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Biomedical subjects

A Gaspardone

Publications and source records attributed to A Gaspardone.

At least 37 records · Page 2Linked to original sources
PubMed1999

Effect of acetylsalicylate on cardiac and muscular pain induced by intracoronary and intra-arterial infusion of bradykinin in humans.

OBJECTIVES: This study assessed the algesic activity of bradykinin (BK) in humans and the effects of acetylsalicylate on muscular and cardiac BK-induced pain. BACKGROUND: Bradykinin is released by the ischemic myocardium and may be involved in the genesis of ischemic pain. METHODS: Increasing doses of BK (from 30 to 960 ng/min) were randomly infused, for periods of 2 min each, into the iliac artery of 10 patients. The same protocol was repeated 30 min after the IV administration of 1 g of acetylsalicylate. In eight other patients with coronary artery disease, the same increasing doses of BK, for periods of 2 min each, were infused into the left coronary artery. The same protocol was repeated 30 min after the IV administration of 1 g of acetylsalicylate. Time to pain onset and maximal pain severity were obtained. RESULTS: Before acetylsalicylate administration, all patients experienced pain during intra-iliac infusion of BK. After acetylsalicylate, eight patients did not experience any pain during BK infusion (p = 0.0014), and in the two remaining patients, time to pain onset and maximal pain severity were similar to those recorded before acetylsalicylate. Before acetylsalicylate administration, all patients experienced pain similar to their habitual angina during intracoronary BK infusion. After acetylsalicylate, six patients did not experience any pain during BK infusion (p = 0.0098), whereas in the two remaining patients time to pain onset and maximal pain severity were similar to those recorded before acetylsalicylate. CONCLUSIONS: Intra-iliac infusion of BK causes muscular pain, and its intracoronary infusion in patients with coronary artery disease causes cardiac pain, which is similar to their habitual angina. The BK-induced pain is abolished or reduced by acetylsalicylate, thus suggesting that acetylsalicylate-sensitive mediators, such as prostaglandins, are involved in its pathogenesis.

Aged↗
PubMed1999

Decreased activity of the red blood cell ATPase-dependent Na+ pump in patients with cardiac syndrome X.

Marked Na(+)/Li(+) countertransport hyperactivity and post-load hyperinsulinaemia have been described in 93% of patients with cardiac syndrome X. We hypothesized that more complex abnormalities in Na(+) traffic across the cell membrane are present in these patients. The aim of the present study was to evaluate the activities of the two main transporters responsible for transmembrane Na(+) transport, i.e. the ATPase-dependent Na(+) pump and the Na(+)-K(+)-2Cl(-) co-transporter, in a selected group of patients with cardiac syndrome X. We evaluated 19 patients with cardiac syndrome X and 14 control subjects. The ATPase-dependent Na(+) pump and Na(+)-K(+)-2Cl(-) co-transport activities were assessed from Na(+)-loaded red blood cells by using nystatine, in the presence of furosemide and ouabain, as appropriate. Erythrocyte Na(+)/Li(+) countertransport activity, serum lipid and post-load (75 g of oral glucose) insulin levels were also evaluated. The V(max) of Na(+)/Li(+) countertransport (P=0.0001) and post-load insulin levels (120 min; P=0.001) were confirmed to be higher in patients with syndrome X than in controls. The V(max) of Na(+)-K(+)-2Cl(-) co-transport was similar in patients and controls. By contrast, the V(max) of the ATPase-dependent Na(+) pump was significantly lower (P=0.002) in syndrome X patients (3.13+/-0.87 mmol.h(-1).l(-1)) than in controls (4.28+/-1.10 mmol.h(-1).l(-1)). Serum total cholesterol and triacylglycerol concentrations were also higher in patients with syndrome X than in control subjects (P<0.0001). Thus decreased activity of the ATPase-dependent Na(+) pump was present in patients with cardiac syndrome X. Such an abnormality has the biological potential to augment microvascular tone and the response to constrictor stimuli via increased intracellular free Ca(2+). Of note, syndrome X patients also manifested Na(+)/Li(+) countertransport hyperactivity which, in turn, is known to induce peripheral insulin resistance and consequent abnormalities in insulin secretion and lipid turnover. Thus cardiac syndrome X appears as a multifaceted syndrome presenting with either metabolic or cardiovascular symptoms, or both, based on the expression of complex abnormalities in Na(+) traffic across the cell membrane.

