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Biomedical subjects

M Chiariello

Publications and source records attributed to M Chiariello.

At least 19 recordsLinked to original sources
PubMed1992

Experimental carotid stenosis and endothelial injury in the rabbit: an in vivo model to study intravascular platelet aggregation.

Previous studies have shown that experimental canine coronary artery stenosis associated with endothelial injury results in a typical pattern of coronary flow characterized by gradual decreases in coronary flow to almost zero values followed by restorations of flow to normal values. This pattern of flow, called cyclic flow reductions (CFRs), is the consequence of recurrent platelet aggregation at the site of the stenosis and endothelial injury and subsequent dislodgement of the thrombus. In the present study, platelet activation and aggregation in vivo was induced by placing an external constrictor around carotid arteries with endothelial injury in anesthetized rabbits. Carotid blood flow velocity was measured continuously with a Doppler flow probe positioned proximally to the constrictor. After placement of the constrictor, CFRs developed in 14 of 14 rabbits with a mean frequency of 16.5 +/- 2.3 cycles/h. CFRs were observed for 30 min, and the animals were treated with either an i.v. bolus of aspirin (10 mg/kg) or R 68070 (20 mg/kg), a drug with simultaneous TxA2 synthase and TxA2/PGH2 receptor blocking properties. Aspirin completely inhibited CFRs in 4 of 7 rabbits, whereas R 68070 eliminated CFRs in 7 of 7 animals. In the 3 animals that did not respond to aspirin, administration of ketanserin (0.25 mg/kg i.v.), a selective serotonin S2 receptor antagonist, completely abolished CFRs. Both aspirin and R 68070 resulted in a marked reduction in serum TxB2 formation and in a complete inhibition of ex vivo platelet aggregation in response to arachidonic acid, whereas aggregation in response to U46619, a TxA2 mimetic, was inhibited only in R 68070-treated rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Influence of atenolol on the relationship between heart rate and QT interval in patients with exercise-induced myocardial ischemia.

The aim of this study was to analyze the relationship between heart rate and QT interval (HR-QT) during exercise in control subjects (Group A) and in patients with coronary artery disease (CAD) with effort angina and without previous myocardial infarction (MI) (Group B). The diagnosis of CAD was confirmed by coronarographic examination. The correlation HR-QT was significant (p < 0.001) in both groups on effort and at recovery. The analysis of the regression HR-QT was carried out separately, both on effort in upright position and at rest in supine position, to avoid the influence of posture on QT length. During effort, the regression line showed lower slope and intercept values in Group B (p < 0.001) than those for Group A. A similar behavior was also observed at rest. Thus, at the highest heart rate, where ECG signs of ischemia (ST depression > 1 mm) frequently occurred, a longer QT interval was present in Group B. Moreover, in Group B, the QT interval in the presence of ECG signs of ischemia was significantly longer (p < 0.01) than in Group A at comparable heart rates both on effort and at rest, thereby confirming the result obtained by comparing both regression lines. The same effort protocol was repeated in Group B patients after acute administration of atenolol 100 mg per os. After atenolol administration, the analysis of the regression HR-QT in Group B clearly showed a shorter QT interval than that obtained in washout period during the baseline test at the highest heart rates where the ECG frequently showed signs of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

Comparison between exercise and trans-oesophageal atrial pacing in patients with coronary artery disease: technetium-99m methoxy isobutyl isonitrile simultaneous evaluation of ventricular function and myocardial perfusion.

