, a vasodilator, according to GNB3 genotypes. Coronary vasomotion was assessed with quantitative coronary angiography. Subjects bearing at least one T allele had greater susceptibility to vasoconstriction in response to methylergonovine maleate than CC subjects, whereas vasodilation in response to isosorbide dinitrate did not differ among the different genotypes. CONCLUSION: The C825T polymorphism of the G-protein beta3 subunit may be a genetic determinant of coronary artery vasomotion in humans.

Coronary Angiography↗
PubMed2000

Coronary Artery Spasm.

Attacks of variant angina usually respond promptly to sublingual administration of short-acting nitrates (nitroglycerin, 0.3 to 0.4 mg, or isosorbide dinitrate, 5 to 10 mg), which may be repeated after 3 to 5 minutes if pain persists. In the rare cases resistant to sublingual nitrates, sublingual nifedipine (5 to 10 mg) or, when readily available, intravenous nitrates (nitroglycerin or isosorbide dinitrate, 2 to 10 mg) or calcium antagonists (verapamil, 5 to 10 mg, or diltiazem, 0.15 mg/kg) can be given. All attempts to prevent ischemic attacks by means of specific receptor blockade in patients with vasospastic angina have been unsatisfactory. This may be either because the doses of the blockers used were insufficient or, more likely, because the blockade of a single receptor-agonist interaction leaves receptors for other vasoconstrictor stimuli unopposed and therefore capable of eliciting spasm. Thus, for instance, alpha-adrenergic, serotoninergic, and thromboxane A(2) antagonists all failed to reduce significantly the number of anginal attacks, although they appeared to be effective in some patients. Until the actual causes of the coronary smooth muscle hyperreactivity to constrictor stimuli are known, treatment of vasospastic angina is based on the use of nonspecific vasodilators. Indeed, the mainstay of pharmacologic treatment of coronary artery spasm is calcium channel blocking agents together with nitrates to cover the periods in which spasm is most likely to occur. These powerful vasodilating agents, at their usual doses, are able immediately and completely to control the recurrences of ischemic attacks in as many as 80% of patients. Moreover, some studies have shown that use of calcium antagonists significantly improves clinical outcome in patients with variant angina.

Journal Article↗
PubMed1982

The effect of vasodilator therapy on systolic and diastolic time intervals in congestive heart failure.

To determine the effects of vasodilator drugs on systolic and diastolic time intervals in patients with congestive heart failure, these noninvasive measurements were made in 50 patients with moderately severe disease before and after vasodilator therapy. These data were compared with direct hemodynamic measurements obtained simultaneously from a flow-directed triple-lumen pulmonary artery catheter placed in each patient. Oral vasodilators included isosorbide dinitrate 20 mg (n-8), hydralazine 75 mg (n-8), and 100 mg (n-8), and first-dose prazosin 2 mg (n-8) and 5 mg (n-8). Ten additional patients received intravenous dose-response infusions of isosorbide dinitrate, nitroglycerin, and nitroprusside. Increases in cardiac output and stroke volume effected a decrease (improvement) in the systolic time interval parameter of ventricular performance, PEP/LVET. The correlation coefficient for vasodilator-induced changes in cardiac output vs changes in PEP/LVET was -0.82 (P less than 0.05) and for changes in stroke volume and PEP/LVET was -0.75 (P less than 0.05). In general, the diastolic time period was not significantly affected by these drugs. The systolic time intervals are a simple and useful method for evaluation of vasodilator therapy in patients with congestive heart failure.

Administration, Oral↗
PubMed1987

[Calcium-blocking effect of nitro compounds in human platelets: correlation with changes in the cyclic guanosine monophosphate level].

