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At least 1,117 records · Page 62Linked to original sources
PubMed1986

New perspectives on the function of coronary artery spasm in acute myocardial infarction: the thromboischemic reentry mechanism. A review of 10 years research on the pathophysiology of AMI.

Research during the last ten years into the pathophysiology of acute myocardial infarction (AMI) has made it gradually clearer that this is a phasic event. A number of independent authors have made this conclusion quite obvious. The authors of this review suggest that the alternating sequence of coronary spasm and dilatation should be described as the "thromboischemic reentry mechanism," which itself leads to waves of reperfusion, producing characteristic episodic changes in some of the parameters of AMI. The spasms are brought about by substances let loose from aggregating platelets. Metabolites released during the concomitant ischemia lead the vessel from spasm to dilatation. Following thrombolytic treatment, the 'staccato' signs of myoglobinemia disappear, because of the withdrawal of the spasmogenic products of the platelets. It could also be shown that the concentration of myoglobin in the serum as a result of the dilating effect of calcium antagonists is twice the mean maximum value that the myoglobin time curve would show without such treatment.

Animals↗
PubMed1987

Cimetidine induces coronary artery spasm in patients with vasospastic angina.

We have previously reported that cimetidine, a histamine H2-receptor blocker, augments the histamine-induced coronary vasoconstriction at the site of spastic segments in the atherosclerotic coronary arteries of swine. To elucidate whether cimetidine has a coronary vasoconstrictive effect in humans, 14 patients with vasospastic angina (group 1) and 14 controls with atypical chest pain (group 2) were examined angiographically. Nitroglycerin-effective spontaneous angina with electrocardiographic ST-T changes and ergonovine-induced coronary artery spasm were confirmed in group 1, but not in group 2. Cimetidine was administered intravenously in a dose of 200 mg. Cimetidine induced coronary artery spasm in 4 patients in group 1 but none in group 2(29% vs. 0%, p less than 0.01). The extent of coronary vasoconstriction induced by cimetidine was greater at the site of spastic coronary segments than that at the site of non-spastic segments in group 1 or all segments in group 2 [14% vs. 4%, (p less than 0.01) or 14% vs. 2%, (p less than 0.01)] as well as the extent of ergonovine-induced coronary vasoconstriction [46% vs. 14%, (p less than 0.01) or 46% vs. 14%, (p less than 0.01)] and nitroglycerin-induced coronary vasodilatation [58% vs. 25%, (p less than 0.01) or 58% vs. 17%, (p less than 0.01)]. As it was suggested that cimetidine has potential vasoconstrictive effects in patients with coronary artery spasm, it should be administered with caution in patients with the vasospastic angina pectoris.

Adult↗
PubMed1985

[Pure arrhythmic form of the pre-infarction syndrome or spasm responsible for myocardial necrosis].

A 74 years old man was admitted as an emergency for syncopal attacks due to recurrent ventricular fibrillation (VF). These attacks were observed at the height of myocardial ischaemia as shown by ST elevation in Leads II, III and RV without associated anginal pain. Inferior myocardial infarction occurred during recurrent VF on the 4th day; the outcome was favourable. Coronary angiography was performed on the 10th day and showed double vessel disease; ergometrine (0.2 mg) induced anginal pain and ST elevation in Leads II, III and AVF. A good clinical result was obtained by calcium antagonists with an 18 months follow-up. Coronary spasm, documented in this case by the ergometrine provocation test, is now recognised as a cause of resting angina, effort angina and also some cases of myocardial infarction. This report suggests that coronary spasm may also induce apparently isolated severe ventricular arrhythmias without associated chest pain, which raises the question as to whether arrhythmias induced by spasm could play a primary role in aggravating myocardial ischaemia, leading to myocardial infarction.

Aged↗
PubMed1979

[Spontaneous coronary spasm with reversible occlusion of the left coronary artery: a case report (author's transl)].

A spontaneous coronary spasm with a complete but reversible occlusion of the left coronary artery could be demonstrated by coronary arteriography in a patient with angina pectoris at rest and during exercise. This will prove that spasms of coronary arteries can cause angina pectoris or even acute myocardial infarction if the spasm is persisting for long enough and if there is no sufficient supply by collateral vessels. This can be a possible reason for akinesia or dyskinesia of the left ventricle associated with normal or near normal coronary arteries.

Angina Pectoris↗
PubMed1979

[Myelography as a cause of persistant cerebral vascular spasm].

