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Biomedical subjects

G Sambuceti

Publications and source records attributed to G Sambuceti.

At least 19 recordsLinked to original sources

Comparative effects of enalapril and verapamil on myocardial blood flow in systemic hypertension.

BACKGROUND: The comparative effects of calcium channel blockers and ACE inhibitors on myocardial blood flow (MBF) in hypertensive patients after long-term treatment are still unknown. METHODS AND RESULTS: Twenty hypertensive subjects with normal coronary arteries were randomly assigned to verapamil 240 to 480 mg/d or enalapril 10 to 40 mg/d. MBF was quantified at rest, during pacing tachycardia, and after dipyridamole by positron emission tomography and 13N-ammonia before and 6 months after treatment after 1 week of pharmacological washout. In both groups, blood pressure and heart rate during flow measurements were not different before and after therapy. Before treatment, mean MBF at rest, during pacing tachycardia, and after dipyridamole infusion was similar in the two groups; however, pacing and dipyridamole flows were significantly lower than those obtained in a control group of normotensive subjects. After treatment, in the enalapril-treated patients, MBF did not change in the three study conditions. In the verapamil-treated patients, MBF did not change at rest and significantly increased during pacing and after dipyridamole. The inhomogeneity of regional MBF distribution, evaluated from the coefficient of variation, decreased at rest after both treatments and, in the enalapril group, also during pacing. No relation was found between changes in MBF and changes in left ventricular mass. CONCLUSIONS: In arterial hypertension, MBF during pacing tachycardia and after dipyridamole is impaired. Successful therapy with verapamil increases MBF response to these stimuli, independent of changes in perfusion pressure and left ventricular mass. These results suggest that verapamil directly improves coronary microcirculatory function in hypertension. Enalapril does not significantly change MBF but reduces the inhomogeneity of regional flow distribution.

Antihypertensive Agents

Coronary vasoconstriction during myocardial ischemia induced by rises in metabolic demand in patients with coronary artery disease.

BACKGROUND: In patients with coronary artery disease, a maximal vasodilation of the coronary microcirculation is generally assumed to occur during myocardial ischemia induced by rises in metabolic demand. However, vasoconstriction has been documented during severe prolonged ischemia in animals. The aim of this study was to investigate coronary vasomotor tone during pacing-induced ischemia in humans. METHODS AND RESULTS: The study included 11 patients with exercise-induced ischemia and single-vessel disease of the left anterior descending artery and 7 control subjects with normal coronary arteries. Blood flow velocity was monitored with a Doppler catheter in the left anterior descending artery. Coronary resistance index was calculated as the ratio between mean arterial pressure and flow velocity. Measurements were obtained at baseline, after intracoronary adenosine (2 mg), and during maximal atrial pacing in the absence and presence of adenosine. After adenosine administration at rest, coronary resistance decreased more in control subjects than in patients (25 +/- 7% of baseline versus 61 +/- 19%; P < .01). Coronary resistance decreased in all control subjects (P < .01) both at maximal pacing (60 +/- 17% of baseline) and after administration of adenosine during tachycardia (31 +/- 13% of baseline). By contrast, all 10 ischemic patients displayed increased coronary resistance at maximal heart rate (221 +/- 131% of baseline; P < .01 versus baseline, P < .01 versus control subjects). At this stage, adenosine decreased coronary resistance to 44 +/- 20% of values observed before injection. Additionally, it reduced ST-segment depression in 5 of 8 patients. CONCLUSIONS: In patients with coronary artery disease, transient myocardial ischemia induced by increased metabolic demand is not associated with maximal vasodilation. Rather, an inappropriate severe microvascular vasoconstriction is present that can be abolished by intracoronary adenosine.

Adenosine

Myocardial and forearm blood flow reserve in mild-moderate essential hypertensive patients.