The effects of nitrates on Ca2+ increase and cyclic nucleotide content in human platelets were studied. Nitroglycerin, isosorbide dinitrate and sodium nitroprusside were found to inhibit the intracellular Ca2+ increase induced by the platelet activating factor, ADP and a stable thromboxane A2 analog--U46619. The inhibiting effect of sodium nitroprusside manifested itself at lower concentrations than those of nitroglycerin and isosorbide dinitrate. Nitroglycerin suppressed the Mn2+ entry into the cells and caused a 2-fold increase of the cGMP content which correlates with the calcium blocking activity. Methylene blue, a guanylate cyclase and glutathione reductase inhibitor, decreased the calcium blocking effect of nitroglycerin and its influence on the cyclic nucleotide content but failed to suppress the inhibitory effect of sodium nitroprusside. The data obtained suggest that the effects of nitrates on platelets are mediated by their influence on guanylate cyclase which leads to a cyclic nucleotide content increase and to a calcium blocking effect.

Blood Platelets↗
PubMed1989

The clinical significance of nitrate tolerance in patients with chronic heart failure.

Tolerance develops during the prolonged use of organic nitrates in patients with chronic heart failure in a fashion similar to its development in patients with angina pectoris, the magnitude of tolerance development being directly proportional to the frequency of dosing. When nitroglycerin is given continuously or when isosorbide dinitrate is administered frequently throughout the day (e.g., every 4h), haemodynamic tolerance develops completely in most patients within 24-48h. Such tolerance can be avoided, however, when these drugs are given intermittently (e.g., every 8 or 12 h). Unfortunately, most clinical trials with isosorbide dinitrate have attempted to produce continuous haemodynamic effects by administering the drug at frequent intervals; this may explain why these trials have produced equivocal results. Two mechanisms have been proposed to explain the development of tolerance in patients with chronic heart failure. According to the first hypothesis, tolerance develops as a result of the depletion of intracellular sulfhydryl groups that are essential to the ability of nitroglycerin to activate guanylate cyclase--the key enzyme in the action of nitrates on blood vessels. According to the second hypothesis, tolerance develops as a result of the activation of endogenous neurohormonal systems; the resulting vasoconstriction limits the direct effects of the nitrovasodilators. A better understanding of both mechanisms may lead to interventions that will circumvent the development of tolerance and enhance the efficacy of long-term nitrate therapy.

Drug Tolerance↗
PubMed1996

Induction of polymorphic ventricular tachycardia by programmed ventricular stimulation in vasospastic angina pectoris.

This study was designed to examine the ventricular vulnerability of patients with vasospastic angina. Fourteen patients (mean age 57 +/- 9 years) with vasospastic angina underwent electrophysiologic testing during the asymptomatic phase (baseline) and after the relief of acetylcholine-induced spasm with isosorbide dinitrates. Twenty patients without structural heart disease served as a control group. By programmed ventricular stimulation, polymorphic ventricular tachycardia (VT) was induced at baseline in 6 of 14 patients, with 1 patient developing ventricular fibrillation and 7 of 14 patients developing repetitive ventricular responses. After isosorbide dinitrate, polymorphic VT was induced in only 1 patient who had ventricular fibrillation at baseline. Repetitive ventricular responses were induced in 3 of 5 patients who had VT at baseline and in 4 of the 7 patients with repetitive ventricular responses at baseline. There was a significant difference in the incidences and severity of induced ventricular arrhythmias between the 2 phases (p <0.01). Among 20 control subjects, repetitive ventricular responses were induced only in 6 patients, but no VT was induced. There was a significant difference in the incidence of induced ventricular arrhythmias and VT at baseline between the vasospastic angina and control groups (p <0.001 and <0.01, respectively). Thus, patients with vasospastic angina had increased ventricular vulnerability, even during the symptom-free period without ischemic events, which could predispose to the development of life-threatening arrhythmias aggravated by vasospastic attacks.

Adult↗
PubMed1995

Progression and regression of coronary stenosis in the long-term follow-up of vasospastic angina.