Adenosine Triphosphatases↗
PubMed1999

Effects of K(ATP) channel blockade by glibenclamide on the warm-up phenomenon.

AIMS: The increased tolerance to myocardial ischaemia observed during the second of two sequential exercise tests, i.e. the warm-up phenomenon, has been proposed as a clinical model of ischaemic preconditioning. As ATP-sensitive K+ channels appear to be a mediator of ischaemic preconditioning in both experimental and clinical studies, the aim of this study was to investigate the role of K(ATP) channels in the warm-up phenomenon. METHODS AND RESULTS: Twenty-six patients with coronary artery disease were randomized to receive 10 mg oral glibenclamide, a selective ATP-sensitive K+ channel blocker, or placebo. Sixty minutes after glibenclamide or placebo administration, patients were given an infusion of 10% dextrose (8 ml x min(-1)) to correct glucose plasma levels or, respectively, an infusion of saline at the same infusion rate. Thirty minutes after the beginning of the infusions, both patient groups underwent two consecutive treadmill exercise tests, with a recovery period of 15 min to re-establish baseline conditions. Before exercise tests, blood glucose levels were similar in placebo and glibenclamide groups (96 +/- 10 vs 105 +/- 22 mg x 100 ml(-1), P=ns). After placebo administration, rate-pressure product at 1.5 mm ST-segment depression significantly increased during the second exercise test compared to the first (220 +/- 41 vs 186 +/- 29 beats x min(-1) x mmHg x 10(2), P<0.01), but it did not change after glibenclamide (191 +/- 34 vs 187 +/- 42 beats x min(-1) x mmHg x 10(2), P=ns), with a significant drug-test interaction (P=0.0091, at two-way ANOVA). CONCLUSIONS: Glibenclamide, at a dose previously shown to abolish ischaemic preconditioning during coronary angioplasty, prevents the increase of ischaemic threshold observed during the second of two sequential exercise tests. These findings confirm that ischaemic preconditioning plays a key role in the warm-up phenomenon and that in this setting is, at least partially, mediated by activation of ATP-sensitive K+ channels.

Adenosine Triphosphate↗
PubMed1999

[Percutaneous transvenous biopsy for the diagnosis of a right atrial myxoma].

Intracardiac tumors are generally diagnosed by transthoracic echocardiography, transesophageal echocardiography and, more recently, magnetic resonance imaging. However, these techniques do not permit a histopathologic diagnosis. When surgery is not indicated because of limited hemodynamic changes but the benign nature of the tumoral mass is questionable, percutaneous transvenous biopsy, when technically feasible, may represent an alternative approach. In this case report, we utilized percutaneous transvenous biopsy to obtain specimens from a right atrial mass in a 39-year-old woman.

Adult↗
PubMed1999

Minor myocardial damage and inflammatory response after three different procedures of left anterior descending artery revascularization.

BACKGROUND: Intracoronary stenting, conventional coronary artery bypass with cardiopulmonary bypass and minimally invasive direct coronary artery bypass without extracorporeal circulation are the three accepted options for revascularizing the left anterior descending coronary artery. We compare the effects of these three procedures in terms of minor myocardial damage and systemic inflammatory response. METHODS: Ninety patients undergoing left anterior descending coronary artery revascularization with these three different techniques (thirty patients per group) were considered. Blood samples were collected preoperatively and immediately postoperatively, and then 24, 48 and 72 hours after the procedures to measure troponin I, creatine kinase, its MB fraction and C-reactive protein levels. RESULTS: Postoperative levels of troponin I and MB-creatine kinase were significantly higher in conventional coronary grafting group than in PTCA-stent and in the minimally invasive surgery groups (p < 0.0003), while in both surgery groups there were higher post-operative levels of total creatine kinase and C-reactive protein (p = 0.0001). CONCLUSIONS: Minimally invasive direct coronary artery bypass surgery and PTCA-stent are similar in terms of virtual absence of minor myocardial damage. Skeletal muscle damage and inflammatory reaction are comparable in surgical patients, but they do not appear to have any clinical relevance.

