Search PubMed⌕ Search

Biomedical subjects

F Tomai

Publications and source records attributed to F Tomai.

At least 55 records · Page 3Linked to original sources
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

Extent and pattern of regression of left ventricular hypertrophy in patients with small size CarboMedics aortic valves.

OBJECTIVE: To assess the extent and pattern of regression of left ventricular hypertrophy after valve replacement for aortic stenosis, we studied 26 patients receiving either 19 or 21 mm CarboMedics valves (group I, 13 patients) or either 23 or 25 mm CarboMedics valves (group II, 13 patients). The studies were done before the operation and after 3 years, and results were compared with those of 10 control patients. METHODS: Left ventricular end-diastolic and end-systolic diameters and volumes, ejection fraction and fractional shortening, and interventricular septum and posterior wall thickness were measured. The ratio between interventricular septum and posterior wall thickness, the ratio between left ventricular wall thickness and left ventricular chamber radius, and the left ventricular mass were then calculated. RESULTS: At follow-up there was a significant reduction in the left ventricular mass, interventricular septum, and posterior wall thickness for both patient groups (p < 0.01). However, only the posterior wall thickness reached normal values; the interventricular septum and the left ventricular mass indices were still significantly greater than in the control group (p < 0.01). Because of the incomplete regression of interventricular septal hypertrophy, the ratio between interventricular septum and posterior wall thickness was similar between both patient groups but it was significantly higher than in control subjects (p < 0.01). The ratio between wall thickness and chamber radius did not decrease significantly in group II patients, in whom it remained above the control values. CONCLUSION: Having a bileaflet aortic prosthesis of one size larger did not seem to significantly influence the pattern and the extent of regression of left ventricular hypertrophy after an intermediate period of follow-up.

Aged↗
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↗
PubMed1996

Hypertriglyceridemia and the apolipoprotein CIII gene locus: lack of association with the variant insulin response element in Italian school children.

Hypertriglyceridemia is a common metabolic disorder with a major inherited component. In some individuals the condition is suspected to occur as a result of overproduction of apolipoprotein (apo)CIII, a major constituent of triglyceride-rich lipoproteins. Population studies have established an association with the apoCIII gene but the identify of the causal mutation remains unknown. In the present study we have examined a series of six 5' polymorphic nucleotides (G-935 to A, C-641 to A, G-630 to A, deletion of T-625, C-482 to T, and T-455 to C) that lie within the promoter region of the apoCIII gene for evidence of possible involvement in disease susceptibility. The polymorphic nucleotides at positions -455 and -482 reside within a negative insulin-response element. We show, in a community-based sample of 503 school children, that a DNA polymorphism (S2 allele) within the 3'-noncoding region of the apoCIII gene was associated with elevated apoCIII and triglyceride levels, but that the polymorphic nucleotides of the promoter were not. In addition, no obvious effect of any extended apoCIII promoter haplotype on plasma apoCIII or triglyceride levels, over and above that conferred by the presence of the S2 polymorphic nucleotide, was detected. These results demonstrate that none of the 5' apoCIII polymorphisms can account for the association of the apoCIII gene locus with hypertriglyceridemia and, moreover, owing to linkage disequilibrium, raise the possibility that the region conferring susceptibility maps downstream, rather than upstream, of the apoCIII gene promoter sequences.

Adolescent↗
PubMed1996

Early coronary artery bypass graft thrombosis in a patient with protein S deficiency.

A 59-year-old white man underwent multiple coronary artery bypass grafts (CABGs) on an emergency basis for severe stenosis of the left main, and occlusion of the right coronary, artery. One month after operation recurrence of angina prompted a new diagnostic evaluation. Occlusion of the grafts was detected at angiography. Accurate hematological screening before reoperation showed decreased levels of protein S. One year after his second operation, the patient is asymptomatic on oral anticoagulant therapy. Tallium-201 scintigraphy shows normal myocardial perfusion.

Angina Pectoris↗
PubMed1996

Effects of A1 adenosine receptor blockade by bamiphylline on ischaemic preconditioning during coronary angioplasty.

