Biomedical subjects

I Simonetti

Publications and source records attributed to I Simonetti.

At least 37 records · Page 2Linked to original sources

PubMed1997

[Carditis associated with Mycoplasma pneumoniae infection. Clinical aspects and therapeutic problems].

A clinical case of carditis associated with Mycoplasma pneumoniae infection in a 65 year-old woman is reported in order to stress some clinical features and therapeutic problems; during a 5-year follow-up. On the basis of this experience it is possible to state that in the pathogenesis an autoimmune mechanism probably plays an important role, whereas in therapy specific antibiotics are not effective and a long-term treatment with anti-inflammatory drugs is necessary.

Aged↗

PubMed1996

Evidence for the existence of a functional cardiac renin-angiotensin system in humans.

BACKGROUND: The presence of mRNA for the essential components of the renin-angiotensin system (RAS) has been found in animal and human hearts. The present study was designed to provide evidence for the existence of a (functional) cardiac RAS. METHODS AND RESULTS: Twenty-four patients with atypical chest pain undergoing coronary angiography for diagnostic purposes were investigated. The cardiac production rate of angiotensins was estimated by measurement of the cardiac extraction of 125I-angiotensin I and 125I-angiotensin II associated with the determination of endogenous angiotensins in aortic and coronary sinus blood in normal, low, or high sodium diets. In a normal sodium diet, angiotensin I and II aorta-coronary sinus gradients were tendentially negative (-1.8 +/- 2.5 and -0.9 +/- 1.7 pg/mL, respectively), and the amounts of angiotensin I and II added by cardiac tissues were 6.5 +/- 3.1 and 2.7 +/- 1.3 pg/mL, respectively. The low sodium diet caused a significant increase in both plasma renin activity (PRA) and angiotensin I concentration in aortic but not in coronary sinus blood, resulting in a more negative aorta-coronary sinus gradient (-9.7 +/- 3.1 pg/mL, P < .01). Angiotensin formation by PRA in blood during transcardiac passage increased (P < .001), whereas angiotensin I formed by cardiac tissues decreased dramatically. Accordingly, in the low sodium diet, 125I-angiotensin II extraction did not change, the cardiac fractional conversion rate of 125I-angiotensin I to 125I-angiotensin II notably decreased (P < .01), and angiotensin II formation by cardiac tissues was undetectable. The high sodium diet caused a decrease in PRA and no changes in cardiac extraction of radiolabeled angiotensins; conversely, angiotensin I formed by cardiac tissues, cardiac Ang I fractional conversion rate, and angiotensin II formed during transcardiac passage significantly (P < .01 for all) increased. CONCLUSIONS: These results provide evidence for the existence of a functional cardiac RAS independent of but related to the circulating RAS.

Adult↗

PubMed1996

Effects of ischemia and reperfusion on QT dispersion during coronary angioplasty.

The effects of ischemia and reperfusion on QT interval dispersion (QTD: QTmax-QTmin in the 12-lead ECG) were analyzed in 15 patients (12 males, 57 +/- 13 years) undergoing coronary angioplasty (PTCA). All patients had single-vessel coronary artery disease (only one > or = 85% stenosis in a major coronary artery) and normal left ventricular function. All were in sinus rhythm with normal atrioventricular and intraventricular conduction on the surface ECG. No patient was on therapy that could affect the QT interval. The ECG was recorded (all 12 leads simultaneously) at 50 mm/s speed before the first balloon inflation, at the end of the first inflation during PTCA, and at 30" and 60" during reperfusion following the first inflation. In order to avoid ischemic preconditioning, only recordings of the first inflation were used. In each tracing QTmax and QTmin were evaluated. All values were rate corrected using a simple linear equation (QT linear corrected = QT + 0.154 [1-RR]). QTD increased significantly during both ischemia and reperfusion. QTmax was not changed by ischemia and was increased by reperfusion. QTmin was reduced by ischemia and increased by reperfusion. These results indicate that both ischemia and reperfusion alter ventricular repolarization, inducing a less homogeneous ventricular recovery pattern.