BACKGROUND: Whether focal vasospasticity plays a pathogenic role in the progression or regression of coronary atherosclerosis is unknown. To determine whether evidence for such a role exists, we studied long-term changes in coronary luminal measurements in patients with vasospastic angina. METHODS AND RESULTS: Quantitative coronary angiography and repeated ergonovine provocation tests were performed 45 +/- 16 months apart in 30 patients. All patients had vasospastic anginal symptoms and coronary spasm on the initial provocation test. On the 30 patients, 16 had persistent symptoms of vasospastic angina and showed coronary spasm at the same site on the follow-up angiogram (group 1), while the remaining 14 whose vasospastic anginal symptoms disappeared at follow-up demonstrated a negative response to ergonovine on the follow-up tests (group 2). There was no significant difference in patients' baseline characteristics between the two groups. Long-term changes in minimal (MLD) and mean (MEAN) luminal diameter were measured (in millimeters) after administration of isosorbide dinitrate in 19 spastic and 93 nonspastic segments in group 1 and in 17 previously spastic and 81 nonspastic segments in group 2. Both MLD and MEAN were measured in 210 coronary segments of the 30 patients at baseline and after administration of ergonovine and isosorbide dinitrate by use of a computer-based quantitative coronary angiography system. Stenosis progression and regression of individual lesions were defined as a change in MLD of > or = 0.40 mm. In group 1, both the MLD and MEAN of 19 spastic segments were significantly smaller (progression) at follow-up compared with the initial angiogram (MLD, 2.21 +/- 0.54 initially versus 1.95 +/- 0.65 at follow-up, P < .01; MEAN, 2.80 +/- 0.56 initially versus 2.56 +/- 0.58 at follow-up, P < .01), whereas the MLD and MEAN of 93 nonspastic segments in group 1 were not significantly different between the initial and follow-up angiograms (MLD, 2.47 +/- 0.67 initially versus 2.44 +/- 0.69 at follow-up, P = NS; MEAN, 2.96 +/- 0.69 initially versus 2.91 +/- 0.68 at follow-up, P = NS). In group 2, the MLD of the 17 previously spastic segments significantly improved (regression) at follow-up (MLD, 1.99 +/- 0.68 initially versus 2.24 +/- 0.54 at follow-up, P < .05); the MLD and MEAN of the 81 nonspastic segments were not significantly different (MLD, 2.36 +/- 0.59 initially versus 2.39 +/- 0.60 at follow-up, P = NS; MEAN, 2.81 +/- 0.58 initially versus 2.81 +/- 0.61 at follow-up, P = NS). In group 1, significant stenosis progression of individual lesions was observed more frequently at spastic than nonspastic segments (6 of 19 versus 10 of 93, P < .05), whereas stenosis regression was observed in no spastic and 3 nonspastic segments (P = NS). In group 2, stenosis progression was observed at 1 previously spastic segment and 4 nonspastic segments (P = NS), while significant stenosis regression of individual lesions was seen more commonly in previously spastic than nonspastic segments (6 of 17 versus 7 of 81, P < .01). CONCLUSIONS: These results have demonstrated in patients an association between persistent vasospastic activity and progression of atherosclerosis and an association between cessation of vasospastic activity and regression of atherosclerosis.

Adult↗
PubMed1999

Antidepressant treatment of patients with diffuse esophageal spasm: a psychosomatic approach.

The cause of diffuse esophageal spasm (DES) has not been clearly established, and effective treatment is lacking. To determine whether a psychosomatic approach can be effective in treating DES patients, nine patients and 26 healthy volunteers were studied. Esophageal manometry and psychological testing were performed in both groups. The psychological background of the DES patients was investigated. Psychiatric diagnoses were made according to the criteria outlined in the Diagnostic and Statistical Manual of Mental Disorders, 3rd edition, revised. The authors started psychosomatic treatment with isosorbide dinitrate for 1 month, then prescribed serotonin reuptake inhibitor antidepressants for an additional month. Anxiety and depression scores were substantially higher for the DES group than for the control group. Five of the nine DES patients (56%) were diagnosed as having major psychiatric disorders. Only one patient showed improvement with isosorbide dinitrate, and eight patients improved with antidepressants. These initial observations suggest that psychosomatic treatment with antidepressants may be effective in the treatment of DES.

Adult↗
PubMed1997

Therapy of congestive heart failure in elderly persons.