A few hours after an ascending myelography with Pantopaque, a woman aged 52 presented light coma with signs of meningeal reaction, left hemiparesis and a central deficit of the left facial nerve. 24 hours later, a computer axial tomography revealed the presence of the contrast media (Pantopaque) in the basal cysterns. Three days after, the right carotid angiography indicated the presence of a diffuse spasm of the intracranial branches of the internal carotid artery, particularly a spasm of the cortical ascending parietal and descending temporal ones, without deplacements. A second CT investigation revealed a slow, but complete recovery of the neurologic functions in the following 10 days. According to the Authors, this clinical observation reproduces the experimental pattern of the cerebral spasm caused by the administration of a spasmogenic chemical factor in the basal cysterns, because of the following clinical aspects: blood absence in the liquor; T wave inversion (the electrocardiographic symptom considered as a predisposing factor); meningeal reaction owing to the irritation of the myelographic contrast and persistent vasospastic answer of the right carotid circle, as it may be seen in the angiographic control.

Angiography↗
PubMed1984

[Results of coronary transluminal angioplasty following Prinzmetal's angina or fixed stenosis with associated spasm].

Transluminal coronary angioplasty (TCA) was carried out in 130 patients (109 men and 21 women) with an average age of 51 years (range 20 to 76 years) between April 1980 and December 1982. The most commonly affected artery was the LAD (100). All patients were on heparin, coronary vasodilators and calcium antagonists before the procedure, and on calcium antagonists and platelet antiaggregant drugs after TCA. The material and methods used were those described by Gruntzig. In this population, we identified a group of patients, Group I, with fixed stenosis and associated coronary spasm--either Prinzmetal angina (13 cases, 6 of which had both ST-T elevation and other ECG changes) or spontaneous spasm with a variable degree of stenosis (2 cases). The stenosis remained greater than or equal to 70% in all cases after intracoronary injection of nitrate derivatives. There were no differences between this group and that of fixed stenosis (Group II) with respect to age and type of diseased vessel (although the right coronary artery was more commonly involved in cases of spasm). The overall primary success rate was 72.8% (14/15--93%--in Group I, and 85/121--70.2%--in Group II: no statistically significant difference). The angiographic relapse rate at 6 months was significantly higher in Group I (8/12: 67%) than in Group II (15/63: 23.8%) p less than 0.02. When "redilatation" with stable success is taken into consideration the difference is not significant (33% and 22.2% respectively). The relapses may be dissociated in Group I (2 cases with recurrent spastic angina and normal angiography).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Long-term efficacy of diltiazem for control of symptoms of coronary artery spasm.

In order to evaluate long-term efficacy of a new calcium antagonist, diltiazem, for therapy of coronary artery spasm, 16 patients with clinical variant angina due to documented coronary artery spasm participated in a 44-week prospective, randomized, double-blind cross-over trial of 240 mg of diltiazem vs. placebo. The study involved eleven 28-day cycles of which one of the first five cycles (phase 1) and one of the last six cycles (phase 2) were placebo, with the remainder being active medication. Response was assessed with the dairy technique, measuring frequency of angina and side effects. When diltiazem was compared with the placebo period during phase 1, there was a 73% decrease in frequency of angina from 1.1 to 0.3 episodes per day (P less than 0.01). When diltiazem was compared with the placebo during phase 2, there was an 80% decrease in frequency of angina from 0.5 to 0.1 episodes per day (P less than 0.05). When phase 1 placebo cycle was compared with phase 2 placebo cycle, there was a 55% decrease in frequency of angina which approached statistical significance (P less than 0.10). This marked disease attenuation demonstrated during the 44-week study reflects the variability of symptoms of variant angina and possibly reflects a carry-over therapeutic effect of the calcium entry blocker. Adverse side effects were absent in our small group of patients. Diltiazem is effective for the long-term control of symptoms of active coronary artery spasm.

Adult↗
PubMed1983

Provocation of coronary artery spasm.

Although a wide variety of provocative agents and physiologic maneuvers may precipitate coronary artery spasm in susceptible patients with Prinzmetal's variant angina, ergonovine maleate testing has been demonstrated to be the safest when followed in a highly structured protocol which mandates not only electrocardiographic monitoring but immediate reversal of spasm by intravenous or intracoronary nitroglycerin. The recent demonstration that calcium channel antagonists can block focal spasm attests to the remarkable clinical efficacy of these agents and suggests that a therapeutic trial with a calcium channel antagonist may preclude the necessity for provocative testing in the future.

Blood Pressure↗
PubMed1984

[Coronary spasm as a mechanism of ischemia or myocardial necrosis immediately after coronary surgery. Considerations on 5 cases and review of the literature].