OBJECTIVE: The role of A1 adenosine receptors in preconditioning in humans is unknown. To establish whether bamiphylline, a selective antagonist of A1 adenosine receptors, abolishes ischaemic preconditioning in man, 36 consecutive patients undergoing single-vessel coronary angioplasty were randomized to receive intravenous infusion of bamiphylline (5 mg.kg-1) or placebo (0.9% NaCl) immediately prior to the procedure. DESIGN: The mean values (+/- 1 SD) of ST segment shifts on the surface and intracoronary electrocardiograms were measured at the end of the first and second balloon inflations, both 2 min long. The severity of cardiac pain was obtained at the same time using a visual analogue scale. RESULTS: In bamiphylline-treated patients, the mean ST segment shift and the severity of cardiac pain during the second inflation were similar to those during the first inflation (14 +/- 15 vs 16 +/- 16 mm, ns and 31 +/- 28 vs 31 +/- 29, ns, respectively). Conversely, in placebo-treated patients both the mean ST segment shift and the severity of cardiac pain during the second inflation were significantly less than those during the first inflation (10 +/- 6 vs 17 +/- 7 mm, P < 0.001 and 25 +/- 21 vs 39 +/- 31 mm, P < 0.01, respectively). Thus, bamiphylline abolishes ischaemic preconditioning observed in man during repeated coronary balloon inflations. CONCLUSION: These results suggest that, in this setting, ischaemic preconditioning is mediated, at least in part, by A1 adenosine receptors.

Adult↗
PubMed1996

Mechanisms of the warm-up phenomenon.

The warm-up phenomenon, described in patients with coronary artery disease, refers to the improved performance following a first exercise test. The aim of this study was to investigate the causes of the warm-up phenomenon. Fifteen patients with coronary artery disease and positive exercise test were enrolled. Patients were off treatment throughout the study. They underwent two consecutive treadmill exercise tests according to the Bruce protocol, with a recovery period of 10 min to re-establish baseline conditions. A third exercise test was then performed 2 h later. Before the onset of ischaemia, the rate-pressure product for a similar degree of workload was similar during the first and second exercise test, while it was lower during the third test (P < 0.05). Time to 1.5 mm ST-segment depression during the second and third exercise test was greater than during the first test (454 +/- 133 and 410 +/- 161 vs 354 +/- 127 s, P < 0.01, respectively). Similarly, the time to anginal pain onset was increased during the second and third exercise tests, compared to the first test (356 +/- 208 and 310 +/- 203 vs 257 +/- 204 s, P < 0.01, respectively). In contrast, rate-pressure product at 1.5 mm ST-segment depression during the second test was higher than that during the first test (232 +/- 47 vs 210 +/- 39 beats.min-1.mmHg.10(2), P < 0.01), while in the third test it was similar to that during the first (209 +/- 43 beats.min-1.mmHg.10(2), P = ns). The warm-up phenomenon observed a few minutes after exercise is characterized by an increase of both time to ischaemia and ischaemic threshold; this adaptation to ischaemia may be due to an improvement of myocardial perfusion or to preconditioning. Conversely, the warm-up phenomenon observed a few hours after repeated exercise is characterized by an increase of time to ischaemia but not of ischaemic threshold and is caused by a slower increase of cardiac workload. Thus, the mechanisms of the warm-up phenomenon may be different, time dependent and related to previous training.

Adaptation, Physiological↗
PubMed1996

Hemodynamic performances of small diameter carbomedics and St. Jude valves.

BACKGROUND AND AIMS OF THE STUDY: Optimal hemodynamic performances are of paramount importance when implanting a mechanical valve in patients with a small aortic annulus. A Doppler echocardiographic study was performed to compare the hemodynamic performances of small CarboMedics and St. Jude valves. MATERIALS AND METHODS: Twenty-nine patients receiving either a 19 mm (n = 10) or a 21 mm (n = 10) CarboMedics valve or a 19 mm (n = 9) St. Jude Med HP valve were evaluated. A Doppler echocardiographic study was performed at rest and two minutes after treadmill exercise with the Bruce protocol. Peak and mean gradients across the valve were estimated; effective orifice area, performance index and discharge coefficient were calculated. Heart rate, blood pressure and cardiac output were all significantly increased with exercise. RESULTS: Peak and mean gradients at rest were significantly higher (p < 0.05) in the 19 mm CarboMedics valve (40.2 +/- 15 mmHg and 22.6 +/- 9 mmHg, respectively) when compared either with 21 mm CarboMedics valve (27.6 +/- 6.8 mmHg and 14.2 +/- 3.4 mmHg, respectively) or with the 19 mm St. Jude HP valve (23.6 +/- 10.4 mmHg and 13.6 +/- 5 mmHg, respectively). Peak and mean gradients were not modified with exercise for the 19 mm CarboMedics valve and significantly increased for the 21 mm CarboMedics and the 19 mm St. Jude HP valves. Although these values were still higher in the 19 mm CarboMedics valve, they did not reach the level of statistical significance when compared with the other two valve groups. CONCLUSIONS: The 19 mm St. Jude HP valve shows hemodynamic performances at rest that are similar to those of the 21 mm CarboMedics valve and superior to those of the 19 mm CarboMedics valve. With exercise both sizes of the CarboMedics valve show an in vivo discharge coefficient close to one, testifying to a full utilization of the internal orifice area.

