Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 3051692

[Angina pectoris].

H Sterz·H Koller·G Kobinia
View original source ↗Export metadata ↓

Abstract

Coronary heart disease has many different clinical courses: it can cause rhythm-disturbances, sudden death, pump-failure, no pain at all (silent ischemia) or typical angina. Heart-pain can occur "on demand" after physical or mental stress with a duration of 3 to 5 minutes with typical location and good response to nitrates. It also can cause atypical forms of angina such as angina on rest, mostly due to coronary spasms. Angina can stable over months and years but can suddenly increase in severity and duration. This form is called unstable angina, which has to be recognized as soon as possible since acute myocardial infarctions evolve rather frequently. Infarction is an irreversible myocardial damage but before it develops many measures can be taken to preserve the jeopardized myocardium. The recognition and differentiation of angina pectoris is therefore of utmost importance.

Explore related subjects

Angina PectorisAngina, UnstableElectrocardiographyHumansMyocardial InfarctionEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

H Sterz, H Koller, G Kobinia. 1988-08-31. [Angina pectoris].. https://pubmed.ncbi.nlm.nih.gov/3051692/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1992

Comparison of painful and painless left ventricular dysfunction recorded during ambulatory ventricular function monitoring in angina pectoris secondary to coronary artery disease.

Left ventricular (LV) function and the electrocardiogram of 55 patients with coronary artery disease and angina were monitored for a mean of 3.2 +/- 1.9 hours with an ambulatory LV function monitor. During the monitoring interval, patients performed daily activities such as sitting, walking, climbing stairs, and eating. Sixty episodes of transient reduction in ejection fraction of > 5% lasting > 60 seconds were observed in 24 patients; 13 episodes were associated with typical angina, but 47 were asymptomatic. Asymptomatic episodes had a shorter duration of ventricular dysfunction (116 +/- 49 vs 189 +/- 113 seconds; p < 0.05), and smaller increases in relative end-diastolic and end-systolic volumes (end-diastolic 0.9 +/- 5.4% vs 4.6 +/- 4.9% [p < 0.05], and end-systolic 21 +/- 11% vs 35 +/- 20% [p < 0.05]) than did symptomatic ones. When a subset of patients with both symptomatic and asymptomatic episodes were analyzed, similar results were observed: in asymptomatic episodes, duration was shorter (82 +/- 31 vs 200 +/- 110 seconds; p < 0.005), ejection fraction decrease was smaller (-7.3 +/- 2.6% vs -11.0 +/- 4.7%; p < 0.05), and end-systolic volume increase was smaller (23 +/- 12% vs 37 +/- 19%; p < 0.05). The data suggest that asymptomatic transient LV dysfunction is less severe and of shorter duration in patients with angina pectoris.

Angina Pectoris↗
PubMed1992

[Angina pectoris after sumatriptan (Imigran)].

Developed for the treatment of migraine, sumatriptan is an agonist of 5-hydroxytryptamine-1-receptors. Though a pressure sensation is a common complaint, significant ECG changes have not been reported after subcutaneous administration of sumatriptan. A case history is given where angina pectoris after sumatriptan self-administration was experienced on two occasions by a 61-year old man with a history of minor myocardial infarction--without post-infarction angina--two years previously. The angina after sumatriptan was accompanied on both occasions by significant ST-segment depression on ECG-monitoring. An extracranial vasoconstrictor action of sumatriptan in patients with ischaemic heart disease is suggested.

Angina Pectoris↗