Endogenous prostaglandin endoperoxides may alter infarct size in the presence of thromboxane synthase inhibition: studies in a rabbit model of coronary artery occlusion-reperfusion.

OBJECTIVES: The aim of this study was to assess whether prostaglandin endoperoxides, which continue to be formed in the setting of thromboxane A2 synthase inhibition, might influence the fate of ischemic myocardium in a model of coronary occlusion and reperfusion. BACKGROUND: It was recently demonstrated that thromboxane A2 synthase inhibitors reduce ischemic myocardial injury through a redirection of prostaglandin (PG) endoperoxides toward the synthesis of "cardioprotective" prostaglandins, such as PGI2, PGE2 and PGD2. However, part of these prostaglandin endoperoxides may also stimulate a receptor, shared with thromboxane A2, mediating platelet aggregation and vasoconstriction. METHODS: New Zealand White rabbits were subjected to 30 min of coronary occlusion, followed by 5.5 h of reperfusion. Fifteen minutes before reperfusion, the animals were randomized to receive 1) saline solution (control animals, n = 8); 2) SQ 29548, a potent and selective thromboxane A2/PGH2 receptor antagonist (n = 8); 3) dazoxiben, a selective thromboxane A2 synthase inhibitor (n = 8); 4) R 68070 (Ridogrel), a drug with dual thromboxane A2 synthase-inhibiting and thromboxane A2/PGH2 receptor-blocking properties (n = 8); or 5) aspirin + R 68070 (n = 8). RESULTS: Dazoxiben and R 68070, but not SQ 29548, significantly reduced thromboxane B2 formation and increased plasma levels of 6-keto-PGF1 alpha, PGE2 and PGF2 alpha. Ex vivo platelet aggregation induced by U46619 (a thromboxane A2 mimetic) was inhibited by SQ 29548 and R 68070 but not by dazoxiben. In control animals, infarct size determined at the end of the experiment by triphenyltetrazolium chloride staining averaged 57.7 +/- 3.2% of the area at risk of infarction. The administration of SQ 29548 did not significantly reduce infarct size compared with that in control animals, whereas dazoxiben and R 68070 significantly reduced infarct size to 36.7 +/- 2.8% and 16.6 +/- 3.6% of area at risk of infarction, respectively (p < 0.001 vs. control values). In rabbits treated with R 68070, infarct size was also significantly smaller than that of dazoxiben-treated rabbits (p < 0.01). This protective effect of R 68070 was completely abolished when the drug was administered with aspirin, infarct size in this group averaging 59.7 +/- 1.6% (p = NS vs. control values). No differences in regional myocardial blood flow, systemic blood pressure, heart rate or extent of area at risk were observed among groups. CONCLUSIONS: Thus, prostaglandin endoperoxides play an important role in modulating the cardioprotective effects of thromboxane A2 synthase inhibitors. The simultaneous inhibition of thromboxane A2 synthase and blockade of thromboxane A2/PGH2 receptors by R 68070 identify a pharmacologic interaction of potential therapeutic importance.

Hemodynamic and hormonal effects of atrial natriuretic factor in patients with essential hypertension.

Hemodynamic and hormonal effects of two graded infusions of alpha-human-(1-28)-atrial natriuretic factor (0.5 microgram/kg prime followed by 0.05 microgram/kg per min for 20 minutes and by 0.1 microgram/kg per min for 20 minutes) were evaluated in 13 patients with mild to moderate essential hypertension. The lower dose of atrial natriuretic factor did not change significantly any of the considered variables, although it tended to reduce aortic mean blood pressure (from 132.6 +/- 5.3 to 125.5 +/- 4.6 mm Hg), cardiac index (from 3.67 +/- 0.2 to 3.54 +/- 0.18 liters/min per m2) and forearm vascular resistance (from 178.6 +/- 15 to 148.3 +/- 10 mm Hg/ml per s). The higher dose of atrial natriuretic factor significantly reduced mean aortic pressure (118.6 +/- 5 mm Hg), cardiac index (3.29 +/- 0.16 liters/min per m2) and stroke volume index (from 45.9 +/- 2.6 to 38.9 +/- 3 ml/m2) and slightly decreased pulmonary wedge pressure, whereas both total peripheral resistance and forearm vascular resistance were not modified. With this latter dose a reduction in aortic pressure was observed in all patients at the steady state, and this was associated with a fall in stroke volume index in 10 of the 13 patients and with a reduction in total peripheral resistance in only 6 patients. Heart rate and right atrial and pulmonary pressures did not change during infusion of atrial natriuretic factor. Plasma renin activity was only slightly reduced by atrial natriuretic factor, whereas plasma norepinephrine rose significantly (from 233 +/- 34 to 330 +/- 58 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac effects of atrial natriuretic peptide in subjects with normal left ventricular function.

