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Biomedical subjects

F Tomai

Publications and source records attributed to F Tomai.

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

Exercise-induced myocardial ischemia triggers the early phase of preconditioning but not the late phase.

The aim of the present study was to establish whether exercise-induced ischemia triggers the second window of protection in 15 patients with coronary artery disease undergoing 2 consecutive treadmill exercise tests and a third test 24 hours later. Our findings confirm that a first exercise-induced ischemic challenge induces the early phase of preconditioning but not the late phase, thus suggesting that either a late protective effect of preconditioning does not exist in the setting of demand ischemia or, if it exists, it must be weaker than the early protective effect.

Aged↗
PubMed1999

Recovery of LV contractility in man is enhanced by preischemic administration of enflurane.

BACKGROUND: Volatile anesthetics enhance postischemic functional recovery in animal models; this effect has not been investigated in man. METHODS: Twenty-two patients undergoing coronary surgery were randomized to enflurane administration (0.5% to 2%) for 5 minutes to reduce systolic blood pressure by 20% to 25% immediately before cardioplegic arrest. Left ventricular contractility was assessed by pressure-area relations using echocardiographic automated border detection during inflow occlusion before and after cardiopulmonary bypass. Linear regression analysis in 16 patients with paired data sets assessed changes in contractility. RESULTS: The relation was highly linear (r = 0.95+/-0.02). A change of slope versus the change in x intercept was detected in controls (mean difference, 16.1 mm Hg/cm2, 95% confidence limits, 5.9 to 26.3; 2.2 cm2, 95% confidence limits, -1.1 to 5.5; p = 0.007), which was different from those of treated patients (mean difference, 0.7 mm Hg/cm2, 95% confidence limits, -2.2 to 3.7; -0.06 cm2, 95% confidence limits, -1.6 to 1.5; p > 0.2). Analysis of covariance in the overall group confirmed a significant effect of treatment (p = 0.002). CONCLUSIONS: Enflurane enhances postischemic functional recovery, possibly through pharmacologic preconditioning of myocardium.

Aged↗
PubMed1999

Coronary flow reserve early and late after minimally invasive coronary artery bypass grafting in patients with totally occluded left anterior descending coronary artery.

BACKGROUND: The impairment of flow reserve of the left anterior descending coronary artery in the early postoperative period in patients receiving a left internal thoracic artery graft has been related to the effects of cardiopulmonary bypass. Indeed, the late improvement in flow has been attributed to a late increase in left internal thoracic artery diameter. METHODS: We evaluated 12 patients who underwent minimally invasive direct coronary artery bypass surgery with the internal thoracic artery used to graft an occluded left anterior descending artery without extracorporeal circulation. Early and 6 months after the operation, patients underwent a second angiogram of the left internal thoracic artery graft and assessment of coronary flow reserve by use of an intracoronary 0.014-inch Doppler guide wire. RESULTS: At the late study, coronary flow reserve had increased compared with the early postoperative data from 1.8 +/- 0.4 (standard deviation) to 2.5 +/- 0.6 (P =.002) because of a significant decrease in baseline averaged peak velocity (32.4 +/- 6.2 vs 21.3 +/- 6.4 cm/s, P =.002), whereas the hyperemic values were similar (51 +/- 6 vs 53.7 +/- 21.9 cm/s, P =.6). The diameters of the thoracic artery (2.1 +/- 0.3 vs 2.2 +/- 0.3 mm, P =. 7) and the left anterior descending coronary artery (1.8 +/- 0.1 vs 1.8 +/- 0.2 mm, P =.5), as well as myocardial oxygen consumption (106 +/- 14 vs 101 +/- 16 mm Hg. beats/min. 10(-2), P =.5), were unchanged. CONCLUSIONS: Our findings suggest that the late improvement in coronary flow reserve is independent of the diameter of the graft and probably reflects an early distal coronary vessel dysfunction, which normalizes with time.

Analysis of Variance↗
PubMed1999

Effects of naloxone on myocardial ischemic preconditioning in humans.