In this study we compared the results of exercise and trans-oesophageal atrial pacing (TAP) technetium-99m methoxyisobutyl isonitrile (99mTc-SESTAMIBI) cardiac imaging in the evaluation of left ventricular (LV) function and myocardial perfusion in patients with angiographically proven coronary artery disease. Ten patients (8 men and 2 women, mean age 59 +/- 6 years) were submitted to 3 separate injections of 99mTc-SESTAMIBI, one under control conditions, one after exercise and one after TAP. LV ejection fraction, as measured by electrocardiogram (ECG) gated first pass, decreased from 49 +/- 5% under control conditions to 42 +/- 6% during exercise (P less than 0.05 versus control) and to 43 +/- 8% during TAP (P less than 0.05 versus control and insignificant change versus exercise). Segmental myocardial perfusion analysis was performed on a total of 150 myocardial segments. On both exercise and TAP 99mTc-SESTAMIBI studies, 103 segments (69% of the total) were normal, 32 (21%) had reversible, and 15 (10%) irreversible, perfusion defects. Relative regional tracer uptake was not statistically different between exercise and TAP in normal regions (91.1 +/- 9.1% versus 90.7 +/- 8.5%, respectively), in regions with reversible (61.9 +/- 12% versus 62.4 +/- 10.4%, respectively) and irreversible perfusion defects (55.8 +/- 7.8% versus 58.8 +/- 9.5%, respectively). Our results demonstrated that 99mTc-SESTAMIBI TAP cardiac imaging shows similar results to 99mTc-SESTAMIBI exercise myocardial scintigraphy in the assessment of LV function and myocardial perfusion in patients with coronary artery disease.

Cardiac Pacing, Artificial↗
PubMed1992

Follow-up of a respiratory rate modulated pacemaker.

The efficacy of 27 respiration sensitive rate modulated pacemakers (Biorate RDP-3 Biotec) implanted in the left pectoral area was evaluated every 3 months during a mean follow-up period of 29 months (range 10-50 months). Rate modulation function was unchanged other than for three patients in whom the auxiliary leads became displaced. Two implants lost ventricular sensing in this nonprogrammable model. In all but the three patients, Holter monitoring demonstrated pacing rate variation corresponding to daily activity. Stress test duration increased from 8.2 +/- 1.5 minutes (in fixed rate VVI rate) to 12.83 +/- 2.0 minutes (in the VVIR mode) (P less than 0.05). Right arm movement increased the pacing rate by 5 +/- 3 beats/min (NS), while the left arm movement increase was 30 +/- 5 beats/min (P less than 0.05). Mental, arithmetic, and nifedipine tests did not change the rate modulated pacing rate. The system responded to a change in respiratory rate by an increase in stimulation rate. A satisfactory response in sensitivity and velocity was present only with medium-high workloads. Interference with rate modulation occurred with movement of the arm ipsilateral to the implanted pulse generator.

Atrial Fibrillation↗
PubMed1992

Effects of ischemia and reperfusion on cardiac tolerance to oxidative stress.

Oxidative stress may affect cardiac function and metabolism. Oxidants are normally inactivated by reacting with reduced glutathione (GSH), with resulting formation and release of oxidized glutathione (GSSG). However, ischemia might affect glutathione metabolism. This might render ischemic hearts less resistant against subsequent oxidant injury during reperfusion, and it might also affect the reliability of GSSG measurements as a means to investigate oxidative stress in reperfused hearts. We compared the metabolic and functional consequences of an oxidant load in control rabbit hearts and in hearts reperfused after 30 min of normothermic total ischemia. In controls, H2O2 infusion (H2O2; 5-30 microM) induced a dose-dependent stimulation of GSSG release and a progressive impairment of cardiac function. At these doses, H2O2 challenge of postischemic hearts resulted in biochemical and functional changes identical to those observed in controls. Release of lactate dehydrogenase (LDH) and of GSH was negligible, similar in both groups. In additional experiments, infusion of H2O2 at a much higher dose (200 microM) elicited a further increase in GSSG release from both groups, although GSSG concentrations were lower in postischemic hearts. The functional effects of the 200 microM H2O2 infusion were similar in both groups, all hearts showing rapid and irreversible deterioration of function. Occurrence of irreversible cell injury was also manifested by a large release of LDH and GSH to a similar extent in both groups. These data demonstrate that cardiac tolerance toward oxidants is largely unaffected by a relatively brief episode of severe ischemia and indicate that GSSG release can be reliably used to investigate oxidative stress in reperfused hearts.

Animals↗
PubMed1992

Role of alpha 2-adrenoceptors in normal and atherosclerotic human coronary circulation.