The effects of atrial natriuretic peptide (ANP) infusion were determined in 9 subjects undergoing cardiac catheterization that did not disclose heart disease. Data were obtained at rest and during the steady-state phase of alpha-human-(1-28)-atrial natriuretic peptide infusion (0.5 micrograms/kg bolus, 0.05 micrograms/kg/min intravenously for 10 minutes). Mean blood pressure decreased from 105 +/- 3 to 98 +/- 4 mm Hg (p less than 0.05); pressure measurements and left ventricular (LV) angiograms suitable for analysis were available in 7 of 9 subjects at matched heart rate. The ANP infusion reduced LV end-diastolic and end-systolic volume indexes from 93 +/- 6 to 80 +/- 6 ml/m2 (p less than 0.01) and from 25 +/- 3 to 17 +/- 1 ml/m2 (p less than 0.05), respectively. The LV ejection fraction increased insignificantly from 72 +/- 5 to 77 +/- 4%. End-systolic pressure/volume ratio showed a slight but not significant increase (from 3 +/- 0.4 to 4 +/- 0.8). Initial plasma levels of ANP (48 +/- 12 pg/ml) increased to 1,890 +/- 423 pg/ml (p less than 0.001) during the infusion and individual hemodynamic responses were not related to plasma ANP concentrations. These data suggest that the administration of ANP has no negative effects on LV function and the ANP-induced changes on cardiac performance are related to the reduced cardiac load.

Effects of oral salt load on arginine-vasopressin secretion in normal subjects.

Arginine-vasopressin (AVP) plays an important role in regulating water balance in humans. Its secretion is under control of several mechanisms, some of which are not completely understood. The purpose of the present study was to evaluate the effects of an acute oral salt load on AVP secretion in normal subjects. Six normal volunteers received 350 mEq of NaCl per os. Pulmonary capillary wedge pressure and right atrial pressure, plasma AVP, plasma sodium and potassium concentration, plasma osmolality, hematocrit, urinary sodium and potassium excretion, and urinary flow were measured at baseline and every 30 minutes for two hours after the salt load. Hemodynamics as well as urinary sodium and potassium excretion did not change over the study. Ninety minutes after the salt load, plasma AVP increased from the basal value of 6.0 +/- 0.9 pg per ml to 10.1 +/- 1.2 pg per ml (mean +/- SE, p less than 0.005) and a significant reduction in diuresis of about 50% was observed. However, plasma osmolality and plasma sodium concentration increased significantly only 120 min after the salt load, from the initial value of 277.7 +/- 2.2 mOsm per kg and 145.3 +/- 1.4 mEq per 1 (mean +/- SE) to 284.8 +/- 2.5 mOsm per kg and 148.7 +/- 1.5 mEq per 1, respectively (p less than 0.01). Ninety minutes after the salt load, no correlation was found between plasma osmolality and plasma AVP concentration, indicating that AVP secretion was independent of changes in systemic blood osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Performance of the XLIMUS sirolimus-eluting coronary stent in very complex lesions.

AIM: In an attempt to improve the stent's safety and effectiveness, development of drug-eluting stents (DES) continues, with new materials and geometry. XLIMUS (CARDIONOVUM GmbH, Germany) is a new DES with the following potential advantages 1) excellent stent platform; 2) biodegradable polymer; and 3) potent antiproliferative drug (sirolimus). METHODS: In this pilot study, we assessed the safety and efficacy of percutaneous coronary interventions (PCI) using the new XLIMUS DES in patients undergoing elective PCI in native coronary vessels for complex de novo lesions, including: 1) severe calcification; 2) severe tortuosity; and 3) chronic total occlusion (CTO). RESULTS: A total of 53 consecutive patients with 59 lesions were analyzed. Severe calcifications occurred in 21% of patients; severe tortuosity in 45%, and CTO in 34%. The device success was obtained in 52 (98%) patients and in 58 (98%) lesions. Globally, the XLIMUS DES was successfully implanted by conventional PCI techniques on the first try with a single guidewire in 48/53 (90.5%) patients and 54/59 (91.5%) lesions. Additional techniques to facilitate stent delivery (i.e., buddy wire, anchoring-balloon, or Guideliner catheter) were required in 5 lesions. In one case the XLIMUS DES finally failed to cross the target lesion. CONCLUSION: This prospective, single-center pilot study suggests that the tracking and lesion crossing performance quality of the XLIMUS DES ensures treatment of complex coronary artery lesions.