Aged↗
PubMed1999

Algogenic effects of the proximal and distal intracoronary infusion of adenosine. Pathophysiologic implications on the mechanisms of ischemic cardiac pain.

BACKGROUND: It has been hypothesized that ischemic cardiac pain might be due to a spatially restricted intense stimulation of non-specific cardiac receptors. If this hypothesis is correct a strong stimulation with an adequate stimulus of a limited myocardial region should cause more pain than a weaker stimulation of a larger myocardial region. METHODS: To test this hypothesis, we carried out a systematic study in 8 male patients (mean age 52 +/- 9 years) with uncomplicated stable angina pectoris and significant isolated proximal left anterior descending coronary artery stenosis in whom the same amount of adenosine, a known mediator of cardiac and muscular ischemic pain, was infused at the proximal and distal site of the left anterior descending coronary artery. Increasing doubling doses (from 108 to 3456 micrograms/min) or adenosine were infused for periods of 2 min each into the left anterior descending coronary artery through a 2.8 F catheter. Adenosine was infused in each patient both proximally to the first diagonal branch and distally to the last diagonal branch of the left anterior descending coronary artery. The initial infusion site, proximal or distal, was randomized. At the beginning of the study patients were asked to promptly report the onset of pain. Time to onset of adenosine-induced pain and maximal pain severity (assessed by a visual analog scale) were recorded. Twelve electrocardiographic leads were recorded throughout the study. RESULTS: Seven patients experienced pain during adenosine infusion both at the proximal and distal level. One patient experienced pain only during adenosine infusion at the proximal site. In all patients pain occurred earlier (176 +/- 125 vs 343 +/- 207 s, p = 0.005) and its severity was greater (51 mm, range 20-95, vs 27 mm, range 0-69, p = 0.002) during infusion at the proximal site. No patient exhibited electrocardiographic changes during the study. CONCLUSIONS: Adenosine infusion at a proximal coronary site causes pain which occurs earlier and is more severe than that experienced during its infusion at a distal site. These findings suggest that the intensity of ischemic cardiac pain is determined by the number of stimulated receptors rather than by the intensity of their stimulation.

Adenosine↗
PubMed1998

Enhanced activity of sodium-lithium countertransport in patients with cardiac syndrome X: a potential link between cardiac and metabolic syndrome X.

OBJECTIVES: This study was aimed at assessing both stimulated insulinemia and the sodium-lithium countertransport in a selected group of patients with cardiac syndrome X. BACKGROUND: Hyperinsulinemia, which is frequently present in patients with cardiac syndrome X, is often associated with an enhanced activity of the sodium-lithium countertransport, an in vitro marker of sodium-hydrogen exchange. METHODS: Fifteen patients with syndrome X and 14 matched controls were studied. After pharmacological washout, sodium-lithium countertransport was assessed from lithium-loaded red blood cells. Postload insulin levels were evaluated by a double-antibody radioimmunoassay. RESULTS: Maximal velocity of sodium-lithium countertransport was higher in patients with syndrome X compared to controls (635+/-200 vs. 324+/-49 micromol/liter/h, p = 0.001). Fourteen of the 15 patients with syndrome X (93%) presented sodium-lithium countertransport values higher than the mean +2 SD of the control group. At 120 min, 12 patients with syndrome X (80%) had plasma levels of insulin >420 pmol/liter, which corresponds to the mean value +2 SD of controls (p = 0.006). CONCLUSIONS: Both enhanced activity of the sodium-lithium countertransport and stimulated hyperinsulinemia are present in the vast majority of patients with cardiac syndrome X. As enhanced activity of the sodium-lithium countertransport has the potential to cause both glucose intolerance and smooth muscle hyperreactivity, it might represent a common cause of the metabolic and vascular alterations frequently found in syndrome X.

Biological Transport, Active↗
PubMed1997

New look to an old symptom: angina pectoris.