Several recent reports suggest that coronary artery spasm may represent a major complication of coronary artery bypass surgery, and that it may have gone unrecognized in the past. During a three-year interval ending July 1983 we have encountered 5 cases in whom reversible S-T changes, angina, arterial hypotension, major arrythmias and/or angiography prompted the diagnosis of coronary arterial spasm early after aorto-coronary bypass surgery. Our experience and the review of 15 previously reported cases reveals that in most cases the clinical presentation was that of an acute, severe, ischemic cardiac event that occurred few hours after termination of cardiopulmonary bypass. A more benign course took place in a minority of cases, although some of them showed evidence of myocardial necrosis on ECG and/or left ventriculography. The mortality rate in the collective series was 20%, and the rate of perioperative non fatal myocardial infarction was 25%. Glyceryl trinitrate administration into the ascending aorta or into the spastic coronary artery appeared to be the most effective way of treating this condition, while the same drug was seemingly uneffective when administered intravenously. The use of calcium antagonists was associated with a favourable outcome in some patients, but on the whole the results were unpredictable. Prompt consideration of the possibility of coronary artery spasm and aggressive treatment are required in order to minimize its impact on perioperative mortality and morbidity rates.

Adult↗
PubMed1984

[Efficacy of medical treatment (isoproterenol + aminophylline) of aneurysm rupture spasm].

Efficiency against spasm of a combined therapy by Isoproterenol Aminophylline is discussed from 97 operated cases (118 aneurysms) and 30 non operated cases (32 aneurysms). This treatment seems efficient and best results are achieved when therapy is started as soon as possible or systematically after surgery. Analysis of spasm and of its treatment is based on criterions which vary from one author to another, and comparison between different series is difficult. In the series here reported, one group with treatment is compared to another one without treatment. This method seems the most reliable. This treatment cannot be considered as the lone efficient therapy against spasm and is usually used beside other techniques such as ICP and Arterial pressure management or early surgery.

Aminophylline↗
PubMed1980

[Mid-systolic click syndrome, coronary spasm and sudden death. General review apropos of a tracing from terminal Prinzmetal's angina, recorded by the Holter method].

The authors review the literature on arrhythmias and ST changes, the principal causes of sudden death in the mid systolic click-late systolic murmur (SC-SM) syndrome, having recorded the ECG during sudden death of a patient with this syndrome by Holter monitoring. This would also appear to be the first reported case of sudden death recorded by this technique. It showed that death was caused by ventricular fibrillation which was preceded by a clinical and electrical episode of Prinzmetal angina. Hypotheses explaining the abnormalities of ventricular repolarisation and rhythm in so-called "idiopathic" SC-SM syndrome are reviewed. Special attention is paid to studies suggesting the participation of coronary spasm and autonomic nervous system disturbances. In conclusion, the authors underline: - the value of ambulatory electrocardiography in patients with the SC-SM syndrome and especially in a defined high risk group; - the value of testing for coronary spasm when coronary angiography is envisaged; - the need for better management with antiarrhythmic therapy. The indications of betablockade are discussed as these drugs are thought to favourise coronary spasm.

Angina Pectoris↗
PubMedDate not supplied

The spectrum of coronary artery spasm. The variable variant.

Angina from coronary artery spasm is not rare. Because new and effective medical therapy is now available, it is imperative that the physician recognize this syndrome when it occurs. Coronary artery spasm can present clinically as unstable rest angina with reversible ST-segment elevation and bradyarrhythmias and tachyarrhythmias. In this setting, Prinzmetal's variant angina is generally promptly recognized and appropriately treated. The diagnosis is variant angina, however, often is not so obvious. Chest pain may be exertional or seem noncardiac in origin. The chest pain syndrome may be chronic and stable as well as unstable. The ECG may show ST-segment depression, rather than elevation. Five cases of coronary artery spasm that emphasize the variable features of variant angina and offer aid for the prompt diagnosis and treatment of the syndrome are presented here.

Angina Pectoris↗
PubMed1981

Hemifacial spasm caused by cholesteatoma.

Hemifacial spasm is a rare disease. Usually a specific etiologic factor is not found and nonspecific treatments are used. A case of hemifacial spasm secondary to a middle ear cholesteatoma is presented. This origin should be considered in any patient who has hemifacial spasm.

Aged↗
PubMed1978

Spontaneous and provoked coronary artery spasm: are they the same?

A 44-yr-old man suffering fro exertional, emotional and spontaneous angina underwent coronary arteriography. During the examination he had a spontaneous attack of angina with ST elevation in the anterior leads. Injection of a contrast medium in the left coronary artery during pain showed marked spasm with anterior descending artery occlusion. The spasm was quickly relieved by nitroglycerin. Intravenous administration of 0.4 mg of ergonovine maleate reproduced the anginal episode with pain, ST elevation in the anterior leads and coronarographic patterns of a spasm occluding the anterior descending artery at the same level. After nitroglycerin, the pain disappeared and the electrocardiographic and coronarographic findings returned to basal conditions.

