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DOI: 10.1055/s-2005-865063
© Georg Thieme Verlag Stuttgart · New York
Gestörte Dehnbarkeit des Hochdruckherzens unter Belastung als früher Marker einer diastolischen Dysfunktion
Reduced left ventricular distensibility as an early sign of diastolic dysfunction in hypertensive heart diseasePublikationsverlauf
eingereicht: 24.8.2004
akzeptiert: 3.2.2005
Publikationsdatum:
10. März 2005 (online)

Zusammenfassung
Fragestellung: Patienten mit arterieller Hypertonie klagen häufig über eine belastungsassoziierte Dyspnoe. Es ist unklar, ob eine systolische, eine früh- oder eine spätdiastolische Funktionsstörung ursächlich ist.
Methodik: Unsere Untersuchung schloss 21 hypertensive Patienten (7 Frauen, 14 Männer, Altersmedian 56 Jahre) und 12 normotensive Patienten (4 Frauen, 8 Männer, Altersmedian 52 Jahre) ein, bei denen eine koronare Makroangiopathie ausgeschlossen wurde. Mittels Herzbinnenraumszintigraphie und Einschwemmkatheter wurden Parameter der systolischen und diastolischen Herzfunktion in Ruhe und unter Belastung analysiert.
Ergebnisse: Beide Kollektive zeigten unter Belastung eine normale Ejektionsfraktion (Hochdruckpatienten 71 % ± 10; Kontrollgruppe 72 % ± 11). Hochdruckpatienten zeigten unter Belastung einen Anstieg des pulmonalkapillaren Verschlussdrucks (17,4 ± 8 vs 11,5 ± 5 mmHg; p = 0,005), ein fixiertes enddiastolisches Ventrikelvolumen (82 ± 21 vs 104 ± 23 ml/m2 p = 0,01) und ein reduziertes Schlagvolumen (58 ± 1,2 vs 73 ± 1,4 ml/m 2; p = 0,007). Füllungsdynamisch zeigten sich im Vergleich zum Normalkollektiv Hinweise für einen forcierten frühdiastolischen Einstrom („peak filling rate” = 6,1 ± 1,6 vs 4,8 ± 1,8 EDV/s; p = 0,04). Dieser könnte Folge einer Übertragung systolischer Energie in die frühe Diastole sein und zum Erhalt der Belastungskapazität des Hochdruckkollektivs beigetragen haben (Herzindex = 8,1 ± 1,8 vs 8,4 ± 2,2 l/min × m 2; ns).
Folgerung: Eine erhöhte Steifigkeit des Herzens unter Belastung ist eine Frühmanifestation des Hochdruckherzens.
Summary
Background: Hypertensive patients often present with exertional dyspnoe. However it is questioned whether it results from a systolic, early- or late diastolic impairment of left ventricular function.
Patients and methods: Our study included 21 hypertensive patients (7 female; 14 male, median age 56 years) and 12 controls (4 female; 8male, median age 52 years). All patients had normal epicardial coronary arteries. Parameters of systolic and diastolic heart function at rest and during exercise were analyzed using a combined hemodynamic and radionuclidangiographic approach.
Results: One principal finding was that the investigated hypertensive patients had a normal ejection fraction during exercise (72 % ± 11 vs 71 % ± 10 in the control group). However these patients showed an exercise induced increase of pulmonary capillary wedge pressure (17,4 ± 8 vs 11,5 ± 5; p = 0,005), a fixed enddiastolic volume (82 ± 21 vs 104 ± 23 ml/m 2 p = 0,01) and a reduced stroke volume index (58 ± 1,2 vs 73 ± 1,4 ml/m 2; p = 0,007). Radionuclid angiography revealed an increased exercise peak filling rate (6,1±1,6 vs 4,8±1,8 EDV/s; p = 0,04) in hypertensive patients. We assume that exercise capacity (cardiac index = 8,1 ± 1,8 vs 8,4 ± 2,2 l/min × m 2; ns) in hypertensive patients without excessive LV hypertrophy is predominantly preserved by an enhanced contractile state and its favorable effects on early diastolic filling.
Conclusion: An increased left ventricular stiffness during exercise is an early manifestation of hypertensive heart disease.
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Dr. med. Gunnar Plehn
Medizinische Klinik II, Kardiologie/ Angiologie, Marienhospital Herne, Universitätsklinik
der Ruhr-Universität Bochum
Hölkeskampring 40
44625 Herne
Telefon: 02323/4991601
Fax: 02323/499301
eMail: gplehn@gmx.de