At the turn of this century, it was proposed that ischemic cardiac pain might be related to distension of the ventricular wall ("mechanical hypothesis"). Three decades later, it was hypothesized that ischemic pain might be elicited by the intramyocardial release of pain-producing substances induced by ischemia ("chemical hypothesis"). Studies carried out in the past 10 years have given strong support to the chemical hypothesis, because they have consistently shown that adenosine is a mediator of ischemic cardiac pain. Adenosine-induced ischemic cardiac pain is mediated primarily by stimulation of A1 receptors located in cardiac nerve endings and is potentiated by substance P. Conversely, the magnitude and rate of left ventricular dilation during ischemia do not predict the severity of angina. It is worth noting, however, that stretching of epicardial coronary arteries appears to potentiate the severity of angina caused by myocardial ischemia. The nervous activity generated by myocardial ischemia is modulated in intrinsic cardiac, mediastinal, and thoracic ganglia. Then it is further modulated in the central nervous system and projects bilaterally to the cortex, as demonstrated in humans by positron emission tomography, where it is decoded as a painful sensation. The causes responsible for the lack of angina during myocardial ischemia are probably different in patients who present both pain-free and painful myocardial ischemia, in patients with predominantly painless ischemia, and in diabetic patients.

Adenosine↗
PubMed1997

Phentolamine prevents adaptation to ischemia during coronary angioplasty: role of alpha-adrenergic receptors in ischemic preconditioning.

BACKGROUND: Experimental studies indicate that alpha-adrenergic receptors are involved in ischemic preconditioning. Their role in humans is unknown. METHODS AND RESULTS: Eighteen patients undergoing angioplasty for an isolated stenosis of the left anterior descending coronary artery were randomized to receive intravenous infusion of phentolamine or placebo during the procedure. Intracoronary ECG and cardiac pain were determined at the end of the first two balloon inflations. Average peak velocity in the contralateral coronary artery during balloon occlusion, an index of collateral recruitment, was also assessed by using a Doppler guide wire. In both phentolamine- and placebo-treated patients, average peak velocity significantly increased from baseline to the end of the first inflation (P<.01), but it did not show any further increase during the second inflation. In phentolamine-treated patients, ST-segment changes and cardiac pain severity during the second inflation were similar to those observed during the first inflation (13+/-9 versus 12+/-8 mm, P=NS, and 51+/-34 versus 54+/-32 mm, P=NS, respectively), whereas in placebo-treated patients, they were significantly less (6+/-4 versus 13+/-7 mm, P<.01, and 26+/-20 versus 49+/-22 mm, P<.05, respectively). CONCLUSIONS: The adaptation to ischemia observed in humans after two sequential coronary balloon inflations is abolished by phentolamine and is independent of collateral recruitment. Thus, it occurs due to ischemic preconditioning and is, at least in part, mediated by alpha-adrenergic receptors.

Adrenergic alpha-Antagonists↗
PubMed1997

A comparison of coronary-artery stenting with angioplasty for isolated stenosis of the proximal left anterior descending coronary artery.

BACKGROUND: Randomized studies have shown that the use of coronary-artery stenting as the initial treatment for coronary stenosis is associated with a lower risk of restenosis than is standard coronary angioplasty. We prospectively investigated the efficacy of these two approaches in selected patients with isolated stenosis of the proximal left anterior descending coronary artery. METHODS: A total of 120 patients with isolated stenosis of the proximal left anterior descending coronary artery were randomly assigned to stent implantation or standard coronary angioplasty. The primary clinical end points were the rate of procedural success (defined as residual stenosis of less than 50 percent and the absence of death, myocardial infarction, and the need for coronary-artery bypass surgery during the hospital stay) and the rate of event-free survival (defined as freedom from death, myocardial infarction, and the recurrence of angina) at 12 months. The angiographic end point was the rate of restenosis 12 months after the procedure. RESULTS: The two treatment groups did not differ significantly with respect to demographic, clinical, or angiographic characteristics. The rates of procedural success were similar in the two groups of patients (95 percent in the stenting group vs. 93 percent in the angioplasty group, P = 0.98). The 12-month rates of event-free survival were 87 percent after stenting and 70 percent after angioplasty (P = 0.04). The rates of restenosis were 19 percent after stent implantation and 40 percent after angioplasty (P = 0.02). CONCLUSIONS: In patients with symptomatic isolated stenosis of the proximal left anterior descending coronary artery, stenting had advantages over standard coronary angioplasty in that it was associated with both a lower rate of restenosis and a better clinical outcome.

