(Circulation. 1995;91:635-640.)
© 1995 American Heart Association, Inc.
Articles |
From the Cardiovascular Division and the Cardiovascular Center, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, and the Veterans Affairs Medical Center, Iowa City, Iowa.
Correspondence to James D. Rossen, MD, Department of Internal Medicine, 4212 RCP, The University of Iowa, Iowa City, IA 52242.
| Abstract |
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Methods and Results Twenty-four diabetic and 31 nondiabetic patients were studied during cardiac catheterization. A Doppler catheter or guidewire was used to measure changes in coronary blood flow velocity in a nonstenotic artery. Maximal coronary blood flow reserve was determined by using intracoronary adenosine or papaverine. Coronary dilation in response to an increase in myocardial metabolic demand was assessed by using rapid atrial pacing. Maximal vasodilator responses to papaverine and adenosine were compared in 12 diabetic patients. Maximal pharmacologic coronary flow reserve was depressed in diabetic (2.8±0.2, n=19) compared with nondiabetic (3.7±0.2, n=21, P<.001) patients. During atrial pacing, the decrease in coronary vascular resistance was attenuated in the diabetic (-14±3%) compared with the nondiabetic (-24±2%, P<.05) patients. Differences in coronary microvascular function between diabetic and nondiabetic patients were not attributable to differences in drug therapy, resting hemodynamics, or incidence of hypertension. In 12 diabetic patients the maximal coronary vasodilator responses to papaverine and adenosine were similar.
Conclusions This study demonstrates both reduced maximal coronary vasodilation and impairment in the regulation of coronary flow in response to submaximal increases in myocardial demand in patients with diabetes mellitus. These microvascular abnormalities may lead to myocardial ischemia in the absence of epicardial coronary atherosclerosis in some circumstances, and thus contribute to adverse cardiovascular events in diabetic patients.
Key Words: diabetes mellitus microcirculation vasodilation blood flow
| Introduction |
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-adrenergic
stimulation was impaired in diabetic rats.9 Attenuation of
coronary vasodilation to adenosine in diabetic animals has been
reported.7 10 Few data on coronary microvascular function in diabetic patients are available. Nitenberg et al11 reported reduced maximal coronary blood flow reserve and impaired endothelial-dependent epicardial coronary vasodilation in a study of 11 diabetic patients. However, since all but one diabetic patient had systemic hypertension in this study, attribution of the abnormalities to diabetes per se was uncertain.
The purpose of the present study was to evaluate coronary microvascular function in patients with diabetes mellitus. The coronary vasodilator response to increased myocardial oxygen demand was evaluated by using atrial pacing stress. Maximal vasodilation was assessed by measurement of pharmacologic coronary flow reserve, similar to the study of Nitenberg et al.11 Finally, we compared maximal vasodilator responses to adenosine and papaverine in diabetic patients to determine if resistance to the vasodilator effects of adenosine is present in diabetics.
| Methods |
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Coronary Flow Velocity Measurement
Changes in coronary blood
flow were assessed by measurement of
flow velocity changes using an intracoronary Doppler
catheter12 or Doppler-tipped angioplasty
guidewire.13 In studies performed with the Doppler
catheter, a 7F or 8F coronary angioplasty guiding catheter was
positioned at the coronary ostium and a 0.014-in. coronary angioplasty
guidewire was advanced into the coronary artery to be studied. A 3F
20-mHz coronary Doppler catheter (NuMed Inc) was advanced over the
guidewire into the proximal vessel and positioned to obtain a
high-quality phasic signal of blood flow velocity. The pulsed Doppler
meter (Bioengineering Department, University of Iowa Hospitals and
Clinics) was range-gated to maximize the amplitude of the mean coronary
blood flow velocity signal. In studies performed with the
Doppler-tipped angioplasty guidewire, a 7F coronary angioplasty guiding
catheter was positioned at the coronary ostium, and the 0.018-in.
12-mHz Doppler wire (Cardiometrics, Inc) was advanced into the coronary
artery to be studied. Audio signals from the Doppler guidewire were
processed with a system that incorporates a real-time spectrum analyzer
to provide a scrolling gray-scale spectral display as well as
determination of instantaneous spectral-peak velocity and the time
average of spectral-peak velocity. Phasic and mean coronary blood flow
velocity signals, mean arterial pressure (in millimeters of mercury)
from the guiding catheter, heart rate, and the surface ECG were
continuously recorded on a multichannel recorder.
Experimental Protocol
Subjects were brought to the cardiac
catheterization laboratory
in a fasting state. Oral hypoglycemic agents were withheld, and the
insulin dose was reduced by one half in patients receiving these
medications on the day of the research study. Prescribed cardiac
medications were continued on the day of the study. Diazepam (5 to 10
mg IV or PO) was given for sedation. No patient received atropine
premedication. The study was performed during infusion of nitroglycerin
at 8 µg/min IV or 5 to 10 minutes after intracoronary administration
of 200 µg nitroglycerin to prevent catheter-induced coronary artery
spasm and avoid changes in coronary artery caliber that would influence
the relation between changes in coronary flow velocity and volumetric
coronary blood flow.
