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Results for “Angina Pectoris, Variant”

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At least 1,315 records · Page 73Linked to original sources
PubMed1979

[Detection of coronary artery spasm by the methylergometrin test. Technic. Results. Indications].

Methylergometrine (Methergin) was given intravenously (0.4 mg) to 118 patients undergoing coronary arteriography. The electrocardiogramme and intraaortic pressure was continuously monitored whilst coronary arteriography was performed, 1,3, and 5 minutes after the injection of the ergot alkaloid. The test was positive if: 1) coronary spasm was observed; 2) if ST segment elevation was recorded with or without pain. Positive tests were obtained in 13 out of 14 patients with Prinzmetal angina. The test was negative in the other patients. However in 3 patients with Prinzmetal angina, the test produced typical coronary spasm without electrocardiographic changes. In Prinzmetal angina the sensitivity of this test was 93 p. 100 with a high specificity: 96-100 p. 100 depending on whether or not electrocardiographical changes associated with spasm are considered. Taking into account current therapeutic methods of treating Prinzmetal angina the indications of this test of coronary spasm are: 1) patients presenting with resting angina whatever the state of their coronary arteries; 2) patients with documented Prinzmetal angina with "angiographically normal" coronary arteries.

Angina Pectoris, Variant↗
PubMed1976

[Indications and contraindications for surgery in coronary insufficiency].

The indications to aortocoronary by-pass technique have during the last two years developed thanks to surgical, emodinamic and clinical exsperiences. The mortality of patients in whom surgery is limited electively to the intervention of aorto-coronary by-pass is at present around 4%. The principal indications to surgery are: a) existence of more than one coronary artery disease; b) a good diameter of the by-passing artery (more than 1 mm) corresponding to the site of the by-pass graft; c) a left ventricular telediastolic pressure lower than 20 mm of Hg; d) left ventricular function with ejection fraction not lesser than 0,40; e) absence of any associated severe and irreversible damages. The comparative data obtained recently from coronary patients medically and surgically treated would show at 4 years a survival rate higher than in those who underwent aorto-coronary by-pass.

Angina Pectoris↗
PubMed2000

Successful treatment of vasospastic angina with a coronary stent.

Calcium antagonists are the treatment of choice in vasospasm angina when no stenosis or mild stenosis are present. We present a case in which ergonovine echocardiography showed vasospasm of the right coronary artery despite optimal medical treatment. Stenting of a mild stenosis in that artery successfully controlled vasospasm and a pre-discharge ergonovine echocardiographic test was negative. The patient remains asymptomatic one year after stenting.

Angina Pectoris, Variant↗
PubMed2000

[Vasospastic angina pectoris following abortion induced by prostaglandin analogue].

A case of vasospastic angina pectoris with loss of consciousness, bradycardia and seizures induced by medical abortion following administration of mifepristone and gemeprost is reported. The patient had a history of smoking and migraine, and former treatment with ergot alkaloids or serotonin agonists had also resulted in chest pain and lipothymia. The case underlines the importance of obtaining a detailed history of vasospastic disorders in women referred for medical abortion.

Abortifacient Agents, Steroidal↗
PubMed1979

[1st degree and 2nd degree blocks (Wenckebach type) during right ventricular stimulation in the course of Prinzmetal's angina].

Right axial deviation and delay between stimulation and ventricular response was observed during pacing of the apex of the right ventricle in Prinzmetal angina. The degree of deformation of the ventricular complex and the length of this delay appear to be related to the severity of the anginan, the length of the preceding diastolic period and the amplitude of stimulation. This observation demonstrates the presence of conduction defects at the heart of ischaemic myocardium and may explain the failure of prophylactic pacing in Prinzmetal angina complicated by paroxysmal atrioventricular block.

Aged↗
PubMed2001

[Prinzmetal angina pectoris associated with 3rd degree atrioventricular block].