Analysis of Variance↗

PubMed1996

[Anticoagulant or antiaggregant therapy in the secondary prevention of myocardial infarct?].

The recent publication of the results of two large trials of secondary prevention of myocardial infarction with oral anticoagulants is causing a revival of interest for oral anticoagulants in this clinical setting. On the basis of these data, oral anticoagulants should be considered not only an effective preventive strategy, but, probably, more effective than antiplatelet agents, currently the standard therapy in the prevention of thrombosis in acute myocardial infarction. There are advantages and disadvantages for both these treatments, and an adequate balancing of expected risks and benefits has to be performed in each single patient. The present review summarizes rationales and main clinical results in the prevention of reinfarction with antiplatelet agents and with oral anticoagulants, and analyzes the reasoning to prefer the formers or the latters in daily clinical practice of secondary prevention of coronary artery disease. Also, an analysis of the benefit/risk ratio of antiplatelet agents (aspirin) and oral anticoagulants in the Italian health system is synthetically presented. Such an analysis can be useful for the formulation of general guidelines and may suggest a modification of currently established and widely popular therapeutic habits in the management of coronary artery disease in Italy.

Administration, Oral↗

PubMed1991

Effects of urokinase and heparin on minimal cross-sectional area of the culprit narrowing in unstable angina pectoris.

The immediate and delayed effects of urokinase and heparin on minimal cross-sectional area of a patent ischemia-producing coronary artery were prospectively investigated in 43 patients with unstable angina. After baseline angiography, patients were randomized to 3 different treatment groups: group I--urokinase (1,000,000 U intravenous bolus dose), followed by heparin infusion 3 hours later; group II--heparin (10,000 U intravenous bolus, followed by continuous infusion); and group III--conventional therapy only (intravenous nitroglycerin, beta blockers and calcium antagonists). Angiography was repeated at 1 hour and at 8 days of treatment and minimal cross-sectional area was determined in the 35 patients who completed the study. In group I, minimal cross-sectional area increased from 0.84 +/- 0.48 mm2 at baseline to 0.94 +/- 0.49 mm2 at 1 hour (p less than 0.05), and to 1.00 +/- 0.51 mm2 at 8 days (p less than 0.01 vs baseline). In group II, a significant increase in minimal cross-sectional area was observed only at the 8-day angiography (0.64 +/- 0.39 mm2 at baseline; 0.67 +/- 0.37 mm2 at 1 hour [p = not significant]; and 0.79 +/- 0.48 mm2 at 8 days [p less than 0.01] vs baseline). In group III, no significant changes in minimal cross-sectional area occurred either at 1 hour or at 8 days. Thus, both urokinase and heparin improved lesion geometry in patients with unstable angina, although a large individual variation was noticed. The effect occurred earlier with urokinase than with heparin.

Aged↗

PubMed1991

Neurohumoral regulation of collateral perfusion.

Mature coronary collaterals, which develop during chronic coronary occlusion, are not simply passive conduits but are capable of active vasomotion. Collateral perfusion must traverse not only these vessels but also proximal and distal coronary vessels. This series of resistances significantly modulates perfusion to collateral-dependent and potentially ischemic myocardium. The collateral vessels themselves possess unique vasomotor characteristics, particularly markedly augmented constriction to vasopressin. The recipient coronary microcirculation develops endothelial dysfunction during collateral development, a phenomenon that may markedly alter neurohumoral regulation of perfusion to collateral-dependent myocardium. Finally, the resistances proximal to the origin of the collateral vasculature, which are negligible at rest, become significant when flow to nonischemic regions (non-collateral-dependent) is increased, predisposing to the collateral steal phenomenon. Although collateral vessels play a crucial role in preventing myocardial infarction and often restore both resting and exercise perfusion to normal, the need to use these vessels is associated with important alterations of regulatory mechanisms in the coronary circulation.