Measurement of Pharmacologic Coronary Flow
Reserve
After measurement of resting coronary blood flow velocity, a
bolus dose of 6 to 10 mg papaverine hydrochloride14 (2
mg/mL 0.9% saline) or 8 to 12 µg adenosine15 (4 µg/mL
0.9% saline) was injected through the guiding catheter into the
coronary ostium, and the resultant increase in coronary blood flow
velocity was recorded. To confirm that maximal hyperemia was produced,
coronary blood flow velocity was recorded during administration of an
additional larger dose of papaverine (2 to 4 mg larger than the initial
dose) or adenosine (4 µg larger than the initial dose). Flow velocity
was allowed to return to control levels between drug doses. Coronary
flow reserve was calculated as the quotient of the peak mean flow
velocity (expressed in units proportional to the Doppler kHz shift)
after vasodilator and the control mean flow velocity during the 15 to
30 seconds preceding vasodilator administration. Coronary flow reserve
was measured in 12 randomly selected diabetic patients sequentially
with both papaverine and adenosine using the protocol described above.
In these patients, the order of drug administration was also randomly
selected.
Assessment of Metabolic Coronary Vasodilation
Metabolic coronary vasodilation was assessed by measurement of
the coronary hemodynamic response to rapid atrial pacing. Atrial pacing
was performed with a 6F bipolar pacemaker positioned at the high right
atrium. The paced rate was increased over 1 to 2 minutes until a 45 to
50 beats per minute increment over the sinus rate was reached or
atrioventricular block developed. Coronary blood flow velocity and mean
arterial pressure were measured during sinus rhythm and when the flow
signal stabilized after at least 2 minutes of pacing at the peak rate.
An index of coronary vascular resistance was calculated as the quotient
of mean arterial pressure (in millimeters of mercury) and coronary flow
velocity expressed in units proportional to the Doppler kHz shift.
Alterations in coronary vascular resistance during pacing were
expressed as percent change from the control value. Despite adherence
to a standardized protocol, pacing resulted in a wide range of
metabolic stress as assessed by changes in the product of heart rate
and mean arterial pressure (rate-pressure product). To control for
this, an index of coronary vasodilation relative to magnitude of
metabolic stress was calculated as the quotient of percent change in
coronary vascular resistance and percent change in rate-pressure
product during pacing.
Data Analysis
Group data are reported as mean±SEM.
Continuous variables were
compared by using Student's t test for paired or unpaired
data as appropriate. Discrete variables were analyzed by
2 test. In assessment of pharmacologic coronary
flow reserve, multivariate stepwise regression analysis was used to
examine the influence of the following variables: diabetes status,
history of hypertension, gender, age, ß-adrenergic antagonist use,
glucose level, control heart rate, control mean arterial pressure, and
control rate-pressure product. In assessment of metabolically mediated
coronary vasodilation, multivariate stepwise regression analysis
was used to examine the influence of the following variables: diabetes
status, history of hypertension, gender, age, ß-adrenergic antagonist
use, glucose level, control heart rate, percent change in heart rate
during pacing, control mean arterial pressure, percent change in mean
arterial pressure during pacing, control rate-pressure product, and
percent change in rate-pressure product during pacing. Differences were
considered significant at the P
.05 level.
| Results |
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2.0 mg/dL.
|
Effect of Diabetes Mellitus on Pharmacologic Coronary Flow
Reserve
Maximal coronary flow reserve was measured using intracoronary
papaverine or adenosine in 19 diabetic and 22 nondiabetic patients. The
heart rate averaged 77±3 bpm in the diabetic and 69±3 bpm in the
nondiabetic (P=.05) patients. Mean arterial pressure
averaged 100±3 mm Hg in the diabetics and 95±3 mm Hg in the
nondiabetics (P=NS). The rate-pressure product was higher in
the diabetic than in the nondiabetic (7731±443 versus 6549±365
bpmxmm Hg, P<.05) patients.
Coronary flow reserve was
lower in the diabetics than in the
nondiabetics (2.8±0.2 versus 3.7±0.2, P<.001; Fig
1
).
|
Since ß-adrenergic antagonists were taken more frequently by nondiabetic than diabetic patients and coronary flow reserve was higher in patients receiving these agents (ß-antagonist, 3.9±0.4; no ß-antagonist, 3.1±0.2, P<.05), the analysis was repeated after excluding patients receiving ß-antagonists. After this exclusion, a reduction in coronary flow reserve in diabetic (n=17) compared with nondiabetic (n=14) patients was still observed (2.8±0.2 versus 3.5±0.2, P<.05). The diagnosis of hypertension was not associated with a reduction in coronary flow reserve in the patients studied (hypertension, 3.2±0.3; no hypertension, 3.4±0.2, P=NS). Coronary flow reserve was reduced in the diabetic patients without hypertension (2.7±0.2, n=4) compared with the nondiabetic patients without hypertension (3.6±0.2, n=12, P<.05).
Multivariate stepwise regression analysis revealed that diabetic status (P=.02), age (P=.01), and control heart rate (P=.05) were independently related to coronary flow reserve. The relation of ß-antagonist therapy with coronary flow reserve was of marginal significance (P=.07).
Effect of Diabetes Mellitus on Metabolic Coronary
Vasodilation
The coronary hemodynamic response to the standardized
atrial
pacing protocol was measured in 24 diabetic and 31 nondiabetic
patients. The control heart rate averaged 79±2 bpm in the diabetic and
73±2 bpm in the nondiabetic (P=.06) patients. The
control
mean arterial pressure was 102±3 mm Hg in the diabetics and 96±2
mm Hg in the nondiabetics (P=.10). The control
rate-pressure product was higher in the diabetic than the nondiabetic
(8087±385 versus 6994±296 bpmxmm Hg, P<.05)
patients.