OBJECTIVES: We attempted to establish whether naloxone, an opioid receptor antagonist, abolishes the adaptation to ischemia observed in humans during coronary angioplasty after repeated balloon inflations. BACKGROUND: Experimental studies indicate that myocardial opioid receptors are involved in ischemic preconditioning. METHODS: Twenty patients undergoing angioplasty for an isolated stenosis of a major epicardial coronary artery were randomized to receive intravenous infusion of naloxone or placebo during the procedure. Intracoronary electrocardiogram and cardiac pain (using a 100-mm visual analog scale) 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 the six patients of each group with a stenosis on the left anterior descending coronary artery. RESULTS: In naloxone-treated patients, ST-segment changes and cardiac pain severity during the second inflation were similar to those observed during the first inflation (12+/-6 vs. 11+/-7 mm, p = 0.3, and 58+/-13 vs. 56+/-12 mm, p = 0.3, respectively), whereas in placebo-treated patients, they were significantly less (6+/-3 vs. 13+/-6 mm, p = 0.002 and 31+/-21 vs. 55+/-22 mm, p = 0.008, respectively). In both naloxone- and placebo-treated patients, average peak velocity significantly increased from baseline to the end of the first inflation (p = 0.04 and p = 0.02, respectively), but it did not show any further increase during the second inflation. CONCLUSIONS: The adaptation to ischemia observed in humans after two sequential coronary balloon inflations is abolished by naloxone and is independent of collateral recruitment. Thus, it is due to ischemic preconditioning and is, at least partially, mediated by opioid receptors, suggesting their presence in the human heart.

Aged↗
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

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

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

Mid-term results of conventional bypass surgery for complex proximal left anterior descending coronary artery stenoses.

BACKGROUND: The significant involvement of proximal left anterior descending (LAD) coronary artery affects patient prognosis and must be treated. Recently, as alternative methods to conventional coronary bypass (CABG), minimally invasive direct coronary artery bypass grafting (MIDCAB) and percutaneous transluminal coronary angioplasty with stent implantation (PTCA/S) have been proposed to reduce costs and patient discomfort. The aim of this study was to obtain early and medium-term results of CABG in patients with complex LAD disease in whom the expected results with PTCA/S or MIDCAB would have been suboptimal. METHODS: We retrospectively examined one hundred consecutive patients subjected to isolated CABG who received either a single graft to LAD or several grafts to LAD and diagonal branches. The choice of CABG was due to poor expectable results with PTCA/S or MIDCAB because of anatomical characteristics of the lesion, inclusion in ongoing randomized study comparing surgical versus non-surgical revascularization, or preference on the part of the cardiologist or patient. RESULTS: Left internal mammary artery (LIMA) was grafted to LAD in 99 (99%) patients; 65 (65%) patients received at least one saphenous graft to the diagonal branches. No death was observed within 30 days from the operation. One (1%) patient had a perioperative non-Q myocardial infarction (MI). At a mean follow-up time of 38 +/- 16 months (range 2-60), there were no cardiac deaths and no new MI. Six patients complained of recurrent angina: in all cases but one (vein graft failure to a diagonal branch), there were no clinical or diagnostic signs suggesting other graft failures. The probability of freedom from early and late events, including cardiac death, MI and recurrence of angina regardless of site, was 99% at 1 year and 86% at 5 years. CONCLUSIONS: At present, conventional CABG seems to be the "gold standard palliation" of LAD disease in most cases. It can be performed safely with excellent early and medium-term results in terms of freedom from cardiac events. Its comparison with percutaneous transluminal techniques and MIDCAB needs to be addressed in further prospective studies.

Adult↗
PubMed1999

Beneficial impact of isoflurane during coronary bypass surgery on troponin I release.