Animals↗

PubMed1991

Coronary dynamics and mental arithmetic stress in humans.

Incidence and mechanisms of psychological stress-induced myocardial ischemia were investigated in a population of 63 patients using mental arithmetic. Fifty subjects (group 1) were selected as a consecutive population of ischemic patients with electrocardiographic documentation of ischemia at rest, on effort, or both. Mental arithmetic induced increases in heart rate, blood pressure, and rate-pressure product in all patients. Transient ischemic electrocardiographic changes occurred in 22 patients (44%; positive mental arithmetic), the majority of whom had both resting and exercise angina. In negative mental arithmetic tests, peak rate-pressure product was always lower than that achieved during exercise (mean +/- SD, 11.9 +/- 3 versus 21.3 +/- 5, p less than 0.01). Of the 22 patients with positive mental arithmetic tests, ischemia occurred in only six, at a rate-pressure product equal to or more than the one achieved during exercise (21.1 +/- 5 versus 19.4 +/- 4, p less than 0.01), suggesting an increase in myocardial O2 demand exceeding the limited increase in flow; in the remaining 16 patients, rate-pressure product values were significantly lower (14.8 +/- 3 versus 22.7 +/- 6, p less than 0.01), suggesting a primary reduction in coronary blood flow that is probably related to an increase in coronary tone. To assess the possible site of such a vasoconstriction, the effect of mental arithmetic on large coronary artery diameter was tested in 13 additional unselected patients (group 2) undergoing coronary angiography for a chest pain syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗

PubMed1991

Physiological assessment of sensitivity of noninvasive testing for coronary artery disease.

The sensitivity of three noninvasive tests for coronary artery disease was assessed by means of quantitative indexes of disease severity in three different groups of patients. The overall population consisted of 110 subjects with limited coronary artery disease and no myocardial infarction. Planar dipyridamole-201Tl scintigraphy was evaluated in 31 patients, computer-assisted exercise treadmill in 28, and high-dose dipyridamole echocardiography testing in 51. Sensitivity was assessed by rigorous gold standards to define disease severity, such as measurement of minimum cross-sectional area and percent area of stenosis, by quantitative computerized coronary angiography (Brown/Dodge method). On the basis of the results of previous studies, the presence of physiologically significant coronary artery disease was indicated by a stenotic minimum cross-sectional area (MCSA) of less than 2.0 mm2 or a greater than 75% area of stenosis. With MCSA as the gold standard, dipyridamole-201Tl scintigraphy, computerized exercise treadmill, and dipyridamole echocardiography testing showed sensitivities of 52%, 54%, and 61%, respectively, in the three different patient cohorts enrolled. With percent area of stenosis as the gold standard, the sensitivity figures obtained for dipyridamole-201Tl, computerized exercise treadmill, and dipyridamole echocardiography testing were 64%, 54%, and 69%, respectively. For each of the three tests, sensitivity increased with increasing lesion severity. Sensitivity was also better in patients with left anterior descending coronary (LAD) disease when compared with patients with left circumflex or right coronary artery disease. Results of these studies, which were obtained with more strict patient selection criteria and by more rigorous gold standards than previous studies, demonstrate that in patients with limited coronary artery disease none of the tests evaluated is definitely superior in sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗

PubMed1990

The brown adipose tissue of hyperthyroid rats. A biochemical and ultrastructural study.

Male Sprague-Dawley rats were treated with triiodothyronine (100 micrograms/100 g/day) for 2, 4, 7, 14 and 21 days and the biochemical and ultrastructural changes of the brown adipose tissue were investigated. Results showed that the tissue weight, DNA and phospholipid content increased very early (by day 2 or 4) and that triglycerides increased later. These hormonal effects are not inhibited by the beta 1-antagonist propranolol. From the morphological point of view, triiodothyronine administration induced the early proliferation and maturation of adipocyte precursors (interstitial cells and preadipocytes). It is concluded that triiodothyronine administration causes a very early hyperplasia in the brown adipose tissue similar to that observed during exposure to cold by mechanisms that may not be secondary to the involvement of norepinephrine.