BACKGROUND: Structural readaptation of systemic resistance-sized arterioles in response to an elevated blood pressure reduces the forearm vasodilator reserve in patients with essential hypertension. The development of a similar process at the coronary microvascular level has frequently been hypothesized, but little information about coronary remodeling during the uncomplicated stage of hypertension has been obtained, and the relationship with concomitant changes in forearm blood flow reserve is not known. OBJECTIVE: To assess the minimal myocardial resistance and its relationship with the minimal forearm resistance in a group of male patients with mild-to-moderate uncomplicated hypertension and carefully matched controls. MATERIAL AND METHODS: The minimal myocardial resistance (Rmin(myocardia), the mean arterial pressure: hyperemic myocardial flow ratio after administration of 0.84 mg/kg dipyridamole, measured by using positron emission tomography and [3N]-ammonia), minimal forearm vascular resistance (Rmin(forearm), a hemodynamic index of arteriolar structure derived from the mean blood pressure and maximal postischemic forearm blood flow by venous plethysmography), echocardiographic cardiac mass and wall thickness were measured in 25 male patients with mild-to-moderate uncomplicated essential hypertension, most of whom had previously been treated, and in seven sex- and age-matched normotensive controls. RESULTS: Rmin(myocardial) (and hyperemia: baseline myocardial flow ratios) did not differ significantly between the two groups, whereas Rmin(forearm) was significantly higher in hypertensives. There was no significant intra-individual correlation between the two parameters. The left ventricular mass index was greater in patients and was related previously to Rmin(forearm) but not to Rmin(myocardial) for the overall sample. In a subgroup analysis, Rmin(forearm) values were 2SD above control values in nine patients and within the normal range in the remaining 16. The myocardial reserve was very similar in the two subgroups. CONCLUSIONS: The myocardial vasodilator reserve appeared to be preserved in these mild-to-moderate uncomplicated hypertensive patients, whereas the forearm vasodilator capacity was reduced, suggesting that the hypertensive readaptation process was not distributed homogeneously over the two vascular beds.

Adaptation, Physiological

Morphological bases for thallium-201 uptake in cardiac imaging and correlates with myocardial blood flow distribution.

To determine the morphological bases of thallium-201 myocardial distribution in chronic cardiac dysfunction and their relation to myocardial blood flow, myocardial slices from ten excised hearts of five chronic ischaemic heart disease patients and five idiopathic dilated cardiomyopathy patients, were imaged on a gamma camera to quantitate the uptake of thallium-201, injected 4 h before surgery, and myocardial blood flow from distribution of technetium-99m-labelled human albumin microspheres injected during surgery. Tracer distribution was correlated with histologically assessed myocardial fibrosis and myocytolysis. Thallium-201 uptake was inversely related to fibrosis (r = -0.73, in ischaemic heart disease, r = -0.65 in idiopathic dilated cardiomyopathy). In ischaemic heart disease, myocardial blood flow was related neither to thallium-201 uptake (r = 0.41) nor to the extent of fibrosis (r = -0.48). In this group, segments with normal or mildly reduced thallium-201 uptake showed significantly lower fibrosis than those with moderate or severe uptake defects (5 +/- 7% and 7 +/- 11% vs 33 +/- 14% and 42 +/- 12%, respectively, P < 0.0001. In a clinical model of chronic ischaemic dysfunction, despite severely depressed myocardial blood flow, extensive areas of myocardium devoid of significant structural impairment are present. Thallium-201 uptake effectively discriminates regions with preserved viability from those with relevant myocardial damage.

Adult

The role of coronary microvascular dysfunction in the genesis of cardiovascular diseases.