Adult↗
PubMed1995

Muscular and cardiac adenosine-induced pain is mediated by A1 receptors.

OBJECTIVES: This study attempted to establish whether bamiphylline, a selective antagonist of A1 adenosine receptors, prevents the algogenic effects of adenosine in humans. BACKGROUND: Experimental findings indicate that the sympathoexcitatory response elicited by adenosine is mediated by A1 receptors. METHODS: An intrailiac infusion of increasing doses (from 125 to 2,000 micrograms/min) of adenosine was given to 20 patients. Adenosine infusion was then repeated after intrailiac infusion of either bamiphylline or saline solution. In 14 other patients with angina, increasing doses of adenosine (from 108 to 1,728 micrograms/min) were infused into the left coronary artery. Adenosine infusion was then repeated after the intravenous infusion of either bamiphylline or placebo. Coronary blood flow velocity was monitored by a Doppler catheter. Data relative to pain severity are expressed as median and all other data as mean value +/- 1 SD. RESULTS: Bamiphylline prolonged the time to pain onset caused by the intrailiac adenosine infusion from 444 +/- 96 to 749 +/- 120 s (p < 0.001) and reduced pain severity from 45 to 24 mm (p < 0.01). After placebo infusion, the time to pain onset and pain severity were similar to that of baseline (428 +/- 112 vs. 430 +/- 104 s, p = 0.87 and 44 vs. 43 mm, p = 0.67, respectively). Bamiphylline prolonged the time to pain onset caused by intracoronary adenosine infusion from 519 +/- 128 to 603 +/- 146 s (p < 0.01) and reduced pain severity from 58 to 28 mm (p < 0.02). After placebo infusion, the time to pain onset and pain severity were similar to that at baseline (542 +/- 87 vs. 551 +/- 79 s, p = 0.14 and 55 vs. 50 mm, p = 0.61). Maximal coronary blood flow velocities before and after bamiphylline administration were similar (47 +/- 22 vs. 49 +/- 24 cm/s, p = 0.36) as well as before and after placebo administrtion (40 +/- 20 vs. 41 +/- 20 cm/s, p = 0.07). CONCLUSIONS: Bamiphylline reduces adenosine-induced muscular and cardiac pain but does not affect adenosine-induced coronary vasodilation. These findings indicate that at the dose used in this study, bamiphylline does not detectably block vascular A2-receptor-mediated adenosine effects in humans, which suggests that the muscular and cardiac algogenic effects of adenosine are mediated mainly by A1 receptors.

Adenosine↗
PubMed1995

Intraoperative antifibrinolysis and blood-saving techniques in cardiac surgery. Prospective trial of 3 antifibrinolytic drugs.

Sixty consecutive patients undergoing elective open-heart surgery were prospectively enrolled in a study to compare the efficacy of 3 different antifibrinolytic drugs to reduce postoperative bleeding and to reduce homologous blood requirements in combination with blood-saving techniques and restrictive indications for blood transfusion. The patients were randomized to 1 of 4 intraoperative treatment regimens: 1) control (no antifibrinolytic therapy); 2) epsilon-aminocaproic acid (10 g IV at induction of anesthesia, followed by infusion of 2 g/h for 5 hours); 3) tranexamic acid (10 mg/kg IV within 30 minutes after induction of anesthesia, followed by infusion of 1 mg/kg per hour for 10 hours); or 4) high-dose aprotinin (2 million KIU IV at induction of anesthesia and 2 million KIU added to the extracorporeal circuit, followed by infusion of 500 thousand KIU/h during surgery). Hemoconcentration and reinfusion of blood drained from the operative field and the extracorporeal circuit after operation were used in all patients. Indications for blood transfusion were hypotension, tachycardia, or both, with hemoglobin values < 8.5 g/dL; or severe anemia with hemoglobin values < 7 g/dL. Compared with the blood loss in the control group, patients receiving aprotinin and epsilon-aminocaproic acid showed significantly less postoperative blood loss at 1 hour (control, 128 +/- 94 mL; aprotinin, 54 +/- 47 mL, p = 0.01; and epsilon-aminocaproic acid, 69 +/- 35 mL, p = 0.03); this trend continued at 24 hours after operation (control, 724 +/- 280 mL; aprotinin, 344 +/- 106 mL, p < 0.0001; and epsilon-aminocaproic acid, 509 +/- 148 mL, p = 0.01). Aprotinin was significantly more efficient than epsilon-aminocaproic acid (p=0.002). Tranexamic acid did not have a statistically significant effect on blood loss. Homologous blood requirements were not significantly different among the groups; postoperative hematologic values and coagulation times were also comparable. Despite the efficacy of aprotinin and epsilon-aminocaproic acid shown in the present study, the blood requirements were not significantly different from those that are found when transfusions are restricted, autotransfusions are used, and blood from the operative field and extracorporeal circuit is concentrated and reinfused. Therefore, intraoperative antifibrinolysis may not be indicated in routine cardiac surgery when other blood-saving techniques are adopted.