[Percutaneous brachial approach in left heart catheterization with 5 French catheters. Preliminary experience]. / Approccio percutaneo brachiale nel cateterismo cardiaco sinistro con cateteri 5 French. Esperienza preliminare.

This describes our preliminary experience with percutaneous brachial approach for cardiac catheterization, by using 5 French (F) preformed catheters. Thirty patients (pts) were studied from the left arm (Group A) with a 5F sheath and 5F Judkins catheters and 30 from the right arm (Group B) with 5F sheath and 5F Amplatz catheters. Pigtail catheters (5F) were used for the left ventricular angiograms in all patients. In 10 patients arterial velocity signals and radial and ulnar artery blood pressures were monitored with the Doppler ultrasonic velocity detector before and immediately after each procedure, and 24 hours later. Arterial puncture was carried out successfully in each patient by using a 18-gauge Potts-Cournand needle. The puncture site was as close as possible to the ante cubital fossa where the artery is less mobile. Both coronary arteries were selectively opacified and the left ventricular angiography was done on every patient. The diagnostic quality of the angiograms was evaluated by the visual analogue scale and the results were not different from those obtained with the femoral approach in our catheterization laboratory. In 3 out of 30 pts in group B it was impossible to obtain a good left coronary opacification with Amplatz catheters for anatomical reasons, thus the right femoral approach was preferred. Brachial artery occlusion occurred in 1 patient from group B and needed surgical thrombectomy carried out to restore normal radial and ulnar pulses.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of O2 deprivation, reduced flow, and temperature on release of ANP from rabbit hearts.

The separate effects of hypoxia and ischemia on atrial natriuretic peptide (ANP) release were evaluated in Langendorff-perfused rabbit hearts. Heart rate, coronary flow, and atrial and ventricular volumes were kept constant. Hypoxia was induced for 20 min at room temperature in seven hearts and at 37 degrees C in a second group of seven hearts. A third group of eight hearts was subjected to global ischemia for 20 min by reducing coronary flow to 1 ml/min at room temperature. All hearts were reoxygenated/reperfused at 37 degrees C for 30 min. Hypoxia at 37 degrees C induced a significant increase in ANP release. In contrast, both room temperature hypoxia and ischemia were characterized by a significant decrease in ANP release, despite hemodynamic alterations similar to those recorded during hypoxia at 37 degrees C. Both reoxygenation and reperfusion induced a prompt reversal of the changes of ANP release observed during the period of oxygen deprivation. These data demonstrate that decreased oxygen availability and reduced coronary flow are not the primary factors affecting release of ANP during ischemia and that alterations of myocardial temperature may play a major role in this phenomenon.

[Effects of atrial natriuretic peptide on left ventricular function in man]. / Effetti del peptide natriuretico atriale sulla funzione ventricolare sinistra nell'uomo.

The effects of atrial natriuretic peptide (ANP) infusion were determined in 9 subjects undergoing cardiac catheterization which did not disclose heart disease. Data were obtained at rest and during the steady-state phase of alpha-human-(1-28)-atrial natriuretic peptide infusion (0.5 microgram/Kg bolus dose, 0.05 microgram Kg/min iv for 20 min). Mean blood pressure decreased from 105 +/- 3 to 98 +/- 4 mmHg (p less than 0.05); pressure measurements and left ventricular (LV) angiograms suitable for analysis were available in 7 of 9 subjects at matched heart rate. The infusion of ANP reduced LV end-diastolic and end-systolic volume indices from 93 +/- 6 to 80 +/- 6 ml/m2 (p less than 0.01) and from 25 +/- 3 to 17 +/- 1 ml/m2 (p less than 0.05), respectively. Left ventricular ejection fraction insignificantly increased from 72 +/- 5 to 77 +/- 4%. End-systolic pressure/volume ratio showed a slight but not significant rise (from 3 +/- 0.4 to 4 +/- 0.8). Initial plasma levels of ANP (48 +/- 12 pg/ml) rose to 1890 +/- 423 pg/ml (p less than 0.001) during the infusion and individual hemodynamic responses were not related to plasma concentrations of the peptide. These data suggest that the administration of ANP has no negative effects on LV function and the ANP-induced changes on cardiac performance are related to the reduced cardiac load.