LVEF should be measured in all elderly persons with CHF Underlying causes and precipitating causes of CHF should be treated. Persons with CHF associated with abnormal LVEF should be treated with a low sodium diet, diuretics, and ACE inhibitors. If CHF persists, digoxin should be added. If CHF still persists, isosorbide dinitrate plus hydralazine should be added. If CHF still persists, a beta blocker should also be added. However, calcium channel blockers should not be used. Persons with CHF associated with normal LVEF should be treated with a low sodium diet, diuretics, and ACE inhibitors. If CHF persists, a beta blocker, isosorbide dinitrate plus hydralazine, or a calcium channel blocker should be added to the therapeutic regimen. If sinus rhythm is present, digoxin should not be used. Persons with CHF and abnormal or normal LVEF unable to tolerate ACE inhibitors should be treated with losartan.

Aged↗
PubMed1994

Response of conductance and resistance coronary vessels to scalar concentrations of acetylcholine: assessment with quantitative angiography and intracoronary Doppler echography in 29 patients with coronary artery disease.

Abnormal vasoreactivity of the large conductance arteries has been observed in the presence of impaired endothelial function. More recently, experimental and clinical reports have shown that in early coronary atherosclerosis the impairment of the endothelium-mediated vasodilatation also involves the resistance arteries. The aim of this study is the correlation of endothelium-dependent vasodilatation of conductance and resistance vessels in coronary arteries without significant stenoses. In 29 patients (aged 57 +/- 9 years, 24 men and 5 women) undergoing coronary angioplasty, a Doppler guide wire and a perfusion catheter were introduced into the proximal segment of an artery with less than 30% diameter stenosis. Selective infusions of papaverine (bolus of 7 mg), acetylcholine (continuous infusion of 0.036, 0.36, and 3.6 micrograms/ml at a flow rate of 2 ml/min), and isosorbide dinitrate (bolus of 3 mg) were sequentially performed. Heart rate, aortic blood pressure, and blood flow velocity were continuously measured. Mean cross-sectional areas of a proximal and a distal arterial segment were measured in baseline conditions, at the end of each infusion of acetylcholine, and at the peak effect of isosorbide dinitrate with quantitative angiography (CAAS System; Pie Medical Data, Maastricht, The Netherlands). Coronary blood flow was calculated from the time-averaged flow velocity and the cross-sectional area at the site of the Doppler sample volume. Coronary flow resistance was calculated as mean aortic pressure divided by coronary flow. All of the concentrations of acetylcholine induced a significant vasoconstriction of the studied artery. At the maximal concentration of acetylcholine all but three patients (90%) showed a reduction of cross-sectional area (-24% +/- 20% and -22% +/- 20% for the proximal and distal segments, respectively, p < 0.00001). Flow velocity showed a significant increase only with the two highest concentrations of acetylcholine. The maximal concentration induced a 105% +/- 138% increase from the baseline flow velocity (p < 0.001). The coronary flow changes after acetylcholine showed a large interpatient variability, with a mean increase from baseline after the highest dose of +43% +/- 85% (range, -60% +/- 239%), with the presence of a flow reduction in 10 patients (35%). No clinical or angiographic variables showed a significant correlation with the cross-sectional area, flow velocity, and flow changes after infusion of acetylcholine.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1997

Treatment of congestive heart failure in older persons.

OBJECTIVE: To review the management of congestive heart failure (CHF), with emphasis on older adults. DATA SOURCES: A computer-assisted search of the English language literature (MEDLINE database) followed by a manual search of the bibliographies of pertinent articles. STUDY SELECTION: Studies on the management of CHF were screened for review. Studies in older people and recent studies were emphasized. DATA EXTRACTION: Pertinent data were extracted from the reviewed articles. Emphasis was on studies involving the older persons. Relevant articles were reviewed in depth. DATA SYNTHESIS: Available data about the management of CHF, with emphasis on studies involving older people, were summarized. CONCLUSIONS: Left ventricular ejection fraction (LVEF) should be measured in all older persons with CHF. Underlying causes of CHF should be treated when possible. Precipitating causes of CHF should be treated. Older persons with CHF associated with an abnormal LVEF should be treated with a low sodium diet and with diuretics plus angiotensin-converting enzyme (ACE) inhibitors. If CHF persists, digoxin should be added to the therapeutic regimen. If CHF still persists, isosorbide dinitrate plus hydralazine should be added. If CHF still persists, a beta blocker should also be used. Calcium channel blockers should not be used. Older persons with CHF associated with a normal LVEF should be treated with a low sodium diet and with diuretics plus ACE inhibitors. If CHF persists, a beta blocker or isosorbide dinitrate plus hydralazine or a calcium channel blocker should be added to the therapeutic regimen. If sinus rhythm is present, digoxin should not be used. The role of angiotensin II receptor antagonists such as losartan in the treatment of CHF is under investigation.