The authors report on the case of a 61 year-old female patient who was repeatedly taken to hospital because of chest pain and temporary loss of consciousness. During her hospitalization there was no ST elevation on the ECG, sinus bradycardia, other times atrial fibrillation was detected. The diagnosis was made by Holter monitoring three years after the onset of complaints. At this time chest pain set in after midnight, which was followed by loss of consciousness. Significant ST elevation and IIIrd degree AV block were detected. The coronarography showed non-significant coronary stenosis. According to the vasospastic patomechanism nitrate, calcium antagonist and acetylsalicylic acid therapy was administered and because of the complete AV block leading to syncope a VVI, M pacemaker was implanted. During the two years passed since the implantation of the pacemaker the patient had chest pain only once and it was not accompanied by syncope.

Adams-Stokes Syndrome↗
PubMed2001

Endothelial dysfunction is an independent factor responsible for vasospastic angina.

In order to evaluate peripheral endothelial function in patients with vasospastic angina (VSA), we measured flow-mediated dilation (FMD) of the brachial artery in patients with VSA and compared it with FMD in patients without VSA. Endothelial dysfunction is considered one of the mechanisms underlying VSA. However, its exact role remains to be clarified. The study included 30 patients with positive spasm-provocational test results without evidence of significant coronary stenosis (VSA group) and 30 patients with negative spasm-provocational test results without evidence of significant coronary stenosis (control group). In each patient, brachial artery diameter responses to hyperemic flow and glyceryl trinitrate spray were measured using high-resolution ultrasound. The carotid intima-media thickness was also measured as a marker of systemic atherosclerosis. FMD was lower in the VSA group (4.8+/-0.5%) compared with the control group (9.4+/-0.7%, P<0.0001). In the VSA group, FMD was not affected by coronary risk factors or the presence of atherosclerotic changes on coronary angiography. Glyceryl trinitrate-induced dilation did not differ between the two groups. The intima-media thickness was comparable between the VSA (0.85+/-0.04 mm) and control groups (0.81+/-0.05 mm). These findings indicated that peripheral endothelial function is impaired only in the VSA group, whereas the atherosclerotic changes were similar in the two groups. We conclude that endothelial dysfunction may be an independent factor responsible for the development of VSA.

Aged↗
PubMed2000

[Effect of left ventricular diastolic dysfunction on pathogenesis of angina decubitus].

OBJECTIVE: To investigate the effect of left ventricular diastolic dysfunction on the pathogenesis of angina decubitus. METHODS: The study population consisted of three groups: (1) group 1, 31 patients with angina decubitus who had ejection fraction > 50%; (2) group 2, 20 patients with coronary artery disease but without angina decubitus; group 2 and 1 were matched for age, EF and extent of coronary artery disease; (3) group 3, 20 patients without cardiovascular diseases. RESULTS: Left ventriculography (LVG) showed that LV first 1/3 filling fraction (1/3 FF) and LV late 1/3 FF were 0.30 +/- 0.12, 0.41 +/- 0.12, 0.46 +/- 0.07 and 0.36 +/- 0.09, 0.31 +/- 0.08, 0.29 +/- 0.06 in groups 1 to 3 respectively. LV first 1/3 FF was significantly lower in group 1 than in group 2 and 3 (both P < 0.001), but LV late 1/3 FF was much higher in group 1 than in groups 2 and 3 (P < 0.05 and P < 0.01, respectively). Left ventricular end-diastolic pressure (LVEDP) was markedly increased before and after LVG in groups 1 and 2 as compared with group 3 (P < 0.001 and P < 0.05, respectively). The difference of LVEDP caused by left atrial contraction (LACD) was much higher before and after LVG in group 1 than in group 3 (P < 0.01 and P < 0.001, respectively). However, there were significant differences in LVEDP and LACD tested between before and after LVG in group 1 (both P < 0.01). No statistical differences were found in LVEDP and LACD tested between before and after LVG in both group 2 and group 3. CONCLUSION: Patients with angina decubitus have LV diastolic dysfunction, which may be closely related to the pathogenesis of angina decubitus.

Adult↗