By experimental design, the increase in heart rate during atrial pacing was similar in diabetic and nondiabetic (45±1 versus 48±2 bpm, P=NS) patients. During atrial pacing in diabetics, mean arterial pressure was unchanged from control (-0.5±1 mm Hg, P=NS), whereas in nondiabetics, mean arterial pressure increased by 4±1 mm Hg (P<.01). While the absolute increase in rate-pressure product in diabetics and nondiabetics was similar (4506±226 versus 5089±245 bpmxmm Hg, P=NS), the increase relative to the control rate-pressure product was smaller in the diabetic than nondiabetic (59±3% versus 77±5%, P<.01) patients.
The reduction in coronary vascular
resistance during pacing was smaller
in diabetics than in nondiabetics. Coronary vascular resistance
decreased by 14±3% in the diabetic patients and by 24±2% in the
nondiabetics (P<.05, Fig 2
). Impairment in
coronary vasodilation during pacing in diabetics was observed after
controlling for the variation in the magnitude of metabolic stress
during pacing; the quotient of percent change in coronary vascular
resistance and percent change in rate-pressure product was
-0.22±0.05
in the diabetic and -0.34±0.03 in the nondiabetic
(P<.05,
Fig 2
) patients.
|
ß-Adrenergic antagonist therapy did not influence the reduction in coronary resistance during pacing (ß-antagonist, -21±3%; no ß-antagonist, -19±2%, P=NS). In the subset of 21 diabetic and 19 nondiabetic patients not receiving ß-antagonist therapy, the reduction in coronary resistance remained attenuated in the diabetic compared with the nondiabetic (-14±3% versus -23±3%, P<.05) group. The diagnosis of hypertension did not influence the reduction in coronary resistance during pacing (hypertension, -18±2%; no hypertension, -21±3%, P=NS). In the subset of 7 diabetic and 19 nondiabetic patients without hypertension, the reduction in coronary resistance remained blunted in the diabetic compared with the nondiabetic (-12±7% versus -24±2%, P=.05) group.
Multivariate stepwise regression analysis revealed that diabetic status (P=.06) and control rate-pressure product (P=.002) were independently related to the change in coronary resistance during pacing. Only diabetic status (P=.05) was independently related to the quotient of percent change in coronary vascular resistance and percent change in rate-pressure product.
Effect of Hypertension on Pharmacologic and Metabolic Coronary Flow
Responses in Diabetic Patients
Of the 24 diabetic patients studied, 17
also had systemic
hypertension. At the time of study, the control heart rate
(hypertension, 78±3 bpm; normotension, 80±5 bpm,
P=NS),
control mean arterial pressure (hypertension, 101±4 mm Hg;
normotension, 102±4, P=NS), and percent change in
rate-mean
pressure product during pacing (hypertension, 59±4%; normotension,
57±8%, P=NS) were similar in the diabetic hypertensive
and
diabetic normotensive patients. Pharmacologic coronary flow reserve was
2.8±0.3 in the diabetic hypertensive and 2.7±0.2 in the diabetic
normotensive patients (P=NS), and coronary vascular
resistance during pacing decreased by 15±3% in the diabetic
hypertensive patients and by 12±7% in the diabetic normotensive
patients (P=NS).
Maximal Coronary Flow Responses to Papaverine and Adenosine in
Diabetic Patients
Coronary vasodilator responses to papaverine and
adenosine as
assessed by maximal coronary flow reserve were comparable in the 12
diabetic patients who received both drugs (papaverine, 2.7±0.3;
adenosine, 2.8±0.3, P=NS).
Pharmacologic Flow Reserve and Metabolic Vasodilation in Diabetic
Patients Receiving Oral Hypoglycemic Agents
Of the 24 patients with
diabetes, 12 were receiving sulfonylurea
oral hypoglycemic agents at the time of the study. Maximal
pharmacologic flow reserve was 2.8±0.2 (n=10) in diabetics not
receiving and 2.7±0.4 (n=9) in those receiving oral hypoglycemic
agents (P=NS). The decreases in coronary vascular resistance
during atrial pacing were identical (14±4%) in both diabetics
receiving (n=12) and those not receiving (n=12) oral
hypoglycemic
agents.
| Discussion |
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The mechanisms leading to impairment in coronary vasodilation are uncertain. Histopathologic studies in diabetic patients describe abnormalities in coronary resistance vessels including arteriolar thickening, perivascular accumulations of connective tissue, and capillary microaneurysms.2 16 Capillary density is reduced in hearts of diabetic patients sustaining myocardial infarction.3 Microvascular morphological abnormalities have also been reported in diabetic animals.4 However, structural abnormalities of the coronary microvascular circulation in diabetes have not been universally observed.17 18
The reduction in metabolic coronary vasodilation during atrial
pacing in diabetics may be related to dysfunction of the coronary
endothelium. Impairment in endothelium-dependent
vasodilation related to diabetes has been described in
animals19 20 21 as well as the human
forearm22 23 and corpus cavernosum.24
Epicardial coronary artery constriction to acetylcholine is augmented
in diabetic patients compared with control subjects.11
Furthermore, the magnitude of coronary vasodilation during pacing
stress is related to endothelium-dependent vasodilation
as assessed by the flow response to intracoronary acetylcholine in
nondiabetic patients with chest pain and angiographically normal
coronary arteries.25 Attenuation of
endothelium-dependent vasodilation related to increased
production of vasoconstrictor prostaglandins has been reported in
diabetic rabbit aorta,20 suggesting that enhanced vessel
wall production of vasoconstrictor substances could also blunt coronary
vasodilation in human diabetics. Finally, increased sensitivity to the
vasoconstrictor effects of
-adrenergic activation has been reported
in experimental diabetes,26 27 28 which
could limit
physiological29 and pharmacologic vasodilation. Additional
studies in diabetic patients evaluating the relation of
endothelium-dependent vasomotion and metabolic
vasodilation, the influence of glycemic control on microvascular
function, adrenergic influences on microvascular dilation, and the
relation between coronary microvascular function and diabetic
microvascular disease in other organs are needed.