Aged↗
PubMed1993

[The problem of tolerance to nitrates and the means to resolve it in patients with exertional stenocardia].

The problem of nitrates tolerance and resistance has been studied for 10 years in a number of clinical pharmacological cross-over studies in patients with stable angina of effort by specially devised pharmacodynamic and pharmacokinetic methods. Both single doses in different medicinal forms and long-term course intake of nitrates were investigated. The results led the authors to the following conclusions: 1) tolerance to isosorbide dinitrate arises in 58% of the patients for 6-12 weeks under regular administration of the drug; 2) transdermal nitroglycerin (nitroderm) and in a less degree oral sustak under long-term treatment regimens become tolerable, whereas a buccal form (trinitrolong) secures a prolonged stable effect; 3) tolerance develops in 2-month administration of oral isosorbide-5-mononitrate; 4) donors of SH-group (methionine) and inhibitors of angiotensin-converting enzyme with SH-group and without it (captopril and perindopril, respectively) in single doses potentiate an antianginal effect of isosorbide dinitrate (even in initial resistance to nitrate), being ineffective in its absence; 5) molsidomine is promising in long-term regimens as an antianginal drug alternative to nitrates.

Angina Pectoris↗
PubMed1990

[Effect of nitrates on left ventricular function and exercise tolerance in patients with mild circulatory failure caused by ischemic heart disease].

In 26 patients with ischaemic heart disease with symptoms of mild chronic circulatory failure (NYHA grade II) aged 56.2 +/- 14.4 years the left ventricular function was tested by two-dimensional echocardiography, the exercise tolerance was determined on cycle ergometer at submaximal workloads, the cardiothoracic index (CTI) and cardiac volume index (CVI) were calculated from chest radiograms. The tests were done before and after 2 and 6 weeks of treatment with isosorbide dinitrate in doses of 49.6 +/- 15.2 mg/day. Isosorbide was found to increase somewhat the ejection fraction (EF), and to raise statistically significantly (p less than 0.05) the velocity of shortening of the circumferential fibres in left ventricular myocardium (mVCF), and to reduce the internal dimensions of the left ventricle (LVIDd and LVIDs), without changing the values of the ejection index (SVI) and cardiac index (CI). Decreased transverse dimensions of the left ventricle was correlated with a significant decrease of the CVI index. No statistically significant effect of isosorbide was noted on the parameters characterizing exercise tolerance but the quotient of the exercise-induced heart rate by the workload (HR/Wat) and the index of myocardial oxygen requirement (HRx Ps) were decreased in a demonstrable way.

Adult↗
PubMedDate not supplied

[An evaluation of the efficacy of nitrates (transdermal and peroral) in the management of the patient with a myocardial contusion].

Although thoracic trauma is frequently accompanied by myocardial injury; this later is often oversighted at early stages of trauma and misdiagnosed by the time complications are present. Myocardial abnormalities have been attributed to a reduction of cardiac flow. Nitroglycerin and isosorbide dinitrate, both agents with a known vasodilator effect on coronary arteries, might improve myocardial ischemic resulting from traumatic contusion. In order to compare safety and efficacy between two nitrates and placebo on myocardial contusion resulting from thoracic trauma, we carried out a comparative, prospective, single blind study. Subjects were randomly allocated to one of the following 3 groups: a) transdermal nitroglycerin, b) isosorbide dinitrate and c) placebo. Medication was dispensed for five days. Major endpoint were electrocardiographic abnormalities at entry and their final modifications. Other were severity injury score and myocardial enzyme levels. Twelve patients were included in each group. Four measured enzymes were high at entry, but MB fraction in the nitroglycerin group showed the most rapid normalization. Creatine phosphokinase and lactic dehydrogenase significantly correlated with severity injury index, but not MB fraction. Electrocardiographic normalization was mainly observed in the nitroglycerin group. Transdermal nitroglycerin systems demonstrated to be effective on recovering from electrocardiographic abnormalities resulting of myocardial contusion.