Adult↗
PubMed1981

Coronary artery spasm and myocardial infarction in the absence of angiographically demonstrable obstructive coronary disease.

Myocardial infarction due to spasm of an "angiographically normal coronary artery" is rare, and its significance as a cause of myocardial infarction in patients without obstructive coronary disease has not been determined. Two patients are described with transmural myocardial infarction, nonobstructive coronary arteries, and suggestive evidence of coronary vasospasm as the cause of infarction. In one patient, angiography was carried out within 7 days of infarction and the documentation of normal coronary arteries argued strongly against a thromboembolic cause for infarction. This patient also had the combination of asthma, hypereosinophilia, and a systemic disease suggesting an immunologic disturbance with increased autoantibody production. A temporal association was noted between the episodes of asthma and those of coronary spasm during exacerbation of the eosinophilia, which raised the speculative issue of "allergic" coronary vasospasm. It is concluded that spasm of a nonobstructed coronary artery may cause transmural myocardial infarction. Further documentation is required in order to place this association in perspective among the other potential cause of infarction in patients with normal coronary artery anatomy.

Adult↗
PubMedDate not supplied

[Variant angina pectoris with demonstration of coronary spasm. Diagnostic and therapeutic considerations].

Eight patients with typical Prinzmetal's angina and angiography proven coronary artery spasm are reviewed. In all cases the angina pain appeared at rest and was accompanied by a simultaneous ST-segment elevation. The coronary angiography results varied from severe multivessel disease (3 cases) to single vessel disease (3 cases), and normal coronary arteries (2 cases). In all patients a coronary spasm was documented, in five cases induced by ergonovine and in three spontaneously; in all patients but in one, the localization of the spasm was concordant with the ST-segment elevation localization. One case with a severe proximal left anterior descending stenosis was grafted; however the pain was not relieved despite treatment with large amounts of propranolol. This patient died after an episode of severe chest pain. Treatment with nifedipine was given to six patients, with excellent results in four cases, and regular response in two. The main physiopathologic diagnostic and therapeutic aspects of the variant angina syndrome are reviewed.

Aged↗
PubMed1994

[Use of sumatriptan (Imigran) in a female patient with coronary spasm].

Sumatriptan (Imigran), an effective drug against symptoms of migraine may cause a sensation of thoracic oppression. In some patients, this is accompanied by ECG alterations. In such cases, the underlying mechanism is probably coronary spasm, although this has never been demonstrated angiographically. The case is described of a young woman who was hospitalized after resuscitation because of ventricular fibrillation. One week previously, after subcutaneous administration of sumatriptan, she had had chest pains for half an hour. A spasm provocation test during coronary angiography gave a positive result. The patient was treated with a calcium antagonist following which she remained free of symptoms. In patients with chest pain after administration of sumatriptan, it is necessary to use this drug cautiously; spasm of the coronary arteries as a cause should be excluded.

Adult↗
PubMedDate not supplied

[Induction of coronary artery spasm by combined cold pressor and hyperventilation test in patients with variant angina].

To examine whether or not a combination of nonpharmacologic provocative tests potentiated the occurrence of coronary spasm, the cold pressor test combined with hyperventilation was studied in 22 consecutive patients with variant angina admitted to our hospital. After a 12-lead electrocardiogram and blood pressure were recorded, the patient was asked to hyperventilate vigorously at a rate of 30 respirations per min for 6 min under continuous electrocardiographic monitoring. Immediately after hyperventilation, the cold pressor test was performed with the patient's right hand submerged in ice water for 2 min. In some patients who showed a positive response to the combined test, a hyperventilation and cold pressor test was performed on another day. Positive response (ST segment elevation > or = 0.1 mV) to the combination test was seen in 18 of 22 patients (82%). Positive response to the hyperventilation test was seen in seven of 11 patients (64%). The response to cold pressor test was all negative in seven patients. The onset of electrocardiographic changes by the combined test occurred an average of 120 sec (30-240 sec) after the end of hyperventilation, whereas the onset by hyperventilation test occurred an average of 210 sec later (60-370 sec). These results suggest the combination of the cold pressor test and hyperventilation test potentiated the occurrence of coronary spasm. The combined cold pressor and hyperventilation test is a powerful and useful nonpharmacologic provocative test for coronary artery spasm in patients with variant angina.

Adult↗