Adult↗
PubMed1997

Effects of A1 adenosine receptor blockade on the warm-up phenomenon.

The increased tolerance to myocardial ischemia observed during the second of two sequential exercise tests, i.e. the warm-up phenomenon, has been proposed as a clinical model of ischemic preconditioning. Adenosine appears to be a mediator of ischemic preconditioning in both experimental and clinical settings. The purpose of this study was to investigate the role of A1 adenosine receptors in the warm-up phenomenon. A double-blind, placebo-controlled, cross-over design was used. Twelve patients with coronary artery disease and positive exercise test were randomized to receive either bamiphylline, a selective A1 adenosine receptor antagonist, or placebo, immediately prior to two consecutive treadmill exercise tests carried out on day 1. Then, on day 2 all patients underwent two consecutive exercise tests immediately after administration of the remaining treatment. During the first exercise test, bamiphylline, compared to placebo, increased the time to and rate-pressure product at 1.5 mm ST-segment depression (from 317 +/- 118 to 423 +/- 127 s, p < 0.05 and from 199 +/- 38 to 230 +/- 36 b/min.mmHg.10(2), p < 0.05, respectively). After both placebo and bamiphylline infusions, time to 1.5 mm ST-segment depression during the second exercise test was greater than that during the first test (445 +/- 121 vs 317 +/- 118 s, p < 0.001 and 483 +/- 128 vs 423 +/- 127 s, p < 0.05, respectively), as was rate-pressure product at 1.5 mm ST-segment depression (228 +/- 40 vs 199 +/- 38 b/min.mmHg.10(2), p < 0.01 and 253 +/- 42 vs 230 +/- 36 b/min.mmHg.10(2), p < 0.05, respectively). In conclusion, bamiphylline, at a dose able to increase ischemic threshold and exercise tolerance compared to placebo, does not prevent the warm-up phenomenon. These findings suggest that, in the setting of the warm-up phenomenon, A1 adenosine receptor blockade is insufficient to prevent ischemic preconditioning.

Aged↗
PubMed1997

Effects of bamiphylline on exercise testing in patients with syndrome X.

An abnormal stimulation of adenosine A1-receptors has been suggested to play a role in the pathogenesis of both chest pain and ischemia-like electrocardiographic changes in patients with syndrome X and a nonselective adenosine antagonist (theophylline) has been reported to be beneficial in these patients. In this study we investigated the acute effects of bamiphylline, a specific A1-receptor antagonist, in 16 patients with syndrome X (14 women, age 57 +/- 6 years), with both angina and ST-segment depression inducible during exercise testing. All patients underwent two treadmill exercise tests (Bruce modified protocol) on 2 separate days, 5 minutes after the end of randomized intravenous infusion of either placebo (saline solution) or bamiphylline (300 mg). Severity of chest pain was assessed by a 100 mm visual analogic scale. There were no significant differences in resting heart rate and blood pressure after bamiphylline or placebo. Rate-pressure product (20 600 +/- 5000 vs 20 200 +/- 5200 bpm.mmHg), time to 1 mm ST depression (549 +/- 196 vs 581 +/- 201 sec), time to angina (519 +/- 209 vs 571 +/- 196 sec), and exercise duration (717 +/- 134 vs 676 +/- 166 sec) were also not significantly different after bamiphylline or placebo, but there was a mild reduction of the severity of exercise-induced chest pain (30 +/- 22 vs 39 +/- 20 mm, p < 0.05) with the active drug. Thus, in patients with syndrome X, bamiphylline does not improve exercise-induced ST changes, suggesting that A1-receptors are not significantly involved in their appearance. In addition, bamiphylline had little effect on anginal pain, suggesting that this cannot be mediated exclusively by A1-receptor stimulation in these patients.

Angina Pectoris↗
PubMed1997

Stent implantation for spontaneous coronary dissection.

Spontaneous coronary artery dissection is a rare cause of acute myocardial infarction and sudden death. We report a case of diffuse spontaneous left coronary artery dissection occurring in the postpartum period, successfully treated by multiple stent implantation. Coronary angiography performed 3 months later showed no evidence of dissection and TIMI flow grade 3 in the treated coronary arteries. At 12-month follow-up the patient was asymptomatic.