BACKGROUND: Experimental studies on the effects of alpha 2-adrenoceptors on regional coronary blood flow in normal and ischemic myocardium are highly controversial. A beneficial effect on regional ischemic myocardium has been demonstrated in different animal preparations with either alpha 2-adrenoceptor blockade or stimulation. Animal studies also demonstrated that postsynaptic alpha 2-adrenoceptors mediate vasoconstriction in coronary and femoral vascular beds. The aims of the study were 1) to investigate the effects of regional alpha 2-adrenoceptor stimulation on regional coronary blood flow in subjects with angiographically normal coronary arteries, 2) to assess the effect of alpha 2-adrenoceptor blockade on coronary circulation in control subjects, and 3) to examine the influence of atherosclerosis on coronary blood flow response to alpha 2-adrenoceptor blockade. METHODS AND RESULTS: The effect of regional administration of BHT 933 (a selective alpha 2-adrenoceptor agonist) was studied in eight subjects with angiographically normal coronary arteries. The coronary blood flow velocity was measured using a subselective intracoronary 3F Doppler catheter and coronary diameter by quantitative coronary angiography. BHT 933 induced a reduction in coronary artery diameter from 2.5 +/- 0.6 mm to 1.8 +/- 0.4 mm (p less than 0.05) as well as in coronary blood flow velocity (from 6.4 +/- 0.9 cm/sec to 4.6 +/- 1.9 cm/sec, p less than 0.01). In some subjects, ST segment abnormalities occurred. In patients with angiographically normal coronary arteries (n = 6), the regional infusion of a selective alpha 2-adrenoceptor blocking agent after beta-blockade did not change coronary diameter or coronary blood flow velocity. In contrast, in patients with significant coronary stenoses (n = 6), regional infusion of an alpha 2-adrenoceptor blocking agent reduced regional coronary artery diameter (from 2.3 +/- 0.5 mm to 2.1 +/- 0.6 mm, p less than 0.01) as well as coronary blood flow velocity (from 5.8 +/- 0.8 cm/sec to 3.7 +/- 0.6 cm/sec, p less than 0.05); in addition, alpha 2-adrenoceptor blockade significantly increased coronary sinus plasma norepinephrine levels (from 300 +/- 144 pg/ml to 429 +/- 207 pg/ml, p less than 0.01). CONCLUSIONS: The selective in vivo stimulation of alpha 2-adrenoceptors produces a reduction in coronary blood flow and diameter in humans with angiographically normal coronary arteries. alpha 2-Adrenergic blockade does not change coronary blood flow in subjects with angiographically normal coronary arteries (suggesting no resting alpha 2-adrenergic vasoconstrictor tone), whereas in patients with coronary artery stenosis, regional coronary blood flow decreases after alpha 2-receptor blockade. Finally, our data also suggest that alpha 2-adrenoceptors participate in the modulation of sympathetic neuronal norepinephrine release in the human heart.

Adrenergic alpha-Agonists↗
PubMed1992

Endothelium-derived relaxing factor modulates platelet aggregation in an in vivo model of recurrent platelet activation.

It has been shown that endothelium-derived relaxing factor (EDRF) may inhibit platelet aggregation in vitro through activation of platelet-soluble guanylate cyclase. To assess whether EDRF may also affect platelet function in vivo, intravascular platelet aggregation was initiated by placing an external constrictor around endothelially injured rabbit carotid arteries. Carotid blood flow velocity was measured continuously by a Doppler flow probe placed proximal to the constrictor. After placement of the constrictor, cyclic flow reductions (CFRs), due to recurrent platelet aggregation, developed at the site of the stenosis. After CFRs were observed for 30 minutes, a solution of authentic nitric oxide (NO, n = 10) was infused into the carotid artery via a small catheter placed proximally to the stenosis. Before infusion of NO, CFR frequency averaged 18.3 +/- 2.9 cycles per hour, and CFR severity (lowest carotid blood flow as percentage of baseline values) was 6 +/- 1%. NO completely inhibited CFRs in all animals, as shown by the normal and constant pattern of carotid blood flow (CFR frequency, 0 cycles per hour, p < 0.001; carotid blood flow, 92 +/- 5%, p = NS versus baseline). These effects were transient; CFRs were restored spontaneously within 10 minutes after cessation of NO infusion. After CFRs returned, S-nitroso-cysteine (S-NO-cys), a proposed form of EDRF, was infused into the carotid artery. S-NO-cys also abolished CFRs in all animals but at a significantly lower dose than NO (0.3 +/- 0.1 versus 12 +/- 4 nmol/min). The role of endogenously released EDRF in modulating in vivo platelet function was then tested in additional experiments. In 10 animals, endogenous release of EDRF was stimulated by infusing acetylcholine into the aortic root during CFRs. Infusion of acetylcholine was also associated with a complete inhibition of CFRs, similar to that observed during exogenous infusion of NO or S-NO-cys. These antithrombotic effects of acetylcholine were completely lost when EDRF synthesis was prevented by administration of the L-arginine analogue NG-monomethyl L-arginine (L-NMMA). Furthermore, in six additional rabbits the basal release of EDRF was blocked by L-NMMA after CFRs had been previously abolished with aspirin or the combination of aspirin and ketanserin, a serotonin S2 receptor antagonist. L-NMMA caused restoration of CFRs in all animals, indicating that even the basal release of EDRF is important in modulating platelet reactivity in vivo. Taken together, the data of the present study demonstrate that endogenous EDRF might importantly contribute to the modulation of platelet function in vivo.