Coronary vasodilation in response to exogenous adenosine is impaired in some animal models of diabetes.7 10 Given the potential role of adenosine in the regulation of coronary blood flow in response to changing oxygen demand, diminished vascular responsiveness to adenosine has been proposed as a link between impaired metabolic vasodilation and diabetes mellitus. However, we found equivalent maximal vasodilation with adenosine and papaverine, suggesting that impairment of metabolic vasodilation in human diabetes is not related to selective resistance to adenosine.
Sulfonylurea oral hypoglycemic agents are antagonists of the ATP-sensitive potassium channel. Basal coronary resistance is increased,30 and hyperemia in response to ischemia is attenuated,31 32 by the oral hypoglycemic agent glibenclamide in dogs. The effects of oral hypoglycemic agents on coronary reactivity in experimental animals and the differences in cardiovascular morbidity between patients treated with insulin and the sulfonylurea tolbutamide in a large multicenter trial33 have led to concern regarding the coronary effects of these agents in diabetic patients. In the present study, no differences in pharmacologic or metabolic coronary vasodilation were observed in diabetic patients treated with oral hypoglycemic agents compared with those receiving other therapy.
While morphological studies in rats demonstrate more marked coronary microvascular abnormalities in hypertensive diabetic animals compared with those with hypertension or diabetes alone,18 we observed no additional impairment in microvascular function in diabetic hypertensive compared with diabetic normotensive patients.
Limitations
In the present study, coronary blood flow
responses were
assessed by using intracoronary Doppler measurements of coronary flow
velocity. Although extensive animal studies have validated the accuracy
of Doppler measurements in the assessment of changes in coronary
flow,12 13 the technique is not capable of measuring
absolute myocardial perfusion. Thus, it is uncertain if the impairment
in vasodilation in diabetics is due to elevation of resting myocardial
perfusion, a reduction in perfusion during the pharmacologic and
metabolic stimuli, or both. However, limited data in diabetic patients
indicate that resting coronary blood flow measured by coronary sinus
thermodilution is similar in nondiabetic control
subjects.34
In our study, the heart rate and arterial pressure in patients with diabetes tended to be higher than in nondiabetics. We35 and other investigators36 have observed that maximal coronary flow reserve is progressively reduced with increases in heart rate but is not influenced by acute increases in arterial pressure. Multivariate regression analysis in the present study revealed that the presence of diabetes was associated with reduced coronary flow reserve independent of the differences in heart rate or other differences between the diabetic and nondiabetic patients.
The diabetic patients enrolled in this study were relatively free of renal and other end-organ complications. The severity of coronary microvascular dysfunction in diabetes may parallel the development of other complications attributable to microangiopathy. Thus, patients with diabetes that is more advanced than in our subjects may have a greater impairment in coronary vasodilator responses.
Clinical Implications
Our studies provide evidence for both
reduced maximal coronary
vasodilation and impairment in the regulation of coronary flow in
response to submaximal increases in myocardial demand in patients with
diabetes mellitus. It is possible that microvascular abnormalities
could lead to myocardial ischemia in the absence of epicardial coronary
atherosclerosis in some circumstances, and could thus contribute to
chronic left ventricular dysfunction and other adverse cardiovascular
events in diabetic patients.
| Acknowledgments |
|---|
Received July 20, 1994; accepted August 31, 1994.
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D. J. Kumbhani, N. A. Healey, H. S. Thatte, S. Nawas, M. D. Crittenden, V. Birjiniuk, P. R. Treanor, and S. F. Khuri Patients with diabetes mellitus undergoing cardiac surgery are at greater risk for developing intraoperative myocardial acidosis J. Thorac. Cardiovasc. Surg., June 1, 2007; 133(6): 1566 - 1572. [Abstract] [Full Text] [PDF] |
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K. Hirata, A. Kadirvelu, M. Di Tullio, S. Homma, A. M. Choy, and C. C. Lang Coronary Vasomotor Function Is Abnormal in First-Degree Relatives of Patients With Type 2 Diabetes Diabetes Care, January 1, 2007; 30(1): 150 - 153. [Full Text] [PDF] |
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S Moir, L Hanekom, Z-Y Fang, B Haluska, C Wong, M Burgess, and T H Marwick Relationship between myocardial perfusion and dysfunction in diabetic cardiomyopathy: a study of quantitative contrast echocardiography and strain rate imaging Heart, October 1, 2006; 92(10): 1414 - 1419. [Abstract] [Full Text] [PDF] |
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T. Szerafin, N. Erdei, T. Fulop, E. T. Pasztor, I. Edes, A. Koller, and Z. Bagi Increased Cyclooxygenase-2 Expression and Prostaglandin-Mediated Dilation in Coronary Arterioles of Patients With Diabetes Mellitus Circ. Res., September 1, 2006; 99(5): e12 - 317. [Abstract] [Full Text] [PDF] |