Adult↗
PubMed1997

Acetylcholine-induced vasodilatation in the human peripheral circulation is independent of ATP-sensitive K+ channels and prostacyclin.

BACKGROUND: Both experimental and clinical studies have shown that the increase in regional blood flow induced by acetylcholine is not completely prevented by inhibitors of the synthesis of endothelium-derived nitric oxide. To establish the role of ATP-sensitive potassium (KATP) channels and prostacyclin in mediating acetylcholine-induced increase in peripheral blood flow in humans, we assessed the effects of acetylcholine on the iliac artery blood flow velocity before and after glibenclamide, an antagonist of KATP channels, or before and after acetylsalicylic acid, an inhibitor of prostacyclin production. MATERIAL AND METHODS: Seventeen patients without evidence of peripheral vascular disease and normal coronary arteries at angiography received intra-iliac incremental bolus injections of acetylcholine (0.2, 2, 20 and 50 micrograms) via a 5F femoral sheath, at the end of routine cardiac catheterization. All injections were repeated 90 minutes after oral administration of glibenclamide (10 mg) in 10 patients of 15 minutes after i.v. infusion of acetylsalicylic acid (1000 mg) in the remaining 7 patients. Right iliac artery blood flow velocity was measured by using an intravascular 0.014-in Doppler guidewire. RESULTS: Before glibenclamide or acetylsalicylic acid administration, acetylcholine infusion increased average peak velocity by 128% (p < 0.001) and by 121% (p < 0.001), respectively. After glibenclamide or acetylsalicylic acid the increases of average peak velocity during acetylcholine infusion (by 121%, p < 0.001, and by 121%, p < 0.001, respectively) were similar (p = ns) to those observed during the control infusion. CONCLUSIONS: In man acetylcholine-induced vasodilatation in the territory supplied by the iliac artery is not prevented by glibenclamide or acetylsalicylic acid, thus suggesting that it is independent of activation of KATP channels and prostacyclin release.

Acetylcholine↗
PubMed1996

Differences of regional coronary flow reserve assessed by adenosine thallium-201 scintigraphy early and six months after successful percutaneous transluminal coronary angioplasty or stent implantation.

This study assesses regional coronary flow reserve using adenosine thallium-201 scintigraphy early and 6 months after angiographically successful percutaneous transluminal coronary angioplasty (PTCA) or stent implantation. Seventeen consecutive men with a significant isolated left anterior descending coronary artery stenosis were scheduled for repeat coronary angiography and adenosine-planar thallium-201 scintigraphy within 24 hours and 6 months after successful PTCA (n = 8) or stent implantation (n = 9). After background subtraction, left ventricular segmental uptake was semiquantitatively assessed on thallium images. The perfusion defect severity was scored from 0 (normal) to 3. Coronary angiograms were analyzed using an automated edge contour detection computer analysis system. Data are expressed as mean value +/- 1 SD, and proportions as percentage. The residual narrowing was 17 +/- 8% after PTCA and 9 +/- 2% after stent implantation (p = 0.02). Twenty-four hours after the procedure, hypoperfused segments were detected in all patients (100%) and in 4 patients (44%) (p = 0.05), respectively. The total number of hypoperfused segments was greater after PTCA than after stent implantation (16 [40%] vs 7 [16%], p = 0.001, respectively) as was the perfusion defect severity (4.4 +/- 3.1 vs 1 +/- 1.2, p = 0.006). Six months after the procedure, 3 of the 5 patients who had undergone PTCA without restenosis still had reversible perfusion defects. None of the stent-treated patients had restenosis or reversible perfusion defects (p = 0.05). Among PTCA-treated patients without restenosis, the total number of hypoperfused segments and the perfusion defect severity were 9 of 25 (36%) and 0.8 +/- 0.8, respectively. Thus, a regional reduction in coronary flow reserve, occasionally observed early after successful stent implantation, is probably due to a transient alteration of small coronary vessels, as was also supported by the absence of perfusion defects 6 months after the procedure. The more severe impairment of regional coronary flow reserve observed early after successful PTCA is probably also due to angiographic underestimation of the residual stenosis, as suggested also by the persistence of reversible perfusion defects 6 months after the procedure in a few patients.

Adenosine↗