Positron emission tomography (PET) offers the unique capability of measuring specific flow (flow per unit of mass) in man by means of a regional, tridimensional, noninvasive approach. Using PET, myocardial perfusion abnormalities secondary to microvascular disorders have been investigated in arterial hypertension (AH), dilated and hypertrophic cardiomyopathy (CM), as well as in ischemic heart disease (CAD). In AH, regional perfusion at rest is within the normal range, while the coronary reserve and flow response to increase in metabolic demand are blunted. These flow abnormalities are independent of the degree of cardiac hypertrophy and the severity of AH; appropriate anti-ipertensive therapy is able to improve the perfusion abnormalities after long term treatment, independently of the effect on myocardial hypertrophy. Both dilated and hypertrophic CM demonstrate abnormal vasodilating capability, which has been shown to be present in the subclinical form of dilated DM; the reduction of coronary reserve is not related to the presence and extent of the hemodynamic impairment in dilated CM, and involves also nonhypertropied myocardium in asymmetric hypertrophic CM. These findings indicate a primary involvement of coronary microcirculation in non advanced forms of dilated and hypertrophic CM. Finally, in patients with CAD, myocardial territories supplied by angiographically normal coronary arteries show abnormal coronary reserve and flow during pacing tachycardia, indicating that, even in absence of epicardial coronary artery obstruction, microcirculation is impaired in subjects with coronary atherosclerosis. This abnormality can smooth perfusion differences between control and jeopardized regions. Accordingly, the absence of a perfusion defect during stress might indicate the presence of either a non significant stenosis or a diffuse impairment in microcirculatory function. Nuclear perfusion imaging with conventional perfusion tracers does not allow measurements of absolute blood flow, rather it provides an estimation of perfusion inhomogeneities. Although the agreement with the angiographic documentation of coronary artery disease has been frequently considered to characterize the diagnostic reliability of these techniques, the evaluation of myocardial perfusion provides an independent tool for the functional assessment of patient with heart disease. The possibility to obtain measurements of regional myocardial blood flow, provided by positron emission tomography, helps to identify the mechanisms affecting flow regulation in the myocardium. This tool thus provides a new rationale for the application of perfusion imaging, to obtain a more precise characterization of these patients, beyond the agreement with the morphological angiographic picture.

Arteriosclerosis

Thallium-201 reverse redistribution at reinjection imaging correlated with coronary lesion, wall motion abnormality and tissue viability.

UNLABELLED: Previous studies based on standard stress-redistribution 201TI scintigraphy provided conflicting results about the clinical significance 201Tl reverse redistribution. Recent observations indicate that the majority of these defects normalize following reinjection reflecting viable myocardium. METHODS: In this study, the meaning of reverse redistribution occurring at reinjection imaging, its relation to standard 4-hr redistribution, coronary lesion, abnormal wall motion and tissue viability were assessed. A region with normal activity in the stress image was considered as having reverse redistribution if 201Tl activity at reinjection imaging was definitely abnormal with a decrease in relative tracer uptake >15% of the peak. From a series of 270 patients, 29 showed reverse redistribution. Of these 29 patients, 27 had evidence of previous myocardial infarction. Coronary lesions were detected in all but 1 patient. Average ejection fraction was 0.38 +/- 0.11. RESULTS: On a segmental basis, 50/377 regions showed the pattern of reverse redistribution. A significant coronary lesion (> or = 50%) was found in 78% of these regions; occlusion rate was 50%, and collateral circulation was found in 35% of occluded vessels. Hypokinesis or akinesis was present in 72% of segments. Tissue viability, defined as an uptake >55% of the peak, was found in 44% of these segments. The 50 segments showing reverse redistribution were divided into two groups according to an abnormal uptake also at 4-hr redistribution (group 1, 25 segments) or appearing only following reinjection (group 2,25 segments). Despite segments of group 1 showing a higher degree of coronary stenosis (80 +/- 32 versus 59 +/- 43%, p < 0.01), a similar rate of coronary occlusion, ventricular dysfunction and maintained viability was found in the two groups. CONCLUSION: Reverse redistribution in chronic coronary artery disease is frequently associated with significant coronary lesion, collateral-dependent dysfunctioning myocardium and preserved tissue viability. The occurrence of reverse redistribution following reinjection expands the indication for viability imaging to all patients with known coronary artery disease and regional wall motion abnormalities who undergo diagnostic and prognostic 201TI scintigraphy.