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D Fukuda, M Yoshiyama, K Shimada, H Yamashita, S Ehara, Y Nakamura, K Kamimori, A Tanaka, T Kawarabayashi, and J Yoshikawa Relation between aortic stiffness and coronary flow reserve in patients with coronary artery disease Heart, June 1, 2006; 92(6): 759 - 762. [Abstract] [Full Text] [PDF] |
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L. Cortigiani, R. Bigi, R. Sicari, P. Landi, F. Bovenzi, and E. Picano Prognostic Value of Pharmacological Stress Echocardiography in Diabetic and Nondiabetic Patients With Known or Suspected Coronary Artery Disease J. Am. Coll. Cardiol., February 7, 2006; 47(3): 605 - 610. [Abstract] [Full Text] [PDF] |
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R. Lautamaki, K.E. J. Airaksinen, M. Seppanen, J. Toikka, R. Harkonen, M. Luotolahti, R. Borra, J. Sundell, J. Knuuti, and P. Nuutila Insulin Improves Myocardial Blood Flow in Patients With Type 2 Diabetes and Coronary Artery Disease Diabetes, February 1, 2006; 55(2): 511 - 516. [Abstract] [Full Text] [PDF] |
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H Yoshitani, M Takeuchi, K Sakamoto, T Akasaka, K Yoshida, and J Yoshikawa Effect of one or more co-morbid conditions on diagnostic accuracy of coronary flow velocity reserve for detecting significant left anterior descending coronary stenosis Heart, October 1, 2005; 91(10): 1294 - 1298. [Abstract] [Full Text] [PDF] |
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R. Florenciano-Sanchez, G. de la Morena-Valenzuela, M. Villegas-Garcia, F. Soria-Arcos, R. Rubio-Paton, F. Teruel-Carrillo, J. Hurtado, and M. Valdes-Chavarri Noninvasive assessment of coronary flow velocity reserve in left anterior descending artery adds diagnostic value to both clinical variables and dobutamine echocardiography: a study based on clinical practice Eur J Echocardiogr, August 1, 2005; 6(4): 251 - 259. [Abstract] [Full Text] [PDF] |
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M. Srinivasan, P. Herrero, J. B. McGill, J. Bennik, B. Heere, D. Lesniak, V. G. Davila-Roman, and R. J. Gropler The Effects of Plasma Insulin and Glucose on Myocardial Blood Flow in Patients With Type 1 Diabetes Mellitus J. Am. Coll. Cardiol., July 5, 2005; 46(1): 42 - 48. [Abstract] [Full Text] [PDF] |
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A. Elhendy, J. M. Tsutsui, E. L. O'Leary, F. Xie, A. C. McGrain, and T. R. Porter Noninvasive Diagnosis of Coronary Artery Disease in Patients With Diabetes by Dobutamine Stress Real-Time Myocardial Contrast Perfusion Imaging Diabetes Care, July 1, 2005; 28(7): 1662 - 1667. [Abstract] [Full Text] [PDF] |
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B. Capaldo, M. Galderisi, A. A. Turco, A. D'Errico, S. Turco, A. A. Rivellese, G. de Simone, O. de Divitiis, and G. Riccardi Acute Hyperglycemia Does Not Affect the Reactivity of Coronary Microcirculation in Humans J. Clin. Endocrinol. Metab., July 1, 2005; 90(7): 3871 - 3876. [Abstract] [Full Text] [PDF] |
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J. O. Prior, M. J. Quinones, M. Hernandez-Pampaloni, A. D. Facta, T. H. Schindler, J. W. Sayre, W. A. Hsueh, and H. R. Schelbert Coronary Circulatory Dysfunction in Insulin Resistance, Impaired Glucose Tolerance, and Type 2 Diabetes Mellitus Circulation, May 10, 2005; 111(18): 2291 - 2298. [Abstract] [Full Text] [PDF] |
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U. Dahlstrom Frequent non-cardiac comorbidities in patients with chronic heart failure Eur J Heart Fail, March 16, 2005; 7(3): 309 - 316. [Abstract] [Full Text] [PDF] |
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E. A. Mokelke, N. J. Dietz, D. M. Eckman, M. T. Nelson, and M. Sturek Diabetic dyslipidemia and exercise affect coronary tone and differential regulation of conduit and microvessel K+ current Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1233 - H1241. [Abstract] [Full Text] [PDF] |
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A. Prasad, G. W. Stone, T. D. Stuckey, C. O. Costantini, P. J. Zimetbaum, M. McLaughlin, R. Mehran, E. Garcia, J. E. Tcheng, D. A. Cox, et al. Impact of diabetes mellitus on myocardial perfusion after primary angioplasty in patients with acute myocardial infarction J. Am. Coll. Cardiol., February 15, 2005; 45(4): 508 - 514. [Abstract] [Full Text] [PDF] |
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G S Werner, U Emig, P Bahrmann, M Ferrari, and H R Figulla Recovery of impaired microvascular function in collateral dependent myocardium after recanalisation of a chronic total coronary occlusion Heart, November 1, 2004; 90(11): 1303 - 1309. [Abstract] [Full Text] [PDF] |
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H.-J. Priebe Triggers of perioperative myocardial ischaemia and infarction Br. J. Anaesth., July 1, 2004; 93(1): 9 - 20. [Abstract] [Full Text] [PDF] |