Acetylcholine↗
PubMed1992

Diagnosis of coronary artery disease with Tc 99m-methoxy isobutyl isonitrile and transesophageal pacing.

Recently the use of a new radioactive agent with physical and biological properties more favorable than those of thallium 201, methoxy-isobutyl-isonitrile (MIBI) labeled with technetium 99m (Tc 99m), has permitted simultaneous performance of perfusion and function studies in ischemic cardiopathy. Transesophageal atrial pacing (TAP) technique has evolved as an alternative provocative test of ischemia. The authors compared the capability of Tc 99m-MIBI myocardial scintigraphy, combined with TAP, with that of Tc 99m-MIBI, combined with maximal stress test, in the diagnosis of ischemic cardiopathy. They studied 11 patients with a clinical history of angina pectoris. Myocardial scintigraphy was performed at rest, after stress test, and after TAP. Finally, all the patients underwent coronary angiography. The analysis of myocardial perfusion images on both Tc 99m-MIBI associated with TAP and with stress demonstrated, in 165 myocardial segments examined: 143 normal, 20 reversible defects, 2 irreversible defects. The concordance of localization between coronarographic data and scintigraphic reversible and irreversible defects was 85%. In conclusion TAP proves to be a valid and sensitive provocative test of ischemia when combined with myocardial scintigraphy and with Tc 99m-MIBI.

Cardiac Pacing, Artificial↗
PubMed1992

Calcium antagonists and experimental myocardial ischemia reperfusion injury.

A number of previous studies have reported that administration of calcium antagonists reduces acute ischemic injury in a variety of experimental models. More recently, however, it has been suggested that the beneficial effects of reperfusing the ischemic myocardium might be blunted by the paradoxical occurrence of a specific form of reperfusion-mediated injury. Although the ultimate mechanisms responsible for this phenomenon have not been completely elucidated, it has been suggested that oxygen radical generation, neutrophil activation, and calcium overload, may all contribute to the development of myocardial damage in postischemic hearts. Several experimental studies suggest that, in addition to their well-known effects on ischemic injury, calcium antagonists may variably affect these mechanisms of reperfusion-mediated cell damage. In particular, evidence has been provided that suggests these drugs may inhibit oxygen radical-mediated peroxidation of membrane lipids and may also reduce activation of stimulated neutrophils. Furthermore, calcium-channel blockers might also prevent calcium overload in reperfused hearts, and they might interfere with reperfusion injury indirectly, secondary to a reduction in the severity of ischemia. From the experimental data available it can be speculated that calcium antagonists might contribute to reducing oxygen radical damage following reflow. At the same time, these drugs may allow the extension of the time window of reperfusion therapy, thus further expanding the benefits of thrombolysis.

Animals↗
PubMed1992

[Evaluation of the therapeutic efficacy of pravastatin in monothereapy and in association with gemfibrozil in hypercholesterolemia associated with moderate hyperglyceridemia].