BACKGROUND: Experimental studies indicate that isoflurane, a commonly used volatile anesthetic, mimics the cardioprotective effects of ischemic preconditioning, probably through ATP-sensitive K+ (KATP) channel activation. The aim of this study was to evaluate the impact of isoflurane during coronary bypass surgery (CABG) on troponin I release. MATERIAL AND METHODS: Forty consecutive patients with chronic stable angina and multivessel disease undergoing isolated CABG were randomized to a control (16 men and 4 women, aged 51 to 73 years, mean 62) or isoflurane (15 men and 5 women, aged 51 to 77 years, mean 65) group before aortic cross-clamping and cardioplegia. Serum levels of troponin I and creatine kinase (CK)-MB, as markers of ischemic injury, were obtained at 24 hours after CABG. Regional wall motion score and left ventricular ejection fraction (LVEF) at transthoracic echocardiography were assessed 5 days postoperatively. Comparisons between groups were performed in the entire population and, subsequently, in those patients with preoperative LVEF < 50%. RESULTS: There were no significant differences between isoflurane-treated patients and controls in cross-clamp time (49 +/- 14 vs 51 +/- 13 min, p = ns), peak values of troponin I (0.9 +/- 0.7 vs 1.4 +/- 1.3 ng/ml, p = ns) and CK-MB (62 +/- 27 vs 64 +/- 27 U/l, p = ns), or postoperative echocardiographic score (26 +/- 7 vs 22 +/- 5, p = ns) and LVEF (53 +/- 10 vs 55 +/- 7%, p = ns). When the comparisons were restricted to those patients with preoperative LVEF < 50%, at 24 hours the isoflurane-treated patients exhibited a smaller release of troponin I and of CK-MB than controls (1.1 +/- 0.7 vs 2.3 +/- 1.3 ng/ml, p = 0.03, and 39 +/- 10 vs 57 +/- 22 U/l, p = 0.04, respectively). CONCLUSIONS: Isoflurane reduces myocardial injury in patients with impaired left ventricular function undergoing CABG; thus, it can be safely used as an additional cardioprotective tool during routine CABG in high-risk patients with poor left ventricular function.

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↗
PubMed1999

Preinfarction angina and myocardial preconditioning.

In the current era of pharmacologic and mechanical reperfusion therapy, several studies have consistently shown that patients with myocardial infarction preceded by angina have smaller infarcts and a better in-hospital outcome after thrombolytic therapy than patients without preinfarction angina. At least three mechanisms may explain these differences between infarctions that are preceded by angina and those that are not: coronary collaterals, reperfusion rate, and ischemic preconditioning. Collaterals alone do not seem to explain the beneficial effects of preinfarction angina, although it is difficult to completely rule out their role in the clinical setting. The possibility that preinfarction angina is not protective per se, but rather is a predictor of a more rapid coronary reperfusion is attractive; however, it should be addressed by further clinical studies. Finally, it is likely that the beneficial effects of preinfarction angina are related to ischemic preconditioning. Although a direct demonstration of this hypothesis is still lacking, clinical features of preinfarction angina, which is characterized by anginal attacks preceding acute myocardial infarction, are very similar to those of ischemic preconditioning, in which brief ischemic episodes precede a prolonged ischemic period. Indeed, the demonstration of ischemic preconditioning in different clinical models of ischemia and reperfusion and the identification of some of its mediators suggest that in patients at high risk of myocardial infarction drugs known to block this endogenous form of protection should be used with caution, while drugs known to elicit preconditioning might have a relevant therapeutic role. However, the optimal timing, administration, and dosage for preconditioning-mimetic drugs in the appropriate clinical setting are still under debate and warrant further investigation.

Angina Pectoris↗
PubMed1998

Levels of troponin I and cardiac enzymes after reinfusion of shed blood in coronary operations.