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M. N. Zairis, A. G. Lyras, S. S. Makrygiannis, P. K. Psarogianni, E. N. Adamopoulou, S. M. Handanis, A. Papantonakos, S. K. Argyrakis, A. A. Prekates, and S. G. Foussas Type 2 Diabetes and Intravenous Thrombolysis Outcome in the Setting of ST Elevation Myocardial Infarction Diabetes Care, April 1, 2004; 27(4): 967 - 971. [Abstract] [Full Text] [PDF] |
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A. Nitenberg, P. Valensi, R. Sachs, E. Cosson, J.-R. Attali, and I. Antony Prognostic Value of Epicardial Coronary Artery Constriction to the Cold Pressor Test in Type 2 Diabetic Patients With Angiographically Normal Coronary Arteries and No Other Major Coronary Risk Factors Diabetes Care, January 1, 2004; 27(1): 208 - 215. [Abstract] [Full Text] [PDF] |
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H. Post, J. Kajstura, B. Lei, W. C. Sessa, B. Byrne, P. Anversa, T. H. Hintze, and F. A. Recchia Adeno-associated virus mediated gene delivery into coronary microvessels of chronically instrumented dogs J Appl Physiol, October 1, 2003; 95(4): 1688 - 1694. [Abstract] [Full Text] [PDF] |
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Z. Bagi, A. Koller, and G. Kaley Superoxide-NO interaction decreases flow- and agonist-induced dilations of coronary arterioles in Type 2 diabetes mellitus Am J Physiol Heart Circ Physiol, October 1, 2003; 285(4): H1404 - H1410. [Abstract] [Full Text] [PDF] |
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E. Picano Diabetic cardiomyopathy: the importance of being earliest J. Am. Coll. Cardiol., August 6, 2003; 42(3): 454 - 457. [Full Text] [PDF] |
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G. S. Werner, B. M. Richartz, S. Heinke, M. Ferrari, and H. R. Figulla Impaired acute collateral recruitment as a possible mechanism for increased cardiac adverse events in patients with diabetes mellitus Eur. Heart J., June 2, 2003; 24(12): 1134 - 1142. [Abstract] [Full Text] [PDF] |
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H. Miura, R. E. Wachtel, F. R. Loberiza Jr, T. Saito, M. Miura, A. C. Nicolosi, and D. D. Gutterman Diabetes Mellitus Impairs Vasodilation to Hypoxia in Human Coronary Arterioles: Reduced Activity of ATP-Sensitive Potassium Channels Circ. Res., February 7, 2003; 92(2): 151 - 158. [Abstract] [Full Text] [PDF] |
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Y. Yu, K. Ohmori, I. Kondo, L. Yao, T. Noma, T. Tsuji, K. Mizushige, and M. Kohno Correlation of functional and structural alterations of the coronary arterioles during development of type II diabetes mellitus in rats Cardiovasc Res, November 1, 2002; 56(2): 303 - 311. [Abstract] [Full Text] [PDF] |
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T. Ono, J. Kobayashi, Y. Sasako, K. o Bando, O. Tagusari, K. Niwaya, H. Imanaka, T. Nakatani, and S. Kitamura The impact of diabetic retinopathy on long-term outcome following coronary artery bypass graft surgery J. Am. Coll. Cardiol., August 7, 2002; 40(3): 428 - 436. [Abstract] [Full Text] [PDF] |
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T. Bartel, Y. a Yang, S. Muller, R. R. Wenzel, D. Baumgart, T. Philipp, and R. Erbel Noninvasive assessment of microvascular function in arterial hypertension by transthoracic doppler harmonic echocardiography J. Am. Coll. Cardiol., June 19, 2002; 39(12): 2012 - 2018. [Abstract] [Full Text] [PDF] |
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G.E. Kochiadakis, E.I. Skalidis, M.D. Kalebubas, N.E. Igoumenidis, S.I. Chrysostomakis, E.M. Kanoupakis, E.N. Simantirakis, and P.E. Vardas Effect of acute atrial fibrillation on phasic coronary blood flow pattern and flow reserve in humans Eur. Heart J., May 1, 2002; 23(9): 734 - 741. [Abstract] [Full Text] [PDF] |
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J. D. Tune, K. N. Richmond, M. W. Gorman, and E. O. Feigl Control of Coronary Blood Flow during Exercise Experimental Biology and Medicine, April 1, 2002; 227(4): 238 - 250. [Abstract] [Full Text] [PDF] |
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J. D. Tune, C. Yeh, S. Setty, and H. F. Downey ATP-Dependent K+ Channels Contribute to Local Metabolic Coronary Vasodilation in Experimental Diabetes Diabetes, April 1, 2002; 51(4): 1201 - 1207. [Abstract] [Full Text] [PDF] |
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A. Nitenberg, S. Ledoux, P. Valensi, R. Sachs, and I. Antony Coronary Microvascular Adaptation to Myocardial Metabolic Demand Can Be Restored by Inhibition of Iron-Catalyzed Formation of Oxygen Free Radicals in Type 2 Diabetic Patients Diabetes, March 1, 2002; 51(3): 813 - 818. [Abstract] [Full Text] [PDF] |
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H. M. O. Farouque, S. G. Worthley, I. T. Meredith, R. A. P. Skyrme-Jones, and M. J. Zhang Effect of ATP-Sensitive Potassium Channel Inhibition on Resting Coronary Vascular Responses in Humans Circ. Res., February 8, 2002; 90(2): 231 - 236. [Abstract] [Full Text] [PDF] |
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K. Hirata, K. Shimada, H. Watanabe, T. Muro, M. Yoshiyama, K. Takeuchi, T. Hozumi, and J. Yoshikawa Modulation of coronary flow velocity reserve by gender, menstrual cycle and hormone replacement therapy J. Am. Coll. Cardiol., December 1, 2001; 38(7): 1879 - 1884. [Abstract] [Full Text] [PDF] |
