title: Evidence for reduced coronary flow reserve in patients with insulin-dependent diabetes. A possible cause for diabetic heart disease in man.
abstract: In diabetic heart disease myocardial, interstitial, coronary and neural structures are often involved. Coronary microangiopathy is supposed to contribute an essential part, which has not yet been clearly analysed.
  
  
  METHODS
  In 9 normotensive patients with insulin-treated diabetes (DP) with clinically suspected coronary heart disease but normal epicardial coronary arteries, coronary microcirculation was studied. Coronary flow was determined as the quotient of base line and minimal coronary resistance after dipyridamole (0.5 mg/kg i.v.), using the argon-gas-chromatography method. Systolic left ventricular function was analysed by ventriculography, diastolic function by M-Mode-echocardiography and Doppler-echocardiograhy. Twelve normotensive subjects served as control group (CON).
  
  
  RESULTS
  In diabetic patients maximal coronary flow was significantly reduced (172 +/- 5 versus 395 +/- 103 ml/min x 100 g, p < or = 0.001) and minimal coronary resistance increased (0.6 +/- 0.19 versus 0.24 +/- 0.06 mmHg x min x 100 g/ml, p < 0.001). Coronary reserve in diabetics was markedly reduced (1.84 +/- 0.39 versus 4.23 +/- 0.52, p < or = 0.001). Global systolic function was normal in all patients (EF: DP: 72 +/- 13 versus CON: 77 +/- 12%, n.s.; cardiac index: DP: 3.2 +/- 0.8 versus CON: 3.3 +/- 1.2 1/ min x m2, n.s.). Diastolic function was impaired in diabetics with an increased relaxation time index (97 +/- 23 versus 45 +/- 18 msec, p < or = 0.01) and an impaired diastolic inflow pattern, indicated by the E/A-ratio (0.75 +/- 0.14 versus 1.66 +/- 0.13, p < or = 0.05).
  
  
  CONCLUSIONS
  The reduced coronary flow reserve in patients with insulin-treated diabetes mellitus may play a crucial role in the pathophysiology of diabetic cardiopathy, causing myocardial ischaemia due to a disturbance of coronary microcirculation leading to diastolic dysfunction and progressing assumably to systolic failure.
authors.affiliation: Department of Medicine, University of Düsscldorf, Germany.
authors.forename: B E
authors.initials: BE
authors.lastname: Strauer
authors.forename: W
authors.initials: W
authors.lastname: Motz
authors.forename: M
authors.initials: M
authors.lastname: Vogt
authors.forename: B
authors.initials: B
authors.lastname: Schwartzkopff
mesh_terms: D002784:Cholesterol / Q000097:blood; D003326:Coronary Circulation; D003327:Coronary Disease / Q000453:epidemiology / Q000503:physiopathology*; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000503:physiopathology*; D003971:Diastole; D005260:Female; D006331:Heart Diseases / Q000453:epidemiology* / Q000503:physiopathology; D006339:Heart Rate; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D012307:Risk Factors; D013599:Systole; D014280:Triglycerides / Q000097:blood; D014655:Vascular Resistance; D016277:Ventricular Function, Left
chemical_list: D014280:Triglycerides; D002784:Cholesterol