[Limitation of the area of necrosis induced by quinacrine after coronary occlusion in the dog]. / Limitazione dell'area di necrosi indotta dalla chinacrina dopo occlusione coronarica nel cane.

Phospholipase activation has been suggested to represent one of the most relevant biochemical steps toward irreversible myocardial injury during ischemia. Accordingly, the time-course of myocardial phospholipid degradation was studied in 167 rats surviving coronary artery occlusion randomly divided into 83 controls and 84 treated with the phospholipase inhibitor quinacrine (75 mg/Kg s.c. every 8 h). The animals were sacrificed at different times ranging from 2 to 48 h post-occlusion and phospholipids and creatine kinase activity (CK) were measured on the supernatant of the left ventricular homogenates. In control animals a rapid fall in phospholipid concentration (from 1.33 +/- 0.12 to 0.67 +/- 0.05 microgram P/mg of protein) and CK activity (from 9.84 +/- 0.49 to 6.93 +/- 0.60 IU/mg of protein) was observed within 4 hours post-occlusion; these parameters remained almost unchanged throughout the rest of the study. In quinacrine-treated animals left ventricular phospholipids and CK also fell during the first hours post-occlusion; however, 24 and 48 h after the occlusion they were significantly higher than in controls (phospholipids: 0.99 +/- 0.05 vs 0.62 +/- 0.04 microgram P/mg of protein, p less than 0.001, and CK: 7.76 +/- 0.54 vs 4.99 +/- 0.37 IU/mg of protein, p less than 0.001, at 48 h). The effect of quinacrine on the extent of necrosis was then assessed in 13 anesthetized dogs undergoing ligation of the left anterior descending coronary artery. To measure the area at risk (RZ), 99Tc-PP labeled albumin microspheres were injected into the left atrium 5 min after coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Are ioxaglate and iopamidol equally safe and well tolerated in cardiac angiography? A randomized, double-blind clinical study.

A randomized, double-blind, parallel-group study was performed in 50 patients undergoing left ventriculography and coronary arteriography to evaluate ECG changes and the effects on left ventricular function of a low-osmolar ionic contrast agent, ioxaglate, as compared with a low-osmolar nonionic contrast medium, iopamidol. Twenty-five patients received ioxaglate (group 1) and 25 patients received iopamidol (group 2). All patients underwent 48 hours of continuous ECG recording beginning 24 hours before the cardiac catheterization. Left ventricular systolic and end-diastolic pressure, peak positive dp/dt, and dp/dt/P ratio were measured immediately before and after left ventriculography and 3 minutes later. Left ventricular systolic pressure did not change after injection of either contrast medium. Left ventricular end-diastolic pressure increased by 30% in group 1 (p less than 0.01) and by 22% in group 2 (p less than 0.01) immediately after left ventriculography. A further increase by 45% in group 1 (p less than 0.01) and by 24% in group 2 (p less than 0.01) was observed 3 minutes later. No differences were observed between values obtained in the two groups. Peak positive dp/dt did not change immediately after injection of either contrast medium but decreased by 5% (not significant) in group 1 and by 7% (p less than 0.02) in group 2 three minutes after left ventriculography. There were no significant differences between the two groups. Analysis of continuous 48-hour ECGs showed that both ioxaglate and iopamidol induced a slight increase (by 8% and 7%, respectively; p less than 0.05) in heart rate during injection with early and complete recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of action of OPC-8490 in human ventricular myocardium.

BACKGROUND: The quinolinone compounds OPC-8212 (vesnarinone), OPC-18790, and OPC-8490 are members of a family of unique positive inotropic compounds that have no positive chronotropic effects. In subjects with heart failure, the prototypic compound OPC-8212 may reduce morbidity and mortality at low doses but increase mortality at high doses. METHODS AND RESULTS: To further characterize the inotropic mechanism(s) of action of these compounds, we investigated the effects of OPC-8490, a water-soluble quinolinone, on the inotropic response, inhibition of phosphodiesterase (PDE), and action potential in human ventricular myocardial preparations. In isolated right ventricular trabeculae and membranes prepared from left ventricular myocardium, OPC-8490 produced dose-related positive inotropic effects, inhibited type III PDE activity, and prolonged action potential. Comparative experiments with other PDE inhibitors, sodium channel agonists, and potassium channel antagonists indicated that the positive inotropic effects are due to PDE inhibition, whereas the action potential effects of OPC-8490 are due to effects on ion channels. CONCLUSIONS: We conclude that OPC-8490 produces selective positive inotropic effects because of type III PDE inhibition combined with ion channel effects, with the latter property inhibiting the positive chronotropic response usually associated with agents that increase intracellular cAMP concentrations.