Adipose Tissue, Brown↗

PubMed1990

Polymorphous ventricular tachycardia: a side effect of intracoronary papaverine.

Polymorphous ventricular tachycardia occurred in 1.3% of patients (5 of 391) who received intracoronary papaverine over a 47 month period. The arrhythmia lasted less than 1 min in all five patients, converting spontaneously in four and requiring electrical cardioversion in one. Ventricular tachycardia occurred in 4.4% of women (4 of 90) and 0.3% of men (1 of 301) (p less than 0.0025). Only one of the patients with ventricular tachycardia had coronary artery disease. To determine whether other clinical or procedural factors predispose patients to this side effect of papaverine, these 5 patients were compared with 25 control patients who were matched for gender and extent of coronary artery disease. The following variables were analyzed: age, baseline serum potassium and calcium levels, left ventricular ejection fraction, baseline heart rate, mean arterial pressure, corrected QT interval, the change in corrected QT interval produced by papaverine and the maximal dose of the drug per kilogram of body weight. Of these variables, only baseline heart rate differed significantly in the two groups of patients. Thus, polymorphous ventricular tachycardia is an infrequent, but important, side effect of papaverine that is usually self-limited. Women with a relatively slow heart rate appear to be predisposed to this side effect.

Coronary Vessels↗

PubMed1989

Regional and global biventricular function during dipyridamole stress testing.

This study assesses the relation between regional ventricular performance (using 2-dimensional echocardiography) and global systolic and diastolic indexes of biventricular myocardial function (using hemodynamic monitoring) during dipyridamole stress testing. Simultaneous 2-dimensional echocardiographic and biventricular hemodynamic monitoring during dipyridamole infusion (0.56 mg/kg over 4 minutes) was performed in 19 patients. All patients had a normal resting function. Eleven of the 19 patients had a positive echocardiography test (new wall motion dyssynergy with dipyridamole) and they formed group 1. Eight patients had a negative echocardiography test (group 2). During baseline conditions, no significant differences were found in the 2 groups: rate pressure product (107 +/- 16 vs 108 +/- 13 mm Hg x beats/min x 1/100), positive left ventricular (LV) dP/dt (1,950 +/- 473 vs 2,262 +/- 430 mm Hg/s), negative LV dP/dt (-2,069 +/- 620 vs -2,205 +/- 245), LV end-diastolic pressure (8.2 +/- 4.4 vs 9.6 +/- 4.0 mm Hg), right ventricular positive dP/dt (368 +/- 133 vs 400 +/- 190 mm Hg/s) and negative dP/dt (-281 +/- 89 vs -383 +/- 147). At peak dipyridamole, the 2 groups were different for LV end-diastolic pressure (20 +/- 10 vs 8 +/- 5 mm Hg, p less than 0.01), LV positive dP/dt (2,100 +/- 688 vs 3,013 +/- 851 mm Hg/s, p less than 0.01) and negative dP/dt (-1,868 +/- 518 vs -2,564 +/- 272, p less than 0.01). At peak ischemia, LV positive dP/dt increased slightly, but not significantly, while negative dP/dt decreased significantly (p less than 0.01) in comparison with resting values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Dose- and time-related vasodilator response of conduit coronary arteries to intracoronary isosorbide dinitrate in human beings.

