Etwa 20 % der Patienten, die wegen Angina pectoris und dem Verdacht auf eine koronare
Herzerkrankung mit einem Herzkatheter invasiv untersucht werden, weisen im Koronarangiogramm
– trotz einer möglichst optimalen Abklärung durch Anamnese, körperliche Untersuchung
und nichtinvasive Diagnostik – normale Herzkranzgefäße auf. Die Ätiologie dieser Angina
pectoris kann anatomisch in 3 Gruppen unterteilt werden: koronare Mikroangiopathien,
epikardiale oder nichtkoronare Erkrankungen. Die mikrovaskuläre Dysfunktion kann Folge
einer arteriellen Hypertonie, eines Diabetes mellitus, einer hypertrophen Kardiomyopathie
oder einer entzündlichen Herzerkrankung sein. Epikardiale Erkrankungen, die eine solche
Angina pectoris mit normalem Koronarangiogramm verursachen, können in endotheliale
Dysfunktion, Koronararterienspasmen und Myokardbrücken unterschieden werden. Grundsätzlich
muss bei einer Angina pectoris bei normalem Koronarangiogramm auch an eine Erkrankung
anderer Organe gedacht werden. Differenzialdiagnostisch müssen daher pulmonale und
gastrointestinale Erkrankungen sowie vertebragene und muskuläre Erkrankungen ausgeschlossen
werden.
Approximately 20 % of patients with cardiac chest pain have a normal coronary angiogram
despite a detailed non–invasive diagnostic. The etiologies of angina pectoris with
normal coronarangiogram can be anatomically classified into three groups: coronary
microvascular dysfunction, epicardial disease and non–coronary disease. Epicardial
disease includes endothelial dysfunction, coronary artery spasm and coronary artery
bridging. Microvascular dysfunction may be secondary to hypertension, cardiomyopathy
or infiltrative disease. Noncoronary artery diseases, which cause angina pectoris
are pulmonary, gastrointestinal or musculoskeletal diseases.
Key words
angina pectoris - normal coronary angiography - myocardial bridge - endothelial dysfunction
- coronary artery spasm - coronary microvascular dysfunction
Literatur
1
Fleet RP, Beitmann BD..
Unexplained chest pain: when is it panic disorder?.
Clin Cardiol.
1997;
20
187-194
2
Yang EH, Lerman A..
Angina pectoris with a normal coronary angiogram.
Herz.
2005;
30
17-25
3
Preik M, Kelm M, Strauer BE..
Management of the hypertensive patient with coronary insufficiency but without atherosclerosis.
Curr Opinion in Cardiol.
2003;
18
255-259
4
Strauer BE..
The significance of coronary reserve in clinical heart disease.
J Am Coll Cardiol.
1990;
15
775-783
5
Strauer BE, Schwartzkopf B, Kelm M..
Assessing the coronary circulation in hypertension.
J Hypertens.
1998;
16
1221-1233
6 Strauer BE.. Das Hochdruckherz. Berlin: Springer 1991
7
Strauer BE..
Koronare Mikrozirkulationsstörungen.
Klin Wochenschr.
1981;
59
1125-1137
8
Schannwell CM, Steiner St, Strauer BE..
Hypertensive mikrovaskuläre Erkrankung.
Herz.
2005;
30
26-36
9
Schannwell CM, Steiner S, Hennersdorf MG, Strauer BE..
Cardiovascular end organ impairment due to hypertension.
Internist.
2005;
46
496-508
10
Schwartzkopff B, Motz W, Frenzel H. et al. .
Structural and functional alterations of the intramyocardial coronary arterioles in
patients with arterial hypertension.
Circulation.
1993;
88
993-1003
11
Abelmann WH, Lorell BH..
The challange of cardiomyopathy.
J Am Coll Cardiol.
1989;
13
1219-1239
12
Warnholtz A, Buse J, Wild P, Münzel T..
Prognostische Bedeutung der endothelialen Dysfunktion.
Kardiologie up2date.
2006;
2
218-225
13
Athanasiadis A, Sechtem U..
Koronarspasmen bei angiographisch normalen Koronararterien.
Dtsch Med Wochenschr.
2004;
129
2657-2659
14
Scanlon PJ, Faxon DP, Audet AM. et al. .
ACC/AHA guidelines for coronary angiography: a report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines developed in collaboration with
the Society of Cardiac Angiography and Interventions.
J Am Coll Cardiol.
1999;
33
1756-1782
15
Maseri A, Crea F, Lanca GA..
Coronary vasoconstriction: where do we stand in 1999? An important, multifaceted but
elusive role.
Cardiologica.
1999;
44
115-118
16
Sueda S, Kohno H, Fukuda H. et al. .
Clinical and angiographical characteristics of acetylcholine–induced spasm: relationship
to dose of intracoronary injection of acetylcholine.
Coron Artery Disease.
2002;
13
231-236
17
Angelini P, Trivellato M, Danis J, Leachman RD..
Myocardial bridges: a review.
Prog Cardiovasc Dis.