The effects of calcium channel antagonist treatment and oxygen radical scavenging on infarct size and the no-reflow phenomenon in reperfused hearts.

Calcium antagonists reduce ischemic injury, and anti-free-radical interventions may reduce reperfusion injury. However, the effects of treatment with both interventions have never been investigated. In the present study, anesthetized rabbits underwent 30 minutes of coronary artery ligation, which was followed by 5.5 hours of reflow. Eight animals in each group received: (1) the calcium antagonist gallopamil during ischemia, (2) the oxygen radical scavenger superoxide dismutase during reperfusion, (3) combined treatment with gallopamil and superoxide dismutase, and (4) saline solution. All groups were similar with respect to collateral flow during ischemia and extent of risk region. Infarct size averaged 60.2% +/- 5.5% of risk region in controls and was significantly smaller (p < 0.001) in rabbits that were treated with either gallopamil (28.1% +/- 3.4%) of superoxide dismutase (29.3% +/- 3.2%). Little further reduction in infarct size was observed with combination therapy (22.9% +/- 3.2% of risk region; p = NS). Superoxide dismutase had no effects on hemodynamics, whereas gallopamil significantly reduced heart rate, mean arterial pressure, and rate-pressure product. However, the reduction in infarct size that was observed in gallopamil-treated rabbits significantly exceeded the expected value in this group after corrections were made for changes in these determinants of ischemic injury. Therefore we investigated whether other factors may have contributed to the beneficial effects of gallopamil. In vitro the drug had no oxygen radical scavenging activity, nor did it exert antioxidant effects. In addition, gallopamil did not affect neutrophil function. In conclusion, in this acute model myocardial cell necrosis was significantly reduced either by administration of a calcium antagonist during ischemia or by removing oxygen radicals during reperfusion. However, superoxide dismutase administration did not further reduce infarct size when given to animals that had been treated with gallopamil. Since gallopamil has no direct effect on several mechanisms of reperfusion injury, these data suggest that calcium antagonists, by decreasing myocardial oxygen demand during ischemia, may indirectly reduce oxygen radical damage during subsequent reperfusion.

Angiotensin II directly stimulates release of atrial natriuretic factor in isolated rabbit hearts.

BACKGROUND: Previous studies have shown that infusion of angiotensin II (Ang II) increases plasma concentrations of atrial natriuretic factor (ANF) in vivo. This phenomenon has been considered secondary to the effects of Ang II on cardiac and systemic hemodynamics. The present study was designed to assess whether Ang II may exert a direct stimulatory effect on ANF release from the heart independent of changes in hemodynamics. METHODS AND RESULTS: Isolated rabbit hearts were perfused in the Langendorff mode. Heart rate, coronary flow, and atrial and left ventricular (LV) volumes were kept constant. After stabilization, Ang II was infused intracoronary at increasing doses (10(-11) to 10(-8) M) in nine hearts and at a single dose of 10(-10) M in 10 hearts. Each infusion lasted for 5 minutes and was followed by a 10-minute washout period. Four hearts received vehicle alone for 80 minutes. Ang II induced a dose-dependent increase in coronary perfusion pressure and in LV developed pressure. ANF release, measured by radioimmunoassay on the extracts of the cardiac effluent, also increased during Ang II infusion and returned to the basal values during the 10-minute washout period. In the control group, coronary perfusion pressure, LV developed pressure, and LV end-diastolic pressure did not change appreciably over the observation period, whereas ANF release progressively decreased during perfusion. CONCLUSIONS: Ang II can directly stimulate cardiac release of ANF in isolated rabbit hearts independently of changes in hemodynamics.

Divergent effects of serotonin on coronary-artery dimensions and blood flow in patients with coronary atherosclerosis and control patients.