BACKGROUND: Reinfusion of shed blood after coronary artery bypass grafting might increase the levels of cardiac enzymes with consequent difficulties in the diagnosis of perioperative myocardial infarction. METHODS: Thirty consecutive patients undergoing coronary artery bypass grafting who bled at least 400 mL within the first 4 hours after operation underwent reinfusion of shed blood. Thirty consecutive patients who were not autotransfused served as control. All patients underwent enzyme determination (total creatine kinase, MB fraction, lactate dehydrogenase, and troponin I) in the shed blood and in circulating blood preoperatively, at arrival in the intensive care unit, and 6, 24, and 48 hours after operation. RESULTS: The shed blood contained significantly higher concentration of cardiac enzymes than the circulating blood at all time intervals (p = 0.0001). The levels of creatine kinase, its MB fraction, and lactate dehydrogenase in circulating blood were significantly elevated in patients receiving autotransfusion up to 24 hours after autotransfusion. The blood levels of troponin I were not significantly different between the two group of patients at all time points. The percent fraction of MB did not increase after autotransfusion. CONCLUSIONS: The measurement of cardiac troponin I is a useful marker for the diagnosis of perioperative myocardial infarction in patients undergoing transfusion of shed blood after coronary operation.

Biomarkers↗
PubMed1998

Regression of left ventricular hypertrophy after aortic valve replacement for aortic stenosis with different valve substitutes.

OBJECTIVE: Stentless biologic aortic valves are less obstructive than stented biologic or mechanical valves. Their superior hemodynamic performances are expected to reflect in better regression of left ventricular hypertrophy. We compared the regression of left ventricular hypertrophy in 3 groups of patients undergoing aortic valve replacement for severe aortic stenosis. Group I (10 patients) received stentless biologic aortic valves, group II (10 patients) received stented biologic aortic valves, and group III (10 patients) received bileaflet mechanical aortic valves. METHODS: Echocardiographic evaluations were performed before the operation and after 1 year, and the results were compared with those of a control group. Left ventricular diameters and function, left ventricular wall thickness, and left ventricular mass were assessed by echocardiography. RESULTS: Group I patients had a significantly lower maximum and mean transprosthetic gradient than the other valve groups (P = .001). One year after operation there was a significant reduction in left ventricular mass for all patient groups (P < .01), but mass did not reach normal values (P = .05). Although the rate of regression in the interventricular septum and posterior wall thickness differed slightly among groups, their values at follow-up were comparable and still higher than control values (P = .002). The ratio between interventricular septum and posterior wall and the ratio between wall thickness and chamber radius did not change significantly at follow-up. CONCLUSIONS: Because the number of patients was relatively small, we could not use left ventricular mass regression after I year to distinguish among patients undergoing aortic valve replacement for aortic stenosis by means of valve prostheses with different hemodynamic performances.

Aged↗
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↗
PubMed1998

Atrial septal defect associated with Albright's hereditary osteodystrophy and other anomalies: a clinical case.

A 36 year-old woman with a history of asthenia and palpitations was admitted to the Cardiac Surgery Department of Tor Vergata University, in Rome. Physical examination revealed short stature, depressed nasal bridge, hypertelorism, hypoacusia, pectus excavatum, diffuse brachydactyly, clinodactyly of the second digit of both the right hand and left foot. A 3/6 holosystolic increasing-decreasing murmur on the pulmonary focus was present at cardiac auscultation. Echocardiogram and cardiac catheterization revealed an ostium secundum atrial septal defect. X-ray examination of the hands exhibited shortening of the third, fourth and fifth metacarpals, shortening of the distal phalanges, shortening of the proximal and middle phalanges of the fifth digits and cone epiphysis of the middle phalanx of the second digits. Radiograph of the feet revealed shortening of the third and fourth and metatarsals on the left side, bilateral shortening of the first metatarsals and of the distal phalanges, cone epiphyses at the proximal base of the first toes. Additional radiographic findings included pectus excavatum and narrowing of the spinal canal. Laboratory investigations disclosed increased plasma levels of parathormone and hypocalcemia. The patient underwent primary closure of the atrial septal defect on cardiopulmonary bypass. Radiographic findings supported the diagnosis of Albright's hereditary osteodystrophy. This is a skeletal malformation involving type I-A pseudohypoparathyroidism and so-called pseudo-pseudohypoparathyroidism. Coexistence of hypocalcemia and high levels of parathormone indicated that our patient was affected with type I-A. About one-fourth of congenital heart diseases are associated with extracardiac anomalies. Although skeletal malformations appear to be the most frequent, the association of a congenital heart defect with Albright's hereditary osteodystrophy has never been described before.

Adult↗