Pravastatin is a new drug that inhibits 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the key enzyme in cholesterol synthesis. It prevents mevalonate synthesis, thus reducing cholesterol. Pravastatin also stimulates the expression of LDL receptors, leading to an activation of this specific pathway of LDL catabolism. Gemfibrozil is a fibrate drug. Although the mechanism of hypolipidemic action of fibrates is not conclusively elucidated, it seems to involve reduction of LDL cholesterol secondary to decreased VLDL production and increased VLDL catabolism. Therefore, it might be hypothesized that combination therapy with both agents could afford greater reduction of cholesterol levels as compared to pravastatin alone. This study compared the efficacy and safety of pravastatin in monotherapy or in combination with gemfibrozil in the treatment of primary hypercholesterolemia with moderate hypertriglyceridemia. Thirty-eight subjects (aged 57 +/- 15 years, 25 M and 13 F) with baseline cholesterol levels > 220 mg/dl, were included in the study. Serum triglyceride levels were greater than 170 mg/dl and lower than 250 mg/dl. All patients initially followed 4 weeks of hypolipidemic diet. The patients were there assigned to receive either 20 mg once a day of pravastatin alone (n 13) or 20 mg of pravastatin in association with 600 mg of gemfibrozil daily (n 11). Fourteen additional patient, treated with diet only, served as a control group. The treatment plan provided 18 months of active treatment with clinical and laboratory controls every month. Both groups of treated patients showed a reduction of total and LDL-cholesterol levels. The HDL-cholesterol levels increased significantly both with pravastatin and with gemfibrozil.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Calcium channel blockers inhibit human low-density lipoprotein peroxidation induced by oxygen free radicals in vitro].

Previous studies have shown that calcium-antagonists may reduce the development of experimental atherosclerosis, and that nifedipine may slow progression of coronary atherosclerosis in man. The mechanisms responsible for this effect are still unclear. It has been recently proposed that oxygen-free radicals can induce peroxidation of human low-density lipoproteins (LDL), and that peroxidized LDL may be an atherogenic stimulus. Chemical modified LDL are internalized by macrophages via specific cell surface receptor that was termed the scavenger receptor, and could induce foam cells transformation in vivo. Previous studies on other systems have shown that calcium-antagonists may effectively inhibit oxygen radical-induced lipid peroxidation. These drugs, though differing widely in their chemical structure, are lipophilic to various degrees and presumably would concentrate in the lipid domain of the phospholipid-rich membranes. Therefore, the aim of the present study was to investigate whether calcium-channel blockers may reduce human LDL peroxidation. Purified human LDL were exposed to oxygen radicals generated by xanthine-xanthine oxidase (18 hours) after a pre-incubation (30 min) in presence of different concentrations of nifedipine, diltiazem and verapamil. Peroxidation was measured from malonyldialdehyde production. The results show that calcium-antagonists prevent LDL peroxidation. Thus, calcium-antagonists may reduce peroxidation of human LDL in vitro, at clinically relevant concentrations. These data suggest that reduced formation of atherogenic peroxidized LDL may be an additional mechanism for the anti-atherosclerotic effects of calcium-antagonists in vivo.

Arteriosclerosis↗
PubMed1992

[Effect of alpha-adrenergic receptor blockade on peripheral vasoconstriction induced by the cold pressor test. Evidence for functional integrity of alpha 1 and alpha 2 adrenergic receptors in patients with congestive heart failure].