BACKGROUND: Studies in animals have shown that serotonin constricts coronary arteries if the endothelium is damaged, but in vitro studies have revealed a vasodilating effect on isolated coronary segments with an intact endothelium. To investigate the effect of serotonin in humans, we studied coronary-artery cross-sectional area and blood flow before and after the infusion of serotonin in seven patients with angiographically normal coronary arteries and in seven with coronary artery disease. METHODS: We measured the cross-sectional area of the coronary artery by quantitative angiography and coronary blood flow with an intracoronary Doppler catheter. Measurements were obtained at base line and during intracoronary infusions of serotonin (0.1, 1, and 10 micrograms per kilogram of body weight per minute, for two minutes). We repeated the measurements after an infusion of ketanserin, an antagonist of serotonin receptors that is thought to block the effect of serotonin on receptors in the arterial wall but not in the endothelium. RESULTS: In patients with normal coronary arteries, the highest dose of serotonin increased cross-sectional area by 52 percent (P less than 0.001) and blood flow by 58 percent (P less than 0.01). The effect was significantly potentiated by administration of ketanserin. In patients with coronary-artery atherosclerosis, serotonin reduced cross-sectional area by 64 percent (P less than 0.001) and blood flow by 59 percent (P less than 0.001). Ketanserin prevented this effect. CONCLUSIONS: Serotonin has a vasodilating effect on normal human coronary arteries; when the endothelium is damaged, as in coronary artery disease, serotonin has a direct, unopposed vasoconstricting effect. When considered with other evidence, these data suggest that platelet-derived factors such as serotonin may have a role in certain acute coronary ischemic syndromes.

Limb vasoconstriction after successful angioplasty of the left anterior descending coronary artery.

BACKGROUND: Coronary vasoconstriction has been described after uncomplicated percutaneous transluminal coronary angioplasty (PTCA). However, it is still unknown whether this phenomenon is limited to coronary circulation. The present study was planned to assess the effects of a successful PTCA on forearm blood flow (FBF) and resistance. The role of alpha-adrenoceptors and calcium antagonist agents on PTCA-induced limb blood flow changes was also investigated. METHODS AND RESULTS: We prospectively studied 37 patients scheduled for elective single PTCA of the left anterior descending coronary artery. All patients had evidence of exercise-induced myocardial ischemia. All vasoactive drugs were withdrawn for at least 48 hours before the study. FBF was measured by calibrated venous occlusion plethysmography. A significant reduction of FBF was observed at 1, 5, and 15 minutes after PTCA (from 3.7 +/- 1.2 to 2.7 +/- 1.5, 3.0 +/- 1.6, and 2.9 +/- 1.9 mL/100 mL tissue per minute, respectively; all P < .05 versus baseline). Vascular forearm resistance also increased at 1, 5, and 15 minutes after PTCA (from 27 +/- 8 to 42 +/- 16, 37 +/- 10, and 43 +/- 19 U, respectively; all P < .05 versus baseline). Phentolamine (12 microgram.kg-1.min-1, n = 7) or verapamil (3.5 micrograms.kg-1.min-1, n = 7) also was infused intra-arterially. PTCA-induced forearm vasoconstriction was completely abolished by pretreatment with regional infusion of phentolamine or verapamil. CONCLUSIONS: After an uncomplicated PTCA of the left anterior descending coronary artery, a reduction in FBF and an increase in forearm vascular resistance were observed. This peripheral vasoconstrictive response was probably due to alpha-adrenergic stimulation and was abolished by intra-arterial infusion of calcium antagonist agents.

[Coronary angioplasty for the recovery of myocardial function after acute myocardial infarction: mid- and long-term results]. / Angioplastica coronarica per il recupero della funzione miocardica post-IMA: risultati a medio e lungo termine.

Sixty-three patients with previous myocardial infarction and documented hypoperfused reversibly dysfunctional myocardium after 201thallium tomography and/or echo-dobutamine were candidates to coronary angioplasty. Patients were enrolled at four hospitals (Naples, Milan, Pisa and Varese) and evaluated by different study protocols, while endpoint (presence of myocardial viability and efficacy of coronary angioplasty to improve dysfunctional myocardium) was similar. Sixty-two patients underwent successful angioplasty, and early evaluation (between 1 and 3 months after procedure) showed the ability of either 201thallium tomography and/or dobutamine echocardiography, to identify hypoperfused reversibly dysfunctional myocardium. Ten patients underwent late (after 8 +/- 2 months) evaluation of both wall motion and myocardial perfusion showing a sustained improvement in 25/32 hypoakinetic myocardial segments. Our data confirm the efficacy of revascularization of hypoperfused dysfunctional myocardial segments by coronary angioplasty. Further studies are warranted to obtain a better patient stratification and to evaluate the long-term results.