Coronary Angiography

Myocardial blood flow response to pacing tachycardia and to dipyridamole infusion in patients with dilated cardiomyopathy without overt heart failure. A quantitative assessment by positron emission tomography.

BACKGROUND: Myocardial blood flow (MBF) impairment has been documented in advanced dilated cardiomyopathy (DCM) in which hemodynamic factors, secondary to severe ventricular dysfunction, may limit myocardial perfusion. To assess whether MBF impairment in DCM may also be present independent of hemodynamic factors, the present study was designed to quantify myocardial perfusion in patients with mild disease without overt heart failure. METHODS AND RESULTS: Absolute regional MBF (milliliters per minute per gram) was measured by positron emission tomography and 13N-ammonia in resting conditions, during pacing-induced tachycardia, and after dipyridamole infusion (0.56 mg/kg over 4 minutes) in 22 DCM patients and in 13 healthy subjects. Patients were in New York Heart Association functional class I-II and showed depressed left ventricular (LV) ejection fraction by radionuclide angiography (35 +/- 8%; range, 21% to 48%), normal coronary angiography, and normal or moderately increased LV end-diastolic pressure (9.2 +/- 5.5 mm Hg; range, 2 to 20 mm Hg). There were no differences in arterial blood pressure, heart rate, and rate-pressure product between patients and control subjects in the three study conditions. Compared with control subjects, DCM patients had lower mean MBF at rest (0.80 +/- 0.25 versus 1.08 +/- 0.20 mL.min-1.g-1, P < .01), during atrial pacing tachycardia (1.21 +/- 0.59 versus 2.03 +/- 0.64 mL.min-1.g-1, P < .01), and after dipyridamole infusion (1.91 +/- 0.76 versus 3.78 +/- 0.86 mL.min-1.g-1, P < .01). LV MBF values were related to baseline LV end-diastolic pressure at rest (r = -.57, P < .01) and during pacing (r = -.67, P < .01) but not after dipyridamole infusion (r = .19, P = .40). Five patients had LV end-diastolic pressure > 12 mm Hg; in 4, myocardial perfusion was severely depressed both at baseline and in response to stress. CONCLUSIONS: In patients with DCM without overt heart failure, myocardial perfusion is impaired both at rest and in response to vasodilating stimuli. The abnormalities in vasodilating capability can be present despite normal hemodynamics; progression of the disease is associated with more depressed myocardial perfusion.

Adult

Perfusional and metabolic effects of nisoldipine as shown by positron emission tomography after acute myocardial infarction.

After myocardial infarction, regional dysfunction can occur in viable myocardial regions because of the presence of baseline hypoperfusion. Recent evidence suggests that these areas may maintain a residual perfusion reserve. The aim of the present study was to evaluate whether oral nisoldipine can increase regional myocardial blood flow (MBF) in dyssynergic but viable myocardium after myocardial infarction. Patients with isolated left anterior descending coronary stenosis were studied 1 month after the first myocardial infarction. Patients underwent [18F]fluorodeoxyglucose imaging, and MBF was measured, using positron emission tomography and [13N]ammonia, at baseline and following dobutamine administration (10 micrograms/kg/min over 5 minutes). MBF measurements were repeated 24 hours after nisoldipine (10 mg twice daily). Preliminary results suggest that necrotic areas showed the largest reduction in baseline MBF. Dyssynergic-viable regions showed a reduced resting MBF but maintained a residual perfusion reserve in response to inotropic stimulation. Thus, nisoldipine selectively improved basal perfusion in dyssynergic-viable myocardium.

Adult

Microvascular dysfunction in collateral-dependent myocardium.