Central sympathetic stimulation results in direct vascular vasoconstriction mediated by activation of alpha-adrenergic receptors. However, it is unknown whether this vasoconstriction is mediated by alpha 1 or alpha 2-adrenoceptor subtypes. In patients with congestive heart failure (CHF), both circulating and neuronally released catecholamines produces vasoconstriction via alpha-adrenergic stimulation. This vasoconstriction produces detrimental hemodynamic effect in CHF patients since it increases right and left ventricular filling pressures and pulmonary and systemic vascular resistances. While the myocardial alpha 1-adrenoceptors seems not to be down-regulated in heart failure, the functional integrity of vascular alpha 1 and alpha 2-adrenoceptors in CHF remains to be elucidated. Accordingly, the present study was designed to assess whether the limb vascular response to alpha 1 or alpha 2-adrenoceptor stimulation is impaired in patients with CHF. We studied 25 control subjects and 19 patients with CHF due to primary dilated cardiomyopathy. Forearm blood flow was measured by venous occlusion plethysmography. Sympathetic stimulation was produced by cold. The intraarterial pump-infusions of BHT 933 (a selective alpha 2-adrenoceptors agonist agent, 0.1, 1, 10 micrograms/kg/min for 5 min) produced the same peripheral vasoconstriction in CHF and in control subjects: 32 +/- 23.9%, 47.3 +/- 20% and 55 +/- 26.1% respectively at I, II, and III dose in CHF and 28.7 +/- 38.6%, 36 +/- 14.5%, and 57 +/- 13.8% respectively at I, II, and III dose in control subjects. The dose response to BHT 933 was not different in the 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1992

Effects of antihypertensive therapy on diastolic dysfunction in left ventricular hypertrophy.

In systemic hypertension, a certain degree of impairment of left ventricular diastolic function is often detectable, and is the consequence of two factors: elevated afterload and left ventricular hypertrophy. The goal of improving diastolic dysfunction can thus be achieved by lowering blood pressure and by inducing a regression in left ventricular hypertrophy. A reduction in blood pressure by intravenous administration of verapamil has proved capable of enhancing left ventricular filling properties in patients with hypertension. This finding has not been corroborated, however, in midterm protocols using an array of drugs (beta-blockers, dihydropyridines, diltiazem, and diuretics). Reduction in left ventricular mass can be achieved by several categories of drugs, and it has been shown that a decrease in mass is accompanied by an improvement in the early diastolic filling pattern. The kind of drug used to accomplish mass reduction seems to be irrelevant as far as the improvement in diastolic function is concerned. The pattern of left ventricular hypertrophy, however, might play a role in influencing the outcome on diastolic mechanics of left ventricular mass decrease.

Adrenergic beta-Antagonists↗
PubMed1992

[Ambulatory monitoring of left ventricular function: the assessment of transient episodes of ventricular dysfunction in patients with ischemic cardiopathy].

BACKGROUND: The recent development of an ambulatory radionuclide detector (VEST) to assess left ventricular (LV) function may enhance the detection of ischemia during routine daily activities in patients with coronary artery disease (CAD). The aim of this study was to evaluate the usefulness of VEST in monitoring LV ejection fraction (EF) responses to daily activities and sustained handgrip test (HG) in patients with CAD. METHODS: 13 patients (12 men and 1 woman) with angiographically proven coronary artery disease were studied by VEST (mean 162 min, range 120 to 250 min). LV responses to different daily activities (walking and climbing stairs) and to HG were evaluated. RESULTS: Walking on a level surface and climbing stairs did not induce significant change in mean LVEF. However, a transient decrease in EF was observed in 4 (31%) and in 5 (38%) of the 13 patients during walking and climbing stairs, respectively. HG induced a significant (p < 0.01) reduction in mean EF. In particular, during HG, EF decreased > or = 5% in 11 (85%) of the 13 patients. A transient spontaneous decrease in LVEF lasting > or = 1 min was observed on 18 occasions in 11 patients with CAD; 5 episodes were symptomatic and 13 asymptomatic. ECG ST segment depression was recorded in 4 of the 5 symptomatic and in 5 of the 13 asymptomatic episodes. CONCLUSIONS: These results suggest that simultaneous monitoring of LV function and ECG may permit a better understanding of the incidence and severity of ischemic symptomatic and asymptomatic episodes.

Aged↗
PubMed1992

Identification of viable myocardium in patients with chronic coronary artery disease: comparison of thallium-201 scintigraphy with reinjection and technetium-99m-methoxyisobutyl isonitrile.