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G. S. Werner, M. Ferrari, B. M. Richartz, O. Gastmann, and H. R. Figulla Microvascular Dysfunction in Chronic Total Coronary Occlusions Circulation, September 4, 2001; 104(10): 1129 - 1134. [Abstract] [Full Text] [PDF] |
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G. Landesberg, M. Mosseri, D. Zahger, Y. Wolf, M. Perouansky, H. Anner, B. Drenger, Y. Hasin, Y. Berlatzky, and C. Weissman Myocardial infarction after vascular surgery: the role of prolonged, stress-induced, ST depression-type ischemia J. Am. Coll. Cardiol., June 1, 2001; 37(7): 1839 - 1845. [Abstract] [Full Text] [PDF] |
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A. Nitenberg, S. Ledoux, P. Valensi, R. Sachs, J.-R. Attali, and I. Antony Impairment of Coronary Microvascular Dilation in Response to Cold Pressor-Induced Sympathetic Stimulation in Type 2 Diabetic Patients With Abnormal Stress Thallium Imaging Diabetes, May 1, 2001; 50(5): 1180 - 1185. [Abstract] [Full Text] |
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S.-i. Saitoh, F. Onogi, K. Aikawa, M. Muto, T. Saito, K. Maehara, and Y. Maruyama Multiple endothelial injury in epicardial coronary artery induces downstream microvascular spasm as well as remodeling partly via thromboxane A2 J. Am. Coll. Cardiol., January 1, 2001; 37(1): 308 - 315. [Abstract] [Full Text] [PDF] |
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R. F. Ammar Jr., D. D. Gutterman, L. A. Brooks, and K. C. Dellsperger Impaired dilation of coronary arterioles during increases in myocardial O2 consumption with hyperglycemia Am J Physiol Endocrinol Metab, October 1, 2000; 279(4): E868 - E874. [Abstract] [Full Text] [PDF] |
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T. Tanikawa, H. Kanatsuka, R. Koshida, M. Tanaka, A. Sugimura, T. Kumagai, M. Miura, T. Komaru, and K. Shirato Role of pertussis toxin-sensitive G protein in metabolic vasodilation of coronary microcirculation Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1819 - H1829. [Abstract] [Full Text] [PDF] |
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T. Hammoud, J.-F. Tanguay, and M. G. Bourassa Management of coronary artery disease: therapeutic options in patients with diabetes J. Am. Coll. Cardiol., August 1, 2000; 36(2): 355 - 365. [Abstract] [Full Text] [PDF] |
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H. Wieneke, M. Haude, J. Ge, C. Altmann, S. Kaiser, D. Baumgart, C. von Birgelen, D. Welge, and R. Erbel Corrected coronary flow velocity reserve: a new concept for assessing coronary perfusion J. Am. Coll. Cardiol., June 1, 2000; 35(7): 1713 - 1720. [Abstract] [Full Text] [PDF] |
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H. Laine, P. Nuutila, M. Luotolahti, C. Meyer, T. Elomaa, P. Koskinen, T. Rönnemaa, and J. Knuuti Insulin-Induced Increment of Coronary Flow Reserve Is Not Abolished by Dexamethasone in Healthy Young Men J. Clin. Endocrinol. Metab., May 1, 2000; 85(5): 1868 - 1873. [Abstract] [Full Text] |
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R. A. M. van Liebergen, J. J. Piek, K. T. Koch, R. J. G. Peters, R. J. de Winter, C. E. Schotborgh, and K. I. Lie Hyperemic coronary flow after optimized intravascular ultrasound-guided balloon angioplasty and stent implantation J. Am. Coll. Cardiol., December 1, 1999; 34(7): 1899 - 1906. [Abstract] [Full Text] [PDF] |
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M. F. Di Carli, D. Bianco-Batlles, M. E. Landa, A. Kazmers, H. Groehn, O. Muzik, and G. Grunberger Effects of Autonomic Neuropathy on Coronary Blood Flow in Patients With Diabetes Mellitus Circulation, August 24, 1999; 100(8): 813 - 819. [Abstract] [Full Text] [PDF] |
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J. A. MILLER Impact of Hyperglycemia on the Renin Angiotensin System in Early Human Type 1 Diabetes Mellitus J. Am. Soc. Nephrol., August 1, 1999; 10(8): 1778 - 1785. [Abstract] [Full Text] |
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I. Yokoyama, S.-i. Momomura, T. Ohtake, K. Yonekura, W. Yang, N. Kobayakawa, T. Aoyagi, S. Sugiura, N. Yamada, K. Ohtomo, et al. Improvement of Impaired Myocardial Vasodilatation Due to Diffuse Coronary Atherosclerosis in Hypercholesterolemics After Lipid-Lowering Therapy Circulation, July 13, 1999; 100(2): 117 - 122. [Abstract] [Full Text] [PDF] |
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J. R. Kersten and D. C. Warltier Modulation of the adaptive response to myocardial ischemia by coexisting disease Am J Physiol Heart Circ Physiol, June 1, 1999; 276(6): H2268 - H2270. [Full Text] [PDF] |
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V. H. Thourani, W. S. Weintraub, B. Stein, S. S.P. Gebhart, J. M. Craver, E. L. Jones, and R. A. Guyton Influence of diabetes mellitus on early and late outcome after coronary artery bypass grafting Ann. Thorac. Surg., April 1, 1999; 67(4): 1045 - 1052. [Abstract] [Full Text] [PDF] |
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T. Akasaka, K. Yoshida, T. Hozumi, T. Takagi, S. Kaji, T. Kawamoto, Y. Ueda, Y. Okada, S. Morioka, and J. Yoshikawa Restricted coronary flow reserve in patients with mitral regurgitation improves after mitral reconstructive surgery J. Am. Coll. Cardiol., December 1, 1998; 32(7): 1923 - 1930. [Abstract] [Full Text] [PDF] |