OBJECTIVES: The aim of this study was to evaluate myocardial blood flow regulation in collateral-dependent myocardium of patients with coronary artery disease. BACKGROUND: Despite great clinical relevance, perfusion correlates of collateral circulation in humans have rarely been estimated by quantitative methods at rest and during stress. METHODS: Nineteen patients with angina and isolated occlusion of the left anterior descending (n = 14) or left circumflex (n = 5) coronary artery were evaluated. Using positron emission tomography and nitrogen-13 ammonia, we obtained flow measurements at baseline, during atrial pacing-induced tachycardia and after intravenous administration of dipyridamole (0.56 mg/kg body weight over 4 min). Flow values in collateral-dependent and remote areas were compared with values in 13 normal subjects. RESULTS: Flow at rest was similar in collateralized and remote myocardium (0.61 +/- 0.11 vs. 0.63 +/- 0.17 ml/min per g, mean +/- 1 SD), and both values were lower than normal (1.00 +/- 0.20 ml/min per g, p < 0.01). During pacing, blood flow increased to 0.83 +/- 0.25 and 1.11 +/- 0.39 ml/min per g in collateral-dependent and remote areas, respectively (p < 0.05 vs. baseline); both values were lower than normal (1.86 +/- 0.61 ml/min per g, p < 0.01). Dipyridamole induced a further increase in perfusion in remote areas (1.36 +/- 0.57 ml/min per g, p < 0.01 vs. pacing) but not in collateral-dependent regions (0.93 +/- 0.37 ml/min per g, p = NS vs. pacing); again, both values were lower (p < 0.01) than normal (3.46 +/- 0.78 ml/min per g). Dipyridamole flow in collateral-dependent myocardium was slightly lower in patients with poorly developed than in those with well developed collateral channels (0.75 +/- 0.29 vs. 1.06 +/- 0.38 ml/min per g, respectively, p = 0.06); however, the former showed higher flow inhomogeneity (collateral/control flow ratio 0.58 +/- 0.10 vs. 0.81 +/- 0.22, respectively, p < 0.02). A linear direct correlation was observed between flow reserve of collateral-dependent and remote regions (r = 0.83, p < 0.01). CONCLUSIONS: Despite rest hypoperfusion, collateral-dependent myocardium maintains a vasodilator reserve that is almost fully utilized during increases in oxygen consumption. A global microvascular disorder might hamper adaptation to chronic coronary occlusion.

Adult

Residual coronary reserve identifies segmental viability in patients with wall motion abnormalities.

OBJECTIVES: The aim of this study was to determine whether the presence of residual coronary reserve can in itself identify viable segments. BACKGROUND: Experimental data suggest that despite hypoperfusion at rest, viable myocardium may exhibit persistence of coronary reserve. Preliminary observations in patients show that in basally dyssynergic areas, a residual vasodilator capability is present despite hypoperfusion at rest and that a flow-mediated increase in regional wall motion identifies residual viability. METHODS: Fourteen patients with evidence of previous myocardial infarction, infarct-related single-vessel coronary artery disease and impaired regional ventricular function at rest underwent positron emission viability imaging by fluorine-18 deoxyglucose. In addition, blood flow at rest and vasodilator capability were regionally evaluated in all patients by means of nitrogen-13 ammonia. RESULTS: Of a total of 252 segments, 133 were dyssynergic at rest. Of these 133 segments, 60 (group 1) showed normal metabolic activity and only mild reduction in myocardial blood flow. The other 73 segments showed a marked reduction in flow; of these, 25 (group 2, viable) had persistent metabolic activity, whereas 48 (group 3, necrotic) did not. Despite similar levels of hypoperfusion at rest, group 2 segments showed a preserved coronary reserve that was virtually absent in necrotic segments (2.6 +/- 1.3 vs. 1.3 +/- 0.5, p < 0.01). This value was similar to that observed in viable group 1 segments (2.5 +/- 1.6, p = NS). CONCLUSIONS: In addition to characterizing myocardium at risk, imaging of coronary flow at baseline and after dipyridamole by positron emission tomography provides helpful information on myocardial viability that may integrate the "static" viability information obtained with the baseline flow/metabolic approach.

