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  • 1
    ISSN: 1432-1440
    Keywords: Coronary angioplasty ; Excercise ; Atrial natriuretic factor ; Pulmonary artery pressure ; Right atrial pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary According to several reports of close correlations between pulmonary artery pressure and ANF plasma levels it would be convenient to replace invasive pressure monitoring by ANF determination. Mean pulmonary artery and right atrial pressures and pulmonary artery as well as peripheral venous ANF plasma concentrations were measured in 24 patients before and after coronary angioplasty (PTCA) continuously at rest and during exercise: At rest, both pressure and ANF-values remained unchanged before and after PTCA. At exercise, there was a decrease of mean pulmonary artery pressure (from 41.3±8.6 to 31.5±7.4 mmHg,p〈0.001), mean right atrial pressure (from 11.9±3.0 to 9.0±2.3 mmHg,p〈 0.001), pulmonary artery (282.5±191.0 to 207.3±157.2 pg/ml,p〈0.05) and peripheral venous (112.7±48.0 to 97.1±53.2 pg/ml, n.s.) ANF concentration after PTCA. We found no correlation between PTCA-induced changes of right arterial pressures and ANF concentrations, while changes of pulmonary artery pressures were significantly correlated to changes of peripheral venous (r=0.79,p〈0.001) as well as pulmonary artery (r=0.59,p〈0.01) ANF concentrations at exercise. In 6 of the 24 patients, however there was an inverse relationship between changes of pulmonary artery pressures and ANF concentrations. — Our data demonstrate a significant correlation between changes of ANF plasma level and pulmonary artery pressure values at exercise after PTCA. In the individual case however invasive pressure monitoring cannot be replaced by determination of ANF plasma levels.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Notfall + Rettungsmedizin 2 (1999), S. 263-266 
    ISSN: 1436-0578
    Keywords: Schlüsselwörter Akuter Myokardinfarkt ; Herzenzyme ; Angina pectoris ; Akutes Koronarsyndrom ; Herzmarker ; Key words Acute myocardial infarction ; cardiac encymes ; Angina pectoris ; Acute coronary syndrome ; cardiac markers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary According to WHO-criteria diagnosing myocardial infarction depends on history (typical chest pain), ECG-changes and elevation of serum enzymes such as creatine-kinase (CK) and its cardiac specific isoenzyme CK-MB. Unfortunately the ECG recorded on admission provides little if any help in as many as 50% of patients presenting with acute myocardial infarction due to abscence of diagnostic changes, bundle branch block, pacemaker stimulation or previous infarcts. When looking at ischaemic heart disease attention will be drawn to the ”acute coronary syndrome”. This term is used for unstable angina and non-Q-wave infarction linked by the pathologic phenomenon of placque rupture and secondary thrombus formation in the atherosclerotic coronary artery. Diagnosing acute coronary syndrome in the abscence of typical ECG-findings (ST-depression, T-wave inversion) and elevation of cardiac enzymes (CK) and thus identifying patients at risk proofs a challenge. In the 90ties new cardiac markers (cardiac specific troponin and myoglobin) have been developed promising improved selection and treatment of patients at risk and reduction of unnecessary hospital admissions.
    Notes: Zusammenfassung Die Diagnose eines akuten Myokardinfarktes basiert traditionell auf der Anamnese (typischer nitrorefraktärer Schmerz), EKG-Veränderungen (ST-Hebungen, T-Wellen-Veränderungen, Auftreten von Q-Zacken, neu aufgetretener Linksschenkelblock) und erhöhten Werten der „klassischen Herzenzyme” Creatinkinase (CK) und CK-MB (WHO-Kriterien). Bei fast jedem zweiten Patienten mit einem akuten Myokardinfarkt ist das Aufnahme-EKG jedoch diagnostisch nicht hilfreich [5]. Ursache hierfür sind fehlende oder nur sehr subtile Veränderungen oder erschwerte Interpretation z.B. bei Linksschenkelblock, reinem Schrittmacher-EKG oder bei Herzwandaneurysma nach früherem Infarkt. Stellen akuter Myokardinfarkt und stabile Angina pectoris die zwei Enden eines Spektrums dar, so finden sich dazwischen fließend weitere Manifestationen der koronaren Herzkrankheit: Die instabile Angina pectoris und der intramurale (non Q-wave) Infarkt werden als „akutes Koronarsyndrom” zusammengefaßt, dem pathogenetisch eine Thrombusapposition bei Placqueaufbruch zugrunde liegt. Die Diagnose eines akuten Koronarsyndroms beschreibt einen Hochrisikopatienten und ist insbesondere bei Fehlen typischer EKG-Veränderungen (ST-Senkungen, T-Wellen-Inversion) und normaler CK nicht immer leicht zu stellen. Dieser diagnostischen Unsicherheit hat man seit Anfang der 90er Jahren mit der Entwicklung neuer selektiver und jetzt zunehmend breit verfügbarer „Herzmarker” versucht Rechnung zu tragen, um Hochrisikopatienten zu erkennen und deren Behandlung zu optimieren. Im Umkehrschluß soll so Patienten mit niedrigem Risiko, einen akuten Myokardinfarkt zu erleiden, eine unnötige Hospitalisierung erspart bleiben.
    Type of Medium: Electronic Resource
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