Microcirculatory coronary dysfunction in type 2 diabetic patients

Citation
A. Nitenberg et al., Microcirculatory coronary dysfunction in type 2 diabetic patients, ARCH MAL C, 93(8), 2000, pp. 937-941
Citations number
15
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
ARCHIVES DES MALADIES DU COEUR ET DES VAISSEAUX
ISSN journal
00039683 → ACNP
Volume
93
Issue
8
Year of publication
2000
Pages
937 - 941
Database
ISI
SICI code
0003-9683(200008)93:8<937:MCDIT2>2.0.ZU;2-6
Abstract
A failure of coronary blood flow to increase during cold presser test has b een shown in patients with coronary atherosclerosis and impaired metabolic coronary vasodilatation in response to atrial pacing has been demonstrated in diabetic patients without significant epicardial artery stenoses. This s tudy was designed to evaluate coronary microvascular adaptation to increase d myocardial oxygen demand in response to sympathetic stimulation in diabet ic patients with angiographically normal coronary arteries. Microvascular coronary adaptation to increased myocardial oxygen demand due to sympathetic stimulation evoked by the cold presser test has been examin ed in 22 type 2 diabetic patients and in 15 control subjects with angiograp hically normal coronary arteries and no other risk factors. Coronary blood flow was calculated by measuring mean flow velocity in left anterior descen ding coronary artery by intracoronary Doppler and cross sectional area of t he artery by digital angiography. Results show that despite a similar incre ase in rate-pressure product in the 2 groups (+22.6+/-12.4% in diabetic pat ients and +31.8+/-8.2% in control subjects, NS), coronary blood flow increa se in left anterior descending artery was significantly lower in diabetic p atients than in control subjects (+14.7+/-19.8% vs +75.5+/-13.5%, respectiv ely, p=0.0001). In addition, when there was a positive correlation between the 2 parameters in control subjects (R=0.651, p<0.01), there was no relati onship in diabetic patients (R=0.054). In conclusion, this study demonstrates that vasodilatation of coronary micr ocirculation in response to sympathetic stimulation evoked by cold presser test is impaired in type 2 diabetic patients without epicardial artery lesi ons. This microvascular impairment during sympathetic stimulation may expla in exercise-induced myocardial perfusion abnormalities observed in these pa tients and may impair microcirculatory coronary vasodilatation during curre nt life stress episodes such as exercise, mental stress or cold exposure.