Aged

Assessment of anatomic and physiological severity of single-vessel coronary artery lesions by dipyridamole echocardiography. Comparison with positron emission tomography and quantitative arteriography.

BACKGROUND: The aim of this study was to compare the results of dipyridamole-echocardiography test (DET: two-dimensional echo monitoring during dipyridamole infusion up to 0.84 mg/kg over a period of 10 minutes) with both anatomic and physiological parameters of coronary artery disease severity, assessed by computer-assisted quantitative coronary arteriography, and regional coronary flow reserve, measured by [13N]ammonia (13NH3) and dynamic positron emission tomography (PET), respectively. METHODS AND RESULTS: We studied 31 patients with a history of chest pain and neither previous myocardial infarction nor resting wall motion abnormalities. Eighteen patients had single-vessel disease (> 50% stenosis of one major coronary vessel), and 13 had normal coronary arteries. The criterion for DET positivity was the appearance of a new transient regional wall motion abnormality. In patients with a positive DET, two parameters were evaluated: the dipyridamole time (ie, the time from the beginning of drug infusion to the development of obvious dyssynergy) and the wall motion score index (WMSI, a semiquantitative integrated estimation of extent and severity of the stress-induced dyssynergy). WMSI was derived by summation of individual segment scores divided by the number of segments interpreted. Quantification of regional myocardial blood flow was obtained by PET measurements of 13NH3 arterial input function and left ventricular myocardial tissue concentration both at control and after dipyridamole (0.56 mg/kg over 4 minutes). Maximal regional blood flow after dipyridamole in the region supplied by the stenotic vessel was significantly lower in the 11 patients with coronary artery disease and positive DET than in the 7 patients with coronary artery disease and negative DET (1.08 +/- 0.33 versus 1.98 +/- 0.37 mL.min-1.g-1, P < .01). In patients with a positive DET, regional coronary flow reserve correlated well with dipyridamole time (r = .87, P < .01) but not with peak WMSI (r = .25, P = NS). Patients with dipyridamole-induced akinesia or dyskinesia (n = 6) had a greater reduction in regional coronary flow reserve than did those showing hypokinesia (n = 5): 1.38 +/- 0.51 versus 2.17 +/- 0.42, P < .05. Percent area reduction was more severe in patients with DET positivity than in those with DET negativity (93.7 +/- 8.7% versus 77 +/- 10.3%, P < .01), and it correlated with regional coronary flow reserve (r = .64, P < .01) and dipyridamole time (r = -.59, P < .01). CONCLUSIONS: In patients with single-vessel disease, DET shows an excellent specificity but a limited sensitivity; in these patients, DET positivity is associated with a physiologically important coronary stenosis. Severity of the anatomic stenosis and impairment in regional flow reserve are greater when the dipyridamole-induced dyssynergy appears earlier during the test. Therefore, a stratification of the anatomo-physiological severity of coronary artery disease can be obtained with DET, based mainly on the temporal allocation of the transient dyssynergy.

Adult

Global alteration in perfusion response to increasing oxygen consumption in patients with single-vessel coronary artery disease.