We compared the results of 201Tl reinjection and those of 99mTc-methoxyisobutyl isonitrile (MIBI) in identifying viable myocardium in 20 male patients with angiographically proven coronary artery disease (CAD) and left ventricular dysfunction (ejection fraction 30% +/- 8%). All patients had irreversible defects on standard exercise-redistribution thallium imaging. Thallium was reinjected immediately after the redistribution study, and images were reacquired. The patients also underwent stress and rest 99mTc-MIBI myocardial scintigraphy (2-day protocol). A total of 300 myocardial regions were analyzed, of which 122 (41%) had irreversible thallium defects on redistribution images before reinjection. Of the 122 myocardial regions with irreversible defects on standard stress-redistribution thallium cardiac imaging, 65 (53%) did not change at reinjection and 57 (47%) demonstrated enhanced uptake of thallium after reinjection. Of the same 122 irreversible defects on stress-redistribution thallium, 100 (82%) appeared as fixed defects and 22 (18%) were reversible on 99mTc-MIBI myocardial scintigraphy. These data indicate that 201Tl cardiac imaging with rest reinjection is superior to 99mTc-MIBI myocardial scintigraphy in identifying viable myocardium in patients with chronic CAD, suggesting that regions with severe reduction of 99mTc-MIBI uptake both on stress and rest images may contain viable myocardium.

Adult↗
PubMed1992

[Left ventricular systolic and diastolic asynchronism in patients with ischemic cardiopathy: its effects on ventricular filling].

To assess whether left ventricular asynchrony would influence filling in coronary artery disease, 27 patients with coronary artery disease and 39 normal subjects were studied by rest radionuclide angiography. Lower ejection fraction and peak filling rate were found in the coronary artery disease group (56% +/- 17% versus 65% +/- 6%, p less than 0.05; 1.8 +/- 0.7 versus 2.9 +/- 1.4 end-diastolic volumes/s, p less than 0.05). Moreover, the patients with coronary artery disease had a prolonged isovolumic relaxation period (114 +/- 86 ms versus 70 +/- 43 ms, p less than 0.05). Two indices of left ventricular asynchrony were evaluated: the coefficient of variation of regional time to end-systole, and the coefficient of variation of regional time to peak filling rate. The coefficient of variation of regional time to peak filling rate was higher in the coronary artery disease group (10.1% +/- 10%) than in the normal subjects (6.2% +/- 3.7%, p less than 0.05). Both these parameters were inversely related to global peak filling rate in the coronary artery disease group. These findings suggest that in patients with coronary artery disease left ventricular systolic and diastolic asynchrony plays a role in determining left ventricular diastolic properties.

Blood Pressure↗
PubMed1991

Digoxin-induced vasoconstriction of normal and atherosclerotic epicardial coronary arteries.

This study evaluated the effect of bolus infusion of digoxin (0.014 mg/kg in 10 minutes, intravenously) on large coronary arteries measured by quantitative digital angiography. Twenty-two patients (mean age +/- standard deviation 47 +/- 12 years) divided into 3 groups were studied. The effects of digoxin infusion (after 10 and 20 minutes) and sublingual administration of isosorbide dinitrate were investigated in group I (patients with angiographically normal coronary arteries, n = 9) and in group II (patients with atherosclerotic coronary arteries, n = 8). To determine whether the effects of digoxin were mediated by activation of alpha-adrenergic receptors, coronary angiography was performed in group III after alpha-adrenoceptor blockade (phentolamine 0.11 mg/kg, intravenously) (n = 5). Ten minutes after the end of digoxin infusion, the cross-sectional area decreased from 7.7 +/- 4.1 to 6.0 +/- 2.2 mm2, and after 20 minutes to 5.6 +/- 2.6 mm2 (p less than 0.05) in group I. Isosorbide dinitrate reverted digoxin-induced vasoconstriction as cross-sectional area increased to 8.5 +/- 3.4 mm2 (p = not significant versus baseline). Twenty minutes after digoxin infusion, heart rate significantly decreased from 79 +/- 16 to 74 +/- 13 beats/min (p less than 0.01). Ten minutes after digoxin infusion, peripheral vascular resistance increased significantly from 1,396 +/- 693 to 1,693 +/- 984 dynes.s.cm-5 (p less than 0.05), whereas cardiac output did not change. Twenty minutes after digoxin infusion, minimal stenosis diameter decreased significantly from 1.6 +/- 0.5 to 1.4 +/- 0.5 mm (p less than 0.05) in group II.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography, Digital Subtraction↗