Administration, Cutaneous↗
PubMed1991

Responses of atherosclerotic human coronary arteries in vivo to the endothelium-dependent vasodilator substance P.

BACKGROUND: The effects of the endothelium-dependent vasodilator substance P (SP) on atherosclerotic human coronary arteries was studied. METHODS AND RESULTS: [125I]-SP binding to luminal cells was shown to be preserved in the atherosclerotic epicardial coronary arteries of four patients. No binding to medial smooth muscle cells was demonstrated. Intracoronary infusions of SP were undertaken in patients with coronary artery disease. SP was infused for 2-minute periods starting at a dose of 2.8 pmol/min rising by doubling increments to 22.4 pmol/min. Analysis of the epicardial coronary artery diameter, using a computerized analysis system (CAAS) of the angiograms, was performed at the end of each infusion. Analysis of seven smooth vessel segments from seven coronary vessels, which were stenosed at more proximal sites, was performed. Significant dose-dependent dilatation was seen (p = 0.04), which was maximal at 5.6 pmol/min SP. No additional dilatation was produced with 2 mg intracoronary isosorbide dinitrate (ISDN). Two of these seven patients showed no response to SP, and only one of these appeared to sustain dilatation with ISDN (2 mg intracoronary). In a second group of six patients with discrete coronary stenoses, analysis at the site of the stenosed segments appeared to reveal dilatation in response to SP in only one instance. One other stenotic segment dilated with isosorbide dinitrate but failed to dilate with SP; the remaining four were fixed. The segment immediately proximal to the stenosis preserved a dose-dependent vasodilator response. CONCLUSIONS: These findings demonstrate that the endothelium-dependent vasodilator substance P can still produce epicardial vasodilatation in vivo in the presence of coronary atherosclerosis.

Autoradiography↗
PubMed1999

In vitro skin permeation of Sinitrodil, a member of a new class of nitrovasodilator drugs.

Clinical trials have shown the potential of benzoxazinones, a new class of organic nitrates, in cardiovascular therapy. In particular Sinitrodil possesses a coronary vascular selectivity greater than that of Nitroglycerin and isosorbide dinitrate. The objective of this study was a preliminary evaluation of the ability of these new organic nitrate derivatives to reach therapeutical steady-state plasma concentrations following a transdermal administration. In vitro permeation studies through human stratum corneum and epidermis have been conducted on two members of this class: Sinitrodil (ITF 296) and ITF 1129. Comparative studies have also been carried out with Nitroglycerin, Isosorbide dinitrate and Nicorandil. Two different fixed concentrations were tested: 0.08% w/v solution and saturated solution. Sinitrodil could be considered a good candidate for transdermal administration on the basis of the in vitro permeation results and of the known therapeutical plasma concentration.

Benzoxazines↗
PubMed1981

[Coronary artery spasms with normal coronary arteries as the cause of recurrent ventricular fibrillations].

Coronary arterial spasms are thought to be responsible for acute myocardial infarction in some patients with normal coronary arteries. A report is presented on a patient with a history of Prinzmetal angina pectoris involving ST-segment elevations in the electrocardiogram and recurrent ventricular fibrillation. Selective coronary arteriography revealed normal coronary arteries. Administration of nifedipin and isosorbide dinitrate brought about prompt relief of pain. One year after cardiac catheterization the patient developed recurrent ventricular arrhythmias when administration of nifedipin was discontinued. It is concluded that coronary arterial spasms may occur in patients with normal coronaries and may cause transient myocardial ischemia with severe ventricular arrhythmias. A history of Prinzmetal angina pectoris is usually present and medical treatment consists in administration of nifedipin and isosorbide dinitrate.

Angina Pectoris↗