BACKGROUND: Recent evidence suggests that, in coronary artery disease (CAD), myocardial blood flow (MBF) regulation is abnormal in regions supplied by apparently normal coronary arteries. However, the relation between this alteration and MBF response to increasing metabolic demand has not been fully elucidated. METHODS AND RESULTS: MBF was assessed at baseline, during atrial pacing tachycardia, and after dipyridamole (0.56 mg/kg IV over 4 minutes) in 9 normal subjects and in 24 patients with ischemia on effort, no myocardial infarction, and isolated left anterior descending (n = 19) or left circumflex (n = 5) coronary artery stenosis (> or = 50% diameter narrowing). Perfusion of both poststenotic (S) and normally supplied (N) areas was measured off therapy by positron emission tomography and [13N]ammonia. Normal subjects and CAD patients showed similar rate-pressure products at baseline, during pacing, and after dipyridamole. In CAD patients, MBF was lower in S than in N territories at rest (0.68 +/- 0.14 versus 0.74 +/- 0.18 mL.min-1.g-1, respectively, P < .05), during pacing (0.92 +/- 0.29 versus 1.16 +/- 0.40 mL.min-1.g-1, respectively, P < .01), and after dipyridamole (1.18 +/- 0.34 versus 1.77 +/- 0.71 mL.min-1.g-1, respectively, P < .01). However, normal subjects showed significantly higher values of MBF both at rest (0.92 +/- 0.13 mL.min-1.g-1, P < .05 versus both S and N areas), during pacing tachycardia (1.95 +/- 0.64 mL.min-1.g-1, P < .01 versus both S and N areas), and after dipyridamole (3.59 +/- 0.71 mL.min-1.g-1, P < .01 versus both S and N areas). The percent change in flow was strictly correlated with the corresponding change in rate-pressure product in normal subjects (r = .85, P < .01) but not in either S (r = .04, P = NS) or N regions (r = .08, P = NS) of CAD patients. CONCLUSIONS: Besides epicardial stenosis, further factors may affect flow response to increasing metabolic demand and coronary reserve in patients with CAD.

Adult

Different tracers and stressors in patients with coronary artery disease: how to standardize clinical questions and nuclear cardiology answers.

The recent introduction of new tracers and stressors has increased the number of combinations of techniques that can be used for the diagnostic and prognostic stratification of patients with coronary artery disease. However, these new techniques still need to be standardized for clinical use. Thallium-201 scintigraphy is at present the most common method to assess transient ischemia and viability in patients. Dynamic exercise and dipyridamole show similar incidence of major cardiac complications and their use can be considered sufficiently safe. Further experimental and multicenter clinical studies are needed for 99mTc-Sestamibi and 99mTc-Teboroxime and for new stressors such as adenosine and dobutamine.

Adenosine

[Global change in the regulation of regional coronary flow in patients with single vessel coronary disease evidenced by positron emission tomography].

AIM OF THE STUDY: Aim of this study is to investigate whether, in patients with coronary artery disease (CAD), regional myocardial blood flow (rMBF) regulation is affected with further mechanisms besides the effects of epicardial coronary stenosis. MATERIAL AND METHODS: RMBF and coronary reserve are measured in 13 normal subjects and in 36 patients with effort angina and isolated (> or = 50% diameter narrowing) left anterior descending (LAD, 27 patients) or left circumflex (LCX, 9 patients) coronary artery stenosis. Measurements are obtained both at baseline and following dipyridamole (0.56 mg/kg in 4 minutes) using positron emission tomography and N13-ammonia. RESULTS: At rest, patients with CAD show similar rMBF values in the stenotic and remote areas (0.71 +/- 0.19 vs 0.77 +/- 0.22 ml/min/gr, respectively, ns); both values are significantly (p < 0.01) reduced with respect to mean rMBF observed in the normal subjects (1.07 +/- 0.21 ml/min/gr). Following dipyridamole, patients with CAD show lower rMBF values in stenotic than in control regions (1.25 +/- 0.54 vs 1.73 +/- 0.80 ml/min/gr, p < 0.01); however, both these values are significantly reduced when compared with mean rMBF in the normal subjects (3.76 +/- 0.88 ml/min/gr, p < 0.01). To evaluate whether reduction in resting myocardial perfusion indicates maximal vasodilatation, patients with CAD are divided into 2 groups: Group 1 with homogeneous baseline perfusion (0.73 +/- 0.2 vs 0.75 +/- 0.24 ml/min/gr, in stenotic and remote areas, respectively, ns), and Group 2 with baseline perfusion defect in the stenotic related territory (0.62 +/- 0.14 vs 0.84 +/- 0.17 ml/min/gr, p < 0.01). Coronary reserve (dipyridamole flow/baseline flow) is similar in the 2 Groups (1.74 +/- 0.66 vs 1.93 +/- 0.45, ns). CONCLUSIONS: These data suggest that, in patients with CAD, other factors beyond hydraulic effects of epicardial coronary stenosis, could modulate rMBF regulation; in fact: 1) myocardium perfused by angiographically normal coronary artery shows reduced values of both resting rMBF and coronary reserve; 2) myocardium supplied by stenotic vessel maintains a residual vasodilating capability despite a reduced baseline perfusion.