1983;
26
75-88
18
Nething K, Merkle N, Liu Y. et al. .
Akuter Vorderwandinfarkt und Koronarspasmus bei Myokardbrücke des Ramus interventricularis
anterior – ausgelöst durch Akupressur?.
Dt Zeitschrift für Sportmedizin.
2005;
56
136-140
19
Low AF, Chia BL, Ng WL, Lim YT..
Bridge over troubling spasm: is the association of myocardial bridging and coronary
artery spasm a distinct entity? Three case reports.
Angiology.
2004;
55
217-220
20
Kelm M, Rath J, Pölitz B, Strauer BE..
Relevanz und Methoden zur Bestimmung der koronaren Flußreserve.
Z Kardiol.
1998;
87
74-79
21
Heller L, Cates C, Popma J. et al. .
Intracoronary doppler assessement of moderate coronary artery disease. Comparison
with 201TI imaging and coronary angiography.
Circulation.
1997;
96
484-490
22
Ge J, Erbel R..
Novel techniques of coronary artery imaging.
Curr Opin Cardiol.
1995;
10
626-633
23
Eggebrecht H, Von C Birgelen, Ge J. et al. .
Postextrasystolic potentiation of vessel compression in myocardial bridging: detection
by intravascular ultrasound.
J Clin Ultrasound.
2002;
30
312-316
24
Ge J, Jeremias A, Rupp A. et al. .
New signs characteristic of myocardial bridging demonstrated by intracoronary ultrasound
and doppler.
Eur Heart J.
1999;
20
1707-1716
25
Hongo Y, Tada H, Ito K. et al. .
Augmentation of vessel squeezing at coronary myocardial bridge by nitroglycerin: study
by quantitative coronary angiography and intravascular ultrasound.
Am Heart J.
1999;
138
345-350
26
Möhlenkamp St, Eggebrecht H, Ebralidze T. et al. .
Muskelbrücken der Koronararterien: mögliche ischämierelevante Normvarianten.
Herz.
2005;
30
37-47
27 Schwarz ER, Klues HG, vom Dahl J. et al. .Functional, angiographic and intracoronary
Doppler flow.
28
Chahine RA..
The diagnosis of coronary artery spasm in the cardiac catheterization laboratory.
Cardiol Clin.
1985;
3
19-28
29
Kültürsay H, Can L, Payzin S. et al. .
A rare indication for stenting: persistent coronary artery spasm.
Heart Vessels.
1996;
11
165-168
30
Antony J, Lerebours G, Nitenberg A..
Angiotensin–converting enzyme inhibition restores flow–dependent and cold pressor
test–induced dilatations in coronary arteries of hypertensive patients.
Circulation.
1996;
94
3115-3122
31
Dahlöf B, Devereux RB, Kjeldsen SE. et al. .
Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction
in hypertension study (LIFE): a randomised trial against atenolol.
Lancet.
2002;
359
995-1003
32
Kjeldsen SE, Dahlöf B, Devereux RB. et al. .
Effects of losartan on cardiovascular morbidity and mortality in patients with isolated
systolic hypertension and left ventricular hypertrophy: a Losartan Intervention for
Endpoint Reduction (LIFE) substudy.
JAMA.
2002;
288
1491-1498
33
Motz W..
Hochdruck und koronare Herzkrankheit. Gibt es neue Therapieoptionen?.
Herz.
2004;
29
255-265
34
Schmieder RE, Martus P, Klingbeil A..
Reversal of left ventricular hypertrophy in essential hypertension. A meta–analysis
of characteristics in symptomatic patients with myocardial bridging: effect of short–term
intravenous beta–blocker medication.
J Am Coll Cardiol.
1996;
27
1627-1645
35
Yusuf S, Sleight P, Pogue J. et al. .
Effects of an angiotensin–converting–enzyme inhibitor, ramipril, on cardiovascular
events in high–risk patients. The Heart Outcomes Prevention Evaluation Study Investigators.
N Engl J Med.
2000;
342
145-153
36
Kondidala S, Guttermann DD..
Coronary vasospasm and the regulation of coronary blood flow.
Prog Cardiovasc Dis.
2004;
46
349-373
37
Fenster B, Tsao P, Rockson S..
Endothelial dysfunction: clinical strategies for treating oxidant stress.
Am Heart J.
2003;
146
218-226
38
Haager PK, Schwarz ER, vom J Dahl. et al. .
Long term angiographic and clinical follow up in patients with stent implantation
for symptomatic myocardial bridging.
Heart.
2000;
84
403-408
39
Iversen S, Hake U, Mayer E. et al. .
Surgical treatment of myocardial bridging causing coronary artery obstruction.
Scand J Thorax Cardiovas.
1992;
26
107-111
1 Losartan Intervention For Endpoint reduction in hypertension
Korrespondenz
PD Dr. Christiana Mira Schannwell
Klinik für Kardiologie, Pneumologie und Angiologie Universitätsklinikum Düsseldorf
Moorenstraße 5
40225 Düsseldorf
eMail: schannwell@med.uni-duesseldorf.de