The time course of the vasodilation of different segments of the epicardial coronary vasculature after three different doses of intracoronary isosorbide dinitrate (ISDN) was investigated in angiographically normal coronary arteries in 10 patients with quantitative coronary angiography. In five patients, 0.1 mg and 0.3 mg ISDN were injected intracoronary 30 minutes apart, and the effect of each dose was assessed at 1, 5, 10, and 15 minutes after the administration by serial angiograms. In five additional patients, a single dose of 3 mg was injected and coronary vasodilation was assessed at 1, 5, 10, 15, and 20 minutes. After each dose, dilation of epicardial coronary arteries occurred within 1 minute, peaked at 5 minutes and progressively decreased thereafter. Relative to control, peak percent diameter increase was (mean +/- SEM) 10% +/- 0.9% (p less than 0.01), 18.5% +/- 1.5% (p less than 0.01), and 26% +/- 2.1% (p less than 0.01) after 0.1, 0.3, and 3.0 mg, respectively. When small (1 to 2 mm), medium (2 to 3 mm), and large (greater than 3 mm) vessels were separately analyzed, peak response was respectively 12% +/- 1.3% (p less than 0.01), 9% +/- 1.9% (p less than 0.01), and 7% +/- 1% (p less than 0.05) after 0.1 mg ISDN; 22% +/- 1.8% (p less than 0.01), 16% +/- 1.3% (p less than 0.01), and 12% +/- 0.8% (p less than 0.01) after 0.3 mg; and 38% +/- 2.4% (p less than 0.01), 22% +/- 2.1% (p less than 0.01), and 17% +/- 2% (p less than 0.01) after 3.0 mg. The duration of the response increased with the dose, but was inversely related to the size of the vessel.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Coronary dilation with standard dose dipyridamole and dipyridamole combined with handgrip.

Intravenous dipyridamole is widely used to produce coronary vasodilation during cardiac imaging procedures. However, the routinely used dose of dipyridamole (0.56 mg/kg IV over 4 min) does not always result in maximal coronary dilation. The addition of isometric handgrip during dipyridamole coronary dilation has been reported to substantially increase coronary blood flow over dipyridamole alone. We compared the coronary vasodilation resulting from infusion of the standard dose of dipyridamole with that resulting from a maximally dilating dose of intracoronary papaverine in 12 patients with angiographically normal coronary arteries. We also assessed the effect on coronary blood flow velocity of the addition of isometric handgrip during dipyridamole coronary dilation. Changes in coronary blood flow velocity were measured with a 3F coronary Doppler catheter. The coronary flow reserve (peak/resting coronary flow velocity ratio) after dipyridamole (3.7 +/- 1.2 [mean +/- SD] was less than that seen after papaverine (4.4 +/- 0.5, p less than 0.05), and the coronary vascular resistance index during dipyridamole coronary vasodilation (0.28 +/- 0.09) was greater than during papaverine (0.22 +/- 0.03, p less than 0.05). The dipyridamole coronary flow reserve was less than 3.0 in four subjects and was 2.0 or less in two subjects. The addition of isometric handgrip to dipyridamole coronary vasodilation produced an 8% increase in mean heart rate and a 17% increase in mean arterial pressure, but coronary flow reserve was unchanged (3.8 +/- 1.1 before handgrip vs. 4.0 +/- 1.1 with handgrip). Quantitative angiography in six patients revealed no change in coronary caliber with the addition of handgrip.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗

PubMed1989

The effect of diltiazem on coronary flow reserve in humans.