Adult↗
PubMed1995

Risk factors in patients with different clinical and angiographic manifestations of ischemic heart disease.

In patients who present with unheralded myocardial infarction both the severity and the extent of coronary atherosclerosis appear to be less than that in patients with chronic stable angina, thus suggesting that, in the latter, protective factors may prevent or delay the evolution towards acute coronary syndromes. Therefore, risk factors were compared in 88 consecutive patients (73 men; mean age 56 +/- 9 years) with unheralded myocardial infarction and a single, discrete, > 70% stenosis in the proximal right, left circumflex or left anterior descending coronary artery (Group 1) and in 55 consecutive patients (46 men; mean age 58 +/- 9 years with chronic stable angina and multiple, diffuse, > 70% stenoses localized both in the right and left coronary arteries (Group 2). Continuous data are presented as mean value +/- 1 SD, proportions as percentages. In Group 1 mean serum levels of total cholesterol, low-density lipoprotein cholesterol and triglycerides were similar to those in mg/dl, p = 0.93 and 160 +/- 87 vs 155 +/- 76, p = 0.74, respectively) while the mean serum level of high-density lipoprotein cholesterol was higher in Group 2 (49 +/- 4 vs 46 +/- 4 mg/dl, p = 0.005). The prevalence of a positive family history of ischemic heart disease, hypertension and smoking habit were similar in the two groups, while the prevalence of diabetes mellitus was higher in Group 2 (29 vs 6%, p = 0.001). Thus, in patients with otherwise similar coronary risk factors, higher levels of high-density lipoprotein cholesterol and diabetes mellitus appear to be associated with a reduced tendency of coronary atherosclerosis to cause acute coronary syndromes.

Aged↗
PubMed1995

Early postoperative myocardial ischemia after coronary artery bypass grafting. Detrimental effects of nitroglycerine infusion.

This study was aimed at assessing the incidence and mechanisms of myocardial ischemia early after coronary artery bypass grafting and the effects of treatment with nitroglycerine. The electrocardiogram of 35 patients (29 males and 6 females, mean age 61 +/- 8 years) with stable angina and multivessel coronary disease, was monitored continuously for 24 hours after uncomplicated coronary artery bypass grafting. Patients were randomized to receive nitroglycerin infusion or placebo. Fourteen of the 35 patients (40%) had 24 transient ischemic episodes (mean duration 11.8 +/- 3.5 min; range 6-20 min with ST segment elevation in 6, ST segment depression in 7 and both ST segment elevation and depression in 1. Seventy-five per cent of the ischemic episodes occurred within the first 6 postoperative hours. The mean ejection fraction prior to surgery and the mean number of stenosed vessels and of the implanted grafts were similar in patients with and without postoperative ischemia (57 +/- 5 vs 57 +/- 6%, p = 0.86; 2.7 +/- 0.5 vs 2.8 +/- 0.4, p = 0.52 and 3.0 +/- 0.9 vs 3.2 +/- 0.7, p = 0.51, respectively) as well as total bypass time and cross-clamp time (123 +/- 38 vs 124 +/- 18 min, p = 0.89 and 67 +/- 20 vs 70 +/- 14 min, p = 0.68, respectively). The values of heart rate and systolic blood pressure at the onset of the ischemic episodes were similar to those recorded 15 min before (103 +/- 16 vs 106 +/- 18 b/min, p = 0.36 and 119 +/- 12 vs 121 +/- 14 mmHg, p = 0.48). Ischemic episodes were recorded in 9 of the 16 patients (56%) randomized to receive nitroglycerine and in 5 only of the 19 patients (26%) randomized to receive placebo (p = 0.05). Thus, transient ischemic episodes occurring early after coronary artery bypass grafting are not preceded by an increase in myocardial oxygen consumption; they appear to be due, therefore, to a primary reduction in coronary blood flow. Treatment with nitroglycerine is associated with a higher prevalence of ischemic episodes, thus suggesting that myocardial ischemia is unlikely to be caused by spasm of large epicardial vessels or grafts. Myocardial ischemia may be caused, instead, by extracorporeal circulation-induced alterations enhanced by the hypotensive effects of nitroglycerine.

Aged↗