Aged

Regional myocardial blood flow in stable angina pectoris associated with isolated significant narrowing of either the left anterior descending or left circumflex coronary artery.

Myocardial perfusion measurements were obtained with positron emission tomography under basal conditions and after intravenous dipyridamole infusion (0.56 mg/kg over 4 minutes) to determine if myocardial perfusion is maximized in areas of resting wall motion abnormalities in patients with stable angina. Thirty-three patients with no history of myocardial infarction, and with coronary stenosis > 50% involving the left anterior descending (n = 24) and left circumflex (n = 9) coronary arteries were evaluated. Quantitative perfusion images were recorded twice in each subject using nitrogen-13 ammonia at baseline and after intravenous administration of dipyridamole. Computer-assisted analysis of left ventriculograms showed abnormal wall motion in the stenosis-related regions in 16 patients (group 1), and normal regional function in 17 (group 2). The flow values in the anterior and posterolateral wall were considered to reflect left anterior and left circumflex coronary artery flow, respectively. Quantitative angiography showed that coronary stenosis severity was higher in group 1 than in group 2 (cross-sectional area reduction 94 +/- 7% vs 87 +/- 11%; p < 0.05). Resting blood flow in the stenosis-related areas was significantly lower than in contralateral regions in group 1 (0.66 +/- 0.19 vs 0.77 +/- 0.26 ml/min/g; p < 0.05), but not in group 2 (0.73 +/- 0.18 vs 0.78 +/- 0.21 ml/min/g; p = NS). Dipyridamole significantly (p < 0.01) increased myocardial blood flow in both stenotic and remote regions in both groups 1 (0.95 +/- 0.41 vs 1.57 +/- 0.70 ml/min/g) and 2 (1.54 +/- 0.53 vs 2.01 +/- 0.84 ml/min/g).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Alteration in regulation of myocardial blood flow in one-vessel coronary artery disease determined by positron emission tomography.

The behavior of myocardial blood flow (MBF) regulation in territories supplied by angiographically normal vessels of patients with coronary artery disease (CAD) has been poorly investigated. Resting MBF and coronary reserve were evaluated in 32 patients with stable angina, no previous myocardial infarction, and isolated left anterior descending or left circumflex coronary artery stenosis (> or = 50% diameter narrowing). MBF was measured, in the absence of any medical therapy, by means of dynamic positron emission tomography and 13N-ammonia. MBF measurements at baseline and after intravenous dipyridamole (0.56 mg/kg administered over 4 minutes), were obtained both in the stenosis-related regions and in contralateral territories. As a control group, 14 normal subjects were evaluated according to the same protocol. At rest, the 32 patients with CAD had similar MBF values in the stenotic and remote regions (0.76 +/- 0.21 and 0.77 +/- 0.19 ml/min/g, respectively, p = NS); both these values were significantly (p < 0.01) reduced with respect to mean MBF in normal subjects (1.03 +/- 0.25 ml/min/g). The dipyridamole study was completed in 30 patients; these patients had lower values of maximal MBF in the stenotic than in the remote regions (1.52 +/- 0.65 vs 1.76 +/- 0.68 ml/min/g, p < 0.05); however, both these values were significantly reduced (p < 0.01) with respect to mean dipyridamole MBF in normal subjects (3.66 +/- 0.92 ml/min/g). Thus, in patients with CAD, resting and maximal MBF can be reduced not only in myocardial territories supplied by stenotic arteries, but also in territories supplied by angiographically normal arteries.

Aged