Calcium channel antagonists have been shown to blunt maximal coronary flow after brief coronary occlusion and during pharmacologic coronary dilation in animals. This property, if present in humans, would result in a reduction in coronary flow reserve in the absence of intrinsic abnormalities of the coronary circulation. A reduction of maximal vasodilator capacity by calcium channel antagonists could also constitute an important anti-ischemic mechanism of action of these agents. To evaluate the effect of calcium channel antagonists on coronary flow reserve in awake humans, we measured coronary flow reserve using the coronary Doppler catheter and intracoronary papaverine at baseline and after diltiazem administered by intravenous (125 or 250 micrograms/kg bolus, 5 micrograms/kg/min infusion, n = 8) or intracoronary (150-600 micrograms bolus, n = 10) routes. Intravenous diltiazem reduced heart rate from 77 +/- 18 to 72 +/- 17 beats/min (mean +/- SD, p less than 0.005) and reduced mean arterial pressure from 96 +/- 11 to 86 +/- 15 mm Hg (p less than 0.005). Intravenous diltiazem resulted in a small decrease in coronary flow reserve (peak-to-resting flow velocity ratio) from 3.9 +/- 1.2 to 3.6 +/- 1.1 (p less than 0.01). After intracoronary diltiazem, mean arterial pressure was unchanged (control 99 +/- 12 mm Hg, diltiazem 97 +/- 13 mm Hg), and heart rate was maintained constant by atrial pacing. Coronary flow reserve was unchanged at 3.8 +/- 0.9 at baseline and after intracoronary diltiazem. Thus, treatment with diltiazem does not invalidate the measurement of coronary flow reserve for diagnostic purposes. Furthermore, these results suggest that attenuation of maximal coronary dilation by diltiazem is not a mechanism responsible for its antianginal effects.

Blood Flow Velocity↗

PubMed1989

Biphasic effect of nitroglycerin on coronary hemodynamics in normal subjects.

Coronary blood flow responses to nitroglycerin (NTG) in patients have been reported to be extremely variable. In dogs, NTG has a striking biphasic effect on coronary hemodynamics, consisting of a brisk increase followed by a decrease in coronary flow. To determine the effect of the drug on the coronary circulation in normal humans, NTG was injected I.C. (50 and 300 mcg) in 11 normals, and its effects on coronary flow velocity were compared to those of I. C. papaverine (6, 8, 10, and 12 mg) and saline (0.5 and 3.0 ml). Coronary flow velocity was measured using a 3F coronary Doppler catheter. The effect of each drug on coronary blood flow was analyzed in terms of both magnitude and duration (s) of the transient vasodilatory response following administration. Changes in coronary flow velocity (expressed as peak/resting velocity ratio) after 6, 8, 10, and 12 mg papaverine were (mean +/- SEM) 2.7 +/- 0.1, 3.4 +/- 0.3, 3.7 +/- 0.2, and 3.9 +/- 0.2, respectively. Very mild changes were observed with saline (1.3 +/- 0.1 and 1.7 +/- 0.1 after 0.5 and 3.0 ml, respectively), while ratios of 2.4 +/- 0.2 and 3.1 +/- 0.3 were obtained after NTG 50 and 300 mcg, respectively. The effect of 300 mcg NTG was significantly greater (p less than 0.01) than that of saline, 6 mg papaverine and 50 mcg NTG, lower than that of 12 mg papaverine and not significantly different from that of 8 and 10 mg papaverine. In terms of duration, the effect of 300 mcg NTG on coronary flow velocity was more prolonged than that of saline and 50 mcg NTG, and shorter than that of 6 to 12 mg papaverine.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗

PubMed1986

Comparison of verapamil and propranolol therapy for angina pectoris at rest: a randomized, multiple-crossover, controlled trial in the coronary care unit.

The effects of oral verapamil (V), 400 mg/day, oral propranolol (P), 300 mg/day, and placebo were compared in 10 patients admitted to the coronary care unit because of frequent attacks of angina at rest. Testing was done according to a randomized, double-blind, multiple-crossover, placebo-controlled trial, consisting of 8 consecutive 48-hour treatment periods with V or P or placebo. Three patients had variant angina, 5 had episodes of both ST-segment elevation and depression and 2 had only ST-segment depression. One patient had no critical coronary stenoses, 1 had 1-vessel disease, 7 had 2-vessel disease and 1 had 3-vessel disease. Electrocardiographic monitoring and tape recording were continued during the 16 days of the trial. A total of 1,602 episodes of transient diagnostic ST shift were recorded during the trial (1,309 episodes of ST-segment elevation, 293 of ST-segment depression); 43% were painless. Mean blood levels of V and P at the end of the active phases were 161 +/- 89 and 120 +/- 45 ng/ml, respectively. In the group as a whole, the average number of diagnostic ischemic ST-segment shifts per 24 hours was significantly reduced relative to corresponding placebo periods during V (2.6 +/- 2.4 vs 11.9 +/- 8.6; p less than 0.01) but not during P treatment (11.9 +/- 8.6 vs 12.0 +/- 7.3). Similar statistically significant reductions were observed in the number of anginal attacks and nitroglycerin tablets consumed. Considering individual patients, V reduced ischemic episodes during both active phases in all patients, whereas P was effective only in 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Dipyridamole-echocardiography test in patients with exercise-induced ST-segment elevation.