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R. A. M. van Liebergen, J. J. Piek, K. T. Koch, R. J. de Winter, and K. I. Lie Immediate and Long-Term Effect of Balloon Angioplasty or Stent Implantation on the Absolute and Relative Coronary Blood Flow Velocity Reserve Circulation, November 17, 1998; 98(20): 2133 - 2140. [Abstract] [Full Text] [PDF] |
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T. Hozumi, K. Yoshida, T. Akasaka, Y. Asami, Y. Ogata, T. Takagi, S. Kaji, T. Kawamoto, Y. Ueda, and S. Morioka Noninvasive assessment of coronary flow velocity and coronary flow velocity reserve in the left anterior descending coronary artery by Doppler echocardiography: Comparison with invasive technique J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1251 - 1259. [Abstract] [Full Text] [PDF] |
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N. S Dhalla, X. Liu, V. Panagia, and N. Takeda Subcellular remodeling and heart dysfunction in chronic diabetes Cardiovasc Res, November 1, 1998; 40(2): 239 - 247. [Abstract] [Full Text] [PDF] |
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R. J. Bache Vasodilator Reserve : A Functional Assessment of Coronary Health Circulation, September 29, 1998; 98(13): 1257 - 1260. [Full Text] [PDF] |
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A. P. Burke, A. Farb, G. T. Malcom, Y.-h. Liang, J. Smialek, and R. Virmani Effect of Risk Factors on the Mechanism of Acute Thrombosis and Sudden Coronary Death in Women Circulation, June 2, 1998; 97(21): 2110 - 2116. [Abstract] [Full Text] [PDF] |
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I. Yokoyama, T. Ohtake, S.-i. Momomura, K. Yonekura, N. Kobayakawa, T. Aoyagi, S. Sugiura, Y. Sasaki, and M. Omata Altered Myocardial Vasodilatation in Patients With Hypertriglyceridemia in Anatomically Normal Coronary Arteries Arterioscler Thromb Vasc Biol, February 1, 1998; 18(2): 294 - 299. [Abstract] [Full Text] [PDF] |
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R. W. Nesto and S. Zarich Acute Myocardial Infarction in Diabetes Mellitus : Lessons Learned From ACE Inhibition Circulation, January 13, 1998; 97(1): 12 - 15. [Full Text] [PDF] |
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P. A. Zimmermann, H. J. Knot, A. S. Stevenson, and M. T. Nelson Increased Myogenic Tone and Diminished Responsiveness to ATP-Sensitive K+ Channel Openers in Cerebral Arteries From Diabetic Rats Circ. Res., December 19, 1997; 81(6): 996 - 1004. [Abstract] [Full Text] |
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N. Maeda, H. Hiraoka, T. Nakamura, F. Matsuura, N. Ouchi, A. Nakata, H. Kobayashi, S. Yamashita, K. Kameda-Takemura, Y. Matsuzawa, et al. Acetylcholine-Induced Coronary Microvascular Vasospasm in a Patient with Angina Pectoris and Normal Coronary Angiogram: A Case Report Angiology, November 1, 1997; 48(11): 995 - 999. [Abstract] [PDF] |
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S. B. King III Is It Important How One Dies? : Questions for Planning Future Revascularization Trials Circulation, October 7, 1997; 96(7): 2121 - 2123. [Full Text] |
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T. B. Investigators Influence of Diabetes on 5-Year Mortality and Morbidity in a Randomized Trial Comparing CABG and PTCA in Patients With Multivessel Disease : The Bypass Angioplasty Revascularization Investigation (BARI) Circulation, September 16, 1997; 96(6): 1761 - 1769. [Abstract] [Full Text] |
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T. Akasaka, K. Yoshida, A. Yamamuro, T. Hozumi, T. Takagi, S. Morioka, and J. Yoshikawa Phasic Coronary Flow Characteristics in Patients With Constrictive Pericarditis : Comparison With Restrictive Cardiomyopathy Circulation, September 16, 1997; 96(6): 1874 - 1881. [Abstract] [Full Text] |
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D. Aronson, E. J. Rayfield, and J. H. Chesebro Mechanisms Determining Course and Outcome of Diabetic Patients Who Have Had Acute Myocardial Infarction Ann Intern Med, February 15, 1997; 126(4): 296 - 306. [Abstract] [Full Text] |
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I. Yokoyama, T. Ohtake, S.-i. Momomura, J. Nishikawa, Y. Sasaki, and M. Omata Reduced Coronary Flow Reserve in Hypercholesterolemic Patients Without Overt Coronary Stenosis Circulation, December 15, 1996; 94(12): 3232 - 3238. [Abstract] [Full Text] |
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N. H.J. Pijls, B. de Bruyne, K. Peels, P. H. van der Voort, H. J.R.M. Bonnier, J. Bartunek, and J. J. Koolen Measurement of Fractional Flow Reserve to Assess the Functional Severity of Coronary-Artery Stenoses N. Engl. J. Med., June 27, 1996; 334(26): 1703 - 1708. [Abstract] [Full Text] [PDF] |
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H. M. O. Farouque, S. G. Worthley, I. T. Meredith, R. A. P. Skyrme-Jones, and M. J. Zhang Effect of ATP-Sensitive Potassium Channel Inhibition on Resting Coronary Vascular Responses in Humans Circ. Res., February 8, 2002; 90(2): 231 - 236. [Abstract] [Full Text] [PDF] |
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