Fourteen consecutive patients with exercise-induced ST-segment elevation in the absence of previous infarction and basal left ventricular asynergy at rest performed a dipyridamole test (infusion of dipyridamole, 0.14 mg/kg/min intravenously for 4 minutes) during 12-lead electrocardiographic (ECG) and 2-dimensional echocardiographic monitoring. In 7 of the 14 patients, dipyridamole infusion consistently induced ST-segment elevation in the leads that showed ST elevation on effort; reversible asynergy (occurring in the region corresponding to the ECG leads with diagnostic changes) could always be documented by echocardiography. In 2 patients dipyridamole induced reversible asynergy in presence of ST-segment depression. In these 9 patients angiography invariably revealed a severe organic stenosis in the coronary artery feeding the region that became transiently asynergic after dipyridamole. In the other 5 patients (all of whom had either spontaneous or ergonovine-induced ST-segment elevation), the dipyridamole test yielded no significant echocardiographic or ECG change; coronary angiography showed absent (2 patients) or significant (3 patients) coronary artery disease. In conclusion, dipyridamole may induce transmural ischemia in humans, as detected by the electrical hallmark of ST elevation; this ECG pattern, in contrast to ST depression, reliably predicts the presence and site of transient regional asynergy. When dipyridamole induces ST-segment elevation, severe basal stenosis is invariably present in the coronary artery supplying the transiently asynergic myocardial region.

Adult↗

PubMed1986

Transient myocardial dysfunction during pharmacologic vasodilation as an index of reduced coronary reserve: a coronary hemodynamic and echocardiographic study.

Regional coronary flow reserve and regional myocardial contractility were evaluated in 29 patients after maximal pharmacologic coronary vasodilation (intravenous dipyridamole, 0.56 mg/kg body weight, administered over 4 minutes). Nineteen patients had a severe (80 to 99%) proximal and isolated stenosis of the left anterior descending coronary artery and 10 patients had normal coronary arteries; all had normal ventricular function under rest conditions. Myocardial contractility was assessed by means of continuous two-dimensional echocardiographic monitoring; coronary reserve was evaluated by coronary sinus thermodilution. After dipyridamole infusion, 9 of the 19 patients with left anterior descending artery stenosis had transient myocardial asynergy involving the septum or apex, or both (Group IA), whereas 10 patients showed no asynergy (Group IB). No impairment of contractility was observed in the 10 patients with normal coronary arteries (Group II). Coronary blood flow was measured under basal conditions and up to 10 minutes after the end of dipyridamole infusion. In patients in Group II, dipyridamole induced an increase in great cardiac vein flow of 167 +/- 68% (mean +/- SD). The 10 patients in Group IB showed a response comparable with that of the control group (Group II) (136 +/- 45% increase in great cardiac vein flow; NS versus Group II), whereas the 9 patients in Group IA had an increase of 46 +/- 30% (p less than 0.01 versus both Group IB and Group II). No significant difference was found in the angiographic severity of the stenosis expressed in terms of minimal cross-sectional area (Group IA = 0.30 +/- 0.13 mm2, Group IB = 0.34 